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or <sh> that correspond with individual phonemes like /p/ and /ʃ/ (rules governing grapheme-phoneme correspondence in English have been classified by Venezky 1970). Patterson/Morton (1985) suggest that this sy stem supplements information about sub-sy llables like -ave in save, that constitute the ‚body ’ or ‚rime’ of a word. Shallice and his colleagues (Shallice/ Warrington/McCarthy 1983; Shallice/McCarthy 1985), on the other hand, claim that phonological reading makes use of a range of sub-word-sized units: grapheme-phoneme correspondences, sub-sy llables, sy llables and morphemes. Evidence from the case reports of surface dy slexia suggests that a range of spelling-sound information is indeed available in phonological reading. Thus, while a surface dy slexic patient reported yb Ka y /Lesser (1985) made use of grapheme-phoneme correspondences on at least some occasions in single-word reading, Shallice, Warrington/ McCarthy (1983) demonstrated convincingly that another patient, given many of the same reading materials to read aloud, relied on subys llabic information about spelling-sound patterns. Their findings converge neatly with evidence from reaction-time studies with normal readers that show the importance of sub-sy llabic knowledge in producing word and nonword pronunciations (e. g. Seidenberg/Waters/Barnes/Tanenhaus 1984; Ka y / Bishop 1987). Even more interesting for this debate is the finding that phonological readers described above, such as patient MP (Bub/Cancelliere/ Kertesz 1985), were able to read aloud even irregular words that they were unable to un-
derstand. MP, for example, was able to read 77% of a set of irregular words. Bub/Cancelliere/Kertesz (1985) discovered that MP’s reading performance was particularly affected by word frequency : she was faster to read aloud high frequency than low frequency words. This factor also influenced the responses that she gave to irregular words: irregular words that were also low in frequency were much more likely to be given regularised pronunciations than corresponding high frequency words. Patient WLP (Schwartz/Saffran/Marin 1980) showed even better performance than MP in reading aloud irregular words; early in her illness she read aloud 95% of a set of irregular words successfully, though her semantic comprehension skills were very poor. For example, she read the irregular word hyena correctly , say ing, Hyena ... hyena ... what in the heck is that? WLP suffered from a progressive dementing disease, and later on in her illness, the percentage of irregular words that she could read decreased to 71%. At the same time, she began to produce substantial numbers of regularisation errors. Shallice and his colleagues explain findings such as these by assuming that a ‚broad’ phonological route, distinguishable from a semantic route, specifies information about morphemic correspondences, as well as smaller units. It is further proposed that larger units, such as morphemes, are more vulnerable to impairment, particularly if they are low in frequency . These assumptions attempt to explain why a progressive disease, such as that observed in WLP, can increasingly restrict the range of correspondences that are available. The response of researchers who favour a phonological reading routine that operates on grapheme-phoneme correspondences and/or sub-sy llable correspondences is not to concede that the routine may have a broader base, but to assume that there is more than one phonological reading sy stem. A l ex i c a l phonological routine, which deals with lexical and morphemic representations, is added to the non-lexical one, so that, within this scheme, there are three reading routes rather than two. Shallice (1988) claims that the difference between this version of the ‚standard’ model and the ‚multiple-levels’ model is “mainly terminological”, and it is certainly clear that both accounts seem equally capable of dealing with most of the findings to do with phonological reading. However, so does a third account, which is a rather more radical
22. Acquired Disorders of Reading
alternative. This approach does away with any phonological routine other than one based on word spelling and pronunciation (e. g. Marcel 1980; McClelland/Rumelhart 1981). According to this view, pronunciation can be constructed for all written letter strings — whether word or non-word — by activating spelling patterns and corresponding sound patterns in visually similar words. The difference between this general approach and a multiple-levels model is that, for the latter, a range of orthographic units are represented within a visual word-form sy stem (with correspondences in a phonological word-form sy stem), whereas, for the former, these units are represented only in as much as they occur in words.
3.
Impairments of Phonological Reading
Some patients with surface dy slexia have difficulty with reading aloud irregular words, but are able to construct plausible pronunciations for non-words. Another variety of acquired dy slexia has been characterised as the obverse side of the same coin. In phonological dyslexia, the ability to read aloud nonwords is severely impaired, while word reading is affected not by regularity , but by grammatical class (Beauvois/Derouesné 1979). For example, AM, reported by Patterson (1982) was able to read only 8% of a set of nonwords, while, on the same occasion, he was able to r e p e a t 83% of a second set. This finding indicates that the problem is not secondary to a speech production difficulty . Neither does there seem to be a problem in visually recognising nonwords to judge from the patient’s normal performance on a visual lexical decision task. In contrast with his nonword reading ability , AM’s performance with nouns, adjectives and verbs was substantially better (86%, 83% and 94%, respectively). A second patient, WB, described by Funnell (1983) averaged about 85% correct in reading words aloud, while he was completely unable to read nonwords. At the same time, WB had very poor semantic understanding (he was unsure, for example, whether mitten or sock was a close associate of glove), suggesting that his ability to read aloud words considerably exceeded his ability to understand fully what they meant. It has been claimed that phonological dy slexic patients like WB, provide convincing evidence for a
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lexical route to phonology that is independent of nonlexical procedures (e. g. Coltheart 1985). (This route involves direct lexical mappings between orthography and phonology — hence the term, direct route reading.) However, the champion of the multiple-levels approach points out a potential problem for this view (Shallice 1988). As a group, phonological dy slexics tend to experience greater difficulty in reading aloud functors than other word classes: AM, for example, was able to read only 72% of functors. It is not hard to see why there might be a difficulty with functors if word reading is mediated by the semantic sy stem (‚meaningless’ functors might not be represented there, for example), but if phonological dy slexic reading depends on a lexical, non-semantic, routine, then why should functors be relatively disadvantaged? This is even more surprising when one recalls that evidence from the surface dy slexic patient described by Bub/Cancelliere/Kertesz (1985), often used to support the notion of direct route reading, indicated that word frequency was an important factor in reading success by the direct route: functors are among the most frequent words in the language. Shallice (1988) turns this question on its head and asks why it is that functors, in particular, tend to cause difficulty for phonological dy slexics. Patterson (1982) has proposed that this is because function word reading depends on intact phonological procedures (we will not go into w hy this may be the case here) which are not available to phonological dy slexics. This view predicts that patients who are severely impaired in reading aloud nonwords will also inevitably experience problems with functors. There is tantalising evidence that this may not be true. Both Shallice/Warrington (1980) and Funnell (1983) describe phonological dy slexic patients who did not have especial difficulty with functors, though in each of these cases a subtle speech production difficulty might actually have been responsible for the nonword reading impairment (Howard 1985; Shallice 1988).
4.
Reading via Semantics
Difficulties in reading aloud nonwords have also been described in the acquired reading disturbance known as deep dyslexia, the third major reading impairment discussed by Marshall/Newcombe (1973). In investigating this disorder, much of the debate has centred on whether it actually constitutes a coherent sy n-
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II. Acquired Organic Pathologies of Language Behavior: Neurolinguistic Disorders
drome or sy mptom-complex, and, if so, which features can be taken as ‚key ’, ‚essential’ and ‚less essential’ (to echo the above discussion about surface dy slexia). As with the other disorders we have discussed, the answer seems to be that deep dy slexia fractionates into a variety of different underly ing impairments, and that the relative importance of various features of the disorder changes with the nature of the impairment. Word reading success in deep dy slexia is considerably lower than in phonological dy slexia and is characterised by a number of different error yt pes. Pre-eminent among them, and taken as the defining or pathognomonic sign, is the semantic reading error (cannibal read aloud as savages, for example, or, merry read as Christmas). For a detailed discussion of the categories of semantic error that can occur, see Coltheart (1980 a). Other major error ty pes are visual errors (e. g. own → now), which include visual and/or semantic errors (e. g. fragment → segment) and visualthen-semantic errors (e. g. sympathy read as orchestra, perhaps via the mediation of sy mphony ), morphological errors (referred to as derivational errors) such as free for freedom, rejected for rejection, and function-word substitutions of one functor for another (e. g. was → and). Whether a word can be read successfully critically depends on how imageable or concrete it is, rather than on how frequent it is (e. g. Richardson 1976). Much also depends on the part-of-speech to which the word belongs: nouns, for example, are read aloud correctly more often than verbs or functors. It appears, however, that this effect can also be attributable to imageability rather than to grammatical word class, since nouns tend to have higher imageability ratings than verbs or functors (e. g. Allport/Funnell 1981). (Note that this variable may not be responsible for the particular difficulty with functors experienced by phonological dy slexics, since imageability is not an important factor governing this disorder.) In addition, the ability to read nonwords is generally totally abolished, single letter naming and sounding is often severely impaired, and great difficulty is experienced in making any kind of phonological judgements from written material (e. g. Patterson/ Marcel 1977). Marshall/Newcombe’s (1973) classic account argued that the absence of phonological reading in deep dy slexia precipitated the production of semantic errors; they suggested
that any available phonological information would have allowed the patient to eliminate such errors. It is further suggested that the reason why semantic errors occur in the first place has to do with the inherently imprecise nature of semantic representations (Saffran/ Schwartz/Marin 1976; Newcombe/Marshall 1980). Thus, deep dy slexia, it is assumed, provides a window on a semantic mechanism that is operating in a relatively normal fashion. A major difficulty with this account is that it now appears that different levels of impairment can underpin deep dy slexia and that different deficits can each result in the production of semantic reading errors. Several authors have proposed that a ‚deep dy slexic’ pattern of reading in general, and the semantic error in particular, can result from different kinds of impairment (e. g. Shallice/Warrington 1980; Shallice 1988). These can be broadly summarised as a ‚input’ difficulty in accessing the semantic sy stem from the visual input lexicon, a ‚central’ difficulty within the semantic sy stem itself, and an ‚output’ difficulty in accessing lexical semantic representations within the speech output lexicon. A large percentage of errors produced by deep dy slexics like KF (Shallice/Warrington 1975) and PS (Shallice/Coughlan 1980) were visual errors (61% and 51% respectively ). The percentage of semantic errors was much lower (4% and 10% respectively ). Shallice (1988) suggests that patients exhibiting a high ratio of visual-to-semantic errors may have an ‚input’ disorder that arises during the course of access to the semantic sy stem. Shallice explicitly rules out an impairment to the visual input lexicon as the cause of the patients’ visual errors, because here one might have expected such errors to occur on high and low imageability words alike (since the deficit would precede the semantic sy stem). This was not the case; visual errors tended to be produced more often in response to low imageability words — the words that gave the patients most difficulty . In line with this proposed locus of impairment, both patients showed much poorer performance on written comprehension tasks than on auditory comprehension tasks. Some deep dy slexic readers appear to have a central semantic difficulty that can affect all modalities of input and output. An example is patient GR (Newcombe/Marshall 1980) who produced semantic errors in picture-to-word matching and in spelling-to-dic-
22. Acquired Disorders of Reading
tation. A further example is the case of KE, recently described by Hillis/Rapp/Romani/ Caramazza (1990). This patient was reported to make comparable ty pes and rates of semantic errors across a variety of tasks: oral reading, reading and auditory comprehension, spelling-to-dictation, writing picture names and say ing picture names, consistent with the proposal of a selective impairment to the semantic system. A third ty pe of ‚output’ deep dy slexic reader is characterised by patient PW (Patterson 1978). PW made considerably more semantic errors than visual errors (54% compared with 13%, respectively ). His performance on comprehension tasks that did not require a verbal response was good, both for written and auditory input. His comprehension of low imageability words was also good, even though he had substantial difficulty in reading them aloud (Patterson/Besner 1984). The difficulty for this patient appears to be at the level of access to word phonology , rather than within the semantic sy stem. A similar explanation is proposed for patient RGB, described by Hillis/Rapp/Romani/Caramazza (1990). Hillis and her colleagues suggest that intact semantic representations activate in vary ing degrees a set of semantically related representations in a phonological output lexicon. If the target word is inaccessible for some reason, another semantically related response may be produced instead. This proposal is similar to the ‚response-blocking’ explanation put forward by Morton/Patterson (1980). These accounts of the variation that can occur in the level of impairment in deep dy slexia have recently been exploited by connectionist-based investigations of acquired dy slexic deficits (see Hinton/Shallice 1991), with some surprising y et promising findings (e. g. Plaut/Shallice 1991). This work is rooted in the view that deep dy slexia reveals certain operations of the normal reading sy stem, with damage to some of its components. However, a radical alternative exists, which claims that deep dy slexia reflects the operation of righthemisphere language processing ys stems (Coltheart 1980 b; Saffran 1980). The righthemisphere hy pothesis has attracted a good deal of controversy over the past decade (e. g. Coltheart 1983; Patterson/Besner 1984). Much of it focuses on revealing the abilities of the right hemisphere reading sy stem in normal subjects (from laterality studies) and on comparing the reading performance of
259
deep dy slexics with right hemisphere reading by a small group of ‚split-brain’ patients (patients in whom cortical connections between right and left hemisphere have been severed in an attempt to relieve intractable epilepsy ). Much of it is inconclusive, as Patterson/Besner (1984) convincingly demonstrate. Indeed, the right hemisphere theory of deep dy slexia was in danger of simply trickling away : as Shallice (1988) noted, “Problems for the theory keep arising. As soon as one leak is temporarily plugged, another bursts through”. However, there has been a recent upsurge of interest in the theory that stems primarily from cerebral blood-flow and PET-scan studies that show far more right than left hemisphere activation in individual deep dy slexic patients (e. g. Coltheart/Weekes/Savage et al. 1991). A challenge for the theory is to account for the fractionation of deficits that occur within the disorder. In conclusion, a variety of different patterns of reading disturbance that can be acquired through brain damage have been described and interpreted with reference to cognitive models of single word recognition and production. Existing findings demonstrate convincingly the fractionation of the basic categories of deep, surface and visual dy slexia, though this work is firmly within the spirit of Marshall and Newcombe’s original enterprise.
5.
References
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Chomsky , N. (1965). Aspects of the Theory of Syntax. Cambridge, MA.: MIT-Press. Coltheart, M. (1978). Lexical access in simple reading tasks. In G. Underwood (Ed.), Strategies of Information Processing. London: Academic Press. Coltheart, M. (1980 a). The semantic error: Ty pes and theories. In M. Coltheart, K. E. Patterson, & J. C. Marshall (Eds.), Deep Dyslexia. 146—159. London: Routledge. Coltheart, M. (1980 b). Deep dy slexia: A righthemisphere hy pothesis. In M. Coltheart, K. E. Patterson, & J. C. Marshall (Eds.), Deep Dyslexia. 326—380. London: Routledge. Coltheart, M. (1983). The right hemisphere and disorders of reading. In A. W. Young (Ed.), Functions of the Right Cerebral Hemisphere. London: Academic Press. Coltheart, M. (1985). Cognitive neuropsy chology and the study of reading. In M. I. Posner & O. S. M. Marin (Eds.), Attention & Performance, Vol. 11. 3—37. Hillsdale, N. J.: Erlbaum. Coltheart, M., Masterson, J., By ng, S., Prior, M., & Riddoch, J. (1983). Surface dy slexia. Quarterly Journal of Experimental Psychology, 35 A, 469—495. Coltheart, M., Weekes, B., Savage, K., Simpson, L., Zurinsky , Y., & Gordon, E. (1991). Deep dyslexia and right hemisphere reading: A regional cerebral bloodflow study. Paper presented to Deep Dyslexia: 12 Years On. London, Birkbeck College. Costello, A. de L. & Warrington, E. K. (1987). Dissociation of visuo-spatial neglect and neglect dy slexia. Journal of Neurology, Neurosurgery & Psychiatry, 50, 1110—1116. Déjerine, M. J. (1892). Contribution a l’etude anatomo-pathologique et clinique des differentes varietes de cecite verbale. Comptes Rendus des Seances et Memoires de la Societe de Biologie, 44, 61—90. Ellis, A. W., Flude, B. M., & Young, A. W. (1987). ‚Neglect dy slexia’ and the early visual processing of letters in words and nonwords. Cognitive Neuropsychology, 4, 439—464. Evett, L. J. & Humphrey s, G. (1981). The use of abstract graphemic information in lexical access. Quarterly Journal of Experimental Psychology, 33 A, 325—350. Friedmann, R. B. & Alexander, M. P. (1984). Pictures, images and pure alexia: A case study . Cognitive Neuropsycholoy, 1, 9—23. Funnell, E. (1983). Phonological processes in reading: New evidence from acquired dy slexia. British Journal of Psychology, 74, 159—180. Goldblum, M. C. (1985). Word comprehension in surface dy slexia. In K. E. Patterson, M. Coltheart, & J. C. Marshall (Eds.), Surface Dyslexia. 175— 205. London: Erlbaum. Henderson, L. (1982). Orthography and Word Recognition in Reading. London: Academic Press.
Hillis, A. E. & Caramazza, A. (1992). The reading process and its disorders. In D. I. Margolin (Ed.), Cognitive Neuropsychology in Clinical Practice. Cary: Oxford University Press. Hillis, A. E., Rapp, B. C., Romani, C., & Caramazza, A. (1990). Selective impairment of semantics in lexical processing. Cognitive Neuropsychology, 7, 191—244. Hinton, G. & Shallice, T. (1991). Lesioning an attractor network: Investigations of acquired dy slexia. Psychological Review, 98, 74—95. Howard, D. (1985). The Semantic Organisation of the Lexicon: Evidence from Aphasia. Unpublished doctoral dissertation. University of London. Humphrey s, G. W. & Riddoch, M. J. (1990). Interactions between object and space sy stems revealed through neuropsy chology . In D. E. Mey er & S. Kornblum (Eds.), Attention and Performance, Vol. 14. Hillsdale, N. J.: Erlbaum. Kartsounis, L. D. & Warrington, E. K. (1989). Unilateral neglect overcome by cues implicit in stimulus display s. Journal of Neurology, Neurosurgery & Psychiatry, 52, 1253—1259. Kay , J. & Bishop, D. V. M. (1987). Anatomical differences between nose, palm and foot, or, the body in question. In M. Coltheart (Ed.), Attention and Performance, Vol. 12. 449—469. London: Erlbaum. Kay , J. & Hanley , J. R. (1991). Simultaneous form perception and serial letter recognition in a case of letter-by -letter reading. Cognitive Neuropsychology, 8, 249—273. Kay , J. & Lesser, R. (1985). The nature of phonological processing in oral reading: Evidence from surface dy slexia. Quarterly Journal of Experimental Psychology, 37 A, 39—81. Kay , J. & Patterson, K. E. (1985). Routes to meaning in surface dy slexia. In K. E. Patterson, M. Coltheart, & J. C. Marshall (Eds.), Surface Dyslexia. 79—103. London: Erlbaum. Kinsbourne, M. & Warrington, E. K. (1962 a). A variety of reading disability associated with right hemisphere lesions. Journal of Neurology, Neurosurgery & Psychiatry, 25, 339—344. Kinsbourne,M. & Warrington, E. K. (1962 b). A disorder of simultaneous form perception. Brain, 85, 461—486. Kremin, H. (1981). Deux strategies de lecture dissociable par la pathologie: Description d’un cas de dy slexie profonde et d’un cas de dy slexie de surface. In C. L. Nespoulos (Ed.), Etudes neurolinguistiques. Toulouse: Le Mirail. Kremin, H. (1985). Routes and strategies in surface dy slexia and dy sgraphia. In K. E. Patterson, J. C. Marshall, & M. Coltheart (Eds.), Surface Dyslexia. Neuropsychological and Cognitive Studies of Phonological Reading. 105—137. London: Erlbaum. McClelland, J. L. & Rumelhart, D. E. (1981). An interactive activation model of context effects in
22. Acquired Disorders of Reading
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Janice Kay, Exeter (U. K.)
23. Acquired Disorders of Writing and Spelling 1. 2. 3. 4.
Historical Introduction Modern Models of Writing Agraphia in Alzheimer’s Disease References
1.
Historical Introduction
As is the case with the field of aphasiology in general, the neuropsy chological study of agraphia originated with the work of nineteenth century European neurologists. Several different models and classifications of agraphia were proposed by these early investigators based on clinico-anatomical observations in patients with focal brain damage (for reviews see Leischner 1969; Marcie/Hécaen 1979). While some of these are purely anatomically based, others also focus on cognitive mechanisms and bear a striking resemblance to current linguistic information processing models of spelling (Charcot 1889; Ellis 1988). Rather than provide an exhaustive review of the various classification sy stems of agraphia, we will only attempt here to highlight certain historic developments relevant to our current understanding of the linguistic processes and brain mechanisms involved in writing and spelling. Although the first discussion of writing disturbances following focal brain lesions is attributed to Marcé (1856), it was Benedikt (1865) who first used the term agraphia. Benedikt (1865) also suggested that parts of the brain that control written and spoken lan-
guage may have different anatomical localization. Ogle (1867) reached a similar conclusion based on his own clinico-anatomical studies of aphasic patients: “The occasional separation of agraphia and aphasia points [...] to the existence of distinct cerebral centers for the faculties concerned in speaking and in writing; while the more frequent coincidence of the two affections leads us to infer that these centers must be closely contiguous”. Ogle distinguished two ty pes of agraphia. In “amnemonic” agraphia, letters are well-formed but are used incorrectly or one word is substituted for another. In “atactic” agraphia, letters are poorly formed and are sometimes unrecognizable. While the views about the independence of writing from speech were rejected by many (Wernicke 1874; Lichtheim 1885; Jackson 1878; Déjerine 1914), Ogle’s clinical distinction between the linguistic and motor disorders of writing was universally endorsed. The next phase of development in the study of agraphia was characterized by attempts to identify the anatomical location of the cortical centers that mediated the linguistic and motor components of writing. This was a natural direction to take, given the prevailing nineteenth century view of language function in the brain which assumed that psy cholinguistic faculties were localizable to distinct cortical regions. The cortical language centers served as memory stores for specific ty pes of linguistic or motor representations and the transmission of information between the lan-
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guage centers occurred via connecting neuronal pathway s. These early theories of brain functioning, advocated by the so-called ‚diagram makers’, provided the impetus for the proliferation of connectionist models of language processing. Within this conceptual framework, Exner (1881) proposed that the cortical center of “motor graphic images” was located at the foot of the second frontal convolution, directly in front of the hand area of the primary motor cortex. The notion of a center for the motor movements of writing, analogous to the motor center for the programming of speech movements (i. e., Broca’s area), was criticized on various grounds both by Wernicke (1886) and Déjerine (1914) but was accepted with only slight modifications by Charcot (1889), Pitres (1894) and Bastian (1898) among others. Despite the controversy about Exner’s writing center, there was a general consensus that the motor movements of writing had to be activated by input from centers that contained linguistic information relevant to the spelling of words. These orthographic representations or “optic word images” were believed by many to be stored in the region of the dominant angular gy rus (Déjerine 1891; Pitres 1894; Henschen 1922; Pick 1931; Nielsen 1946). The putative parietal memory store of learned spellings thus play s a central role in several models of writing. Wernicke (1874; 1886), however, was of the opinion that written language alway s depended on spoken language and maintained that orthographic representations could only be activated indirectly via phonological representations. He also entertained the possibility that once the ability to write has been acquired, the motor movements could be activated directly from ‚sound images’ without the participation of visual orthographic representations. The connectionist models of writing, in their fully developed form, were also explicit about mechanisms for the coordinated activity between the parietal center of orthographic representations and the frontal motor center for the movements of writing (Henschen 1922; Pick 1931; Nielsen 1946). The flow of information between the cortical centers of writing was generally conceptualized as a sensory -to-motor spread of excitation from posterior to anterior brain areas, similar to Wernicke’s (1874) model of spoken language production. The connectionist view is perhaps best articulated by Nielsen (1946): “When one wishes to write, one starts activity
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in the neurons of the left angular gy rus and by this means revives memories of letters and words one wishes to write. Impulses travel for association to all posterior portions of the brain and forward in the external capsule to the writing center at the foot of the second frontal convolution [...] coordinated activity between the writing center and the angular gy rus is necessary not only for the proper execution of the movements of writing but also for the proper concept and spelling of the words”. It is interesting to note that although the connectionists generally assumed that the orthographic representations stored in the dominant angular gy rus were accessed by a wholeword retrieval process, there were also proponents of a subword level phoneme-grapheme conversion procedure in spelling. Grashey (1885), for example, postulated that the writing of words alway s required the serial translation of each sound unit to the corresponding grapheme. This view was later adopted by Wernicke (1886), although he originally posited that the indivisible unit of spelling was the word (Wernicke 1874). A model of spelling based on the use of soundletter correspondence rules was also favored by Luria (1970). Although considerable progress has been made over the y ears in providing more refined and comprehensive neurolinguistic accounts of the writing process, until recently there was relatively little attention devoted to the linguistic analy sis of spelling errors. A notable exception in the older literature is a posthumously published paper by Arnold Pick (1925). Based on a review of previously reported cases and his own observations, Pick makes a clear distinction between phonetic and orthographic writing. Since orthographic knowledge is acquired relatively late in language development, Pick suggests that it may be especially vulnerable to brain pathology . He concludes, in agreement with the earlier views of Heilbronner (1910), that brain damage may selectively impair orthographic writing, while sparing the ability to write ‚purely phonetically ’. Pick also observes that many patients already have an imperfect orthographic knowledge premorbidly and that the disparity between phonetic and orthographic writing may vary considerably in different languages. Although Pick’s remarkable insights received little attention at the time of publication, their relevance for current information processing models of writing is quite striking.
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2.
Modern Models of Writing
2.1. Neurological Models Recent classifications of agraphia have been of two general ty pes, neurological and linguistic. The neurological classifications have emphasized clinical-pathological correlations and the relationship between agraphia and other language disturbances, i. e., aphasia and alexia. This approach has led to the development of three general categories of acquired agraphia: aphasic agraphia, agraphia with alexia and pure agraphia. 2.1.1. Aphasic Agraphia The emphasis on the relationship of agraphia and aphasia has been present since Lichtheim (1885) described one of the earliest neurological models of written language and even before him (Benedikt 1865; Ogle 1867) the relationship was addressed. Aphasic agraphia is usually subdivided into the agraphia of Broca’s aphasia, the agraphia of conduction aphasia, the agraphia of Wernicke’s aphasia and the agraphia of transcortical sensory aphasia (Benson 1979; Clark/Grossfield 1983; Kaplan/Goodglass 1981; Marcie/Hécaen 1979). The characteristics of each ty pe of agraphia are said to be dependent upon the type of aphasia associated with it. 2.1.2. Agraphia with Alexia This disorder is also called parietal agraphia because the two sy mptoms of alexia and agraphia, in the absence of significant aphasia, are said to usually occur together in patients with dominant parietal lobe lesions (Kaplan/Goodglass 1981). These patients are said to yt pically produce poorly formed graphemes when writing and, although in spelling aloud they pronounce letters correctly, they have difficulty spelling. 2.1.3. Pure Agraphia In the traditional neurological models, this is a writing disorder without other significant language disturbance. Most patients with pure agraphia produce well formed graphemes or letters but make different ty pes of spelling errors, depending upon the lesion location. Multiple lesion sites have been implicated in pure agraphia and include the second frontal convolution (Exner’s area) (Aimard/ Devick/Lebel et al. 1975; Vernea/Merory 1975; Hécaen/Albert 1978; Kaplan/Goodglass 1981; Marcie/Hécaen 1979) the superior parietal lobule (Auerbach/Alexander 1981;
Basso/Taborielli/Vignolo 1978), the posterior perisy lvian region (Rosati/DeBastiani 1981) and the region of the left caudate and internal capsule (Laine/Marttila 1981). Pure agraphia, unlike pure alexia which is associated with a fairly consistent lesion site (the dominant occipital lobe) and a fairly consistent pattern of reading disorder (letter by letter reading or inability to read), occurs from multiple lesion sites and consists of multiple ty pes of behavioral abnormalities. One goal of the neurological models has been an attempt to delineate anatomic loci that can be associated with pure agraphia. Although early studies emphasized various cortical regions, more recent studies have emphasized subcortical regions (Laine/Marttila 1981; Tanridag/Kirshner 1985; Kertesz/Latham/ McCabe 1990). The traditional neurological approach to agraphia has helped explain some features found in agraphic patients but there are frequent inconsistencies. First, there is an overlap between sy ndromes in that two ty pes of agraphia, such as one subty pe of aphasic agraphia (Broca’s aphasic agraphia with disturbed letter production) and the agraphia with alexia may have the same description (Kaplan/Goodglass 1981; Marcie/Hécaen 1979). Also, some patients with an agraphia defined by the neurological approach, i. e. Broca’s aphasic agraphia, may have impairment of writing and spelling that more closely resembles the impaired writing and spelling of a patient with Wernicke’s aphasia than the impairment found in other patients with Broca’s aphasia (Roeltgen/Sevush/Heilman 1983). In addition to the difficulties in the behavioral analy sis utilizing the traditional neurologic models, there are difficulties that arise regarding attempts at clinical-pathologic correlation. One lesion locus may be associated with multiple disorders and conversely , the same disorder may be associated with multiple anatomic loci. For example, the dominant parietal lobe has been implicated in the sy ndrome of agraphia with alexia but has also been implicated in the sy ndrome of pure agraphia (Basso/Taborelli/Vignolo 1978; Hécaen/Albert 1978; Kaplan/Goodglass 1981; Leischner 1969; Marcie/Hécaen 1979), and pure agraphia has occurred in patients with lesions in various sites as noted previously. 2.2 Linguistic Models In the past ten to fifteen y ears, investigators have attempted to find models that are not dependent upon other disorders and thereby
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develop a classification of agraphia that is more dependent upon the analy sis of the agraphia rather than the co-occurrence of aphasia or alexia. This approach can best be termed linguistic because of its emphasis on patterns of linguistic performance, including both analy sis of errors made by patients as well as analy sis of performance on words of different linguistic ty pe. The linguistic models also differ from the traditional models in that most put very little emphasis on clinical-pathological localization, although occasional attempts at clinical-pathological correlation have been made (Roeltgen/Sevush/Heilman 1983; Roeltgen/Heilman 1984; Roeltgen/ Rothi/Heilman 1982; Iwata 1984; Kawamura/ Hiray ama/Hasegawa et al. 1987; Rapcsak/ Rubens 1990). Attempts at linguistic analy sis of agraphia have involved two different language groups, Indo-European and Japanese. Although certain features are similar both within the disorders involved as well as the written language sy stems, sufficient differences exist so that they will be treated separately here. In this chapter we discuss the various agraphias in patients with focal lesions and also senile dementia of the Alzheimer ty pe within the framework of a linguistic processing model of spelling and review relevant anatomical data when appropriate. 2.2.1. Linguistic Studies of Agraphia in Indo-European Languages The initial detailed linguistic studies of agraphia were performed by Shallice (1981) and Beauvois & Derouesné (1981). Since then, data from their studies and others have been used to develop linguistic models of the normal writing process. Ellis (1982) provided one of the first such models and others have followed (Margolin 1984; Roeltgen 1985; Roeltgen/Heilman 1984; Patterson 1986; Lesser 1990; Rapcsak/Rubens 1990). All of these models contain many of the same features as that first developed by Ellis, and a prototy pical model is presented in Figure 23.1. Most of the differences among these models are in terminology . However, there are certain important conceptual differences that address some of the features within the model. All of the models emphasize two dissociable sy stems or pathway s through which spellings of words could be produced, a phonological nonlexical sy stem that requires phoneme to grapheme conversion [or phonographeme to letter (Lesser 1990) or phonological
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Fig. 23.1: Diagrammatic model of linguistic spelling systems. Modified after Rapcsak/Rubens (1990)
to orthographic conversion (Patterson 1986; Margolin 1984)] and a lexical (Roeltgen/Heilman 1984; Lesser 1990) [or a lexical-orthographic (Margolin 1984) or orthographic (Patterson 1986; Rapcsak/Rubens 1990)] sy stem. In addition to these two sy stems, a third major component included in all of these models is a semantic sy stem (Roeltgen/Rothi/ Heilman 1986; Roeltgen 1985; Margolin 1984; Lesser 1990; Rapcsak/Rubens 1990) or what has been alternatively called the cognitive sy stem (Patterson 1986). The phonological sy stem is thought to be important for spelling pronounceable nonwords (e. g., flig) and can also serve as a back-up sy stem for spelling regular real words, especially regular words of limited ambiguity . Ambiguity is operationally defined based on the number of alternative graphemes or letters appropriate for each of the phonemes within a word. For example, charm may be spelled in only one way that produces the correct pronounciation. In contrast, cotton may be spelled in multiple way s (e. g., cotton, kotton, kottin) with the same resulting phonology . Although the phonological sy stem is usually presented as a nonlexical sy stem of phoneme to grapheme conversion, some authors have argued that it really represents a lexically based sy stem that allows the spelling of unknown words using analogy (Campbell 1983). The lexical sy stem is important for production of known words and is ty pically necessary for spelling words that are orthographically irregular and words of high ambiguity . Irregular words are words
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that cannot be spelled by direct phoneme-tographeme conversion (e. g., island and yacht). Semantic influence, although not important for the correct spellings of words, is necessary for the incorporation of meaning into what is written by selection of words containing the correct meaning. In addition to these sy stems necessary for the correct letter and word selection, there is one additional cognitive component involved prior to the more peripheral or motoric components of writing or oral spelling, and that sy stem has been labeled the graphemic or orthographic buffer (Caramazza/Micheli/Villa/Romani 1987; Hillis/ Caramazza 1989; Badecker/Hillis/Caramazza 1990; Margolin 1984; Lesser 1990). This last component is defined as a temporary working memory store of abstract letters or graphemes prior to the conversion into concrete letter shapes (for written spelling) or letter names (for oral spelling) (Caramazza/Micheli/Villa/ Romani 1987). These ys stems or pathwa y s that are thought to be important for the production of normal spelling have primarily been developed from the analy sis of patients with acquired agraphia. Patients with these agraphias have produced patterns of performance that appear to be consistent with selective dy sfunction of one of the above postulated sy stems. The disorders include phonological agraphia due to disruption of the nonlexical phonological or phoneme-grapheme conversion sy stem, lexical agraphia due to disruption of the lexical or orthographic sy stem, semantic agraphia due to disruption of the semantic sy stem or disconnection of the semantic sy stem from the other linguistic spelling ys stems and graphemic buffer agraphia, due to disruption of the graphemic buffer. 2.2.1.1. Phonological Agraphia In 1981, Shallice described a patient who had difficulty spelling pronounceable nonwords (e. g., flig) but had preserved ability to write (spell) real words that were orthographically irregular. Shallice termed this sy ndrome phonological agraphia. Others have described patients with similar disorders (Morton 1980; Roeltgen/Sevush/Heilman 1983; Baxter/Warrington 1985; Bolla-Wilson/Speedie/Robinson 1985; Roeltgen/Heilman 1984; Goodman-Schulman/Caramazza 1987; Hatfield 1985; Nolan/Caramazza 1982; Roeltgen/ Rothi/Heilman 1982). These studies include two small series described by Roeltgen and
colleagues (Roeltgen/Sevush/Heilman 1983; Roeltgen/Heilman 1984) and together include more than 15 patients. Among these patients there are certain variabilities, although all patients have had decreased ability to spell or write nonwords and have had no difference in their ability to spell regular and irregular words. The variability among patients has included differing effects of word class, concreteness and imageability . Word class differences have been found in some subjects, such that they can spell or write nouns better than verbs, adverbs and adjectives, all of which are written better than function words. The question has been raised whether this word class effect can be explained merely on the basis of concreteness. However, Baxter/Warrington (1985) have shown in their subject G. O. S. that concreteness can not account for the word class effect. Many subjects also show effects of imageability in that words of high imagery (book) are written better than words of low imagery (hope) even if these words are matched for length and frequency of occurrence (Roeltgen/Rothi/Heilman 1982). A similar effect is found for concreteness, and it is possible that the effects of imageability can be explained on that basis. In addition to the variability found in these patients based on ty pes of words on which they make errors, there are also some differences in the quality of the errors that are produced. Many of the subjects produced real word errors that have been termed ‚derivational’, i. e., responses with the same free morpheme as the stimulus but different bound morphemes (e. g., hunting for hunts or closed for closes) (Roeltgen/Sevush/Heilman 1983; Baxter/Warrington 1985). A second ty pe of error is of particular interest because it suggests the way in which the patient may be accessing the spelling of the word that they are attempting to produce. These are visual errors or errors that demonstrate partial lexical knowledge (Ellis 1982). A visual similarity between the stimuli and the responses was demonstrated yb Roeltgen/Sevush/Heilman (1983) and Hatfield (1985). They concluded that at least some of their patient’s preserved spelling ability was dependent upon visual representations or visual word images. Based on a different method of analy sis, Morton (1980) suggested a similar mechanism. Hatfield (1985) in an in-depth analy sis of a patient with phonological agraphia concluded that what was termed the lexical sy stem or orthographic knowledge is a collection of
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word knowledge that has accumulated through familiarity with the understanding of sound relationships, whole word shapes, word analogies and, perhaps, certain mnemonic rules. In the discussion of lexical agraphia later in this chapter, this heterogeneous collection of abilities becomes very important. Some patients with impaired ability to spell nonwords also make semantic paragraphias (written responses with little phonological or visual resemblance to the stimulus words, e. g., spelling flight when propeller is the stimulus. Bub/Kertesz (1982) termed this sy ndrome deep agraphia because of its similarity to the reading disorder, deep dy slexia. Other patients with phonological agraphia who produce semantic paragraphias have also been described by Marshall/Newcombe (1966), Assal/Buttet/Jolivet (1981), Saffran/Schwartz/ Marin (1981), patient 1 of Roeltgen/Sevush/ Heilman (1983), patient EB of Hatfield (1985) and Van Lancker (1990). These patients also showed effects of imagery , spelling nouns of high imagery better than nouns of low imagery and function word substitution (e. g., spelling and when but is a stimulus). Because deep agraphia includes the error patterns found in phonological agraphia, plus semantic paragraphias, it is possible that deep agraphia represents phonological agraphia plus an additional linguistic dy sfunction. As in the sy ndrome of deep dy slexia (Coltheart 1980; Saffran/Bogy o/Schwartz/Marin 1980), the functional breakdown leading to this important additional finding is not certain. It may be related to a disturbance of the semantic area or semantic ability , an incorrect access to or from semantics or the orthographic lexicon or the utilization of alternative or compensatory right hemispheric spelling strategies (Rapcsak/Beeson/Rubens 1991). One additional area of controversy regarding phonological agraphia is its precise definition. In a prospective study of 43 patients with acquired left hemispheric lesions, Roeltgen (1989; 1991) described patients with a wide range of impairment on nonwords and showed that this impairment in nonword ability highly correlated with overall performance on an independent test of spelling achievement. However, a few subjects had relatively selective impairment of nonword spelling without severe impairment in the spelling of real words. It is uncertain whether the most appropriate operational definition of phonological agraphia should include only the latter
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group of patients with relatively isolated impairment in nonwords or whether it should include those patients who perform poorly on nonwords and also have mild impairments of real word performance. 2.2.1.2. Lexical Agraphia Similar to phonological agraphia, lexical agraphia was first defined in 1981. Beauvois/ Derouesné (1981) described a patient who, in contrast to patients with phonological agraphia, spelled nonwords well but had trouble spelling words that were irregular and ambiguous. By analogy with a similar reading disorder, this selective impairment of the lexical spelling sy stem has also been termed surface agraphia. Also, similar to phonological agraphia, more than 15 patients have been described with lexical agraphia (Beauvois/ Derouesné 1981; Hatfield/Patterson 1983; Roeltgen/Heilman 1984; Goodman-Schulman/Caramazza 1987; Rapcsak/Arthur/Rubens 1988; Friedman/Alexander 1989; Rothi/ Roeltgen/Kooistra 1987; Croisile/Trillet/Laurent et al. 1989; Roeltgen 1989; Alexander/ Friedman/Lo Verso/Fischer 1990; Rapcsak/ Rubens/Laguna 1990). In one study (Roeltgen/Heilman 1984) four patients with lexical agraphia were compared to a random selection of four patients with phonological agraphia and two groups of control patients (brain damaged and not brain damaged). The patients with lexical agraphia had more difficulty spelling irregular words than a group of matched regular words. Control patients and patients with phonological agraphia did not show this effect. The lexical agraphia patients also had more difficulty spelling words of high ambiguity than words of low ambiguity , another finding not seen in the other groups. In contrast, the lexical agraphic patient spelled nonwords as well as controls and better than the patients with phonological agraphia. Also in contrast to the patients with phonological agraphia, who made errors that were usually not phonologically correct, the patients with lexical agraphia usually made errors that were phonologically correct (e. g., spelling gelosy for jealousy). Lastly , patients with lexical agraphia have not shown word class, concreteness or imageability effects. These data are consistent with an impairment of a nonphonological, lexical or orthographic spelling sy stem. The findings from the Roeltgen/Heilman study suggest that the lexical and phonological sy stems may be impaired independently . Therefore, it indicates
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that these sy stems operate in parallel. — There is a certain degree of uncertainty as to the procedure by which these patients retain some ability to spell. Two conflicting positions are the following: First, it is possible that a sublexical phonological ability that performs phoneme-grapheme translation is responsible for the preserved ability . In contrast, given the preserved ability to spell real words, the spelling could occur via a lexical level phonological sy stem, and the nonwords could be spelled by analogy . This is an important issue as demonstrated in the discussion yb Friedman/Ferguson/Robinson/Sunderland (in press) of reading in Alzheimer’s patients. Their results indicated that the patients performed well on reading nonwords that were similar orthographically to real English words but performed poorly on nonwords for which there were no analogous English words. This suggests that use of an analogy sy stem rather than a sublexical grapheme to phoneme conversion was being used by the patients in their study . Results from certain patients with lexical agraphia also supply support for the position that at least certain lexical or orthographical responses are dependent upon visual imagery or visual word images. One of the patients described by Roeltgen/Heilman (1984) stated that her impaired spelling ability was associated with an impairment in the visualization of the words she was attempting to spell. Second, subject BT of Friedman/Alexander (1989) had poor imaging ability of letters. The authors suggest that this poor imaging of letters corresponds with poor imagery of words and the impairment found in lexical agraphia. Similar to the concern regarding the specificity of the sy ndrome of phonological agraphia, there is also a concern regarding the specificity of lexical agraphia. In the same prospective study of patients with left hemispheric lesions described previously , Roeltgen (1989; 1991) described a series of patients with lexical agraphia. Based on previous studies of normal control subjects, these patients did fulfill the criteria of having lexical agraphia. However, for the overall population of patients studied in this group, there was a very high correlation between premorbid education ability and post-lesion achievement ability . In addition, Roeltgen and colleagues have described patients with developmental spelling impairment who have difficulty in spelling that is qualitatively and quantitatively indis-
tinguishable from that seen in patients with acquired lexical agraphia (Roeltgen/Tucker 1988; Blaskey /Roeltgen 1990). Based on these results, Roeltgen (1991) has questioned the degree to which premorbid ability and education contribute to the sy ndrome of acquired lexical agraphia. He has suggested that certain subjects, based on premorbid ability or weakness in the orthographic lexicon, may be at a much higher risk for developing lexical agraphia. Minor cerebral lesions affecting any of those cognitive abilities delineated by Hatfield (1985) (familiarity with phonological components, memorization of word shapes, word analogy and mnemonic rules) can lead to the production of lexical agraphia. If this is the case, lexical agraphia is best considered a heterogeneous sy ndrome, rather than a specific disorder. 2.2.1.3. Semantic Agraphia The initial conceptualization of the linguistic components of spelling was that the two spelling sy stems were phonological and lexicalsemantic (Hatfield/Patterson 1984; Roeltgen/ Sevush/Heilman 1983). The term lexical-semantic was a consequence of the data that indicated a relationship between semantic influence and spelling in subjects with phonological agraphia. However, a series of studies have indicated that semantic influence can be dissociated from the lexical or orthographic output (Roeltgen/Rothi/Heilman 1986; Patterson 1986; Rapcsak/Rubens 1990). Patients in these studies were shown to be able to spell words but were not able to incorporate meaning into what they wrote. Also, their responses were not influenced by part of speech or regularity . The primary method used to study these patients was a homophone spelling test. For this test, a homophone was dictated and then used in a sentence. The patient was asked to spell the correct word. The patients frequently responded with correctly spelled but semantically incorrect homophones (spelling dough when the stimulus was doe or mite when the stimulus was might). In the study by Roeltgen/Rothi/Heilman (1986), the data indicated that the dissociation of the lexical sy stem from the semantic sy stem could be due to either a generalized disruption of semantic processing or to a disconnection of a relatively intact semantic sy stem from the orthographic or lexical output. Also in that study , it was demonstrated that the pattern of performance on nonwords, regular words and irregular words that characterizes lexical
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and phonological agraphia was independent of the semantic agraphia, in that the subjects with semantic agraphia had vary ing ty pes of other linguistic agraphia, including both phonological and lexical agraphia. The patient of Rapcsak/Rubens (1990) had spared general semantic abilities. In addition, their subject had an intact phonological and lexical spelling sy stem. Their results, together with previous results, indicate that the semantic sy stem is dissociable from the lexical and phonological spelling sy stems and that semantic influence on spelling can be selectively disrupted in the absence of damage or disruption to either of the two spelling sy stems. 2.2.1.4. Graphemic Buffer Agraphia Although the graphemic buffer has been proposed in multiple models of writing and spelling, only limited attempts have been made to assess patients with presumed disruption of this sy stem. Most of the studies have been performed by Caramazza and colleagues (Caramazza/Miceli/Villa/Romani 1987; Badecker/Hillis/Caramazza 1990; Hillis/Caramazza 1989). According to Caramazza and colleagues, subjects with disturbance of the graphemic buffer ty pically produce letter omissions, substitutions, insertions and transpositions in words and nonwords with written and oral spelling and in all situations including writing to dictation, spontaneous writing, written naming and delay ed copy ing. This last task consists of showing a word to a subject for a transient period. This is followed by a delay , and the subject is asked to then write the word. Subjects with disturbances of the graphemic buffer produce errors that are not affected by linguistic factors, such as those described in the previous agraphias, including degree of concreteness or imageability , word class, frequency , or regularity . The errors are ty pically influenced by word length, in that more errors are made on longer words than shorter words. In addition, frequently the errors are not evenly distributed across words. Frequently , the graphs of the errors show a bow shaped curve with more errors being produced in the middle of the word than either at the end or at the beginning. Hillis/ Caramazza (1989) suggest that different ty pes of disruption of the graphemic buffer may occur and emphasize the complexity of this process. A further study (Badecker/Hillis/ Caramazza 1990) found that although there
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was a bow shaped curve for errors, there was an influence generated by prefixes and suffixes such that there were decreased errors in these morphemes compared to the expected frequency of errors based on the error patterns in the root morpheme. Therefore, they suggested that information was passed to the buffer in morpheme-sized processing units. A recent study by Lesser (1990) found a dissociation in spelling pattern between oral spelling and written spelling. Written spelling was influenced by whether or not the stimuli were words or nonwords, but was not influenced by the regularity of the words. In contrast, oral spelling was influenced by the regularity but not by whether the stimuli were words or nonwords. Lesser concluded that there are two buffers, one for written spelling and one for oral spelling and that each of these buffers receives input from the letter production sy stems, i. e., the orthographic or lexical sy stem and the phonological sy stem. Such a model is demonstrated in Figure 23.2 This addition to the models of writing represents the first major conceptual change in these models in the last few years.
Fig. 23.2: Interaction of linguistic spelling systems and spelling buffers. Modified after Lesser (1990)
2.3. Possible Anatomic Relationships of Linguistic Agraphias It is controversial as to whether attempts to provide clinical-pathological correlations for the linguistic agraphias is beneficial. Roeltgen/Heilman (1984) have suggested that understanding of the neuroanatomy in the context of the linguistic agraphias may allow better classifications of the agraphias and a better understanding of the nature of agraphia. In contrast, Margolin (1984) has suggested that neuroanatomical correlations, especially those based on CT scan results, should be interpreted with caution given the proximity of the areas of interest as well as variability in the topography of the human cortex. A further criticism can be raised of most previous clinical-pathological correla-
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tions of agraphias, and that is the failure to consider subcortical structures. As noted previously in this chapter, multiple recent studies have described agraphia from subcortical lesions (Laine/Marttila 1981; Tanridag/Kirshner 1985; Kertesz/Latham/McCabe 1990). However, the anatomical correlations proposed principally by Roeltgen and colleagues have not considered subcortical structures (Roeltgen/Heilman 1984; Roeltgen 1985). 2.3.1. Phonological Agraphia Roeltgen and colleagues have attempted to use CT analy sis to help delineate the anatomy of phonological agraphia (Roeltgen/Rothi/ Heilman 1982; Roeltgen/Heilman 1984; Roeltgen/Sevush/Heilman 1983), and these studies have been reviewed by Roeltgen/Heilman (1985). In those studies, it was suggested that patients with phonological agraphia have lesions that are ty pically in the area of the supramarginal gy rus or in the insula deep to that structure. Indeed, one of their subjects had an isolated phonological agraphia (with no additional language deficits) and had on CT a small focal lesion confined to the insula, or possibly extending to the surface of the supramarginal yg rus (Roeltgen/Rothi/Heilman 1982). Consistent with that hy pothesis, other patients described with phonological agraphia have had lesions in the same area (Bub/Kertesz 1982; Nolan/Caramazza 1982; Shallice 1981). However, the patient described by Baxter/Warrington (1985) had a lesion that appears, based on the CT scans, in their paper to be slightly posterior to this region. In a study of a left handed patient with phonological agraphia, Bolla-Wilson/Speedie/Robinson (1985) also described a lesion of the frontal parietal area that included the supramarginal gy rus, but the lesion was in the right hemisphere. In contrast to these results, are results presented by Roeltgen (1989) in which phonological agraphia was attributed to lesions outside of this region (supramarginal gy rus and insula) and included subcortical structures. Based on those data, Roeltgen suggested that the specificity of the clinical-pathological association between phonological agraphia and the supramarginal gy rus may need to be expanded to include subcortical structures as well as individual variations in cerebral architecture and functional representation. 2.3.2. Lexical Agraphia In data also summarized by Roeltgen/Heilman (1985), the anatomic basis for lexical
agraphia was suggested to be the junction of the posterior angular gy rus and the parietal occipital lobule (the superior-lateral aspects of Brodmann’s area 19). In a previous study (Roeltgen/Heilman 1984), they demonstrated that patients with phonological agraphia had lesions that did not overlap the region associated with lexical agraphia, and patients with lexical agraphia did not have lesions that overlapped the region associated with phonological agraphia. They argued that the anatomic dissociation supported the contention that phonological and lexical agraphia were dissociable, both functionally and anatomically . Since that review in 1985, additional patients have been described with lexical agraphia who have had lesions away from the left angular gy rus, including the right parietal region (in a right hander without aphasia) (Rothi/Roeltgen/Kooistra 1987), the left posterior temporal region (middle temporal gy rus) (Croisile/Trillet/Laurent et al. 1989), and the left frontal region (Rapcsak/Arthur/Rubens 1988). In the prospective study of patients with left hemispheric lesions performed by Roeltgen (1989; 1991), the localization of lesions in patients with acquired lexical agraphia was far more varied. These data plus unpublished data of Rapcsak’s, have indicated that multiple sites within the left hemisphere may be associated with lexical agraphia, including the posterior angular gy rus, the dorso-lateral frontal lobe, the caudate, and the thalamus. However, these lesion sites seem to spare the immediate cortical perisy lvian region, including the supramarginal gy rus. In addition, there is a suggestion that the most striking cases have angular gy rus lesions (Roeltgen/Rapcsak, unpublished data). 2.3.3. Semantic Agraphia In their anatomically based neuropsy chological model of writing, Roeltgen/Heilman (1985) indicated that their anatomic data for semantic agraphia did not appear to be as specific as were the anatomic data for the ys ndromes of lexical and phonological agraphia. That conclusion was based on the study of semantic agraphia by Roeltgen/ Rothi/Heilman (1986). Their patients had lesions involving the cortical watershed area, the caudate, the internal capsule and frontal subcortical region, and bilateral medial-frontal and medial-parietal areas and the thalamus. Roeltgen/Rothi/Heilman (1986) suggested that the lesions did not overlap anatomically but were in areas frequently asso-
23. Acquired Disorders of Writing and Spelling
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ciated with transcortical aphasias with impaired comprehension. Consistent with the nonspecificit y associated with semantic agraphia is a recent study by Rapcsak/Rubens (1990) in which a left prefrontal lesion was associated with a disruption of semantic influence on writing. Given the variability in the presentation of the clinical sy ndrome of semantic agraphia and previous studies of semantic ability in aphasia that have indicated multiple way s that semantics can be disrupted, such results are not surprising.
learned by the first grade and can be used for writing any of the words in the Japanese language. Kana sy mbols are ty pically termed phonograms but are probably better described as sy llabograms. Each Kana character has a one-to-one correspondence to a sy llable. Kana characters are ty pically used for writing conjugated endings of verbs, adjectives and adverbs and function words. These grammatical morphemes can only be written using Kana, whereas major lexical items can be written in Kanji and Kana.
2.3.4. Graphemic Buffer Agraphia
2.4.2. Kanji Agraphia
Given that the linguistic studies of patients with agraphia due to the disruption of the graphemic buffer have indicated vary ing ty pes of impairment, a consistent clinicalpathological correlation with this sy ndrome would be unexpected. There are, in fact, a wide variety of lesions described in patients with proposed dy sfunction of the graphemic buffer, including the left frontal-parietal region (Hillis/Caramazza 1989; Lesser 1990), the left frontal region (Miceli//Silveri/Caramazza 1985) and the right frontal-parietaltemporal region (Hillis/Caramazza 1989). Therefore, conclusions regarding clinicalpathological correlation for this sy ndrome are similar to those for semantic agraphia.
Agraphias for both Kanji and Kana have been reported, but the most frequently reported dissociation is impaired Kanji with normal or relatively normal Kana. Most patients with Kanji agraphia have an associated alexia and a brain lesion that is ty pically associated, in Indo-European languages, with pure alexia (left occipital lobe). However, pure Kanji agraphia has been described from lesions of the posterior left temporal regions and the junction of the posterior temporal region with the lateral occipital or the angular gy rus (Kawahata/Nagata 1988) and the left inferior temporal yg rus (Kawamura/Hirayma/Hasegawa et al. 1987). There are limited descriptions of the errors produced by patients with Kanji agraphia. However, the most commonly reported errors include distortion of the grapheme, production of a partial grapheme, simplification of the grapheme and “graphical confusion” (Mochizuki/Ohtomo 1988; Yokoto/Ishiai/Furukawa/Tsukagoshi 1990; Iwata/Sugishita/ Toy okura 1981). The last error ty pe, graphical confusion, are incorrect graphemes with portions replaced by correctly formed but incorrect grapheme components. Despite the striking ‚visual’ or ‚visual-spatial’ character of these errors, they are not ty pically associated with impairment on constructive tasks (Iwata/Sugishita/Toyokura 1981).
2.4. Linguistic Agraphia in Japanese 2.4.1. Background There are two written language sy stems that are used in Japanese, Kanji and Kana. Kanji has been traditionally described as ideogram writing, but a more precise description would be morphogram writing because the sy mbols have both semantic and phonetic value, although there is no sy stematic relationship between the Kanji and speech sound. The sy mbols, which are primarily used for nouns and stems of verbs, adjectives and adverbs, number up to 10,000 in the Japanese language. However, it is expected that only approximately 1,900 of these are learned by the end of the ninth grade and some errors in Kanji writing are common even in educated Japanese individuals (Tanaka/Yamadori/Murata 1987; Iwata 1984; Kawamura/Hira y ama/ Hasegawa et al. 1987; Soma/Sugishta/Kitamura et al. 1989; Iwata/Sugishta/Toy okura 1981). Kana, in contrast, consists of a limited number of sy llabic characters (102) (Paradis/ Hagiwara/Hildebrandt 1985) that are usually
2.4.3. Kana Agraphia The occurrence of selective Kana agraphia is very rare and it has been suggested by some authors (Soma/Sugishita/Kitamura et al. 1989) that there have been no cases of pure Kana agraphia reported. The description that is closest to a case of pure Kana agraphia is the patient reported by Tanaka/Yamadori/ Murata (1987) who described a patient with relatively normal Kanji writing ability but impaired Kana writing ability . In writing
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Kana characters, the patient showed frequent substitutions of other graphemes, as well as perseverations. In addition, when writing words using Kana, there was a very striking length effect such that Kana sy mbols at the ends of the words were written correctly much less frequently than those at the beginnings of the words. Their patient had a lesion of the left inferior parietal lobe, as well as a small lesion in the left corona radiata. These authors interpreted the performance as indicating a difficulty in translating acoustic word images into graphemic forms. 2.4.4. Models of Agraphia in Japanese Based on studies of Japanese agraphia, Iwata/ Sugishita/Toy okura (1981) have offered both an information processing model, as well as an anatomical model, in an attempt to explain Japanese writing. They suggest that in writing Kana, the auditory representation of a word is activated and it in turn activates a ‚somesthetic’ representation and subsequently produces the Kana output. In contrast, they suggest that for Kanji writing, the auditory representation may or may not be activated prior to the activation of a visual-semantic representation of the word. The anatomical model proposed by Iwata (1984) suggests two separate anatomic pathway s for Kanji and Kana. For Kanji, he suggests that the pathway is from Wernicke’s area to or through the posterior inferior temporal region, into the occipital lobe and from there to the angular gy rus before the information flow accesses the peripheral writing mechanisms. In contrast, he suggests that for Kana writing, the information flow is directly from Wernicke’s area to the angular gyrus. 2.4.5. Relationship of Agraphia in Japanese and Agraphia in Indo-European Languages Soma/Sugishita/Kitamura et al. (1989) have suggested that there is an important behavioral similarity between the agraphias in these two language sy stems and that Kanji agraphia represents lexical agraphia in Japanese. In contrast, Tanaka/Yamadori/Murata (1987) argue that it is difficult to establish differences or similarities between the two writing sy stems. In order to address this controversy , it is important to review those similarities and differences that are present. In comparing and contrasting Kanji writing and writing of irregular words, there are
certain similarities. Both Kanji and irregular words have semantic, orthographic and phonological information. Both may be misspelled by normal highly educated people and agraphias associated with these words have been reported following nonperisy lvan lesions. However, they differ in important way s as well. They perform different functions in each of the languages. The irregular words in Indo-European languages may be of any word class or any word ty pe, including both highly concrete and richly semantic words (e. g., yacht) or words that are primarily grammatical in nature (e. g., though). Kanji characters, highly concrete words with rich semantic content, on the other hand, are only used to represent major lexical morphemes. In addition, irregular words in Indo-European languages frequently incorporate the conjugated portion of the word within the morpheme itself, rather than utilizing the addition of separate components. For example, caught an irregular English word carries both the information of the route morpheme (catch) as well as the past tense. A Japanese conjugated form contains both the Kanji and Kana components. From the neuropsy chological standpoint, Kanji and lexical agraphia also differ in that Kanji agraphia almost alway s occurs in the context of alexia. In contrast, in our prospective study of agraphia containing 43 subjects, there were four patients with pure agraphia and three of these four had lexical agraphia (Roeltgen 1989; 1991). Furthermore, of the six patients in the study with lexical agraphia, four had no alexia of any type. Comparison of Kana and phonological spelling is difficult because of the levels of function represented by these sy stems. Kana spelling incorporates phonograms, whereas nonword spelling incorporates phonemes. However, there are certain similarities. First, the ability to produce Kana spelling and nonword spelling utilizes sound to grapheme conversion. Also, both Kana graphemes and letters lack semantic representation. The major difference is that the agraphia associated with each of these is defined very differently . Kana agraphia is defined by dy sfunction at the grapheme level, in that Kana graphemes are not produced. In contrast, phonological agraphia is defined at the word level in that nonwords are not produced correctly. Given some of the difficulties in comparing Kanji and irregular words and Kana and nonwords, and consequently lexical agraphia with Kanji agraphia and phonological
23. Acquired Disorders of Writing and Spelling
agraphia with Kana agraphia, we are inclined to agree with Tanaka/Yamadori/Murata (1987) that comparison or discussion of similarities in agraphias of the two different language systems is difficult.
3.
Agraphia in Alzheimer’s Disease
In his original report, Alzheimer (1907) described a patient with a progressive dementing illness who, in addition to aphasia and alexia, also demonstrated agraphia. Pick (1925) observed that disorders of orthography were indeed often associated with dementia and that orthographic errors increased with the progression of the disease. Several investigators have since confirmed that agraphia is a common feature in Alzheimer’s disease (AD) (Appell/Kertesz/Fisman 1982; Cummings/Benson/Hill/Read 1985; Murdoch/Chenery /Wilks/Boy le 1987; Bay les/ Kaszniak 1987; Faber-Langendoen/Morris/ Knesevich et al. 1988; Horner/Hey man/Dawson/Rogers 1988). It is apparent from these studies that both the linguistic and motor components of writing may become compromised in the course of the illness. Although most agraphic AD patients are also aphasic, the writing impairment is often more severe than the spoken language deficit and at times may precede it (Appell/Kertesz/Fisman 1982; Cummings/Benson/Hill/Read 1985; FaberLangendoen/Morris/Knesevich et al. 1988; Homen/Heyman/Dawson/Rogers 1989). More recent studies of agraphia in AD have attempted to determine the nature of the cognitive-linguistic breakdown in the writing process. Impairments have now been documented at several different levels. At the pragmatic/semantic level, the written narrative of AD patients is often poorly organized, repetitive, irrelevant, uninformative or ‚empty ’ and there is a paucity of written output (Neils/Boller/Gerdeman/Cole 1989; Glosser/Kaplan 1989; Horner/Hey man/Dawson/Rogers 1988; Neils/Kavrie 1990). However, the basic sy ntactic frame of the sentences is relatively well preserved (Glosser/Kaplan 1989). At the single word level, Rapcsak/Arthur/Bliklen/Rubens (1989) found that AD patients spelled regular words and nonwords significantly better than irregular words. In addition, the spelling errors of AD patients on irregular words were frequently phonologicall y plausible. Rapcsak/Arthur/Bliklen/ Rubens (1989) proposed that these findings were consistent with an impairment of the
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lexical spelling sy stem in AD, and reflected either a loss of word representations from the orthographic lexicon or an inability to access these representations. On the other hand, spelling by the phonological spelling sy stem (i. e., phoneme-grapheme conversion) was relatively spared. Others have also documented that irregular words are especially difficult for AD patients and that their spelling errors are often phonologically accurate (Smith/ Sny der/Meeks 1991; Glosser/Kaplan 1989). However, Smith/Sny der/Meeks (1991) also provided evidence that in some AD patients phonological spelling by phoneme-grapheme conversion may not be entirely intact either. Although the studies reviewed above are not directly comparable since they have used different methodologies and have included subjects at various stages of dementia, it is our impression that agraphia in AD does have certain characteristic cognitive-linguistic features that seem to follow a ty pical pattern of progression. In the earliest stages, the writing disturbance is characterized by a general disruption of semantic processing but relative preservation of basic sy ntactic form. The semantic impairment will adversely affect performance on all writing tasks that require semantic mediation. These include spontaneous or descriptive writing, written naming and homophone spelling. With the exception of homophones, however, writing to dictation in early AD may be relatively intact, since this task can be performed without semantic processing (Roeltgen/Rothi/Heilman 1986; Glosser/Kaplan 1989). The next stage of the writing disturbance is characterized by additional impairment at the level of single word orthography . Initially , the orthographic impairment is most severe for irregular words, since these can only be spelled lexically . At this stage, the phonological spelling sy stem (i. e., phoneme-grapheme conversion) is still operational and thus regular word and nonword spelling can still be performed with relative success. Consistent with the relative sparing of the phonological spelling sy stem, spelling errors on irregular words are likely to be phonologically plausible. In more advanced stages of the illness, however, the phonological spelling sy stem may also become compromised. It is apparent from this general outline that, depending on the stage of the illness, a given patient or group of patients might exhibit dy sfunction at the level of overall pragmatic/semantic organization and at the level of single word orthography simul-
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taneously . In addition to the linguistic impairment, the peripheral motor mechanisms of writing may also fail even in patients with only mild to moderate dementia (Rapcsak/ Arthur/Bliklen/Rubens 1989; Horner/He y man/Dawson/Rogers 1988). Whether the progression of the cognitivelinguistic impairment in the writing process conforms to the pattern we have outlined above is y et to be determined by longitudinal studies of agraphia in AD. However, this model is consistent with general observations that language deterioration in AD predominantly affects lexical-semantic and pragmatic abilities, while phonological and sy ntactic operations are relatively spared until the later stages of the illness (Irigaray 1973; Schwartz/ Marin/Saffran 1979; Appell/Kertesz/Fisman 1982; Bay les 1982; Obler 1983). We emphasize that our model does not address explicitly the relationship of memory impairment and agraphia in AD (e. g., storage or access disorders of semantic memory and possible impairment of putative working memory sy stems for the temporary storage of linguistic items such as the phonological and graphemic output buffers). The impairment of different memory sy stems and attentional deficits are likely to contribute significantly to agraphia in all stages of AD and require further study. Pick (1892) was the first to suggest that specific aphasic sy ndromes, similar to those seen following focal brain lesions, may occur in senile atrophy of the brain. He believed that these sy ndromes were caused by the “local accentuation of a diffuse process”. The pattern of language impairment in AD indeed correlates well with the distribution of neuropathological changes in the cerebral cortex. Several anatomical and histological studies have demonstrated that the degenerative process affects the multimodal association cortex of the temporo-parieto-occipital junction most severely and most consistently (Brun/Gustafson 1976; Brun/Englund 1981; Kemper 1984). The neuropathological findings are paralleled by cerebral blood flow and positron emission tomographic studies in AD that show a marked reduction in metabolic activity in the temporo-parieto-occipital areas, as well as an inability to activate these regions during cognitive effort (Hagberg/Ingvar 1976; Ingvar/Risberg/Schwartz 1975; Friedland/Bundinger/Ganz et al. 1983; Chase/Foster/Fedio et al. 1984; Friedland/ Budinger/Koss/Ober 1985; Friedland/Brun/ Budinger 1985). Furthermore, in AD patients
with aphasia, alexia and agraphia, the most significant reduction of metabolic activity is in the temporo-parieto-occipital region on the left side (Gustafson/Hagberg/Ingvar 1978; Foster/Chase/Fedio et al. 1983; Haxb y / Duara/Grady et al. 1985). Given the above considerations, it is not surprising that language dy sfunction is a consistent feature in AD (Appell/Kertesz 1982; Cummings/Benson/Hill/Read 1985; Bay les/Kaszniak 1987) and that the pattern of language impairment closely resembles the aphasic sy ndromes that are seen following focal lesions of the left temporo-parietal association cortex (Obler/ Albert 1981; Benson/Cummings/Tsai 1982). As pointed out by Luria (1974), damage to these cortical regions severely disturbs lexicalsemantic linguistic operations. By the same token, it is likely that the frequently observed preservation of phonological and sy ntactic abilities in AD reflects the relative sparing of immediate perisy lvian language areas by the disease process (Whitaker 1976). In terms of the writing disturbance in AD, the involvement of the left temporo-parietal region by the degenerative process is likely to be responsible for the disruption of lexicalsemantic processing that is evident in tasks of spontaneous or descriptive writing, written naming and homophone spelling. As we have seen earlier, the left angular gy rus is also an important neural substrate of lexical spelling, and the frequent involvement of this region in AD probably accounts for the word-level orthographic impairment (i. e., lexical agraphia). Phonological spelling, on the other hand, depends on the integrity of the immediate perisy lvian language zone (the supramarginal gy rus and insula, in particular) (Roeltgen/ Sevush/Heilman 1983), and the sparing of these regions until later in the disease process may account for the relative preservation of spelling by phoneme-grapheme conversion.
4.
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Henschen, S. E. (1922). Klinische und anatomische Beiträge zur Pathologie des Gehirns. VII. Über motorische Aphasie und Agraphie. Stockholm: Nordiska Bokhandel. Hillis, A. E. & Caramazza, A. (1989). The graphemic buffer and attentional mechanisms. Brain and Language, 36, 208—235. Horner, J., Hey man, A., Dawson, D., & Rogers, H. (1988). The relationship of agraphia to the severity of dementia in Alzheimer’s disease. Archives of Neurology, 45, 760—763. Ingvar, D. H., Risberg, J., & Schwartz, M. S. (1975). Evidence of subnormal function of association cortex in presenile dementia. Neurology, 25, 964—974. Irigaray , L. (1973). Le langage des dements. The Hague: Mouton. Iwata, M. (1984). Neuropsy chological correlates of the Japanese writing sy stem. Trends in Neurosciences, 7, 290—293. Iwata, M., Sugishita, M., & Toy okura, Y. (1981). The Japanese writing sy stem and functional hemispheric specialization. In Neurology, Proceedings of the 12 th World Congress of Neurology. AmsterdamOxford-Princeton: Excerpta Medica. Jackson, J. H. (1878). On affections of speech from disease of the brain. Brain, 1, 305—330. Kaplan, E. & Goodglass, H. (1981). Aphasia-related disorders. In M. T. Sarno (Ed.), Acquired aphasia. New York: Academic Press. Kawahata, N. & Nagata, K. (1988). Alexia with agraphia due to the left posterior inferior temporal lobe lesion — Neuropsy chological analy sis and its pathogenetic mechanisms. Brain and Language, 33, 296—310. Kawamura, M., Hiray ama, K., Hasegawa, K., Takahashi, N., & Yamaura, A. (1987). Alexia with agraphia of Kanji (Japanese morphograms). Journal of Neurology, Neurosurgery, and Psychiatry, 50, 1125—1129. Kemper, T. (1984). Neuroanatomical and neuropathological changes in normal aging and dementia. In M. L. Albert (Ed.), Clinical neurology of aging. 9—52. New York: Oxford University Press. Kertesz, A., Latham, N., & McCabe, P. (1990). Subcortical agraphia. Neurology, 40 (1), 172. Laine, T. N. & Marttila, R. J. (1981). Pure agraphia: a case study . Neuropsychologia, 19, 311—316. Leischner, A. (1969). The agraphias. In P. J. Vinken & G. W. Bruy n (Eds.), Disorders of speech, perception and symbolic behaviour. 141—180. Amsterdam: North-Holland. Lesser, R. (1990). Superior oral to written spelling: Evidence for separate buffers? Cognitive Neuropsychology, 7 (4), 347—366. Lichtheim, L. (1885). On aphasia. Brain, 7 , 433—485.
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Luria, A. R. (1970). Traumatic aphasia. The Hague: Mouton. Luria, A. R. (1974). Language and brain: Towards the basic problems of neurolinguistics. Brain and Language, 1, 1—14. Marcé, M. (1856). Mémoire sur quelques observations de phy siologie pathologique tendant à démontrer l’existence d’un principe coordinateur de l’écriture. Compte-rendu de la Société Biologie (Paris), 3, 93—115. Marcie, P. & Hécaen, H. (1979). Agraphia. In K. M. Heilman & E. Valenstein (Eds.), Clinical neuropsychology (1st Edit.). Ch. 4. 92—127 . New York: Oxford University Press. Margolin, D. I. (1984). The neuropsy chology of writing and spelling: Semantic, phonological, motor, and perceptual processes. The Quarterly Journal of Experimental Psychology, 36 A, 459—489. Marshall, J. & Newcombe, F. (1966). Sy ntactic and semantic errors in paralexia. Neuropsychologica, 4, 169—176. Miceli, G., Silveri M. C., & Caramazza, A. (1985). Cognitive analy sis of a case of pure dy sgraphia. Brain and Language, 25, 187—212. Mochizuki, H. & Ohtomo, R. (1988). Pure alexia in Japanese and agraphia without alexia in Kanji. Archives of Neurology, 45, 1157—1159. Morton, J. (1980). The logogen model and orthographic structure. In U. Frith (Ed.), Cognitive processes in spelling. 117 —133. London: Academic Press. Murdoch, B. E., Chenery , H. J., Wilks, V., & Boy le, R. S. (1987). Language disorder in dementia of the Alzheimer type. Brain and Language, 31, 122—137. Neils, J., Boller, F., Gerdeman, B., & Cole, M. (1989). Descriptive writing abilities in Alzheimer’s disease. Journal of Clinical and Experimental Neuropsychology, 11, 692—698. Neils, J. & Kavrie, S. (1990). Dy sgraphia in early Alzheimer’s disease. Journal of Clinical and Experimental Neuropsychology, 12, 398. Nielsen, J. M. (1946). Agnosia, apraxia, aphasia: Their value in cerebral localization. New York: Paul B. Hoeber. Nolan, K. A., & Caramazza, A. (1982). Modality independent impairments in word processing in a deep dy slexic patient. Brain and Language, 16, 236—264. Obler, L. K. (1983). Language and brain dy sfunction in dementia. In S. J. Segalowitz (Ed.), Language functions and brain organization, 267 —282. Orlando: Academic Press. Obler, L. K. & Albert, M. L. (1981). Language in the elderly aphasic and the dementing patient. In M. T. Sarno (Ed.), Acquired aphasia. 385—398. Orlando: Academic Press.
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Smith, S. T., Sny der, W. B., & Meeks, L. M. (1991). Agraphia in Alzheimer’s disease. Journal of Clinical and Experimental Neuropsychology, 13, 71. Soma, Y., Sugishita, M., Kitamura, K., Maruy ama, S., & Imanaga, H. (1989). Lexical agraphia in the Japanese language. Brain, 112, 1549—1561. Tanaka, Y., Yamadori, A., & Murata, S. (1987). Selective Kana agraphia: A case report. Cortex, 23, 679—684. Tanridag, O. & Kirshner, H. S. (1985). Aphasia and agraphia in lesions of the posterior internal capsule and putamen. Neurology, 35, 1797—1801. Van Lancker, D. (1990). A case of deep dy sgraphia attributed to right hemispheric function. Presented at The Academy of Aphasia. Baltimore, MD. Vernea, J. J. & Merory , J. (1975). Frontal agraphia, (including a case report). Proceedings of the Australian Association of Neurologists, 12, 93—99. Wernicke, C. (1874). Der aphasische Symptomencomplex. Breslau: Max Cohn & Weigert. Wernicke, C. (1886). Nervenheilkunde. Die neueren Arbeiten über Aphasie. Fortschritte der Medizin, 4, 463—482. (Translated by R. De Bleser (1989), Cognitive Neuropsychology, 6, 547—569). Whitaker, H. (1976). A case of isolation of the language function. In H. Whitaker & H. A. Whitaker (Eds.), Studies in neurolinguistics, vol. 2. 1—58. Orlando: Academic Press. Yokota, T., Ishiai, S., Furukawa, T., & Tsukagoshi, H. (1990). Pure agraphia of kanji due to thrombosis of the Labbe vein. Journal of Neurology, Neurosurgery, and Psychiatry, 53, 335—338.
David P. Roeltgen/Steven Z. Rapcsak, Philadelphia, Pennsylvania (USA)/ Tucson, Arizona (USA)
24. Multilingualism and Aphasia 1. 2. 3. 4. 5. 6. 7.
1.
Introduction Patterns of Recovery Three Questions about Language Representation in the Brain Neurofunctional Organization of more than one Language The Measure of Deficits Conclusion References
Introduction
The basic question in the neuropsy chology of bilingualism has been whether the cerebral
representation of language in bilinguals differs from that in unilinguals, and if so, in what specific way s. Some researchers have turned to aphasia in bilinguals for evidence in support of their hy potheses. Others have developed models in an attempt to explain the observed phenomena, in particular the patterns of recovery of the various languages of bilingual and multilingual aphasic patients.
2.
Patterns of Recovery
Six basic patterns of recovery have been observed over the past century : Parallel, when all languages are recovered at the same time
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and to the same extent; differential, when one is recovered better than the other(s); successive, when one is not recovered at all until the other(s) has/have been maximally recovered; selective, when one language is never recovered; antagonistic, when only one language is initially recovered, then is eventually replaced by another language; and mixed, when two languages are sy stematically mixed intrasententially (and even sometimes intramorphemically ) at the level of phonology , morphology , sy ntax and/or the lexicon (Paradis 1977). Some patients exhibiting a selective recovery have been reported to have retained comprehension in the language that was selectively unavailable for production tasks. The available language in some cases of antagonistic recovery has been reported to alternate over periods ranging from 24 hours to 3 weeks (Paradis/Goldblum/Abidi 1982; Nilipour/ Ashay eri 1989) or even 8 months (Paradis/ Goldblum 1989). Moreover, these six patterns are not mutually exclusive: A recovery may change from one pattern into another over time, e. g., from successive to antagonistic (Minkowski 1928), or different patterns may coexist relative to different languages, e. g., alternating antagonism between two languages with successive recovery of a third (Nilipour/Ashay eri 1989). Selective aphasia (aphasia in one language with no measurable deficits in the other(s)), and selective recovery (when one language remains permanently inaccessible) have been interpreted as representing opposite poles on a continuum of differential aphasia (Paradis/Goldblum 1989). In addition, three cases have been interpreted as exhibiting differential aphasia, i. e., a different aphasic sy ndrome in each language (Albert/Obler 1978; Silverberg/Gordon 1979). However, one of them (Silverberg/Gordon, case 1) can really be considered a standard case of selective recovery . The patient is reported to have exhibited conduction aphasia in his native Russian and global aphasia in the little Hebrew he had attempted to acquire with very little success over the previous few y ears. The other two patients were believed to present with Broca’s aphasia in one language and Wernicke’s aphasia in the other. In both cases Hebrew was the language in which the patients were said to have exhibited Wernicke’s aphasia, as reflected by their paraphasias in Hebrew. Their respective native
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languages were English and Spanish, in which they exhibited ty pical agrammatism. However, closer study of these cases suggests that the patients actually exhibited agrammatism in both of their languages, and that the sy mptoms of substitution in Hebrew were erroneously interpreted as evidence of paragrammatism (Paradis 1988). It is also possible that the apparent dissociation of aphasic sy mptoms might have reflected the patient’s differential mastery of the various components of each language before the aphasia. Indeed, some non-brain-damaged speakers of foreign languages can easily pass for Broca or Wernicke patients. It is not unlikely that, given what we now know about the form that agrammatism takes in Hebrew (Grodzinsky 1984), the authors who initially reported cases of differential aphasia would no longer interpret them as such, but as cases of agrammatism in both languages, with possibly different degree of severity in each. Finally , a number of cases have been reported to exhibit paradoxical translation (Paradis/Goldblum/Abidi 1982; De Vreese/ Mota/Toshi 1988) and compulsive translation behavior (Vey rac 1931; Weisenburg/McBride 1935; Jakobson 1964; Schulze 1968; Perecman 1984; De Vreese/Mota/Toshi 1988). Patients are said to exhibit paradoxical behavior when they are able to translate into a language that is not available for spontaneous speech or any other production task, but are unable to do the reverse, i. e., to translate from a language which they do understand (though which they cannot speak spontaneously ) into a language which is available for spontaneous speech. Compulsive translation refers to the patient’s unsolicited spontaneous translation of what they say or of what is said to them. Inability to translate in either direction has also been reported (Goldstein 1948).
3.
Three Questions about Language Representation in the Brain
These various recovery patterns raise three questions that have not alway s been kept distinct: (1) How is it that these patterns are possible in the first place? (2) Why does one particular pattern obtain rather than another in a given patient? (3) Why is one specific language (say , English) preferentially recovered rather than another (say , Japanese)? More specifically , one may ask what neurophy siological mechanisms are responsible for
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the fact that one language can be temporarily or permanently unavailable while the other(s) remain(s) relatively accessible; how it is possible that only one language is accessible for a period of time, and subsequently only the other language is; and what provokes sy stematic mixing. Assuming that we have a satisfactory explanation for the very possibility of the occurrence of all recovery patterns, the next step is to ascertain under what circumstances which of the possible recovery patterns will obtain. Then, assuming that we can explain the mechanism(s) underly ing the various patterns of recovery and that we know the circumstances that determine the particular ty pe of recovery , we may further ask, given any nonparallel pattern, why one specific language is preferentially recovered rather than the other. Most early studies have attempted to answer the third question. A few have attempted to answer the first. None have addressed the second, except, possibly , those that have tried to localize a switch mechanism (see below). 3.1. How are the Various Patterns Possible? The first substantive monograph on aphasia in poly glots is that of Pitres (1895). Pitres addressed two questions. How are the various patterns possible? And what determines which language will be recovered first or best? Most of the literature of the subsequent 80 y ears has concentrated on his contribution to the latter question. On the basis of his review of the literature and of eight cases of his own, Pitres concluded that, contrary to what his precursor Ribot (1881) had proposed in a two-line incidental remark in a book otherwise devoted to diseases of memory , the language preferentially recovered is not the native language (by virtue of the fact that its acquisition is less recent), but is the language most familiar to the patient at the time of insult. This language in many cases indeed happens to be the mother tongue, but then it is recovered not because it was the first acquired, but because it happens also to be the most familiar. This came to be known as “Pitres’ rule”, and was then contrasted with “Ribot’s rule” in a lively debate for y ears to come (Sträussler 1912; Schwalbe 1920; Pick 1921; Hegler 1931; Smirnov/Faktorovich 1949; Lambert/Fillenbaum 1959; Obler/Albert 1977). Papers that claimed to refute either Ribot’s or Pitres’ rule, or both, appeared in quick succession, and other tentative ex-
planations for patterns of loss and recovery were then proposed. Minkowski (1927; 1928), for instance, suggested that the language to be preferentially recovered was the one for which the patient had the strongest positive affective ties. However, exceptions to this proposal abound (Halpern 1950). Moreover, it is very difficult to interpret affective impact. If one wishes to take into account negative as well as positive affect, then just about every case could be interpreted in this light. Yet, in some cases, it is difficult to determine what kind of differential affect there might exist between two languages (e. g., the case described by Zangwill 1979). Pötzl (1925) suggested that the preferentially recovered language was the language most needed by the patient, while Goldstein (1948) proposed that it was the language of the environment, most often that of the hospital. However, while some patients recovered the language of the environment rather than their mother tongue or their most fluent language, just as many did not recover the language of the environment even if it was both their native and most familiar language. 3.1.1. Differential Localization The first question, namely how the various patterns are possible, was formulated most clearly by Scoresby Jackson (1867) who, when referring to the case of “a gentleman who, after a blow on the head, lost his knowledge of Greek and did not appear to have lost any thing else,” asked: “Where was that gentleman’s Greek deposited that it could be blotted out by a single stroke, whilst his native language and all else remained?” (p. 705). In an effort to explain this phenomenon, while quickly adding that it was “of course, mere speculation” on his part, Scoresby Jackson surmised that an individual might acquire his native language “by the aid of the posterior third of his left frontal convolution” and that, with the addition of other languages, “more and more of the convolution is utilized.” (p. 704). This amounted to suggesting that different languages were subserved by different areas of cortex. Pitres (1895) argued at length against the mere hint of such hy pothetical new centres specifically assigned to each of the languages learned by poly glot subjects and, although no one actually proposed that different languages were represented in different locations in the brain, authors continued to argue against this view for a long time
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(Pötzl 1925; Minkowski 1927; Vey rac 1931; Ombredane 1951; Penfield 1953; Penfield/ Roberts 1959; Gloning/Gloning 1965), until the notion was revived in a slightly different form by Albert/Obler (1978) who suggested that there was greater participation of the right hemisphere in the acquisition and use of a second language (Albert/Obler 1978), and by Ojemann/Whitaker (1978) in their interpretation of their electro-cortical stimulation findings. However, there is only contradictory experimental evidence and no clinical evidence in support of differential lateralization of language in bilinguals (Mendelsohn 1988; Solin 1989; Paradis 1990 a). In addition, according to Ojemann/Whitaker, the more automatized language is subserved by a less extensive area of cortex than the less fluent language. That is, both languages share the core areas of the classical language zone, but the less automatic language is also represented in additional areas at the periphery of the language area. Rapport/Tan/Whitaker (1983) reported additional evidence in support of this hy pothesis. So did Berthier/Starkstein/L y yl k/Leiguarda (1990), except that upon closer examination, it can be seen that the latter findings actually provide counter-evidence to such a proposal (Paradis 1990 b). In any case, it may be premature, for methodological reasons, to interpret these results as indicative of differential localization. The electrodes used by Ojemann/Whitaker (1978) for cortical stimulation were bipolar, with electrodes 5 millimetres apart, which, with some spreading at each end, must have interfered with an area of about 20 square millimetres. It is therefore difficult to be sure that exactly the same area of cortex was stimulated on separate occassions. (The various loci were marked by numbered tags that were manually removed for subsequent stimulation at a later time.) A more likely explanation seems to be that, within the core of the language area, language was interfered with every time, but at the periphery , sometimes it was, sometimes it was not, depending on whether the electrodes actually touched the language area, or were displaced from it by a millimetre or so. 3.1.2. The Switch Mechanism Rejecting the notion of a different location for each particular language, Pötzl (1925) proposed that there was a cerebral switch mechanism allowing transition from one language to another. Based on his observation
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that there was a correlation between selective recovery and damage to the left supramarginal gy rus and adjacent temporo-parietal area, Pötzl (1930) concluded that this area subserved that distributing device. Kauders (1929) and Leischner (1948) reached similar conclusions: damage to the switch mechanism causes a patient either to be able to speak only one language or to switch uncontrollably between languages. Yet patients with switching difficulties or mixing in the context of a lesion in the anterior language area — and an intact temporo-parietal region (Minkowski 1927; Stengel/Zelmanovitch 1933; Gloning/Gloning 1965, L’Hermitte/Hécaen 1966) as well as patients without switching disturbances in the context of a damaged temporoparietal area (Gloning/Gloning 1965; L’Hermitte/Hécaen/Dubois 1966; Schulze 1968) have been reported. Thus, if there is a specific bilingual switch mechanism, it is not likely to be localized in the supramarginal gy rus or adjacent temporo-parietal area. In fact, there is no need to postulate anatomical localization or even a ty pe of functional language organization specific to bilinguals other than that which allows every unilingual speaker to switch between register or to select a passive over a cleft construction. 3.1.3. Inhibition/Disinhibition Pitres (1895) proposed a different explanation, namely , that the unrecovered language is not lost, but temporarily or permanently inhibited. This hy pothesis allows for two or more languages to be subserved by the same cortical areas, while remaining neurofunctionally distinct and even possibly subserved by different neural circuits, but inextricably intertwined within the same gross anatomical area. The inaccessibility of one of the languages would thus not be caused by the phy sical destruction of its substrate, but by the neurophy siological inhibition of its neural network. This account has the merit of being compatible with a wide range of data. In fact, it is compatible with all bilingual aphasia recovery patterns. It may also be used to explain normal bilingual verbal behaviour, such as the ability to speak one language at a time, to switch between them, and to mix them at will. In addition, it may be assumed that inhibition is not an all-or-nothing phenomenon. The underly ing cerebral substrate of a given item is unable to “fire” (i. e., be activated) when inhibition exceeds a certain level. When a language item is selected for
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production, it receives excitatory impulses while its competitors are inhibited, or, more accurately , the activation threshold of its competitors is raised (i. e., more excitatory impulses are necessary to cause these items to fire). It may be further assumed that the activation threshold of an item is lower for comprehension than for production (i. e., for a response to an external stimulus in contrast to self-activation).
4.
Neurofunctional Organization of More Than One Language
Therefore, in an effort to account for all reported clinical as well as normal (i. e., nonpathological) phenomena, we will attempt to integrate the subsy stems hy pothesis (Paradis 1981) and the activation threshold hy pothesis (Paradis 1984; 1985) within Green’s (1986) activation, control and resource framework. This should help shed some light on how a speaker-hearer has control over two language sy stems and avoids interference while retaining the ability to mix at will and to translate from one language to another. 4.1. The Organization of Cerebral Substratum At least four hy potheses have been formulated with respect to the way in which two languages are organized in their neuroanatomical and neurophy siological representation (Paradis 1981). T h e ex t e n d e d s y st e m hy p o t h e s i s holds that the languages are undifferentiated in their representations. The bilingual sy stem is in all respects similar to a single language sy stem except that it simply contains more phonemes, morphemes, lexical entries and sy ntactic rules. These are subserved as additional elements of the same kind within the sy stem and are integrated into it. The sy ntactic rules of both languages are stored in the same way as the various sy ntactic rules within a single language. For example, the same mechanism that allows a speaker to select an active rather than a passive or a cleft construction allows the bilingual speaker to select the English over the Japanese structure, the selection of broccoli over cauliflower is of the same nature as the selection of chou-fleur over cauliflower or Blumenkohl. The d u a l sy st e m hy p o t h e s i s holds that each language is subserved by an altogether different neural sy stem. That is, an independent network of neural connections
underlies each language. Phonemes, morphemes and sy ntactic rules of one language are thus subserved by a separate sy stem of connections, independent of the one which subserves the other language. T h e t r i p a rt i t e s y st e m hy p o t h e s i s holds that those items which are identical in both languages are represented in a common underly ing neural substrate, while those that are different are represented in their respective languagespecific neural substrates. The S u b s yst e m s hy p o t h e s i s holds that each language is subserved as a subsy stem of the larger sy stem known as linguistic competence. Language functions form a cognitive sy stem separate from other cognitive sy stems, and each language forms a distinct subset of that sy stem. Language as a sy stem is susceptible to inhibition as a whole, but each subsy stem is also susceptible to selective inhibition (as well as parts of each subsy stem). It is important to note that the subsy stems hy pothesis is the only one compatible with all the observed phenomena. While it is compatible with all patterns of recovery as well as with the ability to mix languages at will, it nevertheless needs additional experimental and/or clinical support. 4.2. The Activation Threshold Hypothesis The activation threshold hy pothesis holds that comprehension and production are subserved by the same neural substrate, but that it takes more ‚energy ’ (or more numerous neural impulses) to voluntarily self-activate a trace (or ‚engram’ or ‚address’, depending on one’s metaphor) than to activate it as a result of impulses triggered by external stimuli. In the normal course of events, the threshold of activation (i. e., the propensity to be activated) of any given trace is a function, among other factors, of frequency and recency of activation. The more frequently a given trace is used, the lower its threshold of activation, hence the easier it is to activate it again and the lesser the amount of energy needed to activate it. The longer it has been since a trace was last activated, the higher its threshold of activation, that is the more difficult it is to activate, and the greater the amount of energy needed to activate it. However, pathology may disrupt the normal pattern of activation threshold. All things being equal, when an item is not activated, its threshold slowly rises until it is activated again, at which time the threshold is lowered and starts rising slowly again from
24. Multilingualism and Aphasia
that point on. If the item is not activated for a very long time, its threshold becomes too high for self-activation, but it can still be activated by external stimulation, thus allowing for comprehension though not for voluntary recall. When a whole language sy stem has not been used for many y ears, as can occur when one emigrates for instance, the speaker is generally said to have retained a “passive knowledge” of that language, namely the ability to understand it without necessarily being able to speak it any more (because of massive word-finding difficulty as well as morphosy ntactic interference from the currently used language). If the period of disuse has not been too lengthy , and if that sy stem is sufficiently reactivated through extensive interaction with speakers of that language, it will become active, namely its activation threshold will be sufficiently lowered for it to be self-activated. If the period of disuse has extended bey ond a certain length (which may vary with the age at which the speaker ceased using the language — in subjects who ceased using the language at a y ounger age, the language has been reported to have become permanently unavailable after shorter periods of time than in subjects who used it until an older age) the activation threshold will have been raised so high that the subject will have lost even the ability to understand that language. It is assumed that the selection of a particular item requires that its activation exceed that of any possible alternatives (Luria 1973; Green 1986). In order to ensure this, its competitors must be inhibited, i. e., their activation threshold must be raised. Thus, as an item is targeted for activation, its competitors are simultaneously inhibited, that is, their activation threshold is raised and consequently more energy is required to activate them (though it is not usually raised so high as to prevent comprehension of incoming signals). In other words, the appropriate item is activated by the raising of the activation threshold of competing items (i. e., all other possible candidates) as much as by actually activating it. Since the availability of an item is a function of the frequency and recency of its activation (Luria 1974), expressions may be more available (because they have been activated more often and/or more recently ) in one language than in another. A word (or any other linguistic item) must reach a certain level of activation in order to become available for use. The activation threshold for the internal
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representation of specific words (or independently for their semantic and morphosy ntactic properties on the one hand, and for their phonological form on the other), or of any other item (e. g., a sy ntactic or morphological rule) may differ from that of other items within the system. It is further assumed that when a bilingual speaker elects to speak one language rather than another, the nonselected language is partly deactivated. That is, the activation threshold of the nonselected language is raised. In cases of aphasia, it sometimes becomes impossible to disinhibit (i. e., to sufficiently lower the activation threshold of) one of the languages, either permanently (as in selective recovery ), temporarily (as in successive recovery ), or alternatingly (as in antagonistic recovery ). The activation threshold may be higher for one language than for the other (differential recovery ). Deactivation of one language (raising its activation threshold) may be difficult, resulting in abundant inadvertant mixing or hybridization. 4.3. Different Grammars for Comprehension and Production? Poly glot speakers have been reported to understand, after insult, a language they are no longer able to speak. Contrary to Albert/ Obler’s (1978, 220) and Green’s (1986, 211) suggestion, such a situation does not necessarily indicate that different functional sy stems underly the comprehension and production of language (bey ond the obvious peripheral auditory and motor involvement). A different threshold of activation is sufficient to account for the occassionally observed clinical dissociation, as well as for the fact that comprehension skills precede production skills during the early stages of language development (Bloom 1974); that perceptual knowledge of a second language is more advanced than productive knowledge (Tarone 1974; Tremaine 1974); that when language is not practiced, production deteriorates more quickly than comprehension (Leopold 1949; Kinzel 1964; Cohen 1989); that in amnestic aphasia, comprehension is recovered before expression (Pitres 1895; Lecours 1975); and that although it is possible for a bilingual to choose to speak either language, it is not possible to choose not to understand either one under any circumstance, as evidenced in all bilingual Stroop tests (Obler/Albert 1978). In addition to the difference in activation threshold, a good deal of comprehension need
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not involve linguistic (e. g., morphosy ntactic) decoding, but educated guessing based on the situational, linguistic, and paralinguistic contexts of the speech event, as well as general knowledge (Bloom 1974). The activation threshold hy pothesis would also explain why recognition is easier than reconstruction, which is easier than evocation or recall (Florès 1970; Piaget 1970). In terms of language use, recognition corresponds to comprehension; reconstruction to comprehension from a degraded stimulus, or part of a stimulus; and recall to the self-activation of the cerebral representation of an item for production (or for inner speech) in the absence of an external stimulus. There is therefore no need to postulate the destruction of an ‚output sy stem’ independent of an ‚input sy stem’ (Green 1986) in addition to the modality -specific peripheral sy stems in order to account for the dissociation between comprehension and production. The cerebral sy stems subserving the comprehension and production of language may be assumed to be separable only in that they are dependent on different activation thresholds. On the other hand, different functional sy stems must be assumed to underlie different languages, since double dissociations between them have been amply documented. 4.4. Resources in the Control of the Use of Language Systems Non-parallel recovery in bilingual aphasia has been postulated since Pitres (1895) not to be the result of selective destruction of the cerebral representation of one language sy stem, but of its temporary or permanent inhibition. Green (1986) argues in favor of this position and underscores the energy dimension of the cerebral control over the use of language sy stems. He maintains that regulation of inhibition/disinhibition (or, in our terms, the respective activation threshold) involves the use (and hence possible depletion) of energy resources. The model assumes the following. When an utterance is produced, the appropriate item comes to dominate other possible candidates by reducing their level of activation, i. e., by inhibiting them (Luria 1973; Luria/ Hutton 1977; Green 1986). When a bilingual speaker elects to speak one language rather than another, the nonselected language is not completely deactivated (Green 1986; Grosjean/Soares 1986); in other words, the threshold of activation is raised sufficiently to pre-
vent interference during production, but not sufficiently to preclude borrowing and mixing, or comprehension in the other language. Practice could probably make a difference. Individuals used to mixing must have developed a lower activation threshold for the nonselected language than individuals who speak each language to different unilingual groups of people and thus never have occasion to mix, in which case the two languages are rigorously kept separate at all times and hence the threshold of the nonselected language is likely to be high. Green (1986) then goes on to assume that words possess particular ‚tags’ that label each item as belonging to one or the other language. Alternatively , we may consider that items in a given language are part of a specific subsy stem, and items of another language part of a different subsy stem, each subsy stem being subserved by a different neural network. These different networks need not be represented in different anatomical locations; they are indeed more likely to be intricately interwoven within the same cortical areas. In any case, Green rightly points out that selection of items in a particular language is partly a matter of increasing the activation of that language but also a matter of suppressing the activation of items in the other language. To further clarify , during the voluntary use of LA, LB is inhibited by LA. Dy sfluencies will occur in LA whenever there is an LB expression which is more available than its equivalent in LA, e. g., when a concept is more “verbalizable” (Clark/Clark 1977) or “codable” (Brown/Lenneberg 1954) in LB than in LA, or when it has been recently used more frequently . In a bilingual speech mode (Grosjean 1985) the speaker will not attempt to suppress the more readily available expression in the other language, and will switch to that language. In a unilingual mode, however, the expression in the other language cannot be produced, and the speaker will continue the search for an expression in the appropriate language, i. e., the speaker will try to inhibit the response in LB in order to activate that in LA, thus possibly causing some dy sfluency (the same ty pe of dy sfluency would be expected by a unilingual having word-finding difficulty ). This model also accounts for the fact that the time required to name simple objects is greater for trilinguals than for bilingual speakers (Mägiste 1986), as LA must externally suppress the activity of the LC sy stem as well as that of LB. In any case there
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are more competitors to be inhibited (sy nony ms/translation equivalents) in a trilingual than in a bilingual, and in a bilingual than in a unilingual — though a unilingual person with a very extensive lexicon also has more competing items than one with a more limited lexicon. It is interesting to note that Mägiste’s data show some overlap between some unilinguals and bilinguals, possibly reflecting the fact that some unilinguals in the sample may have had very large lexicons, potentially as large as the sum of the two (relatively restricted) lexicons of some bilinguals. (A more complex form of regulation is proposed by Green (1986) in the case of translation. Two kinds of inhibition are postulated: internal inhibition of the sy stem by itself, and external inhibition of the antagonistic sy stem. When one is translating from LB to LA, LB needs to be inhibited internally . This issue will not be considered in the limited space available here.) Within Green’s (1986) framework, which we tentatively adopt here, it is assumed that brain damage may limit the availability of the means both to excite and to inhibit a sy stem. The kinds of output produced depend on the relative balance of the means to excite or inhibit a sy stem. Resources are not available for language in general but independently for each specific language, so that the use of one language does not deplete the resources available to the other language(s). The inhibitory sy stem of each language is thus susceptible to selective impairment. The question that remains unanswered is why the (partially depleted) available resources are sometimes equally distributed among the two languages (as in parallel recovery ), sometimes more in one than in the other (as in differential recovery ), sometimes all in one and none in the other (as in selective recovery ), or sometimes alternating between one and the other (as in successive and antagonistic recovery ). That is, what determines the ty pe of pattern? In addition, in non-parallel cases, why does LA lack resources rather than LB (or vice versa)? On what basis are resources assigned to one language rather than to the other, or on what basis are resources shared equally between them? In addition to the question of means (resource, energy ), there is the question of automatic control: How, and on what basis, does the mechanism that controls the distribution of inhibitory resources function? These two fundamental questions remain unanswered. But
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they can now be rephrased as follows: What factors induce the control mechanism to assign all resources to one language and not the other (instead of distributing them equally ), and why to LA rather than to LB? Inhibitory resources allow the regulation of active sy stems. But what is it that regulates and assigns inhibitory resources? And what assigns them in one way rather than in another (reflecting a specific pattern of recovery ), and once the pattern is determined, what determines that one language rather than another will be allocated more inhibitory resources? The non-recovered language remains active in some bilingual aphasic patients but not in others. That is, either comprehension is retained in the absence of production, or both are unavailable. In cases when not even comprehension is possible in one of the languages (i. e., when that language is not active, in Green’s terms), it may be assumed that the threshold of activation for that language has been raised so high that it even prevents activation from outside stimuli. Indeed, some patients have been reported to have lost access to one of their premorbidly fluent languages to such an extent that it appeared as though they had never been acquainted with it before, not only having lost comprehension, but not even being able to repeat sentences in that language any better than someone who was hearing the language for the first time. While some patterns of recovery are indeed explained yb inhibition/disinhibition phenomena (i. e., the raising and lowering of the activation threshold), it must be conceded that, in some cases, when the neural substrate subserving the grammar has been phy sically destroy ed or surgically removed, the grammar (i. e., linguistic competence, the implicit knowledge of the language) is simply no longer there. It is extremely unlikely , however, that this could result in the loss of only one of the patient’s languages, as there is no evidence that two languages are not subserved by circuits within the same (macro-)anatomical area (i. e., in terms of cubic millimeters), even if we allow for possible micro-anatomical differences (in terms of cubic microns), and a fortiori if the very same neurons are involved, albeit in a different neural network. Green’s model, in conjunction with the activation threshold hy pothesis, offers a reasonable account of how the various observed phenomena can occur. Why one rather any other phenomenon does occur remains to be explained, however. We may hope that the
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assessment of large numbers of bilingual aphasic patients, permitting correlational analy ses of recovery patterns and the numerous linguistic, phy siological and pathological variables, will eventually provide us with sufficient data to arrive at an answer.
5.
The Measure of Deficits
Such a project is underway with the sy stematic collection of data from every nonunilingual aphasic patient seen in various hospitals around the world, using the Bilingual Aphasia Test (BAT). The BAT is currently available in over 60 languages and 100 language pair combinations. The various language versions are not mere translations of each other but transpositions that are as linguistically and culturally equivalent as possible. The criterion of equivalence between the different versions varies with each task. The BAT comprises a questionnaire (Part A) to ascertain the context of acquisition and use and the degree of mastery of each language. It measures performance (Part B) at the level of the word, the sentence and the paragraph. Results are grouped according to skill (comprehension, repetition, judgment, lexical access, propositionizing, reading and writing), as well as to level of linguistic structure (phonology , morphology , sy ntax, lexicon, and semantics). For specific language-pairs (Part C), there are word recognition, translation, and grammaticality judgment tasks. (For a thorough description of the BAT, see Paradis/Libben 1987.)
6.
Conclusion
The data thus collected over the next few y ears should allow us to determine whether the organization of two languages in one brain is a function of the structural distance between the languages concerned, and/or of their context of acquisition and/or use, the relative degree to which they have been mastered, the ty pe of aphasia, the severity of the insult, or of any other variable that has been suspected of play ing a potential role. In addition to answering questions about patterns of recovery , the sy stematic collection of data with the BAT should also eventually give us some indications as to whether two languages are represented in the brain as an extended sy stem, two separate sy stems, a tripartite sy stem, or as two subsy stems of the language system.
7.
References
Albert M. L. & Obler, L. K. (1978). The bilingual brain. New York: Academic Press. Berthier, M. L, Starkstein, S. E, Ly ly k, P., & Leiguarda, R. 1990. Differential recovery of languages in a bilingual patient: A case study using selective amytal test. Brain and Language, 38, 449—453. Bloom, L. (1974). Talking, understanding and thinking. In L. Schiefelbusch & L. Lloy d (Eds.), Language perspectives. Baltimore: University Park Press. Brown, R. & Lenneberg, E. H. (1954). A study in language and cognition. Journal of Abnormal and Social Psychology, 49, 454—62. Clark, H. H. & Clark, E. V. (1977). Psychology and language. New York: Harcourt Brace Jovanovich. Cohen, A. (1989). Attrition in the productive lexicon of two Portuguese third language speakers. Applied Psycholinguistics, 20, 135—147. De Vreese, L., Mota, M., & Toshi, A. (1988). Compulsive and paradoxical translation behaviour in a case of presenile dementia of the Alzheimer ty pe. Journal of Neurolinguistics, 3, 233—259. Florès, C. (1970). Mémoire à court terme et mémoire à long terme. In B. Bovet et collaborateurs, La mémoire. Paris: Presses Universitaires de France. Gloning, I. & Gloning, K. (1965). Aphasien bei Poly glotten. Beitrag zur Dy namik des Sprachabbaus sowie zur Lokalisationsfrage dieser Störungen. Wiener Zeitschrift für Nervenheilkunde, 22, 362—97. (Translated in Paradis 1983, 681—716.) Goldstein, K. (1948). Disturbances of language in poly glot individuals with aphasia. In Language and language disturbances. New York: Grune and Stratton. 138—146. Green, D. (1986). Control, activation, and resource: A framework and a model for the control of speech in bilinguals. Brain and Language, 27, 210—223. Grodzinsky , Y. (1984). The sy ntactic characterization of agrammatism. Cognition, 16, 99—120. Grosjean, F. (1985). The bilingual as a competent but specific speaker-hearer. Journal of Multilingual and Multicultural Development, 6, 467—477. Grosjean, F. & Soares, C. (1986). Processing mixed language: some preliminary findings. In J. Vaid (Ed.), Language processing in bilinguals. 145—17 9. Hillsdale, N. J.: Lawrence Erlbaum Associates. Halpern, L. (1950). Observations on sensory aphasia and its restitution in a Hebrew poly glot. Monatsschrift für Psychiatrie und Neurologie, 119, 156—173. Hegler, C. (1931). Zur Aphasie bei Poly glotten. Deutsche Zeitschrift für Nervenheilkunde, 11 7 , 236—239. (Translated in Paradis 1983, 317—319.)
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Jakobson, R. (1964). General discussion. In A. De Reuck & M. O’Connor (Eds.), Disorders of language. Boston: Little, Brown. Kauders, O. (1929). Über poly glotte Reaktionen bei einer sensorischen Aphasie. Zeitschrift für die gesamte Neurologie und Psychiatrie, 122, 651—666. (Translated in Paradis 1983, 286—300.) Kinzel, P. (1964). Lexical and grammatical interference in the speech of a bilingual child. Seattle: University of Washington Press. Lambert, W. E. & Fillenbaum, S. (1959). A pilot study of aphasia among bilinguals. Canadian Journal of Psychology, 13, 28—34. Lecours, A. R. (1975). Aphasie. In Encyclopédie médico-chirurgicale (système nerveux). Paris: EMC, 17019, ALO 7—1975, 7—26. Leischner, A. (1948). Über die Aphasie der Mehrsprachigen. Archiv für Psychiatrie und Nervenkrankheiten, 180, 731—775. (Translated in Paradis 1983, 456—502.) Leopold, W. (1949). Speech development of a bilingual child. Evanston, III.: Northwestern University Press. L’Hermitte, R., Hécaen, H., Dubois, J., Cuoli, A., & Tabouret-Keller, A. (1966). Le problème de l’aphasie des poly glottes: Remarques sur quelques observations. Neuropsychologia, 4, 315—329. (Translated in Paradis 1983, 727—743.) Luria, A. R. (1973). Two basic kinds of aphasic disorders. Linguistics, 115, 57—66. Luria, A. R. (1974). Basic problems of neurolinguistics. In T. A. Sebeok (Ed.), Current trends in linguistics, vol. 12., 2561—2593. The Hague: Mouton. Luria, A. R. & Hutton, J. T. (1977). A modern assessment of the basic forms of aphasia. Brain and Language, 4, 129—151. Mägiste, E. (1986). Selected issues in second and third language learning., In J. Vaid (Ed.), Language processing in bilinguals. 97 —122. Hillsdale, N. J.: Lawrence Erlbaum Associates. Mendelsohn, S. (1988). Language lateralization in bilinguals: Facts and fantasy . Journal of Neurolinguistics, 3, 261—292. Minkowski, M. (1927). Klinischer Beitrag zur Aphasie bei Poly glotten, speziell im Hinblick aufs Schweizerdeutsche. Schweizer Archiv für Neurologie und Psychiatrie, 21, 43—72. (Translated in Paradis, 1983, 205—232.) Minkowski, M. (1928). Sur un cas d’aphasie chez un poly glotte. Revue Neurologique, 49, 361—366. (Translated in Paradis 1983, 274—279.) Nilipour, R. & Ashay eri, H. (1989). Alternating antagonism between two languages with successive recovery in a third in a trilingual aphasic patient. Brain and Language, 36, 23—48. Obler, L. K. & Albert, M. L. (1977). Influence of
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aging on recovery from aphasia in poly glots. Brain and Language, 4, 460—463. Obler, L. K. & Albert, M. L. (1978). A monitor sy stem for bilingual language processing. In M. Paradis (Ed.), Aspects of bilingualism. Columbia, NC.: Hornbeam Press. Ojemann, G. A. & Whitaker, H. A. 1978. The bilingual brain. Archives of Neurology, 35, 409—412. Ombredane, A. (1951). L’aphasie et l’élaboration de la pensée explicite. Paris: Presses Universitaires de France. Paradis, M. (1977). Bilingualism and aphasia. In H. Whitaker & H. A. Whitaker (Eds.), Studies in neurolinguistics, vol. 3. 65—121. New York: Academic Press. Paradis, M. (1981). Neurolinguistic organization of a bilingual’s two languages. The LACUS Forum, 7 , 486—494. Paradis, M. (Ed.) (1983). Readings on aphasia in bilinguals and polyglots. Montréal: Marcel Didier. Paradis, M. (1984). Aphasie et traduction. Μετα: Translators’ Journal, 29, 57—67. Paradis, M. (1985). On the representation of two languages in one brain. Language Sciences, 7 , 1—39. Paradis, M. (1988). Recent developments in the study of agrammatism: their import for the assessment of bilingual aphasia. Journal of Neurolinguistics, 3, 127—160. Paradis, M. (1989). Bilingual and poly glot aphasia. In F. Boller & J. Grafman (Eds.) Handbook of neuropsychology, vol. 2. 117 —140. Amsterdam: Elsevier. Paradis. M. (1990 a). Language lateralization in bilinguals: Enough already ! Brain and Language, 39, 576—586. Paradis, M. (1990 b). Differential recovery of languages in a bilingual patient following selective amy tal injection: A comment on Berthier et al. (1990). Brain and Language, 39, 469—470. Paradis, M., Goldblum, M.-C., & Abidi, R. (1982). Alternate antagonism with paradoxical translation behavior in two bilingual aphasic patients. Brain and Language, 15, 55—69. Paradis, M. & Goldblum, M.-C. (1989). Selected crossed aphasia in a trilingual aphasic patient followed by reciprocal antagonism. Brain and Language, 36, 62—75. Paradis, M. & Libben, G. (1987). The assessment of bilingual aphasia. Hillsdale, N. J.: LEA. Penfield, W. (1953). A consideration of the neurophy siological mechanism of speech and some educational consequences. Proceedings of the American Academy of Arts and Sciences, 82, 199—214. Penfield W. & Roberts, L. (1959). Speech and brainmechanisms. Princeton, N. J.: Princeton University Press.
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Perecman, E. (1984). Spontaneous translation and language mixing in a poly glot aphasic. Brain and Language, 23, 43—63. Piaget, J. (1970). Mémoire et intelligence. In B. Bovet et collaborateurs, La mémoire. Paris: Presses Universitaires de France. Pick, A. (1921). Zur Erklärung gewisser Ausnahmen von der sogenannten Ribotschen Regel. (Translated in Paradis 1983, 156—168.) Pitres, A. (1895). Etude de l’aphasie chez les poly glottes. Revue de Médecine, 15, 873—899. (Translated in Paradis 1983, 26—49.) Pötzl, O. (1925). Über die parietal bedingte Aphasie und ihren Einfluss auf das Sprechen mehrerer Sprachen. Zeitschrift für die gesamte Neurologie und Psychiatrie, 96, 100—124. (Translated in Paradis 1983, 176—198.) Pötzl, O. (1930). Aphasie und Mehrsprachigkeit. Zeitschrift für die gesamte Neurologie und Psychiatrie, 124, 145—162. (Translated in Paradis 1983, 301—316) Rapport, R. L., Tan, C. T., & Whitaker, H. A. (1983). Language function and dy sfunction among Chinese- and English-speaking poly glots: cortical stimulation, Wada testing, and clinical studies. Brain and Language, 18, 342—366. Ribot, Th. (1881). Les maladies de la mémoire, Paris: G. Baillère. Schulze, H. (1968). Unterschiedliche Rückbildung einer sensorischen und einer ideokinetischen motorischen Aphasie bei einem Poly glotten. Psychiatrie, Neurologie und medizinische Psychologie, 20, 441—445. (Translated in Paradis 1983, 753—760.) Schwalbe, J. (1920). Über die Aphasie bei Poly glotten. Neurologisches Zentralblatt, 39, 265. (Translated in Paradis 1983, 155.)
Scoresby Jackson, R. (1867). Case of aphasia with right hemiplegia. Edinburgh Medical Journal, 12, 696—706. Silverberg, R. & Gordon, H. W. (1979). Differential aphasia in two bilingual individuals. Neurology, 29, 51—55. Smirnov, B. & Faktorovitch, N. (1949). K voprosu ob afazii u poliglotov. Nevropatologiia Psikhiatria, 18, 26—28. (Translated in Paradis 1983, 535—538.) Stengel, E. & Zelmanowicz, J. (1933). Über poly glotte motorische Aphasie. Zeitschrift für die gesamte Neurologie und Psychiatrie, 149, 292—311. (Translated in Paradis 1983, 356—375.) Sträussler, E. (1912). Ein Fall von passagerer sy stematischer Sprachstörung bei einem Pol y glotten, verbunden mit rechtsseitigen transitorischen Gehörshalluzinationen. Zeitschrift für die gesamte Neurologie und Psychiatrie, 9, 503—511. (Translated in Paradis 1983, 94—101.) Tarone, E. (1974). Speech perception in second language acquisition: A suggested model. Language Learning, 24, 223—233. Tremaine, R. V. (1975). Syntax and Piagetian operational thought. Washington, D. C.: Georgetown University Press. Vey rac, G.-J. (1931). Etude de l’aphasie chez les sujets poly glottes. Thèse pour le doctorat en médecine, Université de Paris. (Translated in Paradis 1983, 320—338.) Weisenburg, Th. & McBride, K. 1935. Aphasia: A clinical and psy chological study . New York: Hofner (case 4, 160—182) (Translated in Paradis 1983, 376.) Zangwill, O. L. (1979). Two cases of crossed aphasia in dextrals. Neuropsychologia, 17, 167—172.
Michel Paradis, Montréal, Québec (Canada)
25. Communicative Behavior in Aphasia 1. 2. 3. 4. 5.
1.
Introduction Review of the Experimental Evidence Clinical Implications General Conclusions References
Introduction
Language use has considerably improved the communicative ability of human beings and in a first approximation, one may presume that under its diverse forms, aphasia necessarily entails an impairment in the capacity to interact with other people. This intuition
does not follow sound reasoning rules, however, and it deserves several qualifications. Communication is not limited to language. Animals, infants, as well as normal adult subjects are endowed with a wealth of devices enabling social exchanges yb nonverbal means. Inversely , some uses of language are not directed toward a social partner. Internal speech, for instance, may serve self-regulatory or mnemonic functions. Speech impairments as assessed in aphasia examinations are ty pically observed in tasks like confrontation naming whose aim is to elicit expected standard responses, not to test the capability to
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perform the speech act of reference appropriately . Thus, one may wonder whether aphasic subjects retain communicative skills and more particularly , whether they compensate for language disorders by nonverbal behavior. The alternative hy pothesis assumes a supramodal impairment which may concern various aspects of communication (see discussions in Feyereisen 1988; 1991). Communication and language processing involve several components which may be selectively impaired in cases of brain damage. Current models of information processing attempt to describe these components by breaking down complex behavior into elementary operations. Discussing the details of these models is bey ond the scope of this chapter but some critical features of the information processing approach to language may nevertheless be stressed. First, in keeping with the distinction between several components of verbal behavior, multiple forms of aphasia can be described in addition to cases of global aphasia in which all the aspects of language processing are impaired. Accordingly , the term ‚aphasia’ should not be used in the singular form; instead the heterogeneity of the pathologies should be considered (Caramazza 1986; Shallice 1988). Second, language impairments of diverse kinds have different consequences for communication. For the sake of clarity , it is convenient to distinguish between the processes of comprehension and production though they are narrowly linked in natural use of language. Thus, communication may be analy zed into modality -specific components, dealing with input and output processing and with verbal and nonverbal information. Furthermore, during comprehension, different pieces of knowledge are identified and progressively integrated within the conceptual sy stem. For instance, speech understanding involves sublexical processes, word recognition, and semantic activation. Expression relies on operations of a different nature. The intention of the message is activated within the conceptual sy stem, the modality is selected and the form is gradually specified in relation to contextual constraints. There are thus ‚central’ operations dealing with the meaning of the message and more domain-specific processes involved in categorical perception of various classes of stimuli and motor control of various responses. At least in some aphasic subjects, the central cognitive sy stem is spared, thus leaving com-
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munication to rely on intact conceptual processing. For instance, ability to repeat and to understand verbal material is retained in certain patients with anomia, who consequently are less impaired in communication than patients suffering from impairments of the semantic memory . In other cases, written and oral language processing may dissociate. Similarly , unless they suffer from ideomotor apraxia or pantomime agnosia, aphasics may use gestures in order to communicate. Accordingly , ability to process different kinds of verbal and nonverbal information must be assessed empirically on an individual basis and cannot be inferred from, for example, lesion localization or associated deficits. The impaired components of the communication sy stem may nevertheless function with a reduced efficiency . Not every component of an information-processing sy stem works in an all-or-nothing way , but it may operate at vary ing levels of efficiency . Thus, some residual abilities may be retained even in the domain of the impairment. For example, anomic speakers may still have access to the most frequent lexical items and agrammatic subjects may be able to process simple sy ntactic structures. Likewise, in comprehension tasks, aphasic subjects can often respond correctly to some stimuli and incorrectly to others. Furthermore, some automatic processing may be spared even when more controlled access to information is disturbed (see a recent demonstration by Chenery /Ingram/ Murdoch 1990). Thus, language use is not completely abolished by left-hemisphere lesions. Different tasks, as defined by the input to and the output from the sy stem, may be impaired at various degrees because they are more or less demanding. To use an insightful analogy , the term ‚resource’ has been borrowed from microeconomics to name these task demands. In cognitive psy chology , this term refers to attention, to controlled processing, or to load in working memory , all notions that refer to the means the subject can devote to the task. An alternative account assumes data limitations and thus, variations of performance in relation to characteristics of input that may be degraded or, to the contrary , enriched. Then, task difficulty may depend on resource-limited and data-limited processes. Parallelly , severity of aphasia may be characterized either by variation in the amount of resource or data available for a given task (for a related discussion, see Shallice 1988, Chapter 10).
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In order to communicate, aphasic subjects have to adapt to resource limitations and input degradation, and in this respect, communication involves problem solving. Besides compensations which use the spared components of the sy stem, other communicative strategies exploit the residual capacity of the impaired mechanisms and result in performance that demands fewer resources. Multiple routes exist from an idea to its expression and, for instance, a periphrase may convey the same meaning as a precise term. Sentence production results from the selection of a particular frame among alternative way s to express a propositional content. This selection is influenced by contextual constraints since some circumstances require more or less elaborate formulations. The activation of a surface form is also sensitive to contextual influences of a different nature, and on another level, the motor execution of the utterance necessitates local accomodations, too. Thus, if a formulation is momentarily unavailable, it is possible to adapt using other methods. Strategic use of linguistic devices like ellipsis, anaphora, or paraphrase allows the aphasic speaker to by pass lexical and sy ntactic impairments. Especially agrammatism has been interpreted from such a perspective (Kolk/ Heeschen 1990). Similarly , there are several contributions to the activation of the meaning of a spoken utterance. Language comprehension is achieved by the interaction of several sources, input processing (phonological analy sis, word recognition, sy ntactic parsing) and inferential, integrative procedures. Thus, residual speech comprehension can not only be explained by intact conceptual processing, but also by reduced processing demands and by contextual influences when multiple sources of information, verbal and nonverbal, combine. Communication is a collaborative process between at least two subjects. Current models of conversation stress the need for cooperation between different partners to achieve mutual understanding (see e. g. Clark/Schaefer 1989). The normal partner may assist the aphasic subject by supply ing missing words, by requesting confirmation, or by asking y esno questions. Rate of speech, intonation, lexical selection and mean length of utterance can be adapted to the assumed residual capabilities of the disabled speech partner. Furthermore, ill-formed utterances like telegraphic speech or phonetic and phonemic paraphasias may nevertheless be interpreted.
Thus, communicative effectiveness of aphasic subjects sometimes depends on support by an attentive health y listener. Communication also results from a matter of convention. Familiarity with the partner allows the use of simpler or shorter forms because previous experience supplies further, implicit information to the message. The spouse and after some time, the speech therapist of the aphasic subject probably gain some expertise in dealing with distorted utterances. Reciprocally , one may wonder whether aphasic subjects benefit from repeated exposures to situations of communication. Overview. These diverse elements of discussion make the treatment of the issue of ‚communication and aphasia’ more complex. Several accounts of the impairments in communication and of the spared communicative ability of aphasic subjects are made possible. From a structural point of view, selective impairments which spare the nonverbal modalities or some components of the verbal information processing sy stem can be described. More particularly , if the central cognitive processes are intact, the subject will remain able to use ency clopaedic and social knowledge for the purpose of communication. From a dy namic perspective, the development of compensatory , heuristic stategies can be described as adaptations to a reduction of processing resources and impoverishment of input, or resulting from reliance on a healthy partner. In the next section, experimental literature on the communicative behavior of aphasic subjects, first in its receptive, then in its expressive aspects, will be reviewed in relation to the theoretical issues raised in this introduction. Due to space limitations, this review will focus on those recent studies, not treated in the chapter by Foldi/Cicone/Gardner (1983). In a final section, the clinical implications of these findings will be discussed, as far as assessment and rehabilitation of aphasia are concerned.
2.
Review of the Experimental Evidence
2.1. Comprehension Do comprehension disorders in aphasia result from selective impairments of verbal information processing or from a more general deficit which also affects other modalities? Does the nonverbal context facilitate understanding of speech? Does grasping the inten-
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tion of a message dissociate from presemantic processing like phonological analy sis? Unfortunately , these questions have not y et elicited studies on comprehension in interactive situations and on on-line processing of speech. The main evidence available results from experiments dealing with metacommunicative abilities and, in that domain, with the processing of prosody and gestures, among the multiple cues that may facilitate speech comprehension. 2.1.1. Nonverbal Comprehension in Aphasia 2.1.1.1. Auditory Processing Most studies on the reception of vocal cues by brain-damaged subjects were conducted upon the assumption of a right-hemisphere dominance in the processing of emotion and of the nonpropositional aspects of speech. Right-hemisphere damaged subjects may be impaired in several tasks that require prosody to be processed such as voice recognition, perception of linguistic stress and interrogation marks, and comprehension of emotional expressions. However, some left-hemisphere damaged subjects are also impaired in the processing of affective and nonaffective prosody , often in relation to disorders in spokenlanguage comprehension. These data converge with the results of dichotic listening studies in normal subjects to show that both hemispheres contribute to prosody processing. It does not mean that the left and the right parts of brain are equally sensitive to the same components of the auditory input. However, the characteristics of the signal for the processing of which one cerebral region is specialized remain to be identified (see, e. g., Hartje/Willmes/Weniger 1985; Heilman/Bowers/Speedie/Coslett 1984; Tompkins/Flowers 1985; for a review, see Van Lancker 1987). 2.1.1.2. Visual Processing Several studies reported impairments in the perception of facial expressions of emotions in aphasic as compared to normal subjects though in this domain, right hemispheredamaged subjects are often even more severely impaired (for reviews, see Fey ereisen 1986; 1989). Likewise, in gesture-to-picture matching tasks, aphasics perform worse than control subjects, and the extent of the deficit correlates with the severity of naming and auditory comprehension deficits (see e. g., Duff y /Duff y 1981; Rothi/Heilman/Watson
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1985; Fey ereisen 1988 for a review). The most frequent error involves the choice of a picture that has something in common with the correct response. Thus, impaired aphasics understand a part of the meaning of the gesture but not enough to discriminate related concepts (Duffy /Watkins 1984; Varney /Benton 1982). Similarly , impaired subjects can understand some gestures, while failing to understand others (e. g., Daniloff/Noll/Fristoe/ Lloy d 1982; Netsu/Marquardt 1984). Thus, aphasic subjects show similar impairments in the processing of vocal and gestural signals and in the processing of words and pictures in semantic decision or categorization tasks. But, although the existence of nonverbal disorders after left-hemisphere damage is not controverted, the problem remains to identify the impaired mechanism in relation to a model of the operations involved in the task. More particularly , the deficit could involve central semantic processes or result from the association of several modality -specific impairments affecting the presemantic encoding operations. Progress in the neuropsy chological analy sis of nonverbal comprehension is likely to be made from detailed single case studies. Modality -specificity of some disorders is suggested by the observation of impaired discrimination and comprehension of gestures in left-hemisphere damaged subjects without speech comprehension deficits (Rothi/Mack/Heilman 1986). Cases showing the inverse dissociation were also mentioned in some group studies (Varney 1982; Varney / Damasio/Adler 1989). Retained comprehension of gestures when speech comprehension is impaired might relate to similar dissociations between written and spoken language processing. 2.1.2. Integration of Verbal and Nonverbal Information 2.1.2.1. Auditory Information Several vocal cues may facilitate speech comprehension in aphasia. In a word monitoring task, stressed words were responded to faster than unstressed ones (Swinney /Zurif/Cutler 1980). Aphasic subjects suffering from mild or moderate comprehension disorders also performed better in answering y es-no questions when the critical information was emphasized by intonation (Kimelman/Mc Neil 1987). Another kind of interaction between verbal and nonverbal comprehension was demonstrated in experiments bearing on the
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comprehension of emotional cues. When the verbal content itself convey ed affective meaning, left-hemisphere damaged like control subjects performed better if intonation and meaning were congruent and worse when the message was incongruent (Bowers/Coslett/ Bauer et al. 1987; Seron/Van der Kaa/Van der Linden/Remits/Fe y ereisen 1982; Tompkins/ Flowers 1987). 2.1.2.2. Auditory and Visual Information: In the recent y ears, the interaction of visual and auditory information during lip reading has been analy zed mainly in cases of word meaning deafness who, ty pically , have no problem in understanding written language (Campbell/Garwood/Franklin et al. 1990; Shindo/Kaga/Tanaka 1991). Likewise, little or nothing is known about the visual processing of pictorial or actual scenes during sentence comprehension. However, illustrations have been shown to facilitate speech processing in some experimental tasks. In the verification of sentences like a fish is smaller than a whale, the presentation of pictures showing the two arguments reduced the number of errors, even when the verification bore on a less picturable property such as weight (Nicholas/Brookshire 1981). Pictures as well as verbal contexts also facilitated answering questions about sentences but the contextual influences were qualified by interactions with subject and sentence characteristics (Pierce/ Beekman 1985). Reciprocally , semantic decisions about pictures were more accurate when a written word cued the relevant semantic feature (Koemeda-Lutz/Cohen/Meier 1987). Thus, aphasic subjects may benefit from the redundancy of verbal and pictorial information or from focussing of attention on critical aspects of the task. There are few comparable studies on the influence of the gestural context. Better performances in object manipulation tasks after gestural than after oral instructions might simply reflect advantages of imitation over verbal request in the control of motor activity (see, e. g., Beukelman/Yorkston/Waugh 1980). Only two studies have experimentally examined the facilitation of auditory comprehension by gestural cues in word-to-picture matching tasks. Venus/Canter (1987) did not find aphasic subjects performing better in processing words with a concurring gestural cue than in control conditions. This result, however, stems from an analy sis of a group
performance and the gestural context may facilitate speech comprehension in specific cases. In the other study , greater attention was paid to the description of comprehension disorders in the individual aphasic subjects (Fey ereisen/Hazan 1991; see also a summary report in Fey ereisen 1991). However, no case of dissociation between visual and auditory comprehension was present in the group and no specific effect of gestural facilitation was observed. 2.1.3. Heuristic Procedures in Speech Comprehension: the Use of “Context” In a word recognition task, phonemic errors are more frequent when the target word is part of a sentence with an incongruous meaning (Beck 1984). Interactive models of speech comprehension may account for such a result by assuming retroactive influence of semantic activation on speech perception. Similarly , in spoken sentence-to-picture matching tasks, partial processing of content words and of visual, nonverbal information probably activates general knowledge of the world on which the subjects rely on for their responses. Sentences that describe highly improbable events are ty pically more difficult to understand than those which respect semantic rules of selection or common sense. A bias toward the correct understanding of metaphors instead of their literal interpretation may probably be explained in the same way : presented with several possible responses corresponding to different events, aphasic subjects would adopt the general strategy of selecting the most plausible alternative (see, e. g., Caramazza/Zurif 1976; Deloche/Seron 1981; Huber 1990; see also discussions in Caramazza 1988; Grodzinsk y /Marek 1988; Sherman/ Schweickert 1989). A different account of residual comprehension is proposed by Van Lancker (1987) who suggested that different processes may underlie sentence comprehension. Some aphasic subjects would recognize overlearned, familiar sentences as a whole in the same way single words are processed whereas right brain-damaged subjects would parse the sentence into its constituents. As a result, a double dissociation is demonstrated in the processing of idioms like while the cat’s away, the mice will play and of quite novel sentences that require analy sis (Van Lancker/Kempler 1987). Performances in the comprehension of frozen metaphors that are presented out of context
25. Communicative Behavior in Aphasia
may be explained in the same way . From a slightly different perspective, one may also assume that aphasic subjects would have access to the connotative meaning of the lexical items. They would therefore be able to identify the appropriate meaning of potentially ambiguous metaphors (Brownell 1988; Brownell/Simpson/Bihrle et al. 1990). Still other mechanisms are demonstrated with different experimental procedures. In a task of answering questions about directly stated or indirectly suggested items, no difference was observed in relation to the nature of the response and thus, aphasic subjects were shown able to infer information from the sentential context (Brookshire/Nicholas 1984). Their comprehension of sentences was also facilitated by a narrative context by which some constituents were cued, even if this context did not allow a prediction of the event described in the sentence (Hough/ Pierce/Cannito 1989). These compensatory strategies present shortcomings, however, because there are circumstances in which guessing leads to error. For example, ‚prestimulation’, i. e. giving some elements of a sentence before the complete sentence itself, did not affect the number of correct choices among related pictures when all the proposed pictures showed primed items along with distractors (Waller/Darley 1979). Predictibility of a word from context also increased the probability of making semantic errors in answering questions about this word (Pierce/ De Stefano 1987). Heuristic procedures, which aphasic subjects employ to fill in some gaps in comprehension, have mainly been studied for indirect speech acts and linguistic indicators of implicit attitudes (for a more extensive review, see Weylman/Brownell/Gardner 1988). 2.1.3.1. The Comprehension of Indirect Requests The first experimental demonstration of access to contextually convey ed meaning by aphasic subjects was provided in the study of Wilcox/Davis/Leonard (1978). Subjects were presented short videotaped segments in which two characters interacted. One uttered a sentence of the form Will you open the door? or Must you bite the pen?. The other behaved either in an appropriate way , by doing or stopping to do something, or in an inappropriate way . The task was to answer y es or no in accordance to the appropriateness of this behavior. As a group, aphasic subjects with
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high scores in standard tests of auditory comprehension performed better than subjects with low scores and, on the whole, the correlation between the experimental result and the clinical assessment was significant. However, the subjects’ performance was found much better in the experimental task than in comprehension testing. The worse score was 74% of correct responses, much higher than the chance level of 50%. Furthermore, performances were influenced by the presented material. Two variables interacted, sentence formulation and behavior appropriateness. The subjects were globally more often correct when judging a request to do something than to stop something, and in this case, when judging the continuation of action inappropriate rather than its requested cessation appropriate. Thus, the major difficulty was in approving the stopping of an undesirable activity . A plausible interpretation of this result is that subjects were mainly influenced by congruity of action in context and the nonverbal reactions of the speaker but not by the adequacy of the behavior to the verbally expressed request. In that sense, aphasic subjects might have direct access to the intended meaning as infered from context without processing the literal meaning of the verbal message. That hy pothesis was supported in another study using a similar procedure. Sentences of the kind Can you ... were presented either as requests or as questions, i. e. in contexts from which either the performance of the appropriate action or the answer yes was expected. In a sample of five ‚anterior’ aphasics, subjects were found unable to process the literal meaning of the questions, and they were more often correct in inferring the intended meaning of requests, probably from the nonverbal context (Hirst/Ledoux/Stein 1984). Further studies did not use videotapes in their procedures, so the influence of the nonverbal context was reduced. Hence, a different conclusion was drawn and the comprehension was found to be more influenced by linguistic processing than in the previous experiments. Foldi (1987) had subjects rate the likelihood of different dialogs; the verbal responses were illustrated by pictures. Left brain-damaged subjects gave more appropriate responses than right brain-damaged subjects but in the two groups, understanding an indirect request was more difficult than processing direct commands or wh-questions. In another study , only a verbal material was presented and sub-
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jects had to identify the most appropriate answer to a verbal request. Aphasic subjects were more often correct, when the context suggested that the literal meaning of the sentence was intended. They were also influenced by the surface form of the questions, and more often correct when the conventional formulations Can you or Could you were used than with sentences like Is it possible for you ... or Are you able ... (Wey lman/Brownell/ Roman/Gardner 1989). 2.1.3.2. Processing the Indicators of Implicit Attitudes The use of many lexical items relies on pragmatic, context-dependent decisions. For instance, the definite article the is appropriate when the referent is unique in nature, is specified in the remainder of the sentence, or has been mentioned previously . By choosing such a form, the speaker assumes the partner may know something about the referent. Otherwise, the undefinite form a is prefered. Sentences that obey appropriateness rules are ty pically easier to understand than other ones. For example, in front of a sample array of one square and two circles, normal subjects are expected to take longer time to respond to a request like Take the round one than to that in which the undefinite article is used. Furthermore, in that situation, subjects are expected to reduce the ambiguity of the sentence by rely ing on another, nonnamed dimension like the colour of the figure and to select the round figure that is unique to this respect. This pattern of performance was observed in anomic subjects without comprehension disorders but not in other aphasic subjects (Goodenough/Zurif/Weintraub 1977). In these controlled conditions, linguistic impairments prevented access to the implicit meaning of the message because the data for the inference process were limited. A similar conclusion was reached in another experiment. In several respects, sentence comprehension requires reliance on some knowledge shared by the partners. This is also the case with the processing of adverbs like even, also, and mainly used in explicit statements by which some other part of the information is implicitly convey ed. For instance, the sentence Even Alice came refers both to the Alices’s presence and to its somewhat unexpected character, i. e. a propositional attitude assumed by both the speaker and the listener toward the stated fact. In an experimental situation, nonverbal communication may be
prevented and the implicit attitude may be expressed by the surface form of the sentence only . One may thus predict that aphasic subjects who are impaired in the processing of these parts of speech will also be unable to decide about the contextual appropriateness of sentences using words of that class. That hy pothesis was tested in a sentence-to-picture matching task (Hupet/Seron/Frederix 1986). The sentences refered to the color of a figure and the pictures, actually simple rectangles, varied by the number and the size of parts of different colors. Several patterns of performance were observed. Some aphasics behaved like normal subjects whereas other aphasics did not process the adverb and generally selected the figure with the largest surface of the asserted color. Finally , a third subset of aphasic subjects selected a rectangle with a high amount of the asserted color but not necessarily the highest. They were thus appropriate with the sentences using mainly, but not with even sentences. These performances did not sy stematically relate to aphasia ty pe but it is now clear than even within a selected sample of so-called agrammatic patients, a great heterogeneity exists in the processing of the function words. Some agrammatic subjects have no comprehension problems and others may be impaired in the comprehension of some function words only. 2.1.4. Conclusions The several possible accounts of residual comprehension in aphasia do not receive equal support from the literature. Experimental studies do not offer compelling evidence in favour of the nonverbal compensation hy pothesis. However, nonverbal deficites do only concern a subgroup of the aphasic population and their assessment remains an empirical matter, preferably in detailed analy ses of single cases. Another hy pothesis has been the dissociation of pragmatic and linguistic domains, perhaps in relation to different competencies of the right and left cerebral hemispheres in each of these functions. However, if we can admit the possibility that communicative skills may be impaired in cases of brain damage without aphasia, it is much more difficult to understand how aphasic subjects could obtain direct access the speaker’s intention without processing of the message linguistically . Actually , some residual verbal ability is needed and this favors explanations in terms of processing resource. Such an account is also consistent with the frequent su-
25. Communicative Behavior in Aphasia
periority of receptive abilities over expressive ones if we consider that responses in comprehension tasks are less demanding with regard to number of alternatives or complexity of execution. 2.2. Expression 2.2.1. Channel Use in Communication: Speech, Vocalizations and Gestures From current models of information processing, it may be predicted that a breakdown of the central, conceptual sy stem should impair communication in different modalities whereas more specific disorders like an inability to access a word form from its semantic activation may spare nonverbal expression. Accordingly , expressive skills must be assessed empirically in brain-damaged subjects whose drawing, gesturing, writing, and speaking abilities may be impaired to different extent (see, e. g., Gainotti/Silveri/Villa/Caltagirone 1984; Grossman 1988). A great interindividual variability and the specificity of the different nonverbal modalities (that is their independence from language processing) can explain why , for instance, contradictory findings have been reported about the expression of emotion by aphasic subjects in the vocal and facial channels (Borod/Koff/PerlmanLorch/Nicholas 1985 and 1986; Mammucari/ Caltagirone/Ekman et al. 1988; Ry alls/Behrens 1988). From such a perspective, how should one approach the question as to whether aphasic subjects show similar impairments in performing conversational gestures, as in naming, and in apraxia examination? From some pilot studies, it was concluded that linguistic and gestural abilities dissolve simultaneously in aphasia and that left-hemisphere lesions disrupt communication both in the verbal and the gestural modality (e. g. Glosser/Wiener/ Kaplan 1986; see discussions in Fey ereisen 1987; 1991; Mc Neill 1985; 1987; 1989). However, other studies contradicted these observations and aphasic subjects were found to display higher manual activity than normal control subjects. Highest gesture rates have been observed either in nonfluent or in fluent aphasics. Proportion of representational gestures was usually higher in nonfluent aphasics but these subjects sometimes performed more batonic (i. e., nonrepresentational) gestures than fluent aphasics (Fe y ereisen 1983; Le May /David/Thomas 1988; Smith 1987 a, b). In a heterogeneous group of 11 aphasics,
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appropriate usage of gestures did not relate to measures of verbal skills but fluent aphasics tended to perform gestures which supported oral expression while nonfluent aphasics more often substituted gestures for verbal communication (Behrmann/Penn 1984). In another study , higher reliance on gestural mode of communication was observed in severe nonfluent aphasics (Broca’s and global aphasics) as compared to their normal partners and during referential communication task, more gestures were performed by the more severely impaired aphasics whose residual language was less efficient (Fey ereisen/ Barter/Goossens/Clerebaut 1988; Herrmann/ Reichle/Lucius-Hoene et al. 1988). Furthermore, there is some evidence that aphasic subjects control their gestural behavior in relation to communication functions since fewer gestures were performed when visual access to the partner was prevented (Glosser/ Wiener/Kaplan 1988). In summary , only one study has shown reduced gestural activity in aphasics as compared to control (Glosser/Wiener/Kaplan 1986) while several others have shown increased gestural activity in cases of language impairment. Actually , very different patterns of association between gestures and speech may be found in a heterogeneous sample of aphasic subjects and this variability does not relate to speech characteristics like fluency or use of content words. Furthermore, variability also exists among normal subjects who sometimes perform no hand gesture while speaking. Due to the lack of constraints on gestural performance, ‚errors’ cannot be easily identified in brain-damaged subjects. For these different reasons, greatest insight is expected from single cases studies undertaken in more controlled situation than natural conversations y (Fe ereisen/Bouchat/Dér y /Ruiz 1990). 2.2.2. The Role of Context 2.2.2.1. Cueing In normal subjects, the selection of sy ntactic forms and of the lexical items can be influenced by the sentences previously heard or spoken and by associations to this material (see e. g. Bock 1987). This clarifies the common clinical experience that oral performances of aphasic subjects may be improved by contextual cues. For instance, providing open ended sentences increases the proportion of correct naming of pictures (Pease/
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Goodglass 1978). Nevertheless, there is little experimental evidence that speech production is less impaired in natural settings than during out-of-context formal examinations. Semantic priming has been demonstrated in lexical decision task but not in naming tasks. Semantic cues such as priming the word camel with complete sentences like it lives in the desert or it carries heavy loads are generally less effective than a phonemic cue (e. g. Li/ Williams 1990). Similarly , presenting pictures of objects in their functional context or among items of the same semantic category did not significantly facilitate naming whereas objects integrated in composite pictures but without strong semantic links are more often correctly named than isolated objects, at least in some subjects (Hatfield/Howard/Barber et al. 1977; Seron/Monsel/Van der Kaa et al. 1980; Williams/Canter 1982; 1987). It must be emphasized, however, that priming effects were often qualified by interactions with aphasia subty pe and that, any way , large individual differences are observed in the ability to take advantage of the primes. Accordingly , contextual facilitation might better be demonstrated in single-cases than in heterogeneous samples (see e. g. Zingeser/Berndt 1988). 2.2.2.2. Topicalization During sentence production, the speakers select lexical items and sy ntactic frames in function of assumption about the knowledge shared by their partners. Mental dispositions are infered from the situation, from previous interactions, or from the content of the preceding utterances. These presuppositions shape the surface structure of the sentence: use of the definite/indefinite article, pronominalization, word order in active, passive, and cleft sentence, etc. One study dealt with these aspects of sentence production in aphasia (Bates/Hanby /Zurif 1983). Ten subjects (five Broca’s and five Wernicke’s aphasics) were given nine series of three pictures to be verbally described. In each array , only one element, for instance, the agent of the action, varied and the other remained constant. Similar to normal subjects, aphasics increased lexicalization for the variable information and ellipsis for the constant elements. The aphasics also used the definite article more often with the constant term. In contrast, pronominalization was little affected by pragmatic constraints. These results were replicated in a crosslinguistic study (e. g. Wulfeck/Bates/
Juarez et al. 1989). 2.2.3. Communicative Effectiveness and Compensatory Strategies The referential communication task provides an experimental model by which the structure, the development, and the breakdown of conversation skills may be analy zed (Clark/ Wilkes-Gibbs 1986; Krauss/Glucksberg 1977). Two subjects are given similar array s of pictures and are instructed to communicate in the most convenient way in order to arrange the pictures in the same way or to identify the same target picture. Performance is assessed based on speed and accuracy rather than by formal criteria like sentence structure or lexical diversity . This procedure was used in several studies with aphasic subjects. The main result was that these subjects generally succeeded in the task despite their verbal impairments and thus, communicative effectiveness was demonstrated in that population (Busch/Brookshire/Nicholas 1988; y Fe ereisen/Barter/Goossens/Clerebaut 1988; Meuse/Marquardt 1985). Several aspects of the task have to be taken into account in order to qualify that conclusion. First, peculiarities of task requirements must be underlined. In order to communicate, the subject has to give some cues in order to pinpoint the referent among the distractors. Gestures, onomatopoeias, phonemic approximations, or periphrases may be used, all responses that would be considered incorrect in a naming task. Likewise, gestures that are rated as poor performances in apraxia examination may nevertheless be efficient in the referential task (Fey ereisen/Barter/Goossens/ Clerebaut 1988). Second, the pictures presented in the task define a common ground of knowledge and limit the range of possible meanings of the message. It should be easier to find the best match between the provided cues and the different pictures than to identify a referent without any context. However, experimental support for such a hy pothesis is still lacking. Third, communication requires a cooperative partner who may facilitate the transmission of information by asking y es-no questions, by commenting on possible confusions, and by suggesting appropriate formulations. This dimension of the performance remains to be sy stematically controlled by comparing expert and nonexpert partner or by providing different kinds of model and feedback to the aphasic subject.
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2.2.4. Conclusions If “aphasics communicate better than they speak”, which theoretical proposal can account for spared communicative ability despite impaired verbal expression? One suggestion is that to some extent, nonverbal devices may supply alternative means of expression. Another explanation is the reliance on contextual influences which facilitate speech production in interactive situations, as compared to the formal setting of aphasia examination. However, there is no clear demonstration of independence between verbal and nonverbal modalities of communication nor is there firm experimental evidence supporting the contextual facilitation hy pothesis on the aphasic population level. Actually , in many cases of aphasia, verbal and nonverbal behavior is impaired by motor and cognitive deficits, but gestural expression is less severely disturbed than oral expression. Thus, the best explanation for the residual capacities of severe aphasic subjects seems to be the reduced task demand to produce understandable messages. First, to express oneself is less difficult than to produce the specific form required in aphasia or apraxia examination; second, manual signs are probably relatively easier to perform than the verbal ones and third, the partner is contributing to dialogue.
3.
Clinical Implications
Experimental studies on communication in aphasia have renewed the clinical approach to aphasic subjects by suggesting higher consideration than in the past of the pragmatic aspects in language assessment and therapy. 3.1. Assessment Unlike thought disorders manifested in schizophrenia and senile dementia, aphasia is usually assumed to spare the highest-level mechanisms concerning the message elaboration and reception and to impair only the instruments of communication. It remains useful, however, to evaluate the incidence of these instrumental deficits on social interactions because communication problems may be the greatest cause of suffering in aphasic subjects and their main motivation to undergo a rehabilitation process. Questionnaires about the complains of brain-damaged patients and about their functionning in home environment signal needs for help in several domains and thus, reliance on communicating with
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health y partners (Shewan/Cameron 1984; Smith 1985). Three kinds of procedure have been proposed to assess communicative ability of aphasic subjects. 3.1.1. Naturalistic Observations Holland (1982) trained observers to note in a reliable way instances of behavior like “asking questions” and “using spatial indicators” by aphasic subjects in their home environment. Most of these communicative acts were found successful. However, aphasic subjects differed in the amount of communication attempted and in the proportion of failures. Auditory comprehension disorders especially resulted in inappropriate behavior. 3.1.2. Role Playing Aphasic subjects might avoid situations in which they encounter difficulties and thus, it is useful to elicit communicative acts in a greater variety of situations than those observed at home. Communicative competence may be assessed in simulations of daily -life interactions (Blomert/Koster/Van Mier/Kean 1987). The performance of control subjects indicates what is expected from the situation. For instance, in front of a ticket counter at the station, a ‚request’ with the mention of the destination is a necessary component of the appropriate behavior. The precision “second class” may be optional. In the sample studied by Blomert et al., aphasic subjects were found to produce the necessary information normally but less than control subjects the non-essential components. These performances were largely independent from assessment of speech in standard aphasia testing. 3.1.3. Rating Scales and Checklists From the literature on pragmatics, Prutting/ Kirchner (1987) compiled a list of 30 items, which therapists rated for appropriateness based on their observation of spontaneous communication. The list bears on verbal and nonverbal aspects of communication like “maintaining the coherence of topic across the discourse” and “using gestures to support, complement, or replace verbal behavior”. In a sample of 11 left brain-damaged subjects, some parameters like phy sical distance and mutual gaze between the partners were never found inappropriate whereas all subjects were inappropriate in specificity and accuracy of their vocabulary . Another list of 16 items was
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proposed by Lomas/Pichard/Bester et al. (1989) from direct observations of performances in daily life. The patients’ spouses or other familiar people were asked to rate the subject’s ability at different activities like “getting somebody ’s attention” and “communicating his/her emotion”. In another approach to communicative skills in aphasia, subjects were rated on their responses to 20 questions of a standardized interview. One scale dealt with the adequacy of each response and another with the strategy used by the subject (using compensatory paraverbal or nonverbal behavior, asking support, etc.). These performances correlated only moderately with the results of the aphasia examination and non-significantly with the results of the Token test (Herrmann/Koch/Johannsen-Horbach/Wallesch 1989). Copeland’s (1989) Conversation Assessment focussed on 20 speech functions like requesting, agreeing, warning, etc. Prompts were prepared to elicit these speech acts during a 15 minute conversation with the subject. Each function was rated on a five-point rating scale. More specific scales were also proposed, for example, about the spontaneous gestural behavior as estimated by people involved with the aphasic subject. However, the validity of the instrument remains to be assessed by relating these clinical ratings to the actual performances of the subject (Borod/Fitzpatrick/Helm-Estabrooks/Goodglass 1989). 3.2. Therapy 3.2.1. Nonvocal Rehabilitation Techniques Attempts to teach nonvocal communication sy stems in aphasia therapy have a long history . In one direction, artificial ‚languages’ using icons or geometric forms were devised to meet the main communication needs of the subject. These methods are now becoming more sophisticated through the increased availability of microcomputers and the development of programs by which use visual sy stems. They may be helpful for global aphasics who have not retained any expressive means (see, e. g. Steele/Weinrich/Wertz et al. 1989). In another direction, aphasic subjects are trained to use manual sy stems like the American Sign Language or the Amerind. An apparent paradox in these techniques is that they rely on nonverbal abilities which are often impaired in cases of aphasia. Sign acquisition in speechless subjects may be explained, however, if one considers that per-
forming a gesture is less difficult than uttering the corresponding message vocally . A support for such a suggestion can be found in the analy sis of individual differences. To some degree of severity of the language impairment, manual signs may still be learned whereas spoken words do not (see e. g. Coelho/Duffy 1987; 1990). Another evidence stems from the analy sis of sign characteristics like transparency , iconicity , and motor complexity . Even in the gestural modality , some signs are more easily acquired than others (Coelho/Duffy 1986; Daniloff/Fritelli/Buckingham et al. 1986; for reviews, see Christopoulou/Bonvillian 1985; Helm-Estabrook/Emery 1988; Peterson/Kirshner 1981; Rowley 1983). A crucial issue in devising a nonverbal communication sy stem is to evaluate the benefit of the training against its cost for the patient and the healthy partners. From such a point of view, learning a more efficient use of residual verbal abilities may be less expensive if the same objectives can be achieved. This problem was sy stematically addressed by Funnell/Allport (1989) in a study on the use of Blissy mbolics, a visual logographic sy stem, by two aphasic subjects. The subjects were clearly able to learn associations between the geometric sy mbols of the sy stem and pictures of objects. However, acquisition of sy mbols for function words was much less successful. Actually , these performances mirrored the results of language examinations showing spared ability in auditory -visual matching of concrete nouns and severe impairments in processing function words and meaningless sy llables. The authors concluded that sy mbols were simply equivalent to their written counterparts and that there was no benefit in the learning of an artificial sy stem. Treatment was re-oriented towards a better exploitation by the subjects of their residual abilities in processing written language, abilities which have been demonstrated in careful pretherapeutic examinations. 3.2.2. Promoting Aphasic Communicative Effectiveness (PACE) PACE therapy focusses on the incorporation of natural conversation parameters in order to improve communicative ability of aphasic subjects. Four aspects are emphasized and contrasted with traditional rehabilitation techniques: (a) Both the clinician and the patient take active parts as senders and receivers. (b) The exchanged messages bring new information. (c) Any communication modal-
25. Communicative Behavior in Aphasia
ity may be used to convey messages. (d) Performances are rated for communicative effectiveness rather than according to formal criteria (Davis 1989; Davis/Wilcox 1978; 1985). Actually , the PACE therapy relies on an extensive training to referential communication tasks (see section 2.2.3.). The clinician play s an important role in modelling effective messages, for instance, by showing the utility of nonverbal signals, and in inhibiting ineffective way s to transmit information like the inappropriate expansion in some cases of fluent aphasias (see also Penn 1987). Along the same lines, the healthy partner may be given advice in order to improve collaboration to discourse: slowing down speech tempo, using short sentences, reformulating the message, etc. (Green 1984).
4.
General Conclusions
Considerable advances in the pragmatic approach to aphasia have been realized in the recent y ears. Sy stematic studies have attempted to analy se the processes involved in communication and therapeutic implications have been brought out. Increased attention is being paid to individual differences in language impairments and communicative skills. No general claim about ‚communication and aphasia’ is risked here. Instead, heterogeneity of performances is exploited to demonstrate the separability of components forming the cognitive sy stem. Some operations deal with modality -specific input and output processes. Accordingly , the first empirical question addressing the aphasic is about his or her ability to recognize and produce manual and vocal gestures, pictures of objects, spoken and written words, etc. Other processes are implied in the integration of information from different modalities, in using knowledge acquired from past experience, and in selecting the appropriate means to achieve communication goals. A more precise description of this adaptative behavior should be the aim of further research, and finding the best way to improve it, the endeavour of speech therapists. Acknowledgments Pierre Fey ereisen is presently supported as a Research Associate by the National Fund for Scientific Research (Belgium). Gratitude is expressed to Michel Hupet for helpful comments on a previous version of the manuscript. Parts of the chapter were presented in a key note paper at the Fourth International Aphasia Rehabilitation Congress at Edinburgh on September 4, 1990.
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Pierre Feyereisen, Louvain-la-Neuve (Belgium)
26. Text Processing in Aphasia 1. 2. 3. 4. 5. 6. 7. 8.
1.
Introduction Sentence Level within Text Text Level Processing Dissociation between Language Levels Relationship between Language Levels Macrostructure in Text Processing Conclusion References
Introduction
Information relevant to text processing in aphasia has emerged primarily from two perspectives, one related to text representation and the other related to how cognitive and linguistic processes operate on the representation of text. The representation of text and processing of text are closely related; however, for theoretical purposes the two can be discussed separately . For this paper, the terms ‘text’ and ‘discourse’ are used interchangeably to refer to both oral and written forms of connected language. Researchers of text representation attempt to characterize (1) the features that distin-
guish text from non-text, as well as (2) the features that differentiate the various ty pes of text. At a general level, text is defined as connected language. Connected language is frequently characterized as a series of ideas which form an integrated, complete message. That is, text represents a corpus of interrelated chunks of information. In contrast, a unrelated string of sentences or ideas would not typically be labelled as text. A word of caution, however, against too stringent definitional criteria for text is necessary . This bias toward a loose definition for text is particularly relevant when dealing with aphasic populations with marked linguistic disturbances. Impairment of certain linguistic devices interferes with surface level marking of semantic relations across sentences comprising text. Thus, aphasic patients may produce ‘texts’ in which ideas are adjoined but seem only vaguely related since these patients do not have the linguistic devices to signal relations. With this concern in mind, it is important to interpret ‘text’ produced by aphasics using pragmatic criteria of communicative intent rather than surface level cri-
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teria. Justification for a pragmatic basis for defining text is supported by Halliday /Hasan (1976), who suggest that any passage should be interpreted as text if there is the remotest possibility of doing so. At a more specific level, texts are classified according to the particular genre/s represented, e. g. narrative, procedural, conversational and expository text. Research efforts have been directed toward identify ing the unique properties of different text-ty pes in terms of characteristic components, unique organizational structure, and elements of meaning. In contrast to text representation, researchers of text processing focus on the processes involved in manipulating language for purposes of communication. Processing of text covers both production and comprehension, in spoken and written modalities. These two modalities are of interest since they entail different processing demands. Spoken language, for example, ty pically unfolds as it is being formulated. Written text, on the other hand, can be produced over a long period of time with some planning. Processing requirements for text depend on the ty pe of discourse genre and the nature of the task. Processing demands will vary , depending on whether the text is spontaneously -generated, recalled, paraphrased, summarized or reinterpreted in some way. Characterization of text representation is not a simple, straightforward matter, since text processing entails the interactive contribution of multiple components, some realized at a sentential level and others at a discourse level. At a sentential level, both lexical and sy ntactic variables contribute to text organization. For example, manipulation of clauses within sentences is important to the foregrounding and backgrounding of certain information. At a discourse level, unique properties of text operate above and bey ond the sentence level. The dilemma in characterizing text lies in sorting out the aspects of text that depend on sentence-level grammars from those aspects of text that operate independently of sentence-level features. The primary purpose of this chapter is to review the literature relevant to text representation and processing in aphasia. As will be evident from the review, text processing relies on multiple components, some realized by linguistic structures, some by information structures, and others by the interaction of both ty pes. The specific components ad-
dressed in this chapter include: (1) sentential level aspects, (2) text level aspects, and (3) constructs which involve the interaction between these two levels of language. The aspects of text representation which combine both sentential and text level structures are conceptualized by the abstract constructs of cohesion, coherence and macrostructure. Our main objective is to demonstrate that explanations for selective disturbances of text processing in aphasia will be derived from approaches that seek to characterize both the interactions and the dissociations across the components of text comprehension and production. At present, the nature of the interaction across components is not well understood. However, recent studies on cohesion and coherence suggest that breakthroughs are being made in this area. Approaches that seek to identify the interdependencies across language levels will complement and clarify previous documentation of dissociations between levels of language processing.
2.
Sentence Level within Text
Early studies of text processing in aphasia adopted sentential level measures to characterize discourse performance. Specifically , the individual sentences comprising text were analy zed. The justification for such an approach was the belief that higher levels of language were dependent on intactness of lower levels of language. That is, sentential abilities were felt to be dependent on lexicosy ntactic abilities, and discourse abilities were based on sentential ability . This perspective of language processing predicted that discourse difficulties could be explained by problems at a sentential level. The findings of studies of sentential level abilities within texts confirmed deficits in aphasia which were previously identified on isolated sentential measures (Ulatowska/ North/Macaluso-Ha y nes 1981; Ulatowska/ Freedman-Stern/Doy el et al. 1983). However, these sentential measures failed to account for discourse level performance. Observations were made that aphasic patients were able to communicate at a text level better than could be predicted from their performance on sentential measures, suggesting an inverse dissociation between language levels. Unexpectedly , higher levels of language appeared to be better preserved than lower levels. This inverse dissociation between lower and higher levels of language performance observed in
26. Text Processing in Aphasia
aphasic patients suggested that a ‘bottom-up’ theory of language processing was inadequate to explain the observed behavioral phenomena in aphasia. Consequently , researches began to focus on how to objectively document text performance bey ond sentence level measures. One of the earliest studies to document a dissociation between text structure and sentential level performance was a single case study of the written discourse of a Wernicke’s aphasic patient (Ulatowska/Freedman-Stern 1978; Freedman-Stern/Ulatowska/Baker/DeLacoste 1984). Linguistic analy ses revealed sentential level errors in morphology and sy ntax. Analy ses at a discourse level revealed relative preservation of narrative structure in that the necessary components were present. Interestingly , the impairment of linguistic structures within sentences did not preclude effective manipulation of linguistic devices at a discourse level to signal aspects of information structure. For example, the patient was able to linguistically signal digressions from the main story line. This early study demonstrated a way in which textual structure could be evaluated above and bey ond the individual sentences that comprised the text. Subsequently , a number of studies were undertaken to characterize text processing in aphasia. The following section summarizes the general findings from these studies.
3.
Text Level Processing
The majority of investigations of text processing in aphasia have examined narrative discourse. These investigations of narrative discourse have been instigated for various reasons. For one, narratives represent the most basic discourse genre from which other discourse genres, e. g. procedural, are derived. Additionally , the organizational structure of narratives has been the most extensively characterized of all the discourse ty pes. Knowledge of the specific structure provides a theoretical framework for evaluating the disruption of structure above a sentential level. 3.1. Text Production The findings from studies of text processing suggested that aphasic subjects processed the most important information contained in a discourse sample, on both production and comprehension measures. Production studies
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of simple narrative discourse revealed that discourse structure was relatively preserved for mildly and moderately impaired aphasic subjects. The subject populations included both Broca’s and Wernicke’s aphasic patients. Evidence for preservation of discourse structure on production measures was reported both in single case studies (Freedman-Stern/ Ulatowska/Baker/DeLacoste 1984; Ulatowska/Freedman-Stern 1978) and in small group studies (Dressler/Pleh 1988; Ulatowska/North/Macaluso-Ha y nes 1981; Ulatowska/Weiss Boy el/Freedman-Stern et al. 1983; Ulatowska/Freedman-Stern/Do y el 1983). Narrative structure was analy zed using discourse superstructure and sequence of events. Narrative superstructure delineates the components of a narrative, e. g. setting, complicating action and resolution. The sequence of events refers to the temporal unfolding of events in a chronological sequence. In contrast to the relative preservation of narrative superstructure for mildly and moderately impaired aphasic subjects, discourse structure for severely impaired aphasic subjects was not preserved. At this increased severity level, narrative structure was found to be impaired both in terms of omission of the essential superstructure components and disrupted temporal sequence of events (Bond/ Ulatowska/Macaluso-Ha y nes/Ma y 1983). These results suggest that a certain amount of language is necessary to support discourse structure. The mechanisms underly ing the disruption, however, are not well understood. The disruptions in superstructure and event sequence for severely impaired aphasic subjects were attributed to the severe reduction of language rather than a primary underly ing conceptual deficit. The evidence given to support this claim was an apparent intactness of an internal representation of the story in the subject’s mind, manifested in two way s. First, the severely impaired aphasic subjects used formulaic initiators (e. g. once upon a time) and terminators (e. g. the end) to mark the story boundaries. Second, the severely impaired aphasic subjects were able to sequence picture stories on a nonverbal picture arrangement task. These performances supported a preserved conceptual organization for story structure and sequence, at least for the small population of severely impaired aphasic subjects studied. The disruption in narrative text processing for severely impaired aphasic subjects was less marked in conversational discourse. In conversational discourse, discourse structure as
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manifested by range and sequence of speech acts was preserved. Severely -impaired aphasic subjects were able to maintain the discourse structure in a conversation task with only rudimentary sentential language. A possible explanation for preservation of conversation at a discourse level is that many speech acts can be convey ed with only a single word or phrase, and/or because in conversation the structure is a cooperative process (Ulatowska/Allard/Re y es/Chapman 1988). These findings must be interpreted cautiously as the sample size was small. Also, alternative analy ses may prove to be more sensitive to elucidating disruptions of conversational discourse. 3.2. Text Comprehension On measures of text comprehension, aphasic subjects were found to comprehend main ideas embedded in narrative discourse better than less important details. A similar pattern of enhanced comprehension for the main ideas was found for non-brain-damaged control subjects (Brookshire/Nicholas 1984). Comprehension of the most critical information could not be predicted by performance on isolated sentential measures nor by degree of coherency of the text (Wegner/ Brookshire/Nicholas 1984). The findings from other studies on text comprehension in aphasia suggested that aphasic subjects comprehended text level material better than sentential level material. Aphasic subjects apparently benefit from linguistic context in the comprehension of spoken narratives as contrasted with the more limited linguistic context a variable in isolated sentences (Stachowiak/Huber/Poeck/Kerschensteiner 1977). The predominant explanation for the enhancement of textual processing (as compared to the processing of isolated sentences) is that aphasic subjects benefit from the redundancy of information provided by text which is not available in isolated sentences (Cannito/ Jarecki/Pierce 1986; Hough/Pierce/Cannito 1989; Huber/Gleber 1982).
4.
Dissociation between Language Levels
Documentation of relatively preserved discourse structure in aphasic patients for both comprehension and production measures (for simple narratives) stood in sharp contrast to
well documented impairment of sentential structures. This evidence provided insight into how aphasic patients could be communicatively viable despite severe disruption of sentential level abilities. From a theoretical perspective, the findings documented a dissociation between discourse and sentential level abilities on objective measures. From a methodological perspective, this research demonstrated the value of apply ing certain theoretical constructs for evaluating discourse structure above the sentential level. As with many new findings, however, the documentation of relative preservation of discourse structure raised more questions than it answered. While processing of text in aphasia may be preserved relative to sentential processing, there is no question that a relationship between sentential and text processing exists. Although a dissociation between these two levels was established for mildly and moderately impaired aphasic subjects, certain findings support that a relationship exists between sentential and discourse level performance in aphasia. Subjective ratings of narrative discourse were lower for aphasic subjects as compared to normals (Ulatowska/ Hay ashi/Cannito/Fleming 1986). Specifically , aphasic subjects’ discourses were consistently rated as aberrant on clarity and coherence of spoken narratives despite preservation of narrative superstructure. Furthermore, quantitative differences were found between aphasic and normal subjects’ discourses. Compared to normals, aphasic subjects’ discourses showed reduction of information, reduced sentential and discourse complexity , and increased discourse and sentential errors (Berko-Gleason/Goodglass/Obler et al. 1980; Dressler/Pleh 1988; Ulatowska/Hay ashi/Cannito/Fleming 1986; Ulatowska/North/Macaluso-Haynes 1981). One specific pattern which supported a relation between sentential and text level factors was the disruption of reference. Reference in this case refers to the identification of the actors throughout a story by nouns and pronouns. Reference operates across sentences at a textual level, and it is realized through nouns/pronouns at a sentential level. Errors of reference occur when the identification of a particular actor is ambiguous or unclear. Instances of referential ambiguity were traced to increased use of pronouns in mildly and moderately impaired aphasic subjects (Ulatowska/North/Macaluso-Ha y nes 1981; Ulatowska/Weiss Boy el/Freedman-Stern et al.
26. Text Processing in Aphasia
1983; Ulatowska/Freedman-Stern/Do y el et al. 1983). For severely impaired aphasic subjects, the relation between sentential reduction and quality of discourse was more obvious. The reduction of sentential language was deemed responsible for discourse collapse (Bond/ Ulatowska/Macalusco-Hay nes/May 1983). A certain level of sentential intactness and complexity appears to be necessary for supporting discourse structure. In sum, the above examples demonstrate that the relationship between discourse and sentence level structures is important to understanding selective disturbances in text processing in aphasia. As is evident, the relationship is extremely complex. Currently , the most promising approaches to elucidate the impairment and preservation of text processing in aphasia are those that seek to identify the constructs that are critical to text. These approaches utilize the constructs of cohesion and coherence of text and macrostructures. Information relevant to these constructs are summarized below.
5.
Relationship between Language Levels
5.1. Cohesion and Coherence of Text The prime mediator between sentential and discourse level structures is cohesion. Cohesion refers to surface level linkages across sentences or even across larger units of text. Cohesion is achieved by manipulation of various linguistic devices that serve to bind parts of a text into a coherent whole. These devices are called cohesive ties. Cohesive ties form what is called ‘cohesive chains’ as continuity of meaning is found throughout text. Coherence operates at a more conceptual level than the surface markings of cohesion. Nonetheless, cohesive devices contribute directly to coherence, since the ability to produce coherent text requires facility with cohesive devices. The relationship between coherence and cohesion varies depending on the complexity and ty pe of text. For discourse genres with more conventional structures (e. g. narratives), coherence is easier to achieve even when linguistic disturbances of cohesive devices exist. However, as the discourse complexity increases or when discourse genres with less conventional structures (e. g. expository discourse) are utilized,
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it is more difficult to produce coherent text when cohesive devices are disturbed. Studies of cohesion in aphasic texts have been performed using two different ty pes of analy ses, one objective and the other subjective. Objective studies utilized quantitative analy ses of cohesive ties. Berko-Gleason/ Goodglass/Obler et al. (1980), for example, counted cohesive ties of reference and found that reference was differentially impaired for Wernicke’s and Broca’s aphasic patients. Wernicke’s aphasic subjects showed increased frequency of deictic pronouns, whereas Broca’s aphasic subjects exhibited reduced frequency of both deictic and personal pronouns. This same pattern of impairment was confirmed in later discourse studies (Ulatowska/North/Macaluso-Ha y nes 1981; Ulatowska/Weiss Boy el/Freedman-Stern et al. 1983; Ulatowska/Freedman-Stern/Do y el et al. 1983). More recent work on text cohesion of aphasic language has applied a schema developed by Halliday /Hasan (1976) for evaluating cohesion (Armstrong 1987; 1989; Mathews 1987; Piehler/Holland 1984). Using the Halliday and Hasan framework, researchers identified: 1) reduced use of cohesive ties, 2) poor use of local connectors, 3) greater use of deictics, and 4) increased use of pronouns without antecedents or referents in aphasics’ texts as compared to normals’. Additionally , amount and ty pe of cohesive ties were utilized to document different profiles of recovery for a Broca’s and Wernicke’s aphasic patient (Piehler/Holland 1984). One important implication of studies of cohesion was that cohesive ties are not equal in terms of their contribution to cohesion of text. In fact, cohesive ties operate differently in text, although by definition, all cohesive devices provide continuity in meaning across sentences. For example, both reference and connectives are markers of continuity of ideas. However, linguistic devices of reference do not in themselves reveal any thing about the relationship among ideas, whereas connectives explicitly mark relations between ideas. This distinction was evident in an indepth descriptive study of written text for one Wernicke’s patient. The texts produced by this patient exhibited skillfull manipulation of reference but marked disruption in use of connectives (Freedman-Stern/Ulatowska/ Baker/DeLacoste 1984). At present, it is apparent that quantitative measures of cohesive devices alone are inad-
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equate for measuring cohesion in text production. Evidence from a study by Huber/ Gleber (1982) supports the view that surface level cohesive ties do not necessarily improve quality of text. In this study , degree of textual cohesion had no impact on comprehension for aphasic subjects, contrary to expectations. It was argued that the surface level markings of cohesion may not account for overall coherence of the texts. The difficulty in interpreting quantitative measures of cohesive devices is amplified by the lack of data concerning normal cohesion patterns for comparison with cohesion in aphasia. A second ty pe of cohesion analy sis, subjective evaluation, can complement quantitative measures in order to clarify the quality of discourse in relation to cohesion. Subjective analy ses incorporated ratings of overall cohesion and clarity of discourse for aphasic subjects (Ulatowska/North/Mocaluso-Ha y nes 1981; Ulatowska/Weiss Boy el/FreedmanStern et al. 1983; Ulatowska/FreedmanStern/Doy el et al. 1983). However, to date, limited evidence exists concerning correlations between language ratings and counts of cohesive devices. As is evident from the above discussion, quantitative counts of cohesive ties and subjective ratings provide only a partial picture of the relationship between sentence and text level processing. Some recent evidence suggests that this relationship may be clarified by examining clusters of cohesive devices that contribute to key aspects of coherence. For example, two specific features essential to the production of coherent text of the narrative ty pe include temporality and reference. A number of cohesive devices contribute to effective marking of temporality and reference. Temporality and reference operate at a global level, and y et both are realized through linguistic markers of cohesion that operate at a sentential level. Because of this codependence of sentential and text levels, these two aspects may provide additional insight into the interdependency between the two levels of language.
6.
Macrostructure in Text Processing
The construct of macrostructure denotes the global semantic meaning of a discourse (van Dijk 1972). Textual macrostructures are represented by the main ideas of a text and are associated with notions such as theme, gist and topic (Mross 1990). The constructs of macrostructure and superstructure are often
confused primarily because there is some degree of overlap. Both macrostructure and superstructures operate much like an ‘outline,’ providing a global schema for organizing information, both in comprehension and production. On the other hand, superstructures provide the organizational structure, whereas macrostructures provide the semantic content in terms of amount, ty pe and distribution of information (van Dijk 1977). Macrostructure can be tapped at two levels. First, the content of the text itself can be used to evaluate intactness of macrostructure by examining (1) relevant and irrelevant content, (2) distribution of information within superstructure components, and (3) distribution of important information and details. Additionally , macrostructure can be tapped with tasks soliciting titles, summaries, and outlines for texts. These latter tasks require preservation of meaning with reduction of information. It is of interest to note that these tasks can be produced with relatively simple language. For example, titles consist of few words relative to the entire text and represent the global meaning of the story . Outlines are easily expressed in telegraphic language and represent the most important ideas. Research on macrostructure processing in aphasia indicated that macrostructure was impaired as measured by alterations in title and summary productions in comparison to normals (Ulatowska/Freedman-Stern/Weiss Doy el/Macaluso-Hay nes 1983). Aphasic patients produced concrete titles that failed to grasp the global meaning of the story at an abstract level. However, these findings should not be generalized to aphasic patients, at large, since some patients produced acceptable titles. A disruption in macrostructure was not as readily apparent in aphasic patients for simple narrative productions. Amount of language and information was reduced for aphasic patients. This reduction was selective in that the most important information was retained, and less important details were omitted. Perhaps a disruption in narrative macrostructure was obscured because there were not enough details to depart from the macrostructure. The probability of observing impairment of macrostructure for narrative discourse is more likely in posteriorly aphasic patients as compared to anterior patients, since more detail exists in their discourse. While previous evidence suggested that narrative structure was preserved in aphasia
26. Text Processing in Aphasia
(Ulatowska/North/Macaluso-Ha y nes 1981; Ulatowska/Freedman-Stern/Do y el et al. 1983), this pattern referred to superstructure and not macrostructure. Narrative structure may appear intact for aphasic patients because superstructure drives the ongoing processing of narratives. This is to say that superstructure replaces macrostructure in guiding aphasic patients’ narrative structure. Superstructure is more global, less demanding and conceptually simpler than macrostructure. Further evidence to suggest that superstructure replaces macrostructure in narrative processing for aphasic patients is the finding that these patients cannot produce discourse genres with less conventionalized superstructures, e. g. expository . There appears to be a restriction in discourse genres available in aphasia in that expository discourse becomes either narrative or descriptive discourse, and narrative discourse becomes conversational genre. Additionally , aphasic subjects have considerable difficulty combining discourse ty pes. For example, they exhibit problems shifting from conversational to narrative discourse. (Ulatowska/Sadowska 1992).
7.
Conclusion
Most of the earlier text studies in aphasia were done from the perspective of documenting dissociations. Historically , dissociation phenomena of various language components in aphasia have been of great interest both theoretically and clinically , since these phenomena showed selectivity of impairment of particular language functions as a result of an insult to a specific part of the brain. Studies have documented dissociations within morphology , between morphology and sy ntax, and between sy ntax and semantics (MacWhinne y /Bates 1989; Zurif/Caramazza 1976). In text studies, the dissociation between sentence level language and discourse has been described (Freedman-Stern/Ulatowska/Baker/DeLacoste 1984). This chapter has emphasized the interrelationships that exist between levels of language. This new direction may prove to be more revealing in accounting for both impairments and preservations in aphasic discourse and in characterizing the nature of cohesion and coherence in aphasic texts. This approach may one day substantiate the intuition of one of our aphasic patients who remarked: “It took me four hours tp produce this page and a half but it is not a composition
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but just a collection of individual sentences.”
8.
References
Armstrong, E. (1987). Cohesive harmony in aphasic discourse and its significance to listener perception of coherence. In R. H. Brookshire (Ed.), Clinical aphasiology, Vol. 17. 210—215. Minneapolis, MN: BRK Publishers. Armstrong, E. (1989). The potential of cohesion analy sis in the assessment of aphasic discourse. Paper presented at the American Speech-Language Hearing Association Annual Convention. Berko-Gleason, J., Goodglass, H., Obler, L., Green, E., Hy de, M. R., & Weintraub, S. (1980). Narrative strategies of aphasic and normal speaking subjects. Journal of Speech and Hearing Research, 23, 370—382. Bond, S. L., Ulatowska, H. K., Macaluso-Hay nes, S., & May , E. B. (1983). Discourse production in aphasia: Relationship to severity of impairment. In R. H. Brookshire (Ed.), Proceedings of the clinical aphasiology conference. 202—210. Minneapolis: BRK Publishers. Brookshire, R. H. & Nicholas, L. E. (1984). Comprehension of directly and indirectly stated main ideas and details in discourse by brain-damaged and non-brain-damaged listeners. Brain and Language, 21, 21—36. Cannito, M., Jarecki, J., & Pierce, R. S. (1986). Effects of thematic structure on sy ntactic comprehension in aphasia. Brain and Language, 27 , 38—49. Dressler, W. U. & Pleh, C. (1988). On text disturbances in aphasia. In W. U. Dressler & J. A. Stark (Eds.), Linguistic analyses of aphasic language. 151—177. New York: Springer-Verlag. Freedman-Stern, R., Ulatowska, H. K., Baker, T., & DeLacoste, C. (1984). Disruption of written language in aphasia: A case study . Brain and Language, 21, 181—205. Halliday , M. A. K. & Hasan, R. (1976). Cohesion in English. London: Longman. Hough, M. S., Pierce, R. S., & Cannito, M. P. (1989). Contextual influences in aphasia: Effects of predictive versus nonpredictive narratives. Brain and Language, 36, 325—334. Huber, W. & Gleber, J. (1982). Linguistic and nonlinguistic processing of narratives in aphasia. Brain and Language, 16, 1—18. MacWhinney , B. & Bates, E. (1989). Crosslinguistic studies of sentence processing. Cambridge University Press. Mathews, C. (1987). Discourse before and after the onset of aphasia. Paper presented at Clinical Aphasiology Conference.
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Mross, E. F. (1990). Text Analy sis: Macro- and microstructural aspects of discourse processing. In Y. Joanette & H. H. Brownell (Eds.), Discourse ability and brain damage. 50—68. New York: Springer-Verlag. Piehler, M. & Holland, A. (1984). Cohesion in aphasic language. Paper presented at the Clinical Aphasiology Conference. Stachowiak, F. J., Huber, W., Poeck, K., & Kerschensteiner, M. (1977). Text comprehension in aphasia. Brain and Language, 4, 177—195. Ulatowska, H. K., Allard, L., Donnell, A., Bristow, J., Hay nes, S. M., Flower, A., & North, A. J. (1988). Discourse performance in subjects with dementia of the Alzheimer ty pe. In H. A. Whitaker (Ed.), Neuropsychological studies of non-focal brain damage: Trauma and dementia. 108—131. New York: Springer-Verlag. Ulatowska, H. K. & Freedman-Stern, R. (1978). Analy sis of aphasic writing. Paper delivered at the Aphasia Research Group, World Federation of Neurologists, University of Iowa, Iowa City. Ulatowska, H. K., Freedman-Stern, R., Doy el, A., Macaluso-Hay nes, S., & North, A. T. (1983). Production of narrative discourse in aphasia. Brain and Language, 19, 317—334. Ulatowska, H. K., Hay ashi, M. M., Cannito, M. P., & Fleming, S. G. (1986). Disruption of reference in aging. Brain and Language, 28, 24—41. Ulatowska, H. K., North, A. J., & Macaluso-
27. 1. 2. 3. 4. 5. 6.
Hanna K. Ulatowska/Sandra Chapman, Dallas, Texas (USA)
Aphasia and Intelligence Introduction Intelligence or Intelligences? Intelligence and Information-Processing Aphasia and Non-Verbal Deficits Conclusions References
When Wertheimer (1945) told “many report that their thinking words, he only laughed.”
1.
Hay nes, S. (1981). Production of narrative and procedural discourse in aphasia. Brain and Language, 13, 345—371. Ulatowska, H. K. & Sadowska, M. (1992). Some observations on aphasic texts. In: Hwang, S. J. & Merrifield, W. R. (eds.). Language in context: Essay s for Robert E. Longacre. Arlington: The Summer Institute of Linguistics and The University of Texas at Arlington, 51—66. Ulatowska, H. K., Weiss Boy el, A., FreedmanStern, R., Macaluso-Hay nes, S., & North, A. T. (1983). Production of procedural discourse in aphasia. Brain and Language, 18, 315—341. van Dijk, T. A. (1972). Some aspects of text grammar. The Hague: Mouton Press. van Dijk, T. A. (1977). Text and context. Explorations in the semantics and pragmatics of discourse. London: Longman. Wegner, M. L., Brookshire, R. H., & Nicholas, L. E. (1984). Comprehension of main ideas and details in coherent and noncoherent discourse by aphasic and non-aphasic listeners. Brain and Language, 21, 37—51. Zurif, E. B. & Caramazza, A. (1976). Psy cholinguistic structures in aphasia: Studies in sy ntax and semantics. In H. Whitaker & H. A. Whitaker (Eds.), Studies in neurolinguistics. Vol. 1. New York: Academic Press.
Einstein that is alway s in
Introduction
Even the most cursory literature search for references to cognitive or intellectual status in the aphasias will reveal a curious dichotomy of theoretical presuppositions. On the one hand, there is a long tradition of testing patients who have sustained unilateral left or right hemisphere damage with materials orig-
inally devised to measure individual differences in ‚general intelligence’ within the ‚normal’ population. The first substantial work of this nature was Weisenburg/McBride (1935), and there have subsequently been a number of excellent survey s of conceptual impairment in aphasic patients (Zangwill 1969; Hamsher 1981; Kertesz 1988; Vignolo 1989) that update the research consensus (or lack thereof). All these chapters include fairly full reviews of how well or badly different samples of indisputably aphasic patients perform on standard tests of psy chometric intelligence. On the other hand, most of the major textbooks of cognitive neuropsy chology that include extensive discussion of aphasic phenomena make no mention of intelligence. The very term cannot be found in the subject indexes of Ellis/Young (1988), Caplan (1987), Shallice
27. Aphasia and Intelligence
(1988), or McCarthy /Warrington (1990), for example. Research papers within the tradition of which these books are representative do sometimes (but far from invariably ) give psy chometric scores on the patients who are then the subjects of detailed cognitive investigation. The Wechsler Adult Intelligence Scale (WAIS; Wechsler 1958), Progressive Matrices (Raven 1965), and the New Adult Reading Test (Nelson/O’Connell 1978) seem to be the most frequently reported measures; the latter test is widely used as an indicant of premorbid general intelligence (for those patients without significant dy slexic impairment). In (almost) all cases, however, this psy chometric information is given in the ‚clinical background’ section of the paper and subsequently ignored in the design and interpretation of the experiments that document the nature of the patient’s cognitive deficit. What, then, is the likely cause of this striking discrepanc y between two research traditions? Are there substantive empirical and theoretical issues at stake? If so, how do they relate to the methodology of competent investigations of the patient and to practical management?
2.
Intelligence or Intelligences?
Two extreme positions with respect to the n a t u r e of intelligence could be taken up: One is that intelligence is unitary , the other that it is multiple. Although the absolute extremes are not occupied by any reputable psy chometrician, very different relative positions have been advanced (and continue to be debated). Spearman (1927) held that the important component of human intelligence was general intelligence or g. Ex hy pothesi, g play s a significant role in all activities deemed (pretheoretically ) to involve the exercise of intellectual capacity . Thurstone (1938), by contrast, laid far greater stress upon the notion of a set of primary abilities that are r e l at i ve ly independent of each other. In Thurstone’s hierarchical model, general intelligence is just one component that contributes to otherwise distinct primary abilities, which in turn contribute to more restricted taskspecific factors. Psy chometric testing was never primarily intended to shed light upon the patterns of impaired or preserved ability in cases of demonstrable brain pathology (either acquired or developmental). The intent was rather to measure the spread of ability (or abilities) within normal populations of
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different ages. ‚Subnormal’ (or ‚supernormal’) within this framework has no meaning other than scoring significantly below (or above) the average (‚norm’) for a particular reference group (the general population at given ages). Tests were constructed (i. e. items selected) in order to y ield a ‚normal distribution’ of scores that permitted statistical analy sis of the correlations between tests. To a first approximation, Spearman’s g can be regarded as a construct that captures the extent of positive correlation between all tests. Different individual tests are then found to correlate differentially with g. Those that correlate most highly with g include Vocabulary and General Information (from the verbal section of the WAIS), Block Design (from the performance section of the WAIS) and Raven’s Progressive Matrices. These tests are accordingly regarded as the ‚purest’ measures of g. We stress again that psy chometric tests are standardized on the general population. Neuropsy chological inquiry originated in a context that could not be more different. Gall’s theory of ‚multiple intelligences’ was explicitly founded upon the study of ex t r e m e differences between individuals who could in no way be regarded as representative of the ‚general population’ (Marshall 1984). The samples of concern to Gall were saints and mass murderers, idiots and geniuses, psy chotics and supermen. It was the investigation of people with extreme talents (for good or ill) that led Gall to postulate that all basic human competencies had a discrete, responsible organ in the brain. The relatively sizes of these organs in the individual then determined the pattern of domain-specific psy chological strengths and weaknesses in that individual. That Gall initially based his theory upon the somewhat shaky base of craniology is irrelevant. Since it rapidly became clear that injury to different regions of the brain produced qualitatively different patterns of cognitive impairment, the term ‚localization of function’ could replace ‚cerebral organology ’ without necessitating any conceptual shift. From the moment that Hughlings Jackson (1876) formulated the central dogma of human neuropsy chology — the left hemisphere is ‚leading’ for verbal ideation, the right hemisphere for visuo-spatial ideation — the hy pothesis that there could be a ‚brain-centre’ for ‚general intelligence’ began to lose any plausibility . From there it was but a short step to argue that the notion of ‚general in-
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telligence’ was in itself ill-conceived. Under attack from many quarters, general intelligence (and other IQ measures) came to be seen by some psy chologists and many neuropsy chologists as the mere reification of test scores subjected to factor-analysis. After brain injury , patients with focal (or diffuse) damage are no more representative of the general population than are Gall’s extreme cases (irrespective of how ‚normal’ they may have been before sustaining that damage.) Neuropsy chological inquiry has accordingly placed great stress upon demonstrating the existence of ‚double dissociations’ as an indicant of the existence of discrete cognitive modules devoted to specialized domains. If on two tasks A and B, patient X scores well on A but poorly on B, while patient Y scores poorly on A and well on B, this is prima facie evidence for the involvement of two distinct ‚intelligences’ responsible for the two tasks (Shallice 1988). For purposes of discovering the structure of mentation, it is simply irrelevant that within the n o r m a l population, performance on the two tasks may correlate highly (and that both tasks load highly on g). Lezak (1988) therefore argues that in neuropsy chological practice, the use of IQ measures “and that of any scores representing sums or averages of disparate data obtained from tests of brain functions and mental abilities can obscure specific facets of a subject’s neuropsy chological status and can misrepresent it generally.” It might be thought that the above arguments apply only to Spearman’s conception of intelligence and not to Thurstone’s. And this is how Margolin (1992) seems to interpret the issue. The notion of human intelligence as a “unidimensional monolithic attribute or capacity ” has been “officially pronounced dead” and replaced by “the concept of intelligence as a multifaceted multidimensional array of capacities” (Margolin 1992). Descriptively , this is indeed the case (Gardner 1983), although even with respect to Thurstone’s position, the concerns of the psy chometrician and of the cognitive neuropsy chologist are actually diametrically opposed. In the following section we outline the nature of that opposition, with reference to both Spearman and Thurstone.
3.
Intelligence and Information-Processing
One obvious problem in any discussion of intellectual status in the aphasias (or other
language disorders) is how to avoid trivializing the relationship between language and intelligence. If, for example, intelligence is d e f i n e d as that which conventional IQ tests measure, then it will almost invariably be the case that aphasic patients will have a low verbal intelligence quotient (VIQ). Consider, for example, some sample items from the WAIS. It would hardly be surprising if most (or indeed all) patients with a moderately severe aphasia had difficulty in answering the question How does yeast cause dough to rise? (an item from the Information subtest). Likewise, such patients would be expected to have problems in explaining what encumber means (an item from Vocabulary ), or explicating how poem and statue are alike (Similarities). Similarly , digit span is usually (but not inevitably ) impaired after aphasiaprovoking lesions, and arithmetic likewise. It is accordingly difficult to imagine an aphasic patient who would score well on the question If eight machines are needed to finish a job in six days, how many machines would be needed to finish the job in one-half day? (Arithmetic subtest). Now, it is of course possible to r e p o r t lowered scores on such tests in aphasic patients as poor VIQs — the tests were after all taken from a standard IQ test. But does the ‚IQ’ in such descriptions mean any thing over and above the ‚V’ for verbal? To say that aphasic patients have language (verbal) disorders is to give a (rough) definition of ‚aphasia’; it is not to make a discovery about aphasia. From the viewpoint of genuine intelligence testing (in the normal population), however, the ‚IQ’ component of VIQ i s meaningful. Recall that, within Spearman’s framework, Vocabulary and Information have very high loadings on g. It would then follow that the aphasic patient who scores poorly on these tests could have suffered a precipitous fall in g or an impairment to whatever s p e c i f i c abilities are involved in good performance on Vocabulary and Information: no test could measure g and nothing but g; all tests demand information-processing pertinent to the specific task that is given. To show that an interpretation based upon impairment to g is false, it suffices to demonstrate that there is some other task that also loads highly on g (e. g. Block Design) on which the patient performs well. And if, contrariwise, the patient scored badly on Block Design, there would still be no support for the hy pothesis that g had been
27. Aphasia and Intelligence
diminished by brain damage: the patient could simply have conjoint impairment of both sets of disjoint abilities required for Vocabulary and Block Design, respectively . Studies of ‚dementia’ have often been bedevilled by illegitimate reification of g. Thus Hamsher (1981), for example, argues that “The concept of dementia may be viewed as a pathological counterpart to g.” It is, of course, true that ‚dementia’ has often been defined clinically as an impairment to three (or more) cognitive domains. But if a patient manifests aphasia, agnosia and amnesia, it is not clear what is gained by postulating that he or she has suffered “a significant decline in g” (Hamsher 1981) rather than (conjointly ) exhibiting a disorder of language, perception, and memory . Further discussion of this issue can be found in Schwartz (1990) and Gurd/ Marshall (1991). Exactly the same argument goes through with respect to Thurstone’s primary abilities (or group factors). Good performance on one task that loads highly on a particular group factor in conjunction with poor performance on another task that also loads highly on this same factor indicates that a (reified) primary ability has not been impaired. Conjointly impaired performance can likewise indicate that the neuronal instanciation of mechanisms involved in t wo specific factors have both suffered damage. If it is the case empirically that association of impairment for tasks belonging to a common primary ability is more frequent than dissociation, the finding would most likely reflect an anatomical constraint rather than neuropsy chological support for Thurstone’s factorial theory . That is, competences that are psy chologically similar seem often to be represented in neighbouring regions of the brain (Lashley 1937). It remains, however, a logical point (not a matter of empirical observation) that behavioural studies of the patterns of impaired and preserved performance after brain damage can never support claims for the existence of g or any other more specific psy chometric construct. From the standpoint of neuropsy chology , it is purely accidental that the vocabulary items to be defined on the WAIS are part of an intelligence test and not part of an aphasia battery . It is also the case that the nature of the questions asked by neuropsy chologists has little overlap with the nature of those asked in psy chometric IQ testing.
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From the latter standpoint, it suffices to know whether or not the subject can correctly answer the question (e. g. How does yeast cause dough to rise?). For the aphasiologist, however, failure to provide the correct answer is only the starting point of the inquiry . The relevant issues here include: Does the patient have a disorder of phonemic hearing sufficient to block or distort adequate perceptual input? Can the patient access function word vocabulary (how, to)? Can abstract verbs (cause) be understood? The examiner must be able to answer all such questions before it even makes sense to inquire whether the patient has a disorder of semantic memory such that he or she no longer knows how y east causes dough to rise. In short, the question How does yeast cause dough to rise?is not (from the examiner’s standpoint) the same question when given to a 50 y ear-old who has sustained a left middle cerebral artery stroke and a healthy 50 y earold member of the general population. Even if the answer is an indicant of ‚intelligence’ in the latter case, it cannot be so in the former. The distinction is fairly obvious for this particular constrast, but there are other cases where we believe that the same or similar points hold but have gone unrecognized. For example: in a series of publications, Dennis and her colleagues have argued that sy ntactic comprehension is more impaired after left than right surgical hemidecortication for infantile cerebral injury (see Dennis 1980). Dennis interprets these results as showing that the ‚equipotentiality ’ hy pothesis — that the right hemisphere can mediate language as adequately as the left if one hemisphere is removed early enough — is false. Bishop (1983) points out (correctly ) that there are a number of statistical inadequacies in the analy sis of the data (and some overgenerous generalizations therefrom). However, Bishop also argues that Dennis’s results — the failure of some children to comprehend reversible passives — can be explained by the relatively low ‚mental age’ (or ‚intellectual level’) of the children in question. In support of this hy pothesis, Bishop (1983) reports that (in normal children) there is a significant positive association between mental age and performance on reversible passives. Mental age was assessed using the Peabody Picture Vocabulary Test (Dunn 1965). What we find odd about this strategem is the notion that performance on one language task, the PPVT — a measure of receptive vocabulary — can be used to
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ex p l a i n performance on another language task — sy ntactic comprehension. The superficial semblance of explanation is consequent upon nothing more than calling the PPVT scores a measure of ‚mental age’ and then assuming that mental age has explanatory power. This just cannot be right: the undoubted fact that the receptive vocabulary of the normal child increases with chronological age is a datum to be explained. No definition of ‚mental age’ based upon the similarly undisputed fact that the vocabulary of some children increases faster than that of others can turn mental age into an ex p l a n a t i o n of anything. A related example of pseudo-explanation can be found in the literature on language deficits in Parkinson’s disease (PD). A number of authors (including Gurd/Ward 1989) have reported that many patients with PD show deficits on verbal fluency — producing sequences of words within a particular semantic category (e. g. animals) or beginning with a specified letter. Patients produce fewer items than controls and do so at a slower rate. Hanley /Dewick/Davies et al. (1990) replicated this finding. They then showed that the difference between the patient and control samples disappeared if “present verbal ability ” was entered into an analy sis of covariance. Hanley /Dewick/Davies et al. argue that it is possible that the poor performance of the PD patients on verbal fluency tests “is due to lower general ve r b a l ability .” Their measure of general verbal ability is the Mill Hill Sy nony ms Test (Raven 1943), a test of knowledge of word meanings. Again, however, it is unclear how a deficit on one verbal test (Mill Hill Sy nony ms) can be regarded as an ex p l a n a t i o n of a deficit on another verbal test (fluency ). Any association between test scores in either normal or brain-damaged populations is a datum in search of explanation. In the latter population, a theoretically -significant association will be explained by proposing an information-processing account of how the two tasks (that y ield the test scores) depend upon common mechanisms. That account will alway s be subject to revision if some patients show a strong double-dissociation between task performances that cannot be ‚explained away ’ by convincing differential strategic adaptations to a common underly ing impairment. The interpretation of correlated impairments after brain damage as due to a decrement in ‚general intelligence’ or ‚general verbal ability ’ will always be pseudo-explanatory.
4.
Aphasia and Non-Verbal Deficits
There are a number of seemingly non-verbal tests on which some (but not all) aphasic patients have been reported to perform very poorly . The most notable are Gottschaldt’s Hidden Figures Test (Teuber/Weinstein 1956), Progressive Matrices (Basso/De Renzi/Faglioni et al. 1973; Basso/Capitani/Luzzatti/ Spinnler 1981), and varied tests for the comprehension of gesture and pantomime (Duffy / Duffy 1981). The existence of these associations has sometimes been interpreted as indicating that the aphasias are not solely disorders of language. The basic idea that underlies all the different versions of this claim is that some forms of aphasia reflect a breakdown of conceptual thought and reasoning that is not i n t r i n s ic a l ly tied to a linguistic code (lexical semantics, sy ntax, and phonology ). The notion has been variously expressed as a failure to adopt an ‚abstract attitude’ (Goldstein 1948), loss of general intelligence (Marie 1906), and impairment of ‚categorical thinking’ (Vignolo 1989). Both Hughlings Jackson (1878) and Finkelnburg (1870) regarded the sy mptomatology of aphasia itself as a deficit of “sy mbolic formulation and expression” (Hughlings Jackson, 1878), or “asy mbolia” as Finkelnburg (1870) phrases it. Finkelnburg (1870) explicitly relates aphasia to an impairment of the fa c u l t a s s i g n a t r i x (Kant 1798), a faculty that occupies “a kind of middle ground between sensory perception and conceptual thought” (Duffy / Liles 1979). While these ideas are of some interest (and perhaps heuristic value), it is not easy to see how they could be expressed sufficiently clearly to allow empirical data to be brought to bear upon them. In some instances the relevant data-base is itself far from consistent. For example, both Teuber/Weinstein (1956) and Orgass/Poeck/Kerschensteiner/ Hartje (1972) found an impairment on the Gottschaldt Hidden Figures Test that was specific to patients with aphasia after left hemisphere damage. But, by contrast, Mey ers (1948) and Bauer/Beck (1954) could find no such impairment in aphasics as compared to control subjects. The only conclusion that can be drawn at present is that we do not understand the information-processing demands of the test. With respect to Progressive Matrices, the primary data are similarly conflicting, and
27. Aphasia and Intelligence
Zangwill (1964) has emphasized the poor correlation between severity of aphasia and performance on Matrices. Kertesz/McCabe (1975) have reported that many global aphasics are impaired on Matrices and that poor comprehension is the best predictor of that impairment. This conclusion is supported by the results of Gainotti/d’Erme/Villa/Caltagirone (1986). On the other hand, Kinsbourne/ Warrington (1963) and Kertesz (1988) have documented the fact that some aphasics with very poor comprehension can nonetheless obtain well above average scores on Matrices. The most plausible account of the numerous discrepancies between different studies of Matrices is that many of the individual items can be solved by either verbal strategies, visuo-spatial strategies (or some combination thereof). This conclusion is strongly supported by the work of Zaidel/Sperry (1973) who administered Matrices to a series of patients with cerebral commissurotomy . Each independent hemisphere scored well above chance, but each used “different strategies of approach and different modes of central processing.” Costa, (1976) has likewise shown, in patients with left or right unilateral damage, that some items are more easily solved by perceptual matching (Part A) while others place more verbal demands on the deduction of analogies. While these results make good sense, it remains unclear why some authors (e. g. Zaidel/Zaidel/Sperry 1981) wish to impose a psy chometric interpretation upon them. The claim that “‚g’ may contain at least two independent factors, gl and gr”, or that “the data better support the primary abilities model of intelligence” (Zaidel/Zaidel/Sperry 1981) adds little to the results by way of either description or explanation. From a purely psy chometric standpoint, Matrices loads highly on g and on a specific spatial factor. The moral, however, is that many supposedly visuo-spatial problems c a n be solved by verbal means and will be so attempted by some people (not including Einstein). The same point can be made in reverse by the three-term series problem. If one is told that Tom is taller than Dick and Harry is shorter than Dick and then asked Who is tallest?, the problem is explicitly verbal and can be solved by logico-linguistic reasoning. It is nonetheless more easily solved by constructing a mental image of the three heights and reading off the answer directly from the ‚visual’ code (Wason/Johnson-Laird 1972). With respect to the fa c u l t a s s i g n a t r i x,
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Duffy /Duffy (1981) interpret results on pantomime expression and recognition in aphasia as support for the “hy pothesis of a generic sy mbolic ability or process which is prerequisite to, and underlies the use of, specific verbal and nonverbal communicative behaviors.” But this conclusion is surely both too strong and too weak. It is too strong because there are double-dissociations between the two domains. Thus Alajouanine/Lhermitte (1964) have described some severely aphasic patients with essentially intact nonverbal communicative skills; and Hécaen (1978) has shown that conventional gesture codes can be impaired in the absence of equivalent disorders of the linguistic sy stem. As Alajouanine/ Lhermitte (1964) conclude: “Aphasia appears not to bear any necessary relationship to the presence or absence of extralinguistic disorder.” The hy pothesis of impaired ‚generic sy mbolic activity ’ is too weak in that it provides no account of the specific linguistic patterns of aphasic language (Caplan 1987). While the explication of the functional architecture of communicative gesture and pantomime is an interesting problem in its own right (Seron/ van der Kaa/Remitz/van der Linden 1979), it seems fundamentally misguided to conflate communication by gesture and by language.
5.
Conclusions
The main thrust of this chapter has been to argue that psy chometric definitions of intelligence are irrelevant to any understanding of the functional architecture of language skills and their breakdown in aphasia. Language, we have argued, must be regarded as a specific cognitive module (Chomsky 1980; Fodor 1983) and investigated as such. The Gallist philosophy is correct, however much has y et to be discovered in order to give substance to the modular approach. We should nevertheless reiterate that our arguments against the reification of intelligence concern only the extremely odd view that psy chometric intelligence (= score on a behavioural test or tests) can be regarded as an explanatory construct. We have provided no grounds for disbelief in the existence of ‚biological intelligence’ as currently conceived by Ey senck (1986). It could well be true that IQ scores show remarkably high correlations with sy naptic transmission fidelity as assessed by ‚string’ measures of averaged evoked re-
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sponses to flashes of light or pure tones (Blinkhorn/Hendrickson 1982). The validity of such results would, however, shed no light on the structure of language, the character of the processing mechanisms deploy ed in the use thereof, or the nature of the neuronal instanciation of linguistic capacity.
6.
References
Alajouanine, T. & Lhermitte, F. (1964). Non-verbal communication in aphasia. In A. de Reuck & M. O’Connor (Eds.), Disorders of Language. 168—182. London: Churchill. Basso, A., Capitani, E., Luzzatti, C., & Spinnler, H. (1981). Intelligence and left hemisphere disease. Brain, 104, 721—734. Basso, A., De Renzi, E., Faglioni, P., Scotti, G., & Spinnler, H. (1973). Neuropsy chological evidence for the existence of cerebral areas critical to the performance of intelligence tasks. Brain, 96, 715—728. Bauer, K. & Beck, D. (1954). Intellect after cerebrovascular accident. Journal of Nervous and Mental Disorders, 120, 379—395. Bishop, D. V. M. (1983). Linguistic impairment after left hemidecortication for infantile hemiplegia? A reappraisal. Quarterly Journal of Experimental Psychology, 35 A, 199—207. Blinkhorn, S. F. & Hendrickson, D. E. (1982). Averaged evoked responses and psy chometric intelligence. Nature, 295, 596—597. Caplan, D. (1987). Neurolinguistics and Linguistic Aphasiology: An Introduction. Cambridge: Cambridge University Press. Chomsky , N. (1980). Rules and representations. The Behavioral and Brain Sciences, 3, 1—61. Costa, L. D. (1976). Intertest variability on the Raven Coloured Progressive Matrices as an indicator of specific ability deficit in brain lesioned patients. Cortex, 12, 31—40. Dennis, M. (1980). Capacity and strategy for sy ntactic comprehension after left and right hemidecortication. Brain and Language, 10, 287—317. Duffy , R. J. & Duffy , J. R. (1981). Three studies of deficits in pantomimic expression and pantomimic recognition in aphasia. Journal of Speech and Hearing Research, 46, 70—84. Duffy , R. J. & Liles, B. Z. (1979). A translation of Finkelnburg’s (1870) lecture on aphasia as ‚asy mbolia’ with commentary . Journal of Speech and Hearing Disorders, 44, 156—168. Dunn, L. N. (1965). Expanded Manual for the Peabody Picture Vocabulary Test. Minnesota: American Guidance Service Inc. Ellis, A. W. & Young, A. W. (1988). Human Cognitive Neuropsychology. London: Lawrence Erlbaum.
Ey senck, H. J. (1986). Toward a new model of intelligence. Personality and Individual Differences, 7, 731—736. Finkelnburg, F. (1870). Niederrheinische Gesellschaft. Sitzung vom 21. März in Bonn. Berliner Klinische Wochenschrift, 8, 449—450, 460—462. Fodor, J. A. (1983). The Modularity of Mind. Cambridge, Mass.: MIT Press. Gainotti, G., D’Erme, P., Villa, G., & Caltagirone, C. (1986). Focal brain lesions and intelligence: a study with a new version of Raven’s colored matrices. Journal of Clinical and Experimental Neuropsychology, 8, 37—50. Gardner, H. (1983). Frames of Mind: The Theory of Multiple Intelligences. New York: Basic Books. Goldstein, K. (1948). Language and Language Disturbances. New York: Grune and Stratton. Gurd, J. M. & Marshall, J. C. (1991). Neuropsy chology : Cognitive status in progressive neurological illness. Current Opinion in Psychiatry, 4, 612—615. Gurd, J. M. & Ward, C. D. (1989). Retrieval from semantic and letter-initial categories in patients with Parkinson’s disease. Neuropsychologia, 27 , 743—746. Hamsher, K. (1981). Intelligence and aphasia. In M. T. Sarno (Ed.), Acquired Aphasia. 327—359. New York: Academic Press. Hanley , J. R., Dewick, H. C., Davies, A. D. M., Play fer, J. & Turnbull, C. (1990). Verbal fluency in Parkinson’s disease. Neuropsychologia, 28, 737— 741. Hécaen, H. (1978). Les apraxies idéomotrices: Essai de dissociation. In H. Hécaen & M. Jeannerod (Eds.), Du Controle Moteur à l’Organisation du Geste. 343—358. Paris: Masson. Jackson, J. H. (1876). Case of large cerebral tumor without optic neuritis and with left hemiplegia and imperception. Royal London Ophthalmic Hospital Reports, 8, 434—440. Jackson, J. H. (1878). On affections of speech from disease of the brain. Brain, 1, 304—330. Kant, I. (1798). Anthropologie in pragmatischer Hinsicht. Königsberg: Nicolvius. Kertesz, A. (1988). Cognitive function in severe aphasia. In L. Weiskrantz (Ed.), Thought without Language. 451—463. Oxford: Clarendon Press. Kertesz, A. & McCabe, P. (1975). Intelligence and aphasia: Performance of aphasics on Raven’s Coloured Progressive Matrices (RCPM). Brain and Language, 2, 387—395. Kinsbourne, M. & Warrington, E. K. (1963). Jargon aphasia. Neuropsychologia, 1, 27—37. Lashley , K. S. (1937). Functional determinants of cerebral localization. Archives of Neurology and Psychiatry, 38, 371—387. Lezak, D. (1988). IQ: R. I. P. Journal of Clinical and Experimental Neuropsychology, 10, 40.
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Margolin, D. I. (1992). Clinical cognitive neuropsy chology : An emerging speciality . In D. I. Margolin (Ed.), Cognitive Neuropsychology in Clinical Practice. 9—17. Oxford: Oxford University Press. Marie, P. (1906). Revision de la question de l’aphasie: La troisième convolution frontale gauche ne joue acun role spéciale dans la fonction du language. Semaine Médicale, 21, 241—247. Marshall, J. C. (1984). Multiple perspectives on modularity. Cognition, 17, 209—242. Mey ers, R. (1948). Relation of ‚thinking’ and language: an experimental approach using dy sphasic patients. Archives of Neurology and Psychiatry, 60, 119—139. McCarthy , R. A. & Warrington, E. K. (1990). Cognitive Neuropsychology: A Clinical Introduction. New York: Academic Press. Nelson, H. E. & O’Connell, A. (1978). Dementia: The estimation of premorbid intelligence levels using the new adult reading test. Cortex, 14, 234—244. Orgass, B., Poeck, K., Kerschensteiner, M., & Hartje, W. (1972). Visuocognitive performances in patients with unilateral hemispheric lesions. An investigation with three factorial reference tests. Zeitschrift für Neurologie, 202, 177—195. Raven, J. C. (1943). The Mill Hill Vocabulary Scale. London: H. K. Lewis. Raven, J. C. (1965). Guide to Using the Coloured Progressive Matrices. London: H. K. Lewis. Schwartz, M. F. (Ed.) (1990). Modular Deficits in Alzheimer-Type Dementia. Cambridge, Mass.: MIT Press. Seron, X., van der Kaa, M., Remits, A., & van der Linden, M. (1979). Pantomimic interpretation and aphasia. Neuropsychologia, 17, 661—668. Shallice, T. (1988). From Neuropsychology to Mental Structure. Cambridge: Cambridge University Press.
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Spearman, C. (1927). The Abilities of Man. New York: Macmillan. Teuber, H.-L. & Weinstein, S. (1956). Ability to discover hidden figures after cerebral lesions. Archives of Neurology and Psychiatry, 76, 369—379. Thurstone, L. L. (1938). Primary Mental Abilities. Chicago: Chicago University Press. Vignolo, L. A. (1989). Non-verbal conceptual impairment in aphasia. In F. Boller & J. Grafman (Eds.), Handbook of Neuropsychology, Vol. 2. 185— 206. Amsterdam: Elsevier. Wason, P. C. & Johnson-Laird, P. N. (1972). Psychology of Reasoning: Structure and Content. London: Batsford. Wechsler, D. (1958). The Measurement and Appraisal of Adult Intelligence, Baltimore: Williams and Wilkins. Weisenburg, T. & McBride, K. E. (1935). Aphasia: A Clinical and Psychological Study. New York: The Commonwealth Fund. Wertheimer, M. (1945). Productive Thinking. New York: Harper. Zaidel, D. & Sperry , R. W. (1973). Performance on the Raven’s colored progressive matrices test by subjects with cerebral commissurotomy . Cortex, 9, 34—39. Zaidel, E., Zaidel, D. W., & Sperry , R. W. (1981). Left and right intelligence: Case studies of Raven’s progressive matrices following brain bisection and hemidecortication. Cortex, 17, 167—186. Zangwill, O. L. (1964). Intelligence in aphasia. In A. V. S. de Reuck & M. O’Connor (Eds.), Disorders of Language. 261—284. London: Churchill. Zangwill, O. L. (1969). Intellectual status in aphasia. In P. J. Vinken & G. W. Bruy n (Eds.), Handbook of Clinical Neurology, Vol 4. 105—111. Amsterdam: North-Holland.
Jennifer M. Gurd/John C. Marshall, Oxford (UK)
28. Aphasia and Apraxia 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.
Introduction Brain Localization Apraxia and Type of Aphasia Modality Specific Apraxia Testing for Apraxia ‘Linguistic’ Description and Analysis of Parapractic Errors Receptive Aspects of Apraxia Sequential Aspects of Aphasia and Apraxia Linguistic Models of Aphasia in Relation to Apraxia Conclusions References
1.
Introduction
Like the aphasias, the variants of motor apraxia are among the classic sy ndromes in human neuropsy chology . In the vast majority of cases, apraxia arises after lesions in the language-dominant hemisphere. In those rather rare cases in which language is organized in the right hemisphere, apraxia can also develop after a right-sided brain lesion (Poeck/Kerschensteiner 1971; Poeck/Lehm-
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kuhl 1980). A dissociation of hemispheric dominance for praxis and language has been discussed only in exceptional single cases (Heilman/Co y le/Gon y ea/Geschwind 1973; Heilman/Gon y ea/Geschwind 1974). Also, aphasia and apraxia occur very frequently together following a single (either large or small) left hemispheric brain lesion. 1.1. These observations might indicate that the apraxias are language dependent sy ndromes. The term language dependent in this context is ambiguous: on the one hand, it can imply that a sy mptom or sy ndrome is the direct consequence of the aphasic language deficit. Characteristic examples are the inability of aphasic patients to discriminate verbally between left and right (Poeck/Orgass 1967; 1971) or to identify individual fingers verbally (Poeck/Orgass 1969). However the fact that aphasia and apraxia can vary independently of each other argues against this kind of language dependency . That is, after a lesion of the language-dominant hemisphere, apraxia may improve or disappear, whereas aphasia persists. The reverse is also possible. Handedness is not particularly helpful to explain left brain dominance for praxis, since apraxia, with only a few anatomically defined exceptions, affects both hands and feet. On the other hand ‘Language dependency ’ may also mean that a sy mptom or a sy ndrome is brought about by an interruption of fiber tracts between a specific cortical area and the language region (Geschwind 1965). This view would imply that the language region of the brain has conceptual functions bey ond those involved in linguistic expression and comprehension. This assumption is, to a certain extent, supported by the observation that users of American Sign Language are reported to develop different ty pes of sign language aphasia, corresponding to Broca’s and Wernicke’s aphasia, respectively , following lesions in anterior or posterior parts of the language region (Poizner/Klima/Bellugi 1990). However, such a disconnection model is difficult to prove in detail. Furthermore, there are no autopsy studies available for large patient groups. And finally the spatial resolution of available imaging methods as y et is certainly not fine enough to document complete interruption of specific fiber tracts. 1.2. If apraxia is not language dependent in the restricted sense considered above, then the striking association between disorders of
language and of praxis might be explained in a different way. Other possibilities are: — The two disorders are independent and their frequent association is due to the proximity of the cortical areas within which lesions produce the disturbances. — The two disorders are the expression of a common underlying deficit of communication affecting linguistic and gestural behavior in a general sense. This hypothesis recalls Finkelnburg’s (1870) concept of asymbolia. In contrast one might assume a disturbance of motor control mechanisms governing both limb and speech musculature. The last hy pothesis, however, does not account for the linguistic aspects of language disturbances associated with lesions of the left hemisphere. In addition, apraxia also affects movements that have neither sy mbolic value, nor communicative function, such as cutting an apple or drinking a cup of tea. 1.3. The relationship between aphasia and apraxia was aptly discussed as early as the beginning of this century . Liepmann (1913), for one, had already observed that aphasia and apraxia are frequently associated. He linked this association to either impairment in neighboring neural structures or, and this was his preferred position, to disturbances of the same kind (“wesensgleich”). Liepmann stressed that he had conceived of the aphasia in one of his patients as “apraxia of the musculature of speech”. He compared the planning of purposeful movements with the planning of words and sentences, both termed ‘ideation’. Whereas in purposeful movements the ideation had temporal, spatial, as well as visual aspects, in language the ideation had temporal-acoustic ones. Thus, according to Liepmann, only the temporal aspect is common to both activities. Liepmann equated limb-kinetic apraxia with Broca’s aphasia, and he stressed the similarity between various kinds of parapraxic distortions of movements with paraphasic alterations of the motor aspects of language. In particular, he mentioned perseveration, elision, repetition, anticipation, and confusion of semantically similar words or movements. For example, semantically different finite movements reminded him of semantic paraphasias, and the motoric counterpart to word finding disturbances were problems producing the correct movement. Liepmann also stressed that it is difficult to distinguish mnestic and executional
28. Aphasia and Apraxia
disturbances, a consideration which is reminiscent of Geschwind’s seminal paper on the variety of naming disorders (Geschwind 1967).
2.
Brain Localization
Under the aspect of cerebral localization, there is strong overlap between areas involved in the control of speech and of movement. The most interesting of these areas is the Supplementary Motor Area, situated in the medial part of area 6. Indeed, recordings of SMA neuronal activity in conscious, behaving monkey s have demonstrated that SMA’s role in movement control is different from that of the primary motor area in area 4 of the precentral gy rus (Brinkman 1981). The results seem to point to the SMA’s possible role in programming movement. The SMA might actually modulate primary motor area activity , since it is, in fact, located ‘upstream’ from the primary motor area. Correspondingly , in monkey s Brinkman found a deficiency in bimanual coordination after unilateral SMA lesions. That is to say that both hands tended to be used in a sy mmetrical manner instead of sharing the work load between them. Furthermore, the apraxics showed a disability in adjusting their hands for catching purposes which Brinkman interpreted as an inability to sequence flexion and extension components of the movement. Freund (1985) has reported, that in humans, lesion of the mediofrontal cortex including SMA leads to a notable decrease in spontaneous motor activity in the contralateral limbs. These lesions also result in a decrease in language activity , corresponding to Luria’s “dy namic aphasia” (1980) or to ‘transcortical motor aphasia’.
3.
Apraxia and Type of Aphasia
Studies associating motor apraxia with the various subty pes of aphasia will not be discussed in detail here, since in my view, these studies are not very productive, and their results have little, if any , explanatory value. In keeping with this objection, in a large scale study , Lehmkuhl/Poeck/Willmes (1983) were unable to associate presence or absence of apraxia with subtypes of aphasia in any way. An obvious misconception arising from studies such as those mentioned above is the claim that oral apraxia is directly related to
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Broca’s aphasia. In fact, there actually is a very strong positive correlation between the occurrence of phonemic paraphrasias (omission, substitution, anticipation, perseveration and reversal of phonemes) in the setting of any aphasic sy ndrome and apraxic distortions of nonspeech oral movements (DeRenzi/Pieczuro/Vignolo 1966). Oral apraxia is a regular feature of sy ndromes like conduction aphasia or Wernicke’s aphasia. The underly ing brain lesions are localized, according to Vignolo (1977) in the perisy lvian region as opposed to, in Vignolo’s terminology , marginal, i. e. more peripheral, parts of the language area. This close correlation between oral apraxia and phonemic paraphasias suggests that indeed similar brain mechanisms subserve intricate sequential movements in the oral sphere during speech as well as nonspeech motor activity.
4.
Modality Specific Apraxia
In addition to the standard aphasias (Broca’s, Wernicke’s, Global, Amnesic), several nonstandard ty pes of aphasia have been described. From the perspective of brain mechanisms, the modality specific naming disorders are the most interesting. For instance, there are optic aphasia, or naming deficits on visual stimulation, as well as tactile aphasia in conjunction with Braille aphasia. Localization of lesion strongly suggests a disconnection mechanism in these cases. De Renzi/Faglioni/Sorgato (1982) have described modality specific mechanisms in apraxia, in other words, apraxia depending on the kind of stimulus that was given to elicit the gesture. They found a dissociation between the ability to correctly use objects when the stimulus was verbal, visual or tactile, respectively . They concluded that these cases of apraxia resulted from disconnection between cerebral areas where the sensory information is processed and those areas, where movements are programmed.
5.
Testing for Apraxia
At the present stage, studies in apraxia suffer from a regrettable lack of standardized and generally accepted testing procedures. In contrast to existing reliable aphasia test batteries, as of y et there is neither an apraxia test on record based on item analy sis, nor on testretest reliability , nor on interrater stability .
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Furthermore, many researchers base the diagnosis of apraxia on a rather arbitrary cutoff score instead of establishing a cut-off range.
6.
‘Linguistic’ Description and Analysis of Parapractic Errors
Until a few y ears ago, most investigators limited themselves to rating the performance of their patients on apraxia test simply as pass or fail. A more detailed insight into the nature of motor apraxia became possible only when the parapractic movement sequences were subjected to a qualitative analysis. 6.1. Early work on a normal population became available from Efron (1941), who made use of highly differentiated methods of describing movements in a study on gestures. Efron had already noted certain analogies between verbal and gestural behavior, and he used the term ‘linguistic’ to describe the referential aspects of sy mbolic movements. Unfortunately , he limited his analy sis to finite movement sequences and chose not to describe their individual components. This is also true of Ekman/Friesen’s studies (1969; 1972) on the repertoire of nonverbal behavior, in particular of their transcultural investigation of gestural movements. 6.2. The methods of structural linguistics were first applied to normal movements by Birdwhistle (1970), who recognized that body posture, movements, and gestural expression can have fixed patterns, which he catalogued in a hierarchy of elements, similar to the description of language units. Just as phonemes and morphemes are distinguished in linguistics, Birdwhistle differentiated between motor elements he termed ‘kinemes’ and ‘kinemorphes’, and he used a notation sy stem that permitted the exact description of individual elements in a motor sequence. In a field that he called ‘kinesics’, he suggested study ing the group of movements that is significant for communicative processes. 6.3. Ulatowska/Kumin/Kaplan (1974) also attempted to categorize errors in an investigation of sy mbolic gestural behavior (so-called emblems) in aphasic patients and in normal subjects. 6.4. On the basis of these earlier studies,
we (Kerschensteiner/Poeck 1974; Poeck/Kerschensteiner 1975) developed a method that permitted the coding of those individual components that constitute apractic movements. That is, we were able to transcribe these components into graphic sy mbols that could then be analy zed qualitatively and quantitatively . The goal was to describe the ‘vocabulary ’ of apraxia in a manner similar to that of aphasia research, while seeking regularities characteristic either for individual patients or for subty pes of apraxia in certain subty pes of aphasia. The following groups of errors have been distinguished: a) Substitutions: The requested movement is replaced by a finite motor response or by a verbal or sound response. b) Augmentations: The patient makes additional movements or sounds. c) Omissions: These consist either of complete failure to respond or of fragmentary execution of the response. d) Other errors: This is not a uniform category . It includes behaviors that are similar to the ‘conduite d’approche’ of aphasic patients when they try to correct phonological or semantic paraphasias by means of different degrees of approximation. Similarly , apractic patients, when asked to make a hissing noise, may first whistle, then alternate between whistling and a movement by which they inhale air through half-closed lips, before they finally perform the correct movement. Amorphous movements do not fit into any of the categories just named. In our experience, the significance of such movements for the apraxias is less important than what has been reported in the literature. A final very important element of ideomotor apraxia is perseveration. This consists not only of repetition of entire movements, but also of inappropriate introduction of elements of a movement that the patient had performed earlier. The patient perseverates not only from one movement to the immediately following one; rather the tendency to perseverate can be so strong that an element that had been performed correctly (or incorrectly) earlier, recurs eight or ten tasks later. This overview would be too lengthy , if details of the coding and the interpretation of our qualitative analy sis of ideomotor-apractic movement sequences were presented here, particularly in relation to aphasic sy ndromes; the reader is therefore referred to the original publications. One finding, however, deserves special attention. The individual subty pes of aphasia are not accompanied by distinct subty pes of apraxia. Not a single ty pe of ideo-
28. Aphasia and Apraxia
motor apraxia characterized by certain kinds of apractic errors can be distinguished (see also Lehmkuhl/Poeck/Willmes 1983).
7.
Receptive Aspects of Apraxia
7.1. The receptive aspects of apraxia have rarely been investigated thoroughly . Gonzales Rothi/Heilman/Watson (1985) were able to demonstrate that apractic patients with retrorolandic lesions including the parietal areas were impaired in the differential recognition of gestures. They presented videos of pantomimes, and the subjects had to indicate their meaning by chosing the corresponding illustration from a multiple choice set. The drawings were of the kind that if the pantomime was of hammering, one drawing was of a nail, and three were foils. Similarly , in an earlier paper Heilman/Rothi/Valenstein (1982) found that ideomotor apraxic patients with posterior lesions had a gestural discrimination deficit, whereas anterior apraxics did not. Several studies have demonstrated that some aphasics do not recognize gestures. Ferro/Martins/Mariano/Castro-Caldas (1983) studied this performance in 65 left hemispheric stroke patients whose lesions were located by CT scan. In the acute stage frontal lobe and basal ganglia were frequently involved in patients showing inability to recognize gestures. In the later and chronic stages parietal lobe involvement was important. Lesions producing gesture recognition impairment were larger, had more extensive and more frequent parietal involvement and produced less temporal lobe damage than those causing verbal comprehension defects. The latter finding underscores the importance of the multimodal parietal lobe for gesture recognition. 7.2. As indicated above, one of the major issues in gestural behavioral studies is whether the frequent occurrence of gestural impairment after posterior left hemisphere lesions is due to the anatomical coincidence of areas serving both functions or due to an impairment of an underly ing general communicative or cognitive ability . Correlation between gesture and language comprehension varies with ty pe of aphasia. For instance, whereas it is highly significant in global aphasia, it is nonsignificant in Wernicke’s aphasia (Ferro/Santos/Castro-Caldas/Mariano 1980). Moreover,
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among those aphasics with similar language impairments some are impaired in gesture recognition, while others are not. Involvement of centroparietal white matter can cause gesture comprehension disturbance while sparing auditory comprehension at least at the word level. In contrast, severe comprehension defect without gesture recognition disturbance has been associated with temporal lesions and the relative sparing of the parietal lobe. Also, the size of the lesions was shown to play an important role. The loci specifically associated with gesture recognition impairment correspond to parietal supramodal cortical areas that can integrate visual and somesthetic information and the exploration of extrapersonal space. Certain brain areas are mainly associated either with gesture or with language comprehension defects. For other areas (for example part of Wernicke’s area and supramarginal gy rus), both disturbances can be found with comparable frequency . This partial overlap of the areas crucial to those two functions explains some of the striking discrepancies in the literature. All in all, lesions producing auditory comprehension defects are smaller than those causing gesture recognition impairment, suggesting a multicomponent cortical representation of gestures.
8.
Sequential Aspects of Aphasia and Apraxia
On several occasions Poeck/Huber (1977) found evidence that the left hemisphere of humans is particularly involved in the sequential organization of certain ty pes of motor behavior. Based on the results of interestingly devised experiments, Kimura and colleagues (1970; 1973; 1974) had reached the same conclusion. She has elaborated this concept into the assumption that sequential behavior is a supramodal left hemisphere function. In view of this conviction, Kimura/Archibald (1974) have noted “that speaking is another activity characterized by a high degree of precision of movement”. The authors speculate that “it is quite possible that speech disturbances and apraxia are s i m p ly (spacing mine) different manifestations of an impairment of motor sequencing” and that it is “not specifically a sy mbolic, or language sy stem which is affected in aphasia, but the speech sy stem”. Also on another occasion,
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Kimura maintained that “language is a sequential activity”. Contrary to this view, Poeck/Huber (1977) have pointed out that a very important characteristic of the speech code is that the same part of the acoustic signal relay s diverse items of information about successive phonemic segments of the message simultaneously . In support of this assumption MacNeilage (1970) demonstrated that this information processing cannot be achieved simply by serial ordering of fixed articulatory instructions. Language is described in most linguistic models on different levels. Certainly , the information is not processed on each level in isolation, rather it is available from different levels simultaneously . However, sequential activity is certainly characteristic for operations at the phonemic level. Alterations in the sequential order, like anticipation, perseveration, omission, substitution or reversal of phonemes change the meaning of a morpheme profoundly or lead to a meaningless utterance. This holds true for speech errors of normal individuals (Fromkin 1973) as well as for those of aphasics. Up to this point, there are obvious parallels between operations in the realm of speech and gestures, even though reversal of the elements of a movement has rarely , if ever, been demonstrated. However, even at the phonemic level, sequential ordering is only part of the operations performed. The use of phonemes also obey s principles of selection. To my knowledge it has not been possible to demonstrate comparable principles of selection in gestures, even though their elements do have a sequential order. Also, out of the roughly 200 phonetically different phonemes identified in all known languages, the inventory of English includes only some 40 of these (Heike 1972). There are neither dialects, nor different languages in movements, rather individual variations that, by themselves, can vary from one instance to the other and still produce a purposeful or expressive movement. Of course, there are no selection restrictions in gestures; y et even selection restrictions cannot be explained by sequential activity . Severe phonemic jargon in aphasia exhibits both, distortion of the inventory and/or violation of the permitted combinations of phonemes. Parapraxic movements exhibit obvious distortions of the inventory and incorrect combinations of these, but there is no binding or obligatory combinations of kinemes that can be violated. Speech errors certainly are not arbitrary ,
but rather obey certain linguistic regulations. For instance, two reversed phonemes alway s belong to the same category (vowels or consonants), and they usually differ in only one or two phonemic features. Similar basic differences between language and movement have been established by Poeck/Huber (1977) for the lexical and the semantic/sy ntactical level as well as for pragmatic factors that play a great role in language. Thus the claim that aphasic language can be explained solely , in analogy to apraxic errors in movement, as a failure in sequencing cannot be supported. This is not to negate the fact that the left hemisphere play s an important role in the processing of temporal qualities of motor activities as well as of sensory stimuli (Efron 1963).
9.
Linguistic Models of Aphasia in Relation to Apraxia
9.1. Garrett’s model of speech production (1980) distinguishes a general conceptual level, a language specific sentence level and a motor level of articulatory control (see Roy / Square (1985, 9.2.). The conceptual or message level contains processes that are based on the speaker’s perceptual and affective state and his or her general knowledge of the world. Language production takes place under message level control. The message level is the intended locus of the inferential processes that determine structured discourse. At the articulatory level there is the translation from sentence level structures to articulatory structures including those responsible for respiration. 9.2. Roy /Square (1985) describe control mechanisms in limb praxis on the basis of two control sy stems, the conceptual and the production sy stem. For the conceptual sy stem they stress the notion of action fields which surround objects and comprise functional information such as descriptions of purposes and usage. Further, other information, important for categorical knowledge, e. g. perceptual attributes then develops from this functional core. The perceptual attributes of tools and objects provide one source of information. The performer learns through experience with objects that certain perceptual features enable certain actions. The perceptual attributes enable assessment of which actions are possible. The other source of in-
28. Aphasia and Apraxia
formation concerns the environmental/situational context in which tools are normally used. Thus, one possible ty pe of error is a failure to discriminate, as when the performer confuses contextual or perceptual aspects of objects. The production sy stem is concerned with effecting action on the environment. Errors arise principally when the performer is not attending to the unfolding action. These errors occur at ‘key choice points’. The perceptual attributes of tools at surfaces bring about certain restrictions, e. g. the way a pen has to be held in the hand for the act of writing. The performance of actions involves a delicate balance between processes subserved by higher level sy stems which demand attention and the more autonomous operations subserved at lower levels. Thus, Roy ’s theories are based on limb praxis as motor activity involving use of objects. 9.3. Dell (1988) has reviewed a model of retrieval processes in speech production that makes predictions about the factors influencing speech errors possible. For example, the regularities that govern the exchange of phonemes in speech errors are the dimensions of similarity . Also, the major rule sy stems associated with a linguistic level are usually not violated by an error occurring at such a low level. In other words, the resulting non-words are alway s phonologically ‘legal’ sequences and adhere to the phonological rules of the language. Likewise, errors involving lexical items tend to produce sequences that are sy ntactically coherent. Thus, there is strong control over errors emanating from the sy stematic organization of language. Exchange, anticipation, perseveration are phenomena common to aphasia, to speech errors of non-brain lesioned patients and to apraxia. To me it seems to be impossible to draw parallels between the research into speech errors (which betray certain regularities observed by Fromkin (1973) as well as Garrett (1989)) and sequencing errors in apraxic movements which do not follow any recognizable regularity . The problem appears to be that there are rules for the production of language, but there is an almost infinite variety of movements other than emblems. In language production it is possible either to deviate from or adhere to a given grammatical category . The same is not true for movements, however.
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Regularities such as increase in the number of perseverations when people are rushed are not observed in apraxia. Also there is no recognized correspondence to intended sy llables or words. Furthermore, deviations from the intended movement also do not have common features like rhy ming, and rarely do parapraxias belong to the s a m e class as the intended movement. Slips of the tongue frequently create meaningful expressions, which is not often the case in parapraxias. Finally , the similarity of target items play s an important role in determining the frequency of slips, but not of parapraxias. It must be added, however, that the influence of speed on movement has not been studied to the extent of its influence on speaking rate.
10. Conclusions The common interhemispheric and the similar intrahemispheric localization of the underly ing brain lesions calls for consideration of a possible structural relationship between the two sy ndromes. It is true that both activities, language and speech as well as praxis share certain communicative functions. However, praxis also embraces many non-communicative activities. The rules that govern language and speech are not valid for praxis. Consequently , apraxia cannot be described in terms of violation of inherent rules. Movements may well draw from an inventory of motor elements that one might metaphorically term lexicon, and there are elements of movements that might be equated to phonemes, but here the analogy ends. There is no sy ntax of movements, and the present author doubts that one will ever be discovered.
11. References Birdwhistle, R. L. (1970). Kinemics and Context. Philadelphia: University of Pennsylvania Press. Brinkman, C. (1981). Lesions in supplementary motor area interfere with monkey ’s performance of a bimanual coordination task. Neurosciences Letters, 27, 267—270. Dell, G. S. (1988). The retrieval of phonological forms in production: Tests of Prediction from a Connectionist Model. Journal of Memory and Language, 27, 124—142. De Renzi, E., Faglioni, P., & Sorgato, P. (1982). Modality -specific and supramodal mechanisms of apraxia. Brain, 105, 301—312.
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De Renzi, E., Pieczuro, A., & Vignolo, L. A. (1966). Oral apraxia and aphasia. Cortex, 2, 60—73. Efron, D. (1941). Gesture and Environment. New York: King’s Crown. Efron, R. (1963). Temporal perception, aphasia and déja vu. Brain, 86, 403—424. Ekman, P. & Friesen, W. (1969). The repertoire of nonverbal behaviour: Categories, origins, usage and coding. Semiotica, 1, 49—98. Ekman, P. & Friesen, W. (1982). Hand movements. Journal of Communication, 22, 353—374. Ferro, J. M., Martins, I. P., Mariano, G., & CastroCaldas, A. (1983). CT scan correlates of gesture recognition. Journal of Neurology, Neurosurgery, and Psychiatry, 46, 943—952. Ferro, J. M., Santos, M. E., Castro-Caldas, A., & Mariano, G. (1980). Gesture recognition in aphasia. Journal of Clinical Neuropsychology, 2, 277—292. Finkelnburg, R. (1870). Vortrag in der Niederrhein. Gesellschaft der Ärzte. Bonn, Berlin, Klinische Wochenschrift, 7, 449. Freund, H.-J. (1985). Clinical aspects of premotor function. Behavioural Brain Research, 18, 187— 191. Fromkin, V. A. (1973). Introduction. In V. A. Fromkin (Ed.), Speech errors as linguistic evidence. 11—45. The Hague: Mouton. Garrett, M. F. (1980). Levels of processing in sentence production. In B. Butterworth (Ed.), Language Production, vol. 1. 17 7 —220. London: Academic Press. Geschwind, N. (1965). Disconnexion sy ndromes in animals and man, 2. Brain, 88, 585—644. Geschwind, N. (1967). The varieties of naming errors. Cortex, 3, 97—112. Gonzalez Rothi, L. J., Heilman, K. M., & Watson, R. T. (1985). Pantomime comprehension and ideomotor apraxia. Journal of Neurology, Neurosurgery, and Psychiatry, 48, 207—210. Heike, G. (1972). Phonologie. Stuttgart: Metzler. Heilman, K. M., Coy le, J. M., Gony ea, E. F., & Geschwind, N. (1973). Apraxia and agraphia in a left-hander. Brain, 96, 21—28. Heilman, K. M., Gony ea, E. F., & Geschwind, N. (1974). Apraxia and agraphia in a right-hander. Cortex, 10, 284—288. Heilman, K. M., Rothi, L. J., & Valenstein, E. (1982). Two forms of ideomotor apraxia. Neurology, 32, 342—346. Kerschensteiner, M. & Poeck, K. (1974). Bewegungsanaly se bei buccofacialer Apraxie. Nervenarzt, 45, 9—15. Kimura, D. (1973). Manual activity during speaking. I. Right handers. Neuropsychologia, 11, 45— 50. Kimura, D. & Archibald, Y. (1974). Motor func-
tions of the left hemisphere. Brain, 97, 337—350. Kimura, D. & Vanderwolf, C. H. (1970). The relation between hand preference and the performance of individual finger movements by left and right hands. Brain, 93, 769—774. Lehmkuhl, G., Poeck, K., & Willmes, K. (1983). Ideomotor apraxia and aphasia: An examination of ty pes and manifestations of apraxic sy mptoms. Neuropsychologia, 21, 199—212. Liepmann, H. (1913). Motorische Aphasie und Apraxie. Monatsschrift für Psychiatrie und Neurologie, 34, 485—494. Luria, A. R. (1980). Higher cortical functions in man. 2nd edition. New York: Basic Books, Inc. MacNeilage, P. F. (1970). Motor control of serial ordering of speech. Psychology Review, 77 , 182—196. Poeck, K. & Huber, W. (1977). To what extent is language a sequential activity ? Neuropsychologia, 15, 359—363. Poeck, K. & Kerschensteiner, M. (1971). Ideomotor apraxia following right-sided cerebral lesions in a left-handed subject. Neuropsychologia, 9, 359—361. Poeck, K. & Kerschensteiner, M. (1975). Analy sis of the sequential motor events in oral apraxia. In K. J. Zülch, O. Creutzfeldt, & G. C. Galbraith (Eds.), Cerebral Localization. 98—111. Berlin/Heidelberg/New York: Springer. Poeck, K. & Lehmkul, G. (1980). Ideatory apraxia in a left-handed patient with right-sided brain lesion. Cortex, 16, 273—284. Poeck, K. & Orgass, B. (1967). Über Störungen der Rechts-Links-Orientierung. Nervenarzt, 38, 285—291. Poeck, K., & Orgass, B. (1969). An experimental investigation of finger agnosia. Neurology, 19, 801—807. Poeck, K. & Orgass, B. (1971). The concept of the body schema: A critical review and some experimental results. Cortex, 7, 254—277. Poizner, H., Klima, E., & Bellugi, H. (1987). What the hands reveal about the brain. Boston: MIT. Roy , E. A. & Square, P. A. (1985). Common considerations in the study of limb, verbal and oral apraxia. In E. A. Roy (Ed.), Advances in Psychology, vol. 23. Neurops y chological Studies of Apraxia and Related Disorders. 111—161. Amsterdam/New York/Oxford: North-Holland. Ulatowska, H. K., Kumin, L., & Kaplan, E. (1974). Sy mbolic gestural behavior of aphasics and normals under three task conditions. Unpublished manuscript. Vignolo, L. A. (1977). Le Sindromi Afasiche. In Neuropsicologia Clinica, 11—42. Milano: Franco Angeli Editore.
Klaus Poeck, Aachen (Germany)
29. Aphasia and Acalculia
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29. Aphasia and Acalculia 1. 2. 3. 4. 5.
6.
7. 8.
1.
Overview Introduction Is there a Functional Relation between Aphasia and Acalculia? Can Individual Factors Affect Relations between Aphasia and Acalculia? Are there Functional Relations between Disturbed Language and Calculation Components at the Higher Level of Semiotic Systems? Are there Functional Relations between Language and Calculation Components at the Level of Formal Languages? Some Tentatively Concluding Remarks References
Overview
The observation that aphasia often coincides with acalculia has spurned attempts to relate two higher cortical functions, language and calculation. In this article, I shall not present new experiments and data linking aphasia and acalculia. Instead, for each theoretical issue, I will try to integrate the relevant pieces of information available from past research as well as from developmental and neuropsy chological literature. In the course of this article, it will become progressively clear that it currently makes little if any sense to look for general, necessary conditions relating the two domains. Rather, it will be proposed that number processing and calculation be viewed as operations performed on sy mbolic sy stems. Under certain circumstances, such operations can contribute to understanding aspects of other high-level cognitive activities. Indeed, compared to language, arithmetical notations and skills are quite easy to model. This simplicity may highlight some issues under discussion in other more complex domains to be formalized. In such a way , some limited functional relations may be expected from indepth analy sis of single subjects’ language and mathematical processing. I will conclude with some current theoretical issues in the domains of language, memory , etc. which might benefit from this cautious approach.
2.
Introduction
Since oral language is usually required to process and calculate numbers, and orthographic numbers are indispensible when writ-
ing cheques, it is easy to see how disturbances to language can also have an impact on mathematical operations. Moreover, this question goes far bey ond the simple instrumental aspect of language, since arithmetical abilities have been acquired, developed, automated in close relation to language. For instance, one must master counting words before one can learn to add (Secada/Fuson/Hall 1983) and subtract (Fuson 1984), and one learns the multiplication tables by rote. The issue thus also involves the potential effects of acquired language disorders due to brain damage on the more or less autonomous calculation process in adults. First, it is important to note that from a methodological point of view, the question of the relation between aphasia and acalculia may receive quite different answers depending on its level of generality and may be also on individual factors. The first point refers to the varieties of the taxonomies used for classify ing language disturbances on the one hand and calculation deficits on the other hand. The second point simply draws attention to the fact that inter-individual variations in cognitive sty les and skills may result in different architectural relations between language and calculation. I shall now review and comment on different way s of formulating the question of the relationship between aphasia and acalculia. At each step, it must of course be kept in mind that whereas there are two modalities in language (oral, written), there are at least three sy mbolic sy stems for the notation of numbers (the same two as in language, plus the Arabic digit ideographic sy stem, not to mention Roman numerals). For an historical review, see Boller/Grafman (1983).
3.
Is there a Functional Relation between Aphasia and Acalculia?
The answer to this question depends on how narrowly one defines functional relation and on whether one seeks such a relation among brain-damaged patients as a group or as different single cases, and on whether one regards aphasia and acalculia as entities or presenting different syndromes. Up to Henschen (1919), number processing and calculation disorders were simply interpreted within the sy mptom complex of apha-
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sia. His careful review of patients’ performance in language and calculation established that there was no mandatory relationship between the occurrence of aphasia and the concomitant presence of calculation impairments. From Henschen’s point of view, such findings indicated the possible independence of calculation and language, thus justify ing coining the term ‚acalculia’ for referring to the effects of brain damage on this ‚new’ higher cortical function. Within the modern theoretical and methodological information processing approach, this conclusion is still valid since double dissociations of preserved/ impaired abilities in one domain, with the reverse pattern of results in the other domain experimentally demonstrates their functional independence. More recently , Ardila/Rosselli (1990) have proposed a classification of acalculias into 6 different ty pes, one of which being “aphasic acalculia”. The existence of the 5 other ty pes thus constitutes an a contrario argument in support of the non-deterministic relation between the occurrence of aphasia and acalculia and the effects of the former disorder on the latter deficit. Despite the fact that the answer to this first question, viewed at the general level, is clearly no, the issue may still be considered in more detail when the neuropsy chological examination of patients establishes both aphasia and acalculia. The question then becomes: are there relationships between ty pes of aphasia and varieties of acalculia? Is it worth mentioning that Grewel’s studies (1952; 1969) on this topic seem to have also progressed from the general question to the more specific question regarding different sy ndromes since the title of the first study was “Acalculia”, whereas 17 y ears later it changed to “The Acalculias”. Before such detailed analy ses can be made, serious methodological problems must be considered. First, neither language nor calculation disorders have been classified in an unambiguous, theoretically motivated, and universally accepted manner. For instance, the taxonomies of mathematical disabilities vary according to the scientific domain (education, psy chology ...), the area of mathematics concerned (simple calculations, problem solving ...), the level of descriptions of impairments and framework of reference (lesional, functional ...), the etiology of disorders (developmental, acquired ...), the sy ndromes they may constitute (Gerstmann, Alzheimer ...) and other factors (Kosc 1980). The second difficulty is due to the great diversity
of the aspects of number processing and calculation abilities. The assessment batteries for calculation try to tap these different facets by presenting a large variety of subtests: production of more or less automated sequences of counting words; transcoding quantities from one notation sy stem into another (Arabic digits, oral or written numbers); counting, enumeration, estimation of quantities or dot patterns perceptually structured in different way s; access to, and manipulation of the semantic representations of numbers in magnitude comparison or in placing numbers on some analogic number line ...; numerical knowledge, number facts; performing operations with carry ing and borrowing; knowledge of mathematical algorithms, problem solving, numerical reasoning ... (See for instance the batteries devised by Hécaen/Angelergues/Houillier 1961; Hitch 1978; ClarosSalinas/von Cramon 1987; Rosselli/Ardila 1989; Deloche/Seron 1989; Deloche/Seron/ Bergego 1989). As a consequence of the diversity of tasks, mathematical abilities can be impaired in a variety of different way s. Furthermore, computing correlations between calculation error ty pes of so many tasks and the ty pes of aphasia, tends to become venturous, all the more so as there is not as y et any general unified model of number processing and calculation which could account for all tasks. Such a model could enable error ty pes to be defined and identified on theoretically motivated grounds. Such difficulties are clearly indicated by the analy sis of the results reported in studies by Dahmen/Hartje/Büssing/Sturm (1982) and Rosselli/Ardila (1989). In the former case, sophisticated statistical analy sis first seemed to indicate a linguistic factor and a visuo-perceptual factor contributing to calculation errors observed in Broca’s and Wernicke’s aphasics, respectively . However, there was in fact significant interaction between ty pes of aphasia and task-groups factors. In the second study , groups of patients were very small (from 3 to 13). Correlations were also task-dependent and their interpretations were not based on theory. Finally , if some functional relationship between aphasia and acalculia were to hold in any patient, then the patients’ abilities in the two domains should evolve in the same direction. This was clearly not the case of patient *8 in the study by Cohn (1971) since “the patient had recovered more effective language function, but his calculating ability had become more disturbed”.
29. Aphasia and Acalculia
If there is any conclusion to be drawn from this body of arguments and findings, it seems to be that neither at a general level, nor at the level of particular aphasic sy ndromes, should there necessarily exist a simple relation between language deficits and calculation impairments.
4.
Can Individual Factors Affect Relations between Aphasia and Acalculia?
In addition to the variety of mathematical tasks, to the diffuseness of the classifications of language and calculation disturbances and to the single or group study approach discussed above, it may well be that differences in the cognitive sty les of patients affect the tentatively proposed relation between aphasia and acalculia. In fact, identical lesions can result in different forms of acalculia because of the premorbid differences in the way s of performing mental calculations (Grewel 1969). Leonhard (1979) identified three quite different calculation sty les followed by normals. Some people operate automatically on overt or covert verbal number forms. In such cases, a language disorder affecting the verbal sphere should secondarily induce a calculation disorder. This ty pe of relation between aphasia and acalculia was actually reported in two patients with Gerstmann sy ndrome, their calculation errors being caused by verbal paraphasias (Benson/Denckla 1969). However, the functional relationship between paraphasic speech and paraphasias in the domain of number names was in fact clearly observed only in case 1 which presented paraphasic English jargon, but not in case 2 where no overt aphasia was noticed in a minimal lexical disorder marked by a slight wordfinding difficulty . Other normal people report “writing in their mind” the figures involved in calculation. They seem to manipulate numbers in the very same way they would perform operations on Arabic number forms on a sheet of paper. In such cases, alexia or agraphia for letters or words should extend to isolated digits or multidigit numbers. It must, however, be pointed out that the parallel between digits and letters is not y et clear. First, except when producing Arabic numbers in response to numbers presented in the same notation sy stem, all other number processing or calculation tasks oblige these subjects to tran-
327
scode either stimuli or responses (or both) into or from the figure sy stem they operate upon. Following brain damage, such transcoding may of course be impaired, thus introducing an extra source of calculation error. Second, there is a difference between the nature of language and Arabic numbers since the latter sy stem is an ideographic one, a characteristic which is highly relevant for brain machinery (see for instance Besner/Coltheart 1979 for separate orthographic and ideographic processing in normals). In fact, alexia and agraphia do not alway s co-occur in the two sy stems (Grewel 1952). But when dissociations were observed, descriptions of the premorbid calculation sty le of patients were unfortunately lacking, thus rendering the dissociation argument inconclusive. However, the potential role of what people write in their mind is clearly illustrated by Japanese studies showing that in mental calculation verification tasks expert abacus operators may be confused by numbers corresponding to the intermediate configuration steps of the abacus algorithm, whereas non experts were not disturbed (Hatano/Miy ake/Binks 1977). Finally , there is a minority of normal people who refer to some kind of visual stereoty ped diagrams as internal representations of integer number (Galton 1880 a, b; Seron/Pesenti/ Deloche et al. 1992). Such subjects may also have visual diagrams for positioning other sorts of structured serial-ordered verbal material like the months of the y ear. Lesions of the brain affecting visuo-spatial abilities should induce acalculia as a consequence of the general visuo-spatial deficits, since their normal number-representation sy stem and/or the procedures operating on it become impaired. Such a case was reported in which a left-sided occipito-parietal gunshot wound had impaired the patient’s topographical sense, and calculation abilities, resulting in only slight speech difficulties that could not be invoked to explain the calculation disorder (Spalding/Zangwill 1950). In the discussion of the role of premorbid idiosy ncratic calculation strategies on the ty pe of functional relation between impaired higher cortical functions (mainly language, occasionally spatial processes) and calculation thus far, it was assumed that each individual had developed just one path to master calculation. However, the possible influence of other functions like memory on both language and calculation has not y et been mentioned. Indeed, the first point has no empir-
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ical support from developmental psy chology (Lawler 1981) nor from the psy chology of normal (Gonzalez/Kolers 1982) or braindamaged adults (Campbell/Clark 1988). On the contrary , these domains seem to indicate that cognitive structures depend, on the one hand, on the specific experiences encountered bearing in mind that there are many way s of dealing with numbers. On the other hand cognitive structures also interact with each other. Such interactions might involve attention (Grewel 1952), serial order processing (Benson/Weir 1972), perseverations (Grewel 1969), body schema, finger agnosia, visuoconstructive abilities (Collignon/Leclercq/ Mahy 1977), and processing capacities (Benson/Weir 1972). The latter authors reported a case where the patient’s deficit appeared only when a number of steps had to be carried out simultaneously ; the patient had no difficulties performing single steps or other mental operations. Ideally , the question of relating aphasia and acalculia should also consider the two deficits in relation to some theory of spontaneous recovery and of neuropsy chological rehabilitation, since what is observed following brain damage is not produced by an intact brain, and consequently does not necessarily reflect the premorbid architecture of functions of that brain. In other words, depending on the post-onset neurophy siological processes (structural redundancy , closing of the diaschisis, vicariance) that subserve behavioral modifications (restoration of functions, reteaching previous knowledge, building new strategies) the relation between aphasia and acalculia in a patient might equally well fail to mirror the prior hy pothetical functional relation between language and calculation in a normal subject.
5.
Are there Functional Relations between Disturbed Language and Calculation Components at the Higher Level of Semiotic Systems?
As mentioned above, there are a lot of arguments which imply that there are hardly any mandatory functional relationships between aphasia and acalculia. But these conclusions might be misleading for the simple reason that the analy ses of data did not consider the relevant formalization levels in the two domains.
Grewel (1952) pointed out that the different notation sy stems used for representing quantities by different number forms should be considered as semiotic sy stems with their own distinctive features. Accordingly , each numerical sy stem is broken down into several components: (i) the set of sy mbols used; (ii) the semantic interpretation of numbers; and (iii) the sy ntactic rules for combining and manipulating numbers (Grewel 1969). He concluded that the three semiotic sy stems (Arabic digits, verbal and orthographic numbers) might be independently affected by brain damage since “they represent different sy mbolic sy stems with a different sy ntax”. Having thus situated acalculia within the paradigm of semiotic disorders, the initial question of its relation to aphasia may be reformulated. The relationships should be considered between the three different components (lexicon, semantics, sy ntax and computational rules) of each number notation sy stem (arabic, orthographic, verbal numbers) on the one hand, and the corresponding components of language and speech on the other. From a general as well as a formal point of view, divergencies in the linguistic structures of verbal numbers should constitute different sources of difficulty and therefore induce different disturbances in calculation. Grewel (1952) illustrated this point on the different sy stems for teens in English and French. We have reported data in the same direction, for instance in the transcoding of 75 into the Wallonian regular decade-unit structure (septante (70) cinq (5)), as compared to the more complicated phonographic form in French (soixante (60) quinze (15)); see Deloche/Seron (1984 a). In some way s, the semiotic level approach is linked to Finkelnburg’s (1870) (see Duffy / Liles 1979 for translation) theory of asy mbolia. Within such unitary views, different semiotic sy stems should be subserved by common mechanisms, and consequently brain damage should not cause sy stem-specific deficits, but should affect many sy mbolic usages. Ferro/Bothelo (1980) have reported the case of two patients with asy mbolic acalculia whose only deficit in numerical abilities was the misidentification of arithmetic signs. But contrary to expectations in the theoretical framework of asy mbolia, patient *1 clearly showed no extension of impaired processing for other sy mbolic sy stems like letters, numbers, traffic signs, play ing cards, emblems of political parties, horoscope signs, and so on.
29. Aphasia and Acalculia
The authors interpreted their patients’ disorders as cases of alexia for a special lexicon, arithmetical signs. Therefore the semiotic level analy sis, originally formulated by Grewel (1952) for numerical sy stems, does not seem to provide a theoretical framework which reveals simple relations between the consequences of brain damage on the different components described in language and speech on the one hand and their formal corresponding relations in calculation on the other.
6.
Are there Functional Relations between Language and Calculation Components at the Level of Formal Languages?
Stated in contemporary terms of formal language theory , the three components of the different numerical semiotic sy stems described by Grewel (1952; 1969) would refer to the following classification: The set of sy mbols used in a notation sy stem is its lexicon, the interpretation of numbers is its semantics, and the rules governing the well-formedness of lexical primitives into legal number forms is its sy ntax. It seems that Grewel (1952; 1969) considered sy ntax to involve not only the integration of the elements of lexicons into well-formed numbers, but also to extend to the computational rules for performing operations like borrowing from and carry ing over. At the level of formal languages, such computational knowledge should not be included in the sy ntactical sy stems of the different number notations (Arabic digits, phonographic number forms). Such a formal approach to numerical sy stems is intriguing because it identifies components strictly parallel to those described in language and speech, and because the numerical components are far more simple to analy se and formalize than those manipulated in natural languages. Lexicons contain only few primitives (the ten digits from 0 to 9 for Arabic numbers, less than thirty words for verbal and orthographic integers). The semantics of numbers are also straightforward; namely , the meaning of a number is the quantity it refers to. And sy ntaxes are limited to a few grammatical rules (see for instance Deloche/Seron 1986). Moreover, there is a oneto-one correspondence between the different notation forms of any number, which is by
329
no means the case between two different natural languages with the problems due to lexical ambiguities, idiomatic expressions and so on. Several authors have thus proposed explicit descriptions of numerical lexicons, sy ntaxes and semantics, and applied them to transcoding processes between Arabic numbers and verbal or orthographic number forms (Power/Longuet-Higgins 1978; Deloche/Seron 1982 a; Mc Closkey /Caramazza 1987; Cohen/Dehaene 1991). From this standpoint, we have looked for some formal parallels between the level of deficits (lexical, sy ntactic) in language on the one hand, and numerical transcoding errors in aphasic patients on the other hand in both group studies (Deloche/Seron 1982 b; 1986; Seron/Deloche 1984), and in single cases (Deloche/Seron 1984 b; 1985). The group studies seem to indicate some very gross relations between lexical/sy ntactical language processing preserved/impaired abilities of Broca’s or Wernicke’s aphasics and their ty pes of numerical transcoding impairments. However, the numbers of patients with Broca’s or Wernicke’s aphasia were small, and thus firm conclusions could not be established. The double dissociation paradigm seems more appropriate for indicating parallels, in preserved/impaired lexical/s y ntactical performances of brain damaged patients, between language and calculation performances. This line of research of functional relations between language and calculation, aphasia and acalculia may seem promising. However, this relation is not mandatory for lexical processing, since as already indicated alexia and agraphia for letters may occur without corresponding impairments for digits. At the semantic level, the assumption of a unique semantic representation for each number seems quite unrealistic when one considers the constellation of usages and meanings for numbers, which ranges from such items as cardinality , prices, or private bank account numbers, room numbers in an hotel, bus line numbers in the city to nursery rhy mes and numbers in idiomatic expressions. However, the results seem more encouraging for sy ntax. In this domain, we have reported the case of an agrammatic patient where data from linguistic tasks and from (Roman and Arabic) number processing supported Grossman’s (1980) hy pothesis of a central processor for hierarchically structured material in different notation systems (Deloche/Seron 1985).
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7.
Some Tentatively Concluding Remarks
On the one hand, I have presented some methodological and theoretical arguments that seem to indicate that at present a general functional relation between aphasia and acalculia cannot be clearly established. The factors to be considered include the ty pe of idiosy ncratic calculation sty le premorbidly developed by subjects, the potentially differential effects of brain damage on the architectures of language processing and of calculation, the formal levels of analy ses (and diffuseness of classification deficits) where relations between the two domains may be studied, the diversity of meanings attached to numbers depending on context of usage, the ideographic or phonographic natures of notation sy stems, the degrees of generalities expected from single cases or group studies and so forth. On the other hand, since calculation and number processing are well learned and extensively used in every day life, and because of the relative simplicity of the different notation sy stems, one of which is ideographic and almost universal (Arabic numbers), the other being phonographic and thus related to each language, the domain of calculation presents many interesting aspects in developmental psy chology , psy chology , neuropsy chology , artificial intelligence and more generally in the field of cognitive sciences. It seems to me that looking for correlations in order to investigate the lawfulness of mental processes in different domains should first be restricted to the study of many single cases. It is in this way that preserved/impaired calculation abilities may highlight some theoretical issues of concern generally studied in other high level cognitive activities. Among others such issues may encompass the distinctions between operative and figurative cognition (Gardner/Strub/Albert 1975), between conscious and automatic processing (Leleux/ Kaiser/Lebrun 1979), between autonomous and non autonomous mechanisms (Zbrodoff/ Logan 1986), between procedural and declarative knowledge in the field of memory (Squire 1987), between single abstract formatindependent representations in modular sy stems (Sokol/Goodman-Schulman/McCloske y 1989) and integrated networks with formatspecific representations and procedures (Campbell/Clark 1988). Multiple single case analy ses conducted in such directions should not consider calculation to be representative of the other higher cortical functions, but they
should nonetheless provide some insights into the different areas of cognition and thus contribute to significant advances in disentangling the intricacy of human cognitive machinery.
8.
References
Ardila, A. & Rosseli, M. (1990). Acalculias. Behavioural Neurology, 3, 39—48. Benson, D. F. & Denckla, M. B. (1969). Verbal paraphasia as a cause of calculation disturbances. Archives of Neurology, 21, 96—102. Benson, D. F. & Weir, W. F. (1972). Acalculia: Acquired anarithmetia. Cortex, 8 (4), 465—472. Besner, D. & Coltheart, M. (1979). Ideographic and alphabetic processing in skilled readers of English. Neuropsychologia, 14, 467—472. Boller, F. & Grafman, J. (1983). Acalculia: Historical development and current significance. Brain and Language, 2, 205—223. Campbell, J. I. D. & Clark J. M. (1988). An encoding-complex view of cognitive number processing: Comments on McCloskey , Sokol, and Goodman (1986). Journal of Experimental Psychology: General, 117 (2), 204—214. Claros-Salinas, D. & von Cramon, D. (1987). Diagnostik von Störungen im Umgang mit Zahlen (Akalkulie). Fortschr. Neurologie Psychiatrie, 55, 239—248. Cohen, L. & Dehaene, S. (1991). Neglect dy slexia for numbers? A case report. Cognitive Neuropsychology, 8 (1), 39—58. Cohn, R. (1971). Arithmetic and learning disabilities. In H. R. My klebust (Ed.), Progress in Learning Disabilities. 322—389. New York: Grune & Sratton. Collignon, R., Leclercq, C., & Mahy , J. (1977). Etude de la sémiologie des troubles du calcul observés au cours des lésions corticales. Acta Neurologica Belgica, 77, 257—275. Dahmen, W., Hartje, W., Bussing, A., & Sturm, W. (1982). Disorders of calculation in aphasic patients — spatial and verbal components. Neuropsychologia, 20, 145—153. Deloche, G. & Seron, X. (1982 a). From one to 1: An analy sis of a transcoding process by means of neuropsychological data. Cognition, 12, 119—149. Deloche, G. & Seron, X. (1982 b). From three to 3: A differential analy sis of skills in transcoding quantities between patients with Broca’s and Wernicke’s aphasia. Brain, 105, 719—733. Deloche, G. & Seron, X. (1984 a). Some linguistic components of acalculia. In F. C. Rose (Ed.), Advances in Neurology, Vol. 42: Progress in Aphasiology. 215—222. New York: Raven Press.
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Deloche, G. & Seron, X. (1984 b). Semantic errors reconsidered in the procedural light of stack concepts. Brain and Language, 21, 59—71. Deloche, G. & Seron, X. (1985). Sy ntactical knowledge in a case of agrammatism: Evidence from transcoding Roman to Arabic numerals. Brain and Language, 25, 234—245. Deloche, G. & Seron, X. (1986). Grammaticality judgments by aphasics of alphabetically written numeral forms. Psychologica Belgica, 36 (1), 17— 42. Deloche, G. & Seron, X. (1989). Protocole de dépistage des troubles du calcul et du traitement des nombres, EC 301. Paris: La Salpêtrière Hospital. Deloche, G., Seron, X., & Bergego, C. (1989). Traitement des nombres et calcul: Données théoriques et perspectives thérapeutiques. Annales de Réadaptation et de Médecine Physique, 32, 627—637. Duffy , R. J. & Liles, B. Z. (1979). A translation of Finkelnburg’s (1870) lecture on aphasia as “asy mbolia” with commentary . Journal of Speech and Hearing Disorders, 44, 156—168. Ferro, J. M. & Bothelo, M. A. S. (1980). Alexia for arithmetical signs: A cause of disturbed calculation. Cortex, 16, 175—180. Fuson, K. (1984). More complexities in substraction. Journal of Research in Mathematics Education, 15 (3), 214—225. Galton, F. (1880 a). Visualised numerals. Nature, 21, 252—256. Galton, F. (1880 b). Visualised numerals. Nature, 21, 494—495. Gardner, H., Strub, R., & Albert, M. L. (1975). A unimodal deficit in operational thinking. Brain and Language, 2, 333—344. Gonzalez, E. G. & Kolers, P. A. (1982). Mental manipulation of arithmetic sy mbols. Journal of Experimental Psychology: Learning, Memory and Cognition, 8 (4), 308—319. Grewel, F. (1952). Acalculia. Brain, 75, 397—407. Grewel, F. (1969). The Acalculias. In P. J. Vinken & G. Bruy n (Eds.), Handbook of Clinical Neurology, 3. 181—196. Amsterdam: North Holland. Grossman, M. (1980). A central processor for hierarchicall y structured material: Evidence from Broca’s aphasia. Neuropsychologia, 18, 299—308. Hatano, G., Miy ake, Y., & Binks, M. G. (1977). Performance of expert abacus operators. Cognition, 5, 57—71. Hécaen, H., Angelergues, R., & Houillier, S. (1961). Les variétés cliniques des acalculies au cours des lésions rétrorolandiques: Approche statistique du problème. Revue Neurologique, 105, 85—103. Henschen, S. E. (1919). Über Sprache, Musik und Rechenmechanismen und ihre Lokalisationen im Großhirn. Zeitschrift für die gesamte Neurologie und Psychiatrie, 52, 273—298. Hitch, G. J. (1978). The numerical abilities of in-
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dustrial trainee apprentices. Journal of Occupational Psychology, 51, 163—176. Kosc, L. (1980). To the problem of diffuseness in terminology in the field of disturbances and disorders of mathematical abilities. Focus on Learning Problems in Mathematics, 2 (4), 79—83. Lawler, R. W. (1981). The progressive construction of mind. Cognitive Science, 5, 1—30. Leleux, C., Kaiser, G., & Lebrun, Y. (1979). Dy scalculia in a right-handed teacher of mathematics with right cerebral damage. In Y. Lebrun & R. Hoops (Eds.), Problems in Aphasia: Neurolinguistics, 9. 141—158. Lisse: Swets & Zeitlinger B. V. Leonhard, K. (1979). Ideokinetic aphasia and related disorders. In Y. Lebrun & R. Hoops (Eds.), Problems in Aphasia: Neurolinguistics, 9. 11—7 7 . Lisse: Swets and Zeitlinger. McCloskey , M. & Caramazza, A. (1987). Cognitive mechanisms in normal and impaired number processing. In G. Deloche & X. Seron (Eds.), Mathematical Disabilities: A Cognitive Neuropsychological Perspective. 201—219. Hillsdale: Lawrence Erlbaum Associates. Power, R. J. D. & Longuet-Higgins, F. R. S. (1978). Learning to count: A computational model of language acquisition, Proceedings of the Royal Society London, 200, 391—417. Rosseli, M. & Ardila, A. (1989). Calculation deficits in patients with right and left hemisphere damage. Neuropsychologia, 27, 607—618. Secada, W. G., Fuson, K. C., & Halls, J. W. (1983). The transition from counting-all to counting-on in addition. Journal for Research in Mathematics Education, 14 (1), 47—57. Seron, X. & Deloche, G. (1984). From 2 to two: An analy sis of a transcoding process by means of neuropsy chological evidence. Journal of Psycholinguistic Research, 13, 215—236. Seron, X., Pesenti, M., Noel, M. P., Deloche, G., & Cornet, J. (1992). Images of numbers, or when 98 is upper left and 6 sky blue. Cognition, 44. 159—196. Sokol, S. M., Goodman-Schulman, A. R., & McCloskey , M. (1989). In defense of a modular architecture for the number processing sy stem: Reply to Campbell and Clark. Journal of Experimental Psychology: General, 111 (1), 105—110. Spalding, J. M. K. & Zangwill, O. L. (1950). Disturbance of numberform in a case of brain injury . Journal of Neurology, Neurosurgery and Psychiatry, 13, 24—29. Squire, L. R. (1987). Memory and Brain. New York: Oxford University Press. Zbrodoff, N. J. & Logan, G. D. (1986). On the autonomy of mental processes: A case study of arithmetic. Journal of Experimental Psychology: General, 115 (2), 118—130.
Gérard Deloche, Paris (France)
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30. Short-Term Memory in Aphasia 1. 2. 3. a
4. 5.
1.
Introduction Memory Disorders in Aphasic Patients Do Memory Impairments Play Specific Role in Sentence Repetition, Comprehension, and Expression? Summary References
Introduction
There is no doubt that language processing is highly complex. It involves at least the coordinated execution of multiple linguistic processes that subserve each of several segmental ty pes of information represented in language. It is possible, however, that even a fully elaborated account of these linguistic processes may not be adequate to explain our efficient use of language material. Thus, our ability to understand, repeat or express a sentence may turn as well on some facility with processes not ty pically thought to be ‘linguistic’ such as learning and memory . Several studies have begun to probe whether memory play s a role in sentence processing, and more recently , to incorporate memory in some specific fashion in a model of sentence processing. The ultimate goal is that a more realistic processing account of language use can be achieved, that is, a description of the cognitive and linguistic elements that interact in order for us to understand, repeat, or express a sentence. This review will specificall y examine whether short-term memory play s a role in sentence processing. In order to focus the scope of such a review, I will concentrate on data obtained from observations of adults with brain damage attempting to process sentence material. Space limitations prevent a discussion of the cerebral topographic representation or neurotransmitter basis for memory functioning in language. The data discussed below can be interpreted to support the claim that short-term memory play s a role in sentence processing, and in some cases may even be said to play a specific role in a particular language task, but it may be premature to state that memory deficits can account entirely for impaired sentence comprehension, repetition, or expression.
2.
Memory Disorders in Aphasic Patients
There is ample evidence that aphasics have a
memory impairment. Some of this evidence will be reviewed below. It is unclear, however, whether this memory deficit necessarily contributes to aphasics’ language difficulties, or whether the memory impairment is a by stander that happens to co-occur but without any direct impact on language processing. Indeed, it is possible that an aphasic disorder may prevent patients from learning or recalling verbal material. 2.1. Do Aphasics Have a Memory Impairment? The technique of Peterson/Peterson (1959) has frequently been used to document a shortterm memory (STM) impairment. This involves the presentation of the stimulus material, following which the subject performs a task such as mental arithmetic for a specified period of time, and then stimulus recall is probed. The mental arithmetic prevents explicit rehearsal of the stimulus material prior to recall, and the length of time between presentation and recall establishes the decay characteristics of the memory trace. Consider some representative early studies of memory in aphasia. Butters/Samuels/ Goodglass/Brody (1970) found that aphasics are significantly impaired in their recognition of visual and auditory single phonemes and consonant trigrams using the Peterson/Peterson (1959) technique. Goodglass/Gleason/ Hy de (1970) asked aphasics to point to a series of pictures corresponding to a list of nouns read to them. Anomic, conduction, and Wernicke’s ty pes of aphasics exhibited significantly better pointing span scores than socalled Broca’s aphasics. Although not without fault, findings such as these have been taken as evidence that a verbal memory impairment can be seen in aphasic patients. Consider in more detail the significance of these memory deficits in aphasics. It is possible that the memory impairment reflects some general properties of the language material which may be difficult for aphasics. For example, some have focused on the observation that words are sequentially ordered in a sentence, and it may be difficulty remembering this sequential order that accounts in part for aphasics’ sentence processing difficulty . De Renzi/Nichelli (1975) asked brain-damaged patients to repeat a series of digits orally, point to a written sequence of orally presented digits, and point to a series of pictures corresponding to an orally presented series of
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words. Broca’s, Wernicke’s and global ty pes of aphasics were significantly more impaired than non-aphasic patients with left hemisphere insult on all of these span tasks. However, aphasic and non-aphasic groups did not differ in their ability to repeat a spatially presented pointing sequence. These authors argued that aphasic patients’ deficits are due to difficulty holding verbal information in a specific sequence or order. However, such an account would have to explain how nonaphasic patients with frontal lobe insult also exhibit deficits in the temporal organization of information in memory (Milner/Petrides/ Smith 1985). Within the domain of language, moreover, there are language processing devices represented in the grammatical or semantic features of a language processor which help circumvent dependence on the linear character of the input string. Another approach has been adopted by Cermak and his associates. Cermak has cast aphasics’ memory impairment within a general model of memory . Cermak/Moreines (1976) presented a list of words to aphasics, and asked the patients to indicate when a word had been repeated in the list. Aphasics encountered increasing difficulty recognizing a repeated word as the number of words between the initial presentation and the subsequent repetition increased. Cermak/Tarlow (1978; also Riege/Metter/Hanson 1980) attempted to prove the specificity of this finding for language processing by demonstrating the effect only for the presentation of verbal material but not non-verbal material. Cermak/ Moreines (1976; Cermak/Stiassny /Uhly 1984) also found that aphasics were even more compromised when asked to detect repeated rhy mes or repeated words from the same semantic category . When patients were allowed more processing time or given instructions prior to list presentation, improvement was seen in the detection of semantically similar items but not rhy mes. Riege/Metter/Hanson (1980) performed an analy sis of patients’ errors on their detection task, and found that many false positives were phonemically based. Results such as these have been interpreted within the framework of a ‘depth of processing’ approach (e. g. Craik/Lockhart 1972) that suggests a differential impairment in the encoding of phonemic information in comparison to semantic information. It may be possible, however, to explain patterns of results such as these without rely ing on an in-
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dependent theory of memory . Thus, these data do not rule out the possibility of a compromised language processing device where access to a phonologically -based code for a word is relatively compromised when compared to access via a semantically -based code (Blumstein/Baker/Goodglass 1977). Others have taken this ty pe of criticism quite seriously . These investigators have suggested that the aphasic patients’ memory sy stem is relatively intact, but that their language impairment may lead to the appearance of a deficit on certain memory tasks. Rothi/ Hutchinson (1981), for example, found that aphasics encounter difficulty encoding the verbal information represented in the stimulus material used for their assessment of word list memory . Locke/Deck (1978) found that superspan list learning varied depending on whether or not the lists were composed of words that the patients could use for naming. Ostergaard/Meudell (1984; also Heilman/ Scholes/Watson 1976) found that Broca’s aphasics and Wernicke’s aphasics are severely compromised on a word span task. An assessment of the locus of patients’ errors indicated that Broca’s aphasics do not exhibit a primacy effect. The rehearsal of encoded material may be troublesome for Broca’s aphasics because of their ‘expression’ difficulty (Martin 1990). It is important to point out that aphasic patients’ memory impairments are not necessarily restricted to the verbal domain. Boller/De Renzi (1967; Gainotti/Caltagirone/ Miceli 1978) found that left hemisphere-damaged patients are significantly more impaired than right hemisphere-damaged patients in their recall of visually presented information such as meaningful and meaningless pictures. Kelter/Cohen/Engel (1977) found that fluent aphasics are impaired in their recall of meaningful pictures as well as snowflake patterns, while non-fluent aphasics encounter difficulty only in their recall of the snowflake patterns. Ostergaard/Meudell (1984) found that Broca’s aphasics encountered difficulty remembering faces. Goodglass/Denes/Calderon (1974) have suggested that aphasics are unable to use any form of covert verbal mediation to support their participation in non-linguistic processes such as their memory of non-verbal material. These observations call to question the material specificity of aphasics’ memory disorder and the role which this ty pe of memory impairment may play in aphasics’ language processing difficulties.
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Episodic memory thus may be impaired in aphasics. Does this mean that this memory disorder play s a causal role in their language deficit? It is possible that it is actually the aphasia that interferes with the ability to acquire, encode, and/or retrieve the verbal material. Indeed, even if aphasics do have an episodic memory impairment, this is not restricted to the verbal domain and thus may not be related to their language difficulty.
3.
Do Memory Impairments Play a Specific Role in Sentence Repetition, Comprehension, and Expression?
One of the general problems potentially limiting our ability to specify the relationship between memory and language is that the verbal material used in the above assessments of memory may not be truly ‘linguistic’ in nature. Though elegant experimentally , it may be difficult to leap from the random lists of letters or words to the highly organized phonologic or grammatical information which is so critical to our daily language. This problem may be circumvented by manipulating sentence material instead of consonants and trigrams. A second general problem is the ty pe of memory evaluated in these studies. The conscious attempt to learn and recall specific facts is generally referred to as ‘episodic memory ’. When try ing to understand or express a sentence, however, we do not ordinarily try to remember the sentence as we might learn a fact. Instead, there may be a transient mental representation of a sentence while it is being processed or otherwise manipulated mentally . It is this fleeting trace of a sentence which is addressed below. 3.1. Working Memory in Sentence Processing The theory often implicated in sentence processing is the model of ‘working memory ’ described by Baddeley (1986). A ‘central executive’ is said to manage the selective input of a stimulus into an information processing sy stem. One component of the central executive regulates the distribution of finite attentional resources. There is also a limited storage component. When this is overwhelmed, either because of excessive processing demands or a large volume of input data, excess information can be stored temporarily in an associated slave sy stem. The specific salve sy stem
which is recruited varies depending on the modality or material of the input data, and in the case of language is thought to be an ‘articulatory loop’. The articulatory loop in turn is composed of two elements — a phonological store and an articulatory rehearsal mechanism. The rehearsal mechanism can refresh the content of the phonological store. Working memory thus may serve as a interface between a perceptual device and a computational mechanism such as a sentence parser. While remarkably powerful and clearly capable of accounting for a wide variety of phenomena, it is just this universal applicability that may prove to be a shortcoming of the working memory model. The roles of short-term memory (STM) postulated in sentence comprehension, repetition, and sentence expression often appear to be quite similar, but this is not necessarily the case. Sentence processing may be supported by a general purpose STM such as the working memory model, or there may be a series of specialpurpose STM processors with slightly different characteristics that are particularly suited to the needs of, say , a grammatical processing device (e. g. Berwick/Weinberg 1984; Marcus 1980). Below I explore the possibilities that language-impaired patients have deficits in working memory that interfere with language functioning, and that amnesic patients with deficits in working memory have language disorders. 3.2. The Role of Short-Term Memory in Sentence Repetition One ty pe of task where language and memory are thought to interact is sentence repetition. In repeating a sentence, the subject must remember the initial parts of the sentence while the remainder of the sentence continues to be presented. In a sense, then, one part of a sentence may be play ing the role of filler material that interferes with active rehearsal during the process of remembering the entire sentence. From this perspective, sentence repetition may resemble the Peterson/Peterson technique. Nevertheless, sentence repetition is sensitive to the processing of linguistic material that has phonologic, grammatical, and semantic attributes. It is for this reason that sentence repetition differs from the repetition of an equally long list of unrelated words. Analy ses of performance profiles in conduction aphasia have served as the natural arena for study ing the relative role of these
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mnestic and linguistic processes in sentence repetition. Green/Howes (1977) reviewed the clinical features of the 52 cases of conduction aphasia in the literature at the time of their report. According to these authors, the major characteristics of conduction aphasia include a severe impairment in repetition despite normal or mildly impaired auditory comprehension and mild to moderate deficits of spontaneous speech. Secondary deficits include mild to moderate difficulty with reading comprehension and serial speech, but moderate to severe deficits in oral reading, writing, and naming. An error analy sis indicates that literal and verbal paraphasias, jargon, and grammatical errors occur in equal proportions in conduction aphasics’ repetition, spontaneous speech, naming, and oral reading. While there may be some agreement on the broad clinical picture of conduction aphasia, there is little consensus on the nature of the disrupted mechanism that underlies the repetition deficit. The classic explanation roughly states that there is limited information transfer from an input device to an output device (Geschwind 1965; Kinsbourne 1972). Goldstein (1948) specifically suggested that there may be a disruption of ‘inner speech’ which results in difficulty relating non-verbal mental phenomena to external speech. Relatedly , Alajouanine/Lhermitte (1964) have characterized the repetition impairment in terms of an unstable phonological trace. Hecaen/Dell/ Roger (1955; Dubois/Hecaen/Angelergues et al. 1964) elaborated these claims by specify ing that thoughts may have structural attributes that can be ordered, selected, and otherwise regulated. It is argued by these investigators that conduction aphasics cannot appreciate the sequence of mental forms constituting the information which must be repeated. Moreover, certain ty pes of words appear to be particularly difficult for conduction aphasics to repeat in an utterance or to use in spontaneous speech. For example, low frequency words are said to be more difficult to repeat than high frequency words, sentences with conjunctions and complex structures may be more difficult than simple utterances, and verbs may be more difficult than nouns which are more difficult than initial articles. Shallice/Warrington (1977), Warrington/ Logue/Pratt (1971), and Warrington/Shallice (1969) have published an elegant series of case descriptions which point to an entirely different ty pe of explanation for the repetition deficit in conduction aphasia. These investigators
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have suggested that the repetition deficit is due to an auditory -verbal STM impairment. This ty pe of explanation is a direct extension of Baddeley ’s (1986) working memory model, applied in this case to the auditory -verbal domain. Specifically , these authors found that their patients are profoundly limited in their auditory digit span, a standardized task that has been taken to measure STM. Moreover, this impairment was much more evident in the auditory modality than when equivalent strings were presented in the visual modality . Using the Peterson/Peterson technique, a decrement in performance was observed at longer delay conditions. The authors were careful to rule out several other possible explanations for their patients’ impairments, demonstrating that the deficit can not be attributed to a perceptual, comprehension, or expression deficit. Tests of long-term memory such as paired associate learning and logical memory subtests of the Wechsler Memory Scale failed to reveal significant abnormalities, suggesting a relatively specific STM problem. On the basis of these findings, it was claimed that the repetition deficit in conduction aphasia can be attributed to a selective defect of auditory verbal STM. Tzortzis/Albert (1974) and Strub/Gardner (1974) have seized on several inconsistencies in these observations in an attempt to demonstrate that the deficit in conduction aphasia is linguistic in nature rather than mnestic. Conduction aphasics’ performance on digit span tasks replicated the results described above. However, Tzortzis/Albert (1974) and Strub/Gardner (1974) emphasized that there is more difficultly repeating items in the correct sequence than simply reproducing the items regardless of the sequence. A decrement in performance was also seen with more rapid rates of presentation. Strub/Gardner’s analy sis of incorrect responses indicated many paraphasic errors rather than the omission of items that might be expected in a memory impairment. Patients demonstrated an advantage for the repetition of meaningful and more familiar material, and they were able to recognize whether paired sequences of digits are similar. Characteristics such as these do not support strong claims that the deficit in conduction aphasia is due to a STM impairment. Conduction aphasics also encountered difficulty on tasks assessing structural aspects of linguistic material such as later portions of the Token Test. Impairments in the repetition of non-verbal material such as musical notes,
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meaningful sounds, and rhy thms called to question the specificity of the memory disorder for language material. There were also impairments on perceptual identification tasks, suggesting reduced appreciation of the input stream. Focusing on the relative difficulty repeating sequences correctly compared to the relative success repeating items in an order-free fashion, Tzortzis/Albert (1974) supported Hecaen/Dell/Roger’s (1955) claim that conduction aphasics are compromised because of difficulty reproducing the organizational attributes of the target material. However, this ty pe of explanation fails to account for the patients’ consistent ability to repeat visually presented material more accurately than auditory material. Strub/Gardner (1974) felt that conduction aphasics exhibit difficulty decoding the auditory input signal for transformation into phonological shapes. This was based in part on the finding of a significant decrement in performance with more rapid rates of presentation and the difficulty with perceptual identification tasks. Caramazza/Berndt/Basili/Koller (1981) attempted to compare the mnestic and linguistic hy potheses in their examination of a conduction aphasic MC. Unfortunately , there was not a clear outcome supporting one hy pothesis or the other. MC exhibited a reduced digit span, as did the other patients described above. The pattern of MC’s errors revealed more sensitivity to list length than to the length of the delay between presentation and response, interpreted as support for a STM impairment. An analy sis of repetition errors revealed a primacy effect but not a recency effect, consistent with the STM hy pothesis, but a recognition task probing each of the serial positions in a digit sequence revealed equivalent treatment of initial and terminal items. An advantage for visually -presented sequences over auditoril y -presented sequences of material was seen in MC’s memory performance, consistent with the Warrington/ Shallice data and Strub/Gardner’s observations, but there was also better repetition performance when scored in an order-free fashion as compared to scoring that penalized for incorrect sequencing of material. A materialspecific repetition effect was seen for the presentation of some auditory materials but not others. Thus, lists of functors were repeated very poorly compared to lists of nouns, but high frequency noun sequences were repeated as accurately as low frequency noun se-
quences. While MC exhibited impairments on assessments of structural aspects of language material such as grammar, he exhibited little difficulty on tasks requiring lexical processing. Caramazza tentatively concluded that the STM hy pothesis is the best available account of conduction aphasia. Allport (1984) also compared the mnestic and linguistic hy potheses in several conduction aphasics. As with Strub/Gardner (1974), but unlike Caramazza/Berndt/Basili/Koller (1981), Allport found an effect for word frequency . There was also an effect for word imagability , but no disadvantage for the repetition of functors. An auditory discrimination task revealed significant difficulty , and an analy sis of repetition errors revealed many literal paraphasias. In contrast to Caramazza/ Berndt/Basili/Koller (1981), Allport (1984) concluded that the repetition deficit in conduction aphasia is due to an impairment decoding the auditory input signal, and that this impairment in fact underlies the STM deficit. It is difficult to resolve competing claims such as these. Several tasks such as digit span have been administered to all of the cases discussed above. However, a common set of baseline tasks and a common method of analy sis have not been identified. Without this common body of information, it remains difficult to determine whether there are two populations of conduction aphasics, as suggested by Shallice/Warrington (1977). These authors indicate that one group of conduction aphasics may have a prominent ‘reproduction’ deficit, that is, difficulty specifically repeating single words composed of many sy llables (see below), but the second group may have a ‘true repetition’ deficit. Moreover, while the above studies correlated performance on STM tasks with repetition performance, there has been very little manipulation or qualitative analy sis of the sentential material which conduction aphasics are attempting to repeat. Ostrin/Schwartz (1986) responded to this challenge in their study of sentence repetition in six agrammatic aphasics. Their patients had difficulty repeating a target sentence, but their detailed analy sis in fact indicated an important interaction between linguistic elements and the retained memory trace of the target. The NP1-V-NP2 sentences that were presented as targets varied in terms of a grammatical variable (they were in the active voice or passive voice) and the sentences varied in terms of a semantic variable (they were reversible sentences (NP1 and NP2 could be
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interchanged) or non-reversible sentences (NP1 and NP2 could be interchanged) or nonreversible sentences (NP1 could not be exchanged with NP2) which were either plausible or implausible). It should be noted that a change in the voice of an implausible item would make the item plausible. The results revealed that subjects made more errors in their attempts to repeat passive than active sentences, and most errors were in the repetition of closed class items. These findings alone are ambiguous with respect to the mnestic and linguistic hy potheses: Passive voice items are longer, and difficulty here may be due in part to a limited STM, but the material — specific difficulty with closed class items appears more consistent with a linguistically based impairment. An error analy sis revealed different ty pes of responses to the semantic variable depending on the voice of the target, and this analy sis suggests one possible resolution of the mnestic-linguistic conflict. In the active voice, omissions of free grammatical morphemes accounted for the errors in reversible and plausible items, but mixed morphology errors (combining together elements of active and passive voice) were seen in implausible items. The order of major sentential constituents was maintained. Ostrin/Schwartz argued that, for the mixed morphology ty pe of error to occur in the implausible items, patients must have a memory trace of the target after which they can pattern their responses. This must consist of some mental representation of surface word order or its argument structure. The authors go on to state that patients must also have a bias toward producing semantically coherent sentences. In order to maintain word order while respecting semantic coherency , patients apparently add an element of the passive voice to their responses on implausible items presented in the active voice. That is, patients attempt to modify the voice of an active implausible item toward the passive in order to make the item seem plausible. The same ty pe of explanation is used to account for the mixed morphology errors in the passive voice. The authors did not state whether the patients are told beforehand that they will hear some implausible items, nor did they monitor whether the patients are aware of the anomalous nature of the implausible items. Thus, the role of a decoding deficit in these patients is not clear. Nevertheless, in terms of defining the role of mnestic and linguistic processes in sentence repetition, the important point of
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this study is that an analy sis of patients’ repetitions suggests an interaction of partially compromised grammatical and STM processors. 3.3. The Role of Short-Term Memory in Sentence Comprehension While a potential role for memory in sentence repetition seems fairly obvious, it has become apparent only more recently that STM may also contribute significantly to sentence comprehension. It is somewhat trivial to state that memory may be a factor in the comprehension of very long sentences, but recent observations suggest the possibility that STM may also play a role in supporting the comprehension of certain grammatical features of a sentence regardless of sentence length. 3.3.1. Sentence Comprehension in Stroke Patients Linguistic analy ses of the aphasias have often led to characterizations of so-called Broca’s aphasics as agrammatic. Thus, these patients were said to omit grammatical morphemes from their spontaneous speech and to express themselves with utterances consisting of one or two nouns and possibly a verb — so-called telegraphic speech. This was thought to be a characteristic of their writing, repetition, and oral reading as well. In comprehension, moreover, it was claimed that Broca’s aphasics encounter considerable difficulty interpreting sentences which turn on grammatically -specified relationships between the words constituting the utterance. While there have been some observations of modality -specific grammatical impairments (Miceli/Mazzucchi/ Menn/Goodglass 1983; Nespoulous/Dordain/Perron et al. 1988), the hy pothesis has nevertheless been forwarded that Broca’s aphasics may not be competent with respect to sy ntactic appreciation (Berndt/Caramazza 1980). This ‘sy ntactic loss’ hy pothesis has recently been called to question. One ty pe of objection has focussed on the difficulty which this theory has for the different levels of performance that are seen across different sentence ty pes: If a sy ntactic capacity is lost, it is argued, then it ought to be lost across-theboard. Kolk/van Grunsven (1985) examined eleven Dutch-speaking aphasics who were generally representative of patients with a socalled Broca’s aphasia. On a sentence-picture matching task where active, locative, and passive sentences were used, they observed dif-
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fering levels of accuracy for each sentence ty pe across patients. A second ty pe of objection has focused on the observation that each patient exhibits a vary ing degree of impairment depending on the sentence ty pe. Relatedly , variability has been observed across identical sets of items administered to the same subject repeatedly , such as on successive day s. Kolk/van Grunsven argued that intersubject and intra-subject variability such as this are incompatible with the ‘sy ntactic loss’ hypothesis. Several attempts to explain these ty pes of variability have been proposed. Since these are not ‘on-line’ tasks, it is possible that patients can rely on a variety of non-specific ‘strategies’ to understand sentences. Caramazza/Zurif (1976) pointed out that Broca’s aphasics can reliably match a sentence to a picture if non-reversible nouns are used in the sentence’s arguments. This allows only one possible semantic interpretation of the sentence, even if the sentence is relatively complex grammatically . Bootstrapping strategies such as reliance on SVO word-ordering (which is ty pical in English) and dependence on sentential relations derived from thematic roles have also been proposed (e. g. Caplan 1983). It can be countered that these heuristic strategies may be very tedious, and their intricacy can potentially occupy a large amount of processing space, so they may not be very efficient or even useable in the real world. There is also evidence arguing against the likelihood that patients use even simple word order or semantic bootstrapping strategies (Kolk/van Grunsven 1985; Schwartz/Saffran/ Marin 1980). Another approach to the problem of variability has been to attribute sentence comprehension impairments to a deficit at some performance level of processing such as shortterm memory . It is not difficult to conceive of a working memory mechanism which takes as its input the speech signal and retains a mental representation on which further processing may be performed (Clark/Clark 1977). A STM disorder could easily account for the variability in intra-subject and inter-subject performance, for example, since sentence comprehension performance would vary depending on the limited number of features of the sentence that happened to be remembered. This ty pe of STM mechanism was first investigated in conduction aphasics’ sentence comprehension (Saffran/Marin 1975; Heilman/Scholes/Watson 1976; Caramazza/Bas-
ili/Koller/Berndt 1981). The comprehension deficit in conduction aphasia was attributed to the auditory -verbal STM impairment thought to underlie their repetition. More recentl y , studies of agrammatic aphasics have been performed to determine whether agrammatic comprehension can be attributed to an auditory -verbal STM impairment. Linebarger/Schwartz/Saffran (1983) asked four agrammatic aphasics to make grammaticality judgments of sentences containing a wide variety of grammatical structures. While their patients were generally quite successful, two ty pes of sentences proved inordinately difficult. These grammatical constructions seemed to require that the entire sentence be held in memory since information presented at the beginning of the sentence and at the end of the sentence had to be compared (e. g. The little boy fell down, didn’t it?’). Linebarger/Schwartz/Saffran questioned the ‘sy ntactic loss’ hy pothesis, and emphasized the role of a STM mechanism in the appreciation of some aspects of the grammar of a sentence. Similarly , in the Kolk/van Grunsven (1985) study mentioned above, the authors did not find that the grammatical features of the sentences discriminated between successful and poor sentence comprehension. Instead, their agrammatic patients encountered more difficulty on longer sentences than shorter sentences, regardless of grammatical complexity . Kolk/van Gunsven attributed poor performance to the greater processing demands made by longer sentences on a defective STM device. Others have cast some doubt on sweeping claims such as these, and have underlined the importance of determining the precise role which a STM mechanism may play in sentence comprehension. Martin (1987), for example, evaluated three nonfluent patients whose speech was consistently and severely agrammatic and three nonfluent aphasics who were judged not to be agrammatic since their speech included some simple sentences that were grammatically correct (two patients) or consisted only of stereoty ped utterances (the third patient). On a sentence-picture matching task using active, passive and relative-clause ty pes of sentences, the agrammatic patients performed at worse levels than the nonfluent patients who were not agrammatic. All nonfluent patients had equally reduced digit spans. Martin argued that the disrupted STM mechanism reflected in reduced digit span is not necessarily the same
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mechanism proposed to support sentence comprehension (also Caplan/Vanier/Baker 1986). Martin / Wetzel / Blossom-Stach / Feher (1989) attempted to test the relative success of the sy ntactic loss hy pothesis and the STM hy pothesis at explaning agrammatic aphasics’ sentence comprehension impairment. Three sentence-picture matching paradigms were used where active and passive sentences of vary ing lengths were presented. Foils included reversals (subject and object depicted in the incorrect role) or lexical substitutions (an unmentioned bit of information depicted in a picture choice). Martin argued that the ‘sy ntactic loss’ hy pothesis would predict better performance on active sentences than passives, but that the STM hy pothesis would predict better performance on shorter sentences than longer sentences. The results revealed that the vast majority of errors were due to the incorrect selection of reversal foils. In this context, three of the four aphasics encountered significantly more difficulty on passive items than active items. However, only one of the four patients actually performed at chance levels in sentence-picture matching. None of the patients demonstrated significantl y better performance on the shorter items than the longer items, but the small number of errors involving lexical substitution foils occurred exclusively on longer sentences, suggesting a partial memory deficit. The patterns of performance seen in this study thus failed to provide support for strong versions of either the sy ntactic loss hypothesis or the STM hypothesis. The role of memory in grammatical comprehension has also been evaluated by examining the ability of agrammatic patients to learn a new word. Grossman/Carey (1987) taught a low frequency word bice — an adjective referring to the dark green portion of the color spectrum — to seven patients who were classified as Broca’s aphasics by the Boston Diagnostic Aphasia Examination (Goodglass/Kaplan 1983). This was accomplished by first exposing each patient to the new word, paired with a dark green pen and a brown pen, in the sentence Take the bice pen — not the brown pen but the bice pen — and draw a picture of some clothes. This statement in this context provided all of the information necessary for patients to learn the new word’s phonological shape (bice), the new word’s meaning (that it refers not to brown but to dark green), and the new word’s
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grammatical form class (in the phrase the bice pen, bice modifies the noun pen so it is an adjective). About ten minutes after the exposure period, patients were probed for their knowledge of the new word’s grammatical form class and its meaning. To assess the ability to learn the new word’s grammatical form class, patients were asked to judge sentences where bice was used in an adjectival slot or a verb slot. This was compared with their judgments of sentences containing a known adjective or a nonsense sy llable in adjectival or verb slots. It was found that each of the Broca’s aphasics encountered significant difficulty demonstrating that they had learned the new word’s form class. This failure to learn that bice was a kind of adjective also had ramifications for their mental representation of the meaning of bice. In order to assess what they learned about the meaning of the new word, patients were asked to classify as bice or not bice objects that were bice-colored, bice-related in color (e. g. focal green, dark blue), or unequivocally not bice-colored (e. g. orange, red). In addition, the objects were different shapes: long and-thin (as in the initial pen used to illustrate bice), round or oblong (an object that was not pen-shaped), and shapeless swatches of colored paper. All but one of the Broca’s aphasics exhibited a graded judgment criteria for classify ing the objects. They classified bice-colored objects as bice more often than bice-related objects, which in turn were more often considered bice than objects which were unrelated in color to bice. This differed from their classification of green-colored objects, where there was a sharp discontinuity between objects considered green and non-green objects. All but one of the Broca’s aphasics also classified long-and-thin-shaped objects as bice more often than roundish objects, which in turn were classified as bice more often than color swatches. The authors reasoned that these patients hadn’t learned that the word was an adjective, so they also hadn’t learned that the word referred to a single property of the objects they were sorting. Findings such as these can be interpreted as indicating that a selective decoding impairment may have a significant impact on what can be learned or remembered. However, there is an alternate explanation — that a compromised attention component of the central executive may be limited in its ability to focus on the important features that should be captured for lexical acquisition. Both of
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the accounts stand in contrast to the role often attributed to STM in sentence processing — a mechanism that supports time-consuming process such as mapping across representational formats, or a post-interpretive process that supports the clarification of ambiguous material (Caplan/Waters 1990; McCarth y /Warrington 1987; Saffran/Martin 1990). Regardless of the correct interpretation, these observations could not be made without a word learning technique that eliminates bootstrapping strategies. Taken together, there is some evidence that sentence comprehension deficits may be due in part to a STM impairment. This evidence is far from definitive. Indeed, the alternate argument remains to be excluded. Caplan/ Waters (1990) have argued that STM has a marginal role in normal sentence comprehension, and a selective linguistic impairment in decoding the input string or performing the necessary grammatical computations may determine in part what can be remembered. One additional way to evaluate the role of STM in language processing is to assess amnesic patients who have a sentence comprehension deficit. To the extent that selective aspects of STM may be compromised in different groups of amnesics, these evaluations may also help us understand the precise role of each STM component in sentence comprehension.
vious sy ntactic deficits in their spoken language, and both can understand a range of sy ntactic structures in short sentences. It is argued that a sy ntactic deficit per se can not explain the difficulties experienced by these patients, and that their sentence comprehension impairment is attributable to a compromised STM mechanism. Findings such as these have been called to question. Butterworth/Campbell/Howard (1986) and Howard/Butterworth (1989) have reported a patient RE with an auditory -verbal STM impairment who has little difficulty understanding sentences. In reviewing the literature, these authors argue that many of these STM-impaired patients may have sentence comprehension impairments for other reasons, such as an independent grammatical processing deficit, and indeed that there is great heterogeneity across patients with socalled STM deficits. It is also possible that several of the STM-impaired patients may not have a STM impairment which is exclusively phonologic and/or auditory : TB, for example, also has a reduced visual digit span. In sum, there is debate about the need for a STM processor in sentence comprehension based on assessments of patients with discrete STM deficits.
3.3.2. Sentence Comprehension in Amnesic Patients
STM has also been shown to be compromised in patients with probable dementia of the Alzheimer ty pe (pDAT). Thus, several experiments have demonstrated a reduction in immediate serial recall of digits (Kaszniak/Garron/Fox 1979), letters (Morris 1984), and words (Corkin 1982). This is due in part to a moderate decrease in the recency effect (Martin/Brouwers/Cox/Fedio 1985). In order to define the locus of this impairment within the STM mechanism, each of the components of working memory have been examined in more detail. Morris (1984) demonstrated that pDAT patients are as sensitive to the effects of phonological similarity on a letter list recall task as control subjects, suggesting that the phonological store is relatively preserved in pDAT. Morris (1987) has shown that short words are recalled better than long words on a memory span task, and that concurrent articulation suppresses this effect, both paralleling the effects seen in neurologically -intact adults. This suggests that the articulatory loop rehearsal mechanism is relatively intact. By comparison, Baddeley /Logie/Bressi et al.
Assessments of aphasics have not provided a definitive picture of the role of STM in sentence comprehension. Other investigators have focussed instead on the evaluation of sentence comprehension in patients with STM impairments. Vallar/Baddeley (1984; 1987) described PV, a patient with a very limited phonological STM, no articulatory rehearsal capacity , and apparently little ability to recode visually presented information. PV has considerable difficulty understanding relatively long sentences where the subject and object are reversible, and she has difficulty detecting errors of anaphoric reference where one or two sentences are placed between the item and its subsequent reference. A second patient, TB, also has very limited phonological STM, despite normal phonological processing. He has profound difficulty verify ing complex or lengthy sentences presented auditorily , but improves somewhat with visual presentation. Both patients are without ob-
3.3.3. Sentence Comprehension in Alzheimer’s Disease
30. Short-Term Memory in Aphasia
(1986) have shown that pDAT patients’ performance on immediate recall tasks suffers when they are asked to perform concurrent tasks. Using the Peterson/Peterson (1959) technique with different ty pes of intervening material, Morris (1986) claimed that dividing their attention with increasingly difficult task results in progressively inferior performance. These findings have been taken as support for the argument that the central executive is compromised in pDAT. It should be noted, however, that alternate explanations have been offered for results such as these (Broadbent 1983; Monsell 1984). Moreover, memory span deficits are also seen on a pointing span task (Corkin 1982), suggesting that these phenomena are not specific to a language processing sy stem. Careful analy ses of errors on span tasks have also revealed a reduction in the primacy effect (Martin/Brouwers/Cox/ Fedio 1985), and there is a strong correlation between performance on span tasks and the overall degree of dementia (Corkin 1982; Kopelman 1985). The central executive component of working memory may be compromised in pDAT, but these data must be interpreted cautiously. In this context, there have been several assessments of sentence comprehension in pDAT. Clinically , it is claimed that grammatical structure in language expression is impaired late in the disease process in some patients, including inappropriate tense agreement and the breakdown of phrase markers in spontaneous speech (Constantinidis/ Richard/de Ajuriaguerra 1978; Irigara y 1967). Observations of mildly and moderately impaired patients seem to support the claim that the bulk of patients’ difficulty is in the processing of semantic aspects of sentences. Appell/Kertesz/Fisman (1982) and Cummings/Benson/Hill/Read (1985) administered aphasia screening batteries to pDAT patients, for example, and found relatively profound impairments in the domains of naming/wordfinding and lexical semantic comprehension/ expression. Kertesz/Appell/Fisman (1986) directly compared the language performance patterns of pDAT patients with stroke patients, and found that pDAT patients resembled aphasics with Wernicke’s, transcortical sensory , and anomic sy ndromic profiles, but that none of the demented patients resemble so-called Broca’s aphasics or transcortical motor aphasics. Bay les (1982) has also suggested relatively preserved appreciation of a sentence’s grammatical features in pDAT,
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since pDAT patients were able to correct ‘sy ntactic’ errors in sentences but not ‘semantic’ errors. It should be noted that the sentences with semantic errors used by Bay les apparently violated sy ntactic rules as well, including strict subcategorization and argument structure constraints. Nebes (1989) asked pDAT patients to recall short sentences that were normal, that exhibited disrupted semantic structure, and/or had disrupted ys ntactic structure. They found that recall of the sy ntactically disrupted sentences is similar in pDAT and normal subjects. However, they also found that semantic disruption did not differentially affect pDAT and control subjects. While these findings suggested relatively preserved grammatical processing, Appel/ Kertesz/Fisman (1982) found significant impairments on the ‘sequential commands’ subtest of the Western Aphasia Battery (Kertesz 1982), and Cummings/Benson/Hill/Read (1985) found significant impairments on the ‘complex commands’ subtest of the Boston Diagnostic Aphasia Examination (Goodglass/Kaplan 1983). Hier/Hagenlocker/ Shindler (1985), analy zing pDAT patients’ descriptions of “The Cookie Theft Scene” (Goodglass/Kaplan 1983), found that the mean length of utterances, the use of subordinate clauses, and the use of prepositional phrases are all reduced. Findings such as these may be consistent with a grammatical processing impairment, but the extent to which these deficits may also be attributed to an impaired working memory sy stem or to some other cognitive impairment in pDAT remains unclear. One recent study , however, has found specific impairments on a sentence comprehension task that implicate difficulty with grammatical aspects of sentence comprehension (Chawluk/Grossman/Calcano-Perez et al. 1991). These investigators administered an extensive set of sentences to six pDAT patients who were mildly impaired according to the MMSE, had digit spans of about 5, and were relatively intact in their sentence repetition. The sentences, composed of high frequency nouns and verbs, were cast in three sy ntactic frames: Simple, terminal subordinate where a relative clause was placed at the end of a simple sentence, and center-embedded subordinate where a relative clause was placed in the center of a simple sentence. Half of each ty pe of sentence was in the active voice and the remainder in the passive voice.
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The information in each sentence was probed with a simple question that was in the active or passive voice (e. g. The eagle chased the hawk. Which bird was chased?). The results revealed an error rate of 26%, significantly inferior to the performance of control subjects. A detailed analy sis of the error pattern revealed that pDAT patients responded randomly on items where the voice of the sentence did not correspond to the voice of the question. Given their ability to repeat sentences such as these, one possible interpretation of this finding is that a compromised central executive was overwhelmed by the mental manipulation required to compare thematic roles in the sentence and its question when these did not correspond in voice. Alternate explanations include attributing the deficit to a non-specific effect of limited information processing or a defect in performing the necessary grammatical comutations. Regardless of the specific explanation, the finding of a sentence processing impairment in Alzheimer’s disease opens the way to characterizing the nature of sentence processing that may occur in the setting of a compromised central executive. 3.3.4. Sentence Comprehension in Parkinson’s Disease Parkinson’s disease (PD) is a common neurodegenerative condition that results in a movement disorder consisting of tremor, rigidity , and brady kinesia. It has been stated that the cognitive impairment in PD can be characterized as a so-called subcortical dementia, where deficits can be seen in the domains of memory , visuo-spatial processing, executive functioning such as attention and organizational capacit y , and brad y phrenia (Cummings 1990). An aphasia is said to be among the exclusionary criteria of subcortical dementia (Cummings/Darkins/Mendez et al. 1988). Thus, the presence of a language processing deficit in PD ought to be attributable to some non-linguistic cognitive impairment, such as limited STM. Lieberman/Friedman/Feldman (1990) administered the Rhode Island Test of Language Structure to PD patients who had a moderate motor disorder. Several of their patients had high rates of comprehension errors on sentences that were moderately complex sy ntactically . The impaired patients also were demented, but the authors did not characterize the dementia or report the results of memory measures. Grossman/Carvell/Gollomp et al.
(1991, 1992) assessed the ability of mildly impaired, non-demented PD patients to answer simple questions about target sentences such as The eagle chased the hawk that was fast. Which bird was chased?. The sentences varied in terms of phrase structure, voice, and semantic constraint. Probes were also designed to assess the ability to compare information from adjacent and non-adjacent segments of the target sentence. Patients were also asked to detect errors in some similarly constructed sentences. Significant impairments in PD patients’ overall performance were found when compared with control subjects. Indeed, discriminant analy ses revealed that 65% of PD patients differ from control subjects. Performance on sentences deteriorated as they became more demanding grammatically , an order of difficulty seen in 83% of the patients. There was little effect for sentence length, and errors occurred regardless of whether the information being probed could be found in adjacent or non-adjacent portions of the sentence. These negative findings argued against the possibility that a limitation in the size of a STM buffer can explain their impairment. However, the PD patients encountered difficulty detecting the presence and nature of errors in grammatical morphemes in the sentences. This suggested that a compromised attentional mechanism within a grammatical processor may be contributing to PD patients’ sentence comprehension difficulties. Ge y er/Grossman (submitted) confirmed this ty pe of sentence processing impairment in another group of mildly impaired, nondemented PD patients. In this experiment, patients were asked to make truth verification judgments of probes that followed sentences (e. g. The pirate sank the ship. The ship sank — True or False). The items contained one of two ty pes of verbs: a simple transitive verb, where its subject in a transitive sentence is also its subject in an intransitive sentence; or a lexical causative verb, where its object in a transitive sentence is its subject in an intransitive sentence, as in the above example. These verbs were embedded in active voice, passive voice, or periphrasic (as in The pirate made the ship sink) sentential frames. All PD patients performed at normal levels on a short version of the Token Test. Sixty percent of PD patients encountered significant difficulty determining the accuracy of probes about sentences containing lexical causative verbs, and compromised individuals exhibited simi-
30. Short-Term Memory in Aphasia
lar performance profiles with equivalent levels of absolute impairment in all but one case. While lexical causatives were more difficult than simple transitives in both active and passive voice sentences, the 2 verb ty pes were treated equivalently when embedded in the periphrastic ty pe of sentence. Moreover, lexical causatives in the periphrastic voice were easier to understand than lexical causatives in the passive voice. These findings suggest that a defect in performing grammatical computations cannot fully account for PD patients’ sentence comprehension difficulties. The periphrasic voice may have helped PD patients disambiguate the aty pical mapping from sy ntactic roles to thematic roles in lexical causative verbs, a kind of process that is said to be subserved by working memory (Berndt/Salasoo/Mitchum/Blumstein 1988; Saffran/Martin 1990; Schwartz/Saffran/Marin 1980). Grossman/Carvell/Peltzer (submitted) assessed the role of working memory and a mapping function in grammatical comprehension in PD as well. In the first experiment, non-demented patients with mild PD were asked to judge sentences containing a mass noun (e. g. water) or a count noun (e. g. pencil) modified by a quantifier such as much or few. In half of the items, the noun was modified appropriately by a mass adjective or a count adjective, but in the remainder the noun and the adjective did not agree. In half of each ty pe of count item, moreover, the ‘s’ modify ing the noun was used appropriately and in the remainder inappropriately . In the second experiment, patients were asked to match a sentence containing a count term or a mass term (e. g. Point to the container with many) with one of four pictures (a large amount of a mass substance, a large amount of a count substance, a small amount of a mass substance, or a small amount of a count substance). The results revealed on the first experiment that 45% of PD patients encounter significant difficulty detecting sentences where a noun and its adjective do not agree. In these patients, the impairment was due to difficulty detecting an adjective-noun mismatch or difficulty identify ing an inappropriate use of a modify ing ‘s’. Importantly , sentences exhibiting both ty pes of errors simultaneously were judged accurately by PD patients. This effect is not consistent with a grammatical computation impairment, but instead suggests a threshold effect as might be seen in a limited
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working memory . On the second experiment 70% of PD patients were impaired, indicating significant difficulty mapping sentences onto pictures. An error analy sis indicated that patients frequently err by choosing the wrong ty pe of substance, but they rarely err by choosing the wrong amount of substance. These findings emphasize the difficulty experienced by these patients in mapping sy ntactic roles onto thematic roles, lending support to the claim that working memory may play a role in the sentence comprehension deficits of PD patients. In sum, there is some evidence that STM may play a role in sentence comprehension. This conclusion, however, is far from unequivocal. In aphasics, for example, the nature of the interaction between mnestic and linguistic factors remains to be established. It is also unclear whether the role is as simple as a limitation in the size of a STM buffer or involves a more dy namic process such as actively attending to appropriate grammatical information. Such a role may be linked to a so-called central executive, as suggested by the data from Alzheimer’s disease patients. 3.4. The Role of Memory in Sentence Expression The traditional treatment of sentence expression difficulty has emphasized the identification of the modality through which expression cannot be accomplished. For example, alexia is used to refer to an impairment in reading written material, and agraphia refers to an impairment in written expression. The initial descriptions of these phenomena were concerned with determining whether an alexia or agraphia occurred in isolation (so-called ‘alexia without agraphia’ or ‘pure agraphia’) or the two deficits co-occurred. More recent clinical descriptions of neurologically -impaired adults have described alexic and agraphic impairments in more detail. Thus, surface alexia or agraphia (Hatfield/ Patterson 1983; Patterson/Marshall/Coltheart 1985) is said to describe that group of patients where known words with unusual spelling patterns cannot be read or written accurately (e. g. who, said). By comparison, words and novel lexemes with transparent grapheme-phoneme correspondence rules are read and written accurately (e. g. stad, lif). Their reading and writing errors are often regularizations of irregular words (e. g. guest → ‘just’). Moreover, they are more likely to read mildly irregular words correctly in com-
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parison to very irregular words (e. g. yacht) and are influenced by word frequency , letter frequenc y , and part-of-speech (Bub/Cancelliere/Kertesz 1985; Goodman/Caramazza 1986; Shallice/Warrington/McCarth y 1983). Graded irregularity and frequency effects such as these have suggested the possibility of reading and writing models which turn on the use of units that are larger than the grapheme or phoneme, and may even entail reading/writing by analogy to known words that are similar in appearance to the target word (Marcel 1980; Friedman 1988; Patterson/ Morton 1985). The reverse pattern of performance is called phonological alexia or agraphia (Beauvois/Desrouesne 1979; Funnell 1983; Roeltgen/Heilman 1984). These individuals find it difficult to read and write novel words with transparent grapheme-phoneme correspondence rules, but are accurate at reading or writing known words even if their spelling pattern is quite irregular. Some of these patients nevertheless find functors difficult to read and write (Bub/Kertesz 1982; Patterson 1982). Among the alternate explanations is the proposal that the word includes form class or other category -specific information that can be used to mediate some aspects of reading and writing (Bub/Chertkow 1988; Friedman 1988). On the basis of observations such as these, a minimal computational apparatus for reading and writing can be hy pothesized. This may include a phonological output lexicon to mediate oral reading of known words, a graphemic output lexicon for writing known words, and a set of grapheme-phoneme correspondence rules to mediate the oral reading of novel written words and the writing of novel dictated words. The overall architecture of this expression mechanism, although widely held, may not be computationally adequate to support oral or written expression or account for the entire spectrum of impairments said to occur in neurologically -impaired patients with reading and writing disorders. The most common strategy has been to postulate additional processing elements, such as a memory component (Ellis 1982; Miceli/Silveri/Villa 1985; Morton 1980; Newcombe/Marshall 1980). A STM buffer such as this may be needed to retain the code of an output lexicon while the identity of each letter or sound is chosen prior to expression. Consider some of the case studies of acquired dy sgraphia that underline the necessity
for hy pothesizing a STM buffer mechanism. A graphemic buffer, for example, is said to hold the information from a graphemic output lexicon while a letter name conversion mechanism translates the abstract graphemic representation into an orally spelled word or an allographic conversion mechanism translates the graphemic representation into a written word. Caramazza/Miceli/Villa/Romani (1987) described a patient LB who was thought to have a functional lesion to the graphemic buffer. LB made the same ty pes of errors in writing, ty ping, and oral spelling, suggesting that the deficit was due to an impairment prior to the planning and execution of a motor program. LB also erred when asked to write spontaneously , write dictated words, and produce the written name of an object, suggesting that the deficit occurred after the orthographic information had been retrieved. Spelling errors were not responsive to any lexical properties such as imagability , word frequency , or grammatical form class. Similarly , error ty pes did not reflect any consistent semantic, morphologic, or phonologic characteristics, consistent with the possibility that the graphemic buffer is a post-lexical mechanism. Errors consisted of letter deletions that became increasingly frequent as the word was longer, and they were more likely to occur in the middle of a word. Related patterns of spelling errors have been described in other patients (Hillis/Caramazza 1989; Posteraro/Zinelli/Mazzucchi 1988). These recent observations, as well as additional analy ses of LB, have suggested that the original characterization of the graphemic buffer must be recast. Caramazza/ Miceli (1990) provided additional descriptions of LB that indicated the sensitivity of his spelling errors to the sy llabic context in which they occurred. For example, LB made more errors on words with complex consonant-vowel patterns (e. g. CCVCVV) than words with a, regular consonant-vowel pattern (e. g. CVCVCV). Errors in the regularCV words were overwhelmingly transpositions and substitutions, but deletions and insertions were equally frequent for complexCV words. LB also tended to apply doubled letters to the incorrect consonant within a word (e. g. sorella → sorrela), although a letter-doubling error rarely occurred in words that did not already have a doubled letter. Findings such as these suggested that the graphemic buffer does not simply hold an ordered sequence of graphemes, but must also
30. Short-Term Memory in Aphasia
be sensitive to certain rule-determined properties of words. Thus, the graphemic buffer apparently represents the consonant-vowel status of graphemes and the graphosy llabic structure of words. Similarly , based on detailed analy ses of spelling errors in morphologically complex words, Badecker/Hillis/ Caramazza (1990) have also demonstrated that information is stored in the graphemic buffer in morpheme-sized packages. There is additional evidence that the graphemic buffer may not simply be a passive storage vehicle. The distribution of ty pes of errors in words and non-words was quite similar in these patients, for example, but some had more difficulty spelling non-words than words. Some patients were also affected by lexical factors such as word frequency . Observations such as these suggest that other factors may contribute to the functioning of the graphemic buffer, and again raise the specific possibility of a role for writing by analogy to the corpus of words in the patient’s written vocabulary . Errors were also differentially distributed in words as a function of the location of the causative brain lesion in some patients (Hillis/Caramazza 1989). This effect for spatial location suggests a role for an attentional mechanism in the graphemic buffer. Several of the individuals exhibited impairments in other cognitive domains which bear an important family resemblance to their language expression deficit. Consider, for example, the errors in drawing abstract figures from memory made by DH (Hillis/ Caramazza 1989) and the dy scalculia, drawing apraxia, and poor verbal memory of SE (Posteraro/Zinelli/Mazzucchi 1988). These additional neuropsy chological deficits call to question the specificity of something like a graphemic buffer for language expression. Thus, there is considerable evidence for the existence of a buffer mechanism that holds a transient mental representation of a word during its spelling, but many questions remain about the specific nature of this buffer. A phonologic buffer has been postulated to hold phonologic material while a conversion mechanism prepares the material for expression. A phonologic buffer play s a role in 3 expressive modalities: writing words to dictation, mediated by the phonologic output lexicon; reading non-words orally , mediated by a grapheme-phoneme conversion mechanism; and repeating non-words orally . In the case of written output, material is held in the phonologic buffer while a phoneme-graph-
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eme conversion sy stem transcodes phonemes for the graphemic buffer. For oral output, the phonologic buffer retains the set of phonemes while an articulatory process prepares the information for expression. Evidence for a functional lesion of the phonologic buffer would come from the converging inability to perform all 3 of these expression tasks in the face of an ability to write known words to copy or dictation, that is, expression tasks that depend only on the graphemic buffer. Caramazza/Miceli/Villa (1986) present such converging evidence from patient IGR. Errors were more evident in longer words and overwhelmingly consisted of single letter substitutions. Similarly , many errors were made in the repetition of non-words (data are not provided for the repetition of familiar words), and errors were ty pically single phoneme substitutions. These findings are largely consistent with the proposed location of the phonologic buffer in the language expression sy stem. Findings inconsistent with the proposed characteristics of this STM mechanism included that this patient made many more errors writing non-words than words. Moreover, the length of delay on a delay ed writing task did not have an effect. Errors in oral reading resembled the target response phonologically and consisted of deviations by 1 or 2 letters, also consistent with some expected properties of the phonologic buffer. However, oral reading errors were more common for non-words than words, a finding inconsistent with the proposed location and role of the phonologic buffer. An examination of the ordinal location of errors indicated a relative predominance of reading errors at a word’s initial position when compared to writing and repetition, but errors otherwise occurred in the middle positions of words. Since IGR had a right hemisphere lesion, it is possible that this patient was display ing some left-sided inattention. As with the graphemic buffer, there may be some influence of an attentional mechanism on the phonologic buffer. Moreover, the persistent finding of inferior performance with nonwords emphasizes the need to incorporate additional attributes in these buffers or develop an alternate functional architecture that can incorporate this finding. Additional evidence for a phonological buffer may come from an analy sis of patients with a so-called reproduction conduction aphasia (Caplan/Vanier/Baker 1986; Kohn 1984; McCarthy /Warrington 1984). These in-
II. Acquired Organic Pathologies of Language Behavior: Neurolinguistic Disorders
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dividuals are affected by word length and produce many phonemic paraphasias that often consist of single phoneme errors, characteristics thought to be associated with a phonologic buffer. The ‘output’ nature of their disorder is emphasized by the fact that they often repeat words multiple times in an attempt to reproduce the target, and their performance on span tasks is generally quite good. As with IGR, the patients of Caplan and McCarthy /Warrington had much more difficulty with non-words than words, suggesting that other factors involving alternate procedural and/or computational mechanisms must be taken into consideration in the characterization of the phonologic buffer. Moreover, a study by Pate/Saffran/Martin (1987) found that errors occurred differentially depending on the context and nature of the phonologic material being repeated (e. g. murderous vs murder us). This suggested that the phonologic buffer is not a passive reservoir but may be sensitive to the nature of the information being represented. As in the case of the graphemic buffer, then, additional word has begun to suggest some of the internal characteristics of outout buffer mechanisms that retain information in preparation for oral expression. In sum, there is some evidence from a handful of case studies that suggests the existence of graphemic and phonologic output buffer mechanisms for language expression. The nature of these buffers, however, is far from clear. While some observations have begun to clarify the internal nature of these devices, others have suggested that we are far from the point of feeling confident about the precise role of these devices in the functional architecture underly ing expression. There has not been an adequate interpretation of the persistent advantage of words over nonwords, for example.
4.
Summary
Do memory impairments play a role in the language processing deficits seen in aphasia? Investigators interested in memory and language initially treated sentential material as but one example of a broader set of stimuli. Thus, the sequence of words in a sentence was taken to be representative of any ty pe of sequence, and difficulties were thought to occur because of the compromised appreciation of the ordered material (De Renzi/Nichelli
1975). Aphasiologists often felt that reasonably detailed linguistic analy ses would probably be adequate for an appropriate schema characterizing sentence processing. Indeed, there was even some reason in ignore claims about the potential impact of aphasics’ memory impairments on their language performance since several studies had indicated that memory deficits were not restricted to the verbal domain (Boller/De Renzi 1967; Gainotti/Caltagirone/Miceli 1978). More recently , investigations of sentence repetition in conduction aphasia have served as a forum for debating whether a linguistic deficit or mnestic deficit can explain the repetition difficult y (Caramazza/Berndt/Basili/ Koller 1981; Shallice/Warrington 1977; Strub/ Gardner 1974). Linguists have pointed to several shortcomings in the arguments of the ‘memory loss’ advocates; mnemonists have also pointed out inconsistencies in the thinking of the ‘linguistic loss’ advocates. Fortunately , more recent work (Ostrin/Schwartz 1986) has adopted the rational view that both linguistic and STM processors probably contribute to sentence repetition. This work has thus initiated the next step in our attempts to characterize a reasonable model of sentence processing, that is, determining how memory and language processes may work together in supporting sentence repetition. One hy pothesis is that there may be a partial memory trace of the sentence which the patient is attempting to repeat. The semantic and grammatical capabilities of the listener may bias the content of the memory trace. Other studies have considered the role of memory in sentence comprehension. Again, there has been a contrast between, on the one hand, ‘sy ntactic loss’ advocates who have observed sentence comprehension impairments to increase in correlation with increasing grammatical complexity in a sentence (Benson/Geschwind 1986; Berndt/Caramazza 1980), and on the other hand, ‘memory loss’ advocates who see increasingly frequent sentence comprehension impairments as the sentences become longer and therefore more difficult to remember (Kolk/van Grunsven 1985; Linebarger/Schwartz/Saffran 1983). One possible resolution may be that a working memory device w i t h i n the grammatical processor is compromised (Grossman/Carvell submitted; Kolk/van Grunsven 1985). This may prevent appropriate identification of grammatical morphemes, the storage of appropriate information in a STM buffer, and thus de-
30. Short-Term Memory in Aphasia
grade the quality of grammatical computations. It also appears that STM processors may be necessary for language expression. Earlier characterizations of these STM devices suggested only slave buffers that interface 2 processing components. However, even these mechanisms appear to have internal characteristics indicating that they actively participate in the exchange of information from processor to processor. It is noteworthy , as implied throughout the discussion, that the STM devices involved in comprehension, repetition, and expression are quite different in many respects. The variability depends in large part on the nature of the task being performed. Such non-uniformity is inconsistent with ‘working memory ’ as conceived by Baddeley (1986) in that a single working memory mechanism does not appear to subserve these diverse manifestations of STM in language processing. I should briefly mention that this componential approach to the role of memory in sentence processing assumes a great deal about the overall architecture of the cognitive elements contributing to these language tasks. A very different approach has recently been developed — parallel distributed processing (McClelland/Rumelhart 1986). According to this model, a lay ered device using large numbers of densely interconnected units ‘learns’ about the probabilities inherent in a corpus based on several exposures to the material. During each learning session, feedback is given to the device in response to its answers to questions. The task-specific device then modifies the weights on the set of internal connections between lay ers. The learningfeedback cy cle is repeated many times until the device’s answers approach 100% accuracy. This radicall y different approach has proven extraordinarily powerful. In one experiment intended to model dy slexia, for example, the number of units in the middle lay er of a three-lay ered device was decreased. This modified processor appeared ‘dy slexic’ in that it was less capable of making appropriate decisions about the acceptability of letter strings as words despite an equal number of learning sessions (Patterson/Seidenberg/McClelland 1988). More remarkable y et was the finding that the “lesioned” device produced the same pattern of errors that is seen clinically in phonologic alexia. Despite the power of this approach, there are many potential
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problems (Pinker/Prince 1988). The middle lay ers of these devices are ‘hidden’, for example, so that the precise cognitive role play ed by these lay ers is far from clear. Detailed examinations of various linguistic constructs claimed to be learned by parallel distributed processing devices — such as the regular versus irregular past — in fact may not be reliably represented. With respect to dy slexia, it is unclear why only one form of dy slexia has emerged from lesioned devices. Despite these shortcomings, the ‘parallel distributed processing’ approach represents an important alternative to the componential model. In sum, the data suggest that memory probably play s a role in sentence processing — probably an important role. The strong forms of arguments characterizing memory as explanatory for all aspects of sentence processing impairment may not be supported over the long run. Instead, the data are beginning to outline some of the specific way s in which mnestic and linguistic processes may interact in our attempts to appreciate a sentence. It is the precise description of this interaction which holds the hope of providing a computationally adequate characterization of the processes subserving sentence appreciation. Author’s note: This work was supported in part by the United States Public Health Service (DC00039 and AG09399) and by the McCabe Foundation. I would like to express my appreciation to Patricia Giampapa for her help with preparing this manuscript.
5.
References
Alajouanine, T. & Lhermitte, F. (1964). Les composantes phonemiques et semantiques de la jargonaphasie. International Journal of Neurology, 4, 277—286. Allport, D. A. (1984). Auditory -verbal short-term memory and conduction aphasia. In H. Bouma & D. G. Bowhuis (Eds.), Attention and performance X. New York: Academic Press. Appell, J., Kertesz, A., & Fisman, M. (1982). A study of language functioning in Alzheimer patients. Brain and Language, 17, 73—91. Baddeley , A. D. (1986). Working memory. Oxford: Oxford University Press. Baddeley , A. D., Logie, R., Bressi, S., Della Sala, S., & Spinnler, H. (1986). Dementia and working memory . Quarterly Journal of Experimental Psychology, 38A, 603—618.
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31. 1. 2. 3. 4. 5. 6. 7. 8.
1.
Aphasia Therapy Introduction Intuitive Therapies Model-Based Approaches Communication Therapy Evaluation Delivery of Services Conclusion References
Introduction
A spate of research papers and editorials published in medical journals in the UK in the late 1970s and early 1980s prompted a new examination of the practice and evaluation of aphasia therapy , the ripples from which spread around the world. Three papers in particular (David/Enderby /Bainton 1982; Lincoln/McGuirk/Mulley et al. 1984; Meikle/ Wechsler/Tupper et al. 1979) came to the conclusion that the therapy for aphasic patients provided as part of the speech therapy service in Britain was not effective, or at least was no more effective than the help which volunteers could provide if given some advice. Coming at a time of economic cutbacks, and pressures on health services to work within cost-effective budgets, these papers evoked strong reactions. One, taken by some phy sicians, health managers and their advisers, was to question the need for referring aphasic patients for specialist help, and to promote interest in catering for the needs of this section of the population by encouraging volunteer helpers. There was also discussion of increasing the numbers of paid ‘speech therapy assistants’, and of creating generic therapists who could cope at a basic level with a range of ‘paramedical’ needs, such as social work, phy sical therapy , speech therapy and occupational therapy . A second, more reasoned, reaction was to examine the methodological validity of the studies. It was argued that they were apply ing, inexactly and inappropriately , a design of randomised controlled trials developed for other purposes, which presumed, in particular, that the subjects used were homogeneous in respect of the critical variable (aphasia), and that the treatment engaged was similarly homogeneous and exactly specified. Neither of these conditions had in fact applied (Howard 1986; Pring 1986). Randomised allocation of aphasic subjects to the different treatment conditions rests on the questionable assumption
that aphasia is essentially a unitary condition. Treatment regimes in all these studies were described vaguely as classical, traditional, conventional, or as flexibly adapted to the patient’s needs, but with no further information. Replication of the studies, on these grounds alone, would therefore be impossible. 1.1. A Paradigm Shift? The result of such heart-searching has been to accelerate a paradigm shift in the study of therapy for aphasia (therapy here being used in its broadest sense of any kind of intervention aimed at alleviating the patient’s communicative dy sfunction). It consolidated the moves which were already being made on three fronts towards a more scholarly approach to the examination of aphasia therapy . These were: first, the matching of defined categories of patients with therapy programmes which were published in detail and were replicable; second, the application of psy cholinguistic models of language processing to the examination of aphasic individuals, with a model-based specification of the disorder and of the aims of therapy ; and third, the sy stemization of therapy which focusses on communication rather than language, and which therefore also gives primacy to the aphasic individuals’ partners in every day life. What all these approaches have in common, and what justifies the claim of a paradigm shift, is the emphasis on sy stematic analy sis, though the methods used depend on the discipline with which each approach is allied. For these three ‘schools’ of therapy they are, respectively , the disciplines of neurology , cognitive psy chology and sociolinguistics. In all these schools, aphasia therapy is not seen as intuitive and ad hoc, but as based on motivated and recursive assessment of the individual, sy stematically testing hy potheses about the nature of the disorder. This assessment is not necessarily psy chometric in its nature (cf. also art. 11.), and the discussion of each of these three schools of therapy will attempt to show how the approach to assessment, as well as to therapy, differs.
2.
Intuitive Therapies
Before we look at these three particular schools, however, a word of explanation is needed as to how the circumstances should
31. Aphasia Therapy
have arisen which lead to the articles mentioned at the beginning of this chapter, in which aphasia therapists lent themselves to what they believed was an honest exposure of the inadequacies of the service they were offering. Their conclusions seemed to support the recommendation that, since it appeared that face-to-face therapy with aphasic patients could be conducted as effectively by guided volunteers as by skilled therapists, therapists’ roles should become those of assessors and supervisors of less-qualified helpers rather than direct practitioners of therapy . The reason was that, for some time, the dominant practice of aphasia therapy had been intuitive, with therapists responding reactively to patients’ patterns of language behavior. Therapy required, not so much expert knowledge, as a sy mpathetic rapport, good judgement as to when to encourage and when to hold back, and a stock of language exercises, classed as to whether they were aimed at helping speech, auditory comprehension, reading or writing. Specialised postgraduate training in aphasia therapy was short on the ground (and still is). The only attempts at theories of aphasia were unitary theory (which proposed that aphasia could not be divided into ty pes) or neurologically -based theories. The only one of these that had direct relevance to therapy was that of Luria (1970) which was little known outside Eastern Europe until the 1980s. Very little experimental work had been published on the effectiveness of different ty pes of therapy for different ty pes of aphasic patients. With a predominantly intuitive and empirical approach to therapy , therefore, the difference between many speech therapists (for whom aphasia was just one of their areas of practice) and dedicated, experienced volunteers was less great at this time than the professional/amateur boundary might suggest. 2.1. Stimulation Therapy This is not to imply that there had not been any attempts to introduce a sy stematic rationale to aphasia therapy before the 1970s (in addition to the delay ed world-wide impact of the Lurian approach, to which we shall refer later) (see Howard/Hatfield 1987, for an excellent review of the history of aphasia therapy ). One of these was developed by the ‘stimulation’ school of aphasia therapy , initiated by Wepman (1951) and developed by Schuell/ Jenkins/Jiménez-Pabón (1964). This was based on a quasi-phy siological concept of
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brain damage, in which it was held that the language sy stem in the brain operated with reduced efficiency , and that stimulation was the only means by which the therapist could make complex events occur in this damaged brain sy stem. This unitary conception of brain function was mirrored in a unitary conception of aphasia, the defining characteristics of which were a reduction in available vocabulary and in comprehension. Vocabulary items were not lost, but were inaccessible at will. This conceptualisation of aphasia, and its consequent implications for remediation, differed from the earlier emphasis, which had focussed on speech production difficulties, and assumed that abilities were lost and had to be re-taught. In the stimulation school of therapy the key to remediation for all aphasic patients was intensive auditory stimulation, predominantly at word rather than sentence level, from which the patient’s own responses would be produced as an overflow rather than being forced. The therapist was encouraged to repeat words to the patient over and over again — to the order of 20 times. The obvious surface differences between individual aphasic patients was explained by say ing that they had (or had not) additional peripheral disorders overlaid on the ‘simple’ aphasia which was the true, unitary aphasia — peripheral disorders which could be visual affecting reading, visuospatial affecting writing, sensorimotor affecting the praxis of articulation, for example. The full therapeutic repertoire, therefore, incorporated exercises using all modalities. The aim was to build on automatic production in order to develop voluntary control. Despite the current unpopularity of unitary theory , the stimulation approach remains influential in clinical practice, although now much modified from the stress on intensive repetition of words by the therapist. At the time of its introduction the popularity of this therapy can be attributed to several features. It was linked with the first comprehensive assessment to be designed specifically for aphasia (the Minnesota Test for the Differential Diagnosis of Aphasia), and to a formal proposition about the nature of aphasia based on results from this test. It provided advice on a number of therapeutic exercises and on interactions with the patient. The book in which it was popularised, with authors from the disciplines of psy chology and neurology as well as speech pathology (Schuell/Jenkins/ Jiménez-Pabón 1964), reveals a warmth and insightfulness into the care of aphasic people,
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and a respect for their courage, which makes it attractive to members of a caring profession. We can see the changes that have occurred in therapy derived from this school in the recommendations for therapy published by Shewan/Bandur (1986). Although in reporting the group results of 28 patients who received Language Oriented Therapy (LOT), these therapists used the Boston classification (Broca’s, Wernicke’s aphasia etc.), the ty pes of treatment used were not married to these sy ndromes. The schemes of treatment (specified in commendable detail, and with materials and procedures provided in the book) were modality based in a similar way to Schuell’s recommendations i. e. they are classed as treatments for auditory processing, visual processing, gestural/gestural-verbal communication, oral expression and graphic expression. The patient is to be assessed on a standard test or otherwise, so that deficits in these language behaviors can be recorded, and individual therapy programmes then be targeted at the deficits in the modalities. The general philosophy of aphasia is similar to that of Schuell i. e. that the language sy stem is impaired or disturbed and that access to it is also faulty. Although in its lack of a specific match of treatment to theory , we feel justified in classing this approach still under the heading of ‘intuitive’, it represents a serious attempt to provide a clinically practicable methodology for therapy and to evaluate the effectiveness of the approach used. 2.2. Behavioral Therapy Where earlier approaches to therapy had assumed that language had to be retaught or to be reactivated through stimulation, behavior therapy as applied to aphasia rests on the intuition that language is essentially intact, and can be revealed if the behavioral blockages are removed. Much of the influence of behaviorism in the 1960s and early 1970s was on apply ing the principles of behavior modification such as shaping and reinforcement as a teaching method using programmed learning, often with teaching machines (Holland 1970; Sarno/Silverman/Sands 1970). This aspect of behaviorism has its most modern form in the more flexible use of microcomputers and interactive discs as teaching machines. Robertson has reviewed the development of computers as a medium of therapy , commenting that their use for teaching precise aspects of language to aphasic patients has
so far been restricted “Because of the lingering adherence to more generalized notions of wide-ranging and non-specific language reabilitation” (Robertson 1990, 388). He does, however, cite an unpublished study by Stachowiak and his colleagues in Bonn in which results from a large randomized controlled trial suggested that adding extra hours of general computerized speech therapy improved effectiveness. As well as providing a medium through which therapy can be delivered in clinic or home (Petherham 1991), microcomputers can also, of course, provide an alternative means of communication (see Kraat 1990) for a review) or a supplement to communication, as in providing word-finding prompts (Bruce/Howard 1987; Colby /Christinaz/Parkison et al. 1981). Behaviorism provided more than ideas for improving the teaching media used in rehabilitation. It influenced the content of therapy through its tenet that language behavior, like other behaviors, could be shaped by modelling and reinforcement by tokens, praise, or simply accurate feedback as to success (Goodkin 1969; Goldstein/Ruthven 1983). In some cases also, aphasia could be accompanied by learned fears of communicating, and could therefore be reduced by the same desensitization techniques that were used with stutterers or people with phobias (Ince 1968; Damon/Lesser/Woods 1979). Similarly relaxation (Marshall/Watts 1976), laughter (Potter/ Goodman 1983) or hy pnosis (Thompson/ Hall/Sison 1986) might be effective as facilitators. Behaviorism’s most significant influence on aphasiology in the 1970s was probably in its stress on quantification and ‘objectivity ’, an overtly anti-theoretical perspective, as expressed by Sidman (1971, 413): “The phenomena of aphasia can be classified empirically , without biassing the observations by preconceptions of what language ‘really ’ is. The data will then be available to any theory ”. One result of this attempt at empirical objectivity was the categorisation of patients by their quantifiable production of speech rather than by their more-difficult-tomeasure comprehension, as fluent or nonfluent. Another was the formulation of tests which aimed to meet the standards laid down for psy chological tests (Porch 1967) and to compare stimulus and response sy stematically (Sidman 1971). But its influence on therapy also remains. Porch (1986), maintaining like Schuell that aphasia represents a reduction in the processing efficiency of the brain, de-
31. Aphasia Therapy
scribes how the results of his test can be used in therapy . But his recommendations relate to general management and are atheoretical. Patterns of performance within subtests (‘slowrise’ compared with rapid fatiguability ) and across subtests can be used to predict the potential which the patient could achieve; therapy should be directed at parallel items to those in the subtests in which the patient was able to perform accurately but only after delay or further prompts. An effective recent application of behavioral principles in aphasia therapy was reported by Doy le/Goldstein/Bourgeois/Nakles (1989). It is particularly interesting because it overtly marries behaviorism with some of the tenets of functional communication therapy , which we shall describe later. It remains, however, within what we have called intuitive approaches to therapy , in that the therapy was not based on a rationale which distinguished individual patients’ patterns of aphasia, or on a coherent theory of the nature of aphasia. y Do le/Goldstein/Bourgeois/Nakles’s paper describes how four stroke patients with Broca’s aphasia were trained to ask questions. The technique was primarily to “give the subject an opportunity to talk” on one of three topics (health, leisure and personal information). The patients were told explicitly to ask as many questions of their conversational partner as they could. They were praised if they asked an intelligible (however ungrammatical) question, and were also ‘rewarded’ with an answer. If the patient had not formulated a request for information within 20 seconds despite the partner’s nonverbal encouragement through ey e contact, the partner modelled a request for the patient to imitate; cue cards could be used if necessary . To maintain the naturalness of the requests for information on the topics, a large number of volunteers were used as partners, as well as three therapists who functioned as the trainers. The researchers report that “following the initiation of treatment, all subjects demonstrated a rapid and marked increase in the use of requests during trainer probes” y (Do le/Goldstein/Bourgeois/Nakles 1989, 165) i. e. during 5-minute conversation samples in a nontreatment setting. The patients were also rated as being significantly more talkative, after the initiation of treatment, by a group of 12 students who were asked to assess videotaped samples presented in random order. The criterion for success was func-
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tional communication, not language structure, and the authors note that “improved efficiency of requesting occurred within the context of negative effects with regard to grammatical completeness and question morpheme usage” (Do y le/Goldstein/Bourgeois/ Nakles 1989, 169). The behavioral philosophy behind this approach to therapy is that aphasic patients can communicate if instructed to do so and given appropriate modelling and reinforcement. This successful study indicates that this may apply at the level of the social and pragmatic use of language, but does not necessarily circumvent the aphasic person’s difficulties with language structure as such. It suggests, in fact, a trade-off between the two, with the implication that an emphasis on grammatical structure in therapy could even make functional communication less effective. The various alternative visual communication sy stems which have been used with aphasic patients, such as Blissy mbols, VIC and its computerised adaptation C-VIC have concentrated on communication of the message, with minimal loading on grammatical effort other than word or sy mbol order (Gardner/Zurif/Berr y /Baker 1976; Funnell/ Allport 1989; Weinrich 1991). Two of the formalised programmes of therapy which have recently emerged from the influential Boston group also apply the behaviorist philosophy that language can be brought under control by instruction and feedback, i. e Voluntary Control of Involuntary Utterances (VCIU) and Treatment of Aphasic Perseveration (TAP). In VCIU (Helm-Estabrooks 1983b) patients whose speech is largely restricted to stereoty pies are asked to read voluntarily any words they have been heard to read involuntarily , as in semantic paralexias. The list is supplemented by emotional words, which are usually considered to be better preserved; the patients are then asked to use these words in other way s, thus moving to voluntary production of them. TAP (Helm-Estabrooks/Emery /Albert 1987) employ s strategies to avoid perseveration in naming such as drawing patients’ attention to the phenomenon and explaining it, slowing the pace of presentation of items and tearing up a piece of paper which has the perseverated word written on it. A more radical approach to preventing perseveration is to avoid circumstances which promote it in some patients, such as the rather unnatural task of naming pictures.
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3.
Model-Based Approaches
In contrast to the approaches we have reviewed so far, three model-based approaches have been developed, which attempt to relate individual patients’ sy mptoms to coherent models of aphasia. Two of these are neurological in motivation, one psychological. 3.1. Syndrome-Linked (Lurian) Luria’s phy siologically based concept of the operation of mind proposed a sy stem of distributed neural networks which served the ‘higher cortical functions’ such as language. Such a network has a degree of plasticity ; if one component is damaged, a similar output from it can sometimes be achieved through reconstitution of the network using the other components. Whereas the approaches to therapy we reviewed above can be categorised as re-teaching, reactivating or revealing, the Lurian approach is essentially one of reconstitution through re-organization. With such a theory of potential plasticity , and working often with y oung head-injured soldiers, Luria had a much more active interest and participation in aphasia therapy than currently do most Western neurologists. Luria’s techniques, however, though developed in the 1930s and described in Russian in the 1940s, were not made available in English until the 1960s (Luria 1963; 1966), and were therefore influential on clinical practice predominantly only in Eastern Europe until recently . Luria developed a classification of aphasias into (originally ) six sy ndromes, associated with neuroanatomical sites according to the location in which damage interrupted the network. His proposals for therapy were therefore the first to be sy ndrome-linked and matched to the underly ing concept of the nature of that particular disorder. With a ffe r e n t m o t o r a p h a s i a, for example, the underly ing disorder was considered to be in the kinaesthetic basis of the articulation of speech; therapy included substituting visual input for the kinaesthetic feedback through diagrams of articulatory gestures. This externally assisted reorganisation could then become internalised and automatised as part of the reconstituted network. Similarly visual input could be helpful in the impairment of phonological discrimination which underlay s e n s o r y a p h a s i a. A well-known application of therapy for e f fe r e n t m o t o r a p h as i a by a student of Luria’s is the “preventive method” (Be y n/Shokhor-Trotska y a 1966),
which stresses the need to use predicative words and phrases early in therapy , so as to avoid the development of telegrammatic speech. A more recent adaptation of the Lurian approach in Finland has taken the notion of reorganisation as apply ing more generally to the whole language sy stem, and has resulted in the development of an integrated multi-modal Language Enrichment Therapy programme (Salonen 1980), which shares some similarities with the general stimulation approach. 3.2. Syndrome-Linked (Bostonian) The most structured sy ndrome-linked therapies for aphasia have been developed in the last two decades at the Boston V. A. Hospital in Massachusetts. From this base the neurologist Geschwind (1965) repopularised the classical localizationist doctrines of the late 19th century , and the division into aphasia of the sy ndromes of B r o c a’s, We r n i cke’s, c o n d u c t i o n, a n o m i c, t r a n s c o r t i c a l and g l o b a l a p h a s i a s. The sy ndromes were linked with linguistic levels by the clinical psy chologists Goodglass/Kaplan (1972), with Broca’s aphasia identified (as well as with articulatory disorder) with a disorder of sy ntax, Wernicke’s with a lexical-semantic disorder, conduction with an output phonological deficit particularly affecting repetition, and anomic with difficulty in lexical retrieval. Transcortical aphasia (in its isolation, motor and sensory forms) was a complete or partial separation of the whole language sy stem from thought. The speech pathologists at Boston have published a number of formal programmes aimed at ameliorating some of these ys ndromes. Melodic Intonation Therap y (MIT) is used for patients with a Broca’s aphasia in which the ‘articulation’ difficulties of apraxia of speech are prominent (HelmEstabrooks 1983a). This draws on the theory that the right cerebral hemisphere, considered to be the neural substrate for some aspects of music, may take over some language functions after severe left hemisphere damage, or may be able to assist recovery in the left hemisphere. (An extreme form of therapy based on this notion is Brain Function Therapy (Buffery /Burton 1982) in which multimodal stimulation is directed at the right hemisphere with masking stimuli to the left hemisphere; other, more pragmatic “rightbrain stimulation” therapies for aphasia use drawing (Pillon/Signoret/Van Eeckhout/ Lhermitte 1980) and visual imagery (Fitch-
31. Aphasia Therapy
West 1983)). For the sy ntactic aspects of Broca’s aphasia, Helm-Estabrooks (1981) has devised the Helm Elicited Language Sy ntax Stimulation (HELPSS) programme, which provides graded exercises aimed at eliciting sentences of different complexities, first with modelling, then with a lead-in prompt. Like other forms of stimulation therapy this is based on the premise that patients have not lost a particular ability (in this case the use of sy ntax) but need practice in accessing it. The comprehension problems of Wernicke’s aphasia can be tackled by another Boston programme, Sentence Level Auditory Comprehension (SLAC) (Naeser/Haas/Mazurski/ Laughlin 1986), in which the focus is on making phonemic discriminations between pairs of words, first-presented without, then with, a sentence context. This uses a tape play back sy stem, the Language Master, and is suitable for self-teaching for some patients, as feedback as to correctness is provided. For globally aphasic patients, Visual Action Therapy (VAT) (Helm-Estabrooks/Fitzpatrick/Barresi 1981) may be suitable, as a preliminary to other therapies. This has the aim of reintegrating the patient’s mental functioning, in order to cope with the processing of stimulus, sy mbol and response. It therefore has a rather different purpose from the direct teaching of the use of a sign sy stem such as Amerind (Skelly 1979) or a visual sy stem of communication, such as we have described earlier, as an alternative means of communication — whatever secondary effect these may have on the language sy stem itself. With VAT patients learn to associate representational drawings (first of their own hand and then of a series of objects) with the objects themselves and with gestures indicating the use of these objects. The programme culminates in the patient making a gesture to indicate an object which is out of sight. Since this is a re-integrating therapy , globally aphasic patients are expected to improve not only in the use of gesture but in auditory comprehension and other aspects of language as well. Helm-Estabrooks (1983b) indicates that VAT may be particularly suitable for a sub-ty pe of ‘global’ aphasia which can be identified as secondary to subcortical damage. In the same edited book as Helm-Estabrooks’ paper, several other authors offer their general guidelines for sy ndrome-linked therapy , apply ing the Boston classification. As sub-ty pes of sy ndromes have emerged, programmes have be-
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come more directly targeted. Kohn/Smith/Arsenault (1990), for example, give an account of the successful use of sentence repetition as a means of treatment for a patient with the ty pe of conduction aphasia which is characterised by “a general speech production deficit in phonemic planning” (Kohn/Smith/Arsenault 1990, 58) rather than reduced auditory verbal short-term memory. Also emerging from Boston, though at present less closely identified with its sy ndromes, is pharmacological therapy for aphasia (Bachman/Albert 1990). This is not a novel approach (it was, for example, one advocated by Luria, and Bachman/Albert cite more recent studies in Russia, Romania and Germany ), but it has recently been reactivated in Boston. So far only uncontrolled studies of the use of bromocriptine have been reported, using patients classed as having a chronic non-fluent aphasia. Some improvement in naming and vocabulary , with a reduction in pauses in spontaneous speech, has been reported in most cases, with a dramatic improvement in one individual. Bachman and Albert’s anatomo-ph y siological explanation for such a recovery is that dopaminergic centres in the midbrain project to the supplementary motor area in the dorsal-medial part of the left frontal lobe. If the dy sfluency or initiation difficulties result from damage to this area or the projections to it, replacement therapy with a dopamine agonist such as bromocriptine may be of benefit. The sy ndrome that this particular pharmacological therapy would be linked with in this case would be transcortical motor aphasia. The Boston classification is currently in use world-wide, and other programmes have emerged elsewhere which have been linked loosely to these sy ndromes, as they have become more closely aligned with linguistic levels of language. Howard/Hatfield (1987) review a number of studies from Germany which describe specific therapies for impaired phonemic organisation, agrammatism and global aphasia, and are suggested as appropriate for groups of patients who share these distinctive linguistic deficits. Many of these programmes have been influenced by linguists, and Howard/Hatfield distinguish these European aphasiologists as forming a ‘neurolinguistic’ school of therapy . The sy ndrome-linked therapy of MIT has also been developed for use with French aphasic patients (Van Eeckhout/Pillon/Signoret et al. 1982).
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3.3. Cognitive Neuropsychological The model which underlies the therapies described in the last two sections is primarily a neurological one, with some sophistication introduced by linguists in elaborating it by incorporating linguistic levels. The psy cholinguistic approach to therapy (or cognitive neuropsy chological, as it is often called in order to distinguish it from the non-specific use of ‘psy cholinguistic’ by therapists such as Shewan and Bandur) is based on models which have a different root i. e. in cognitive psy chology . Since these models are reviewed in another chapter of this volume (cf. art. 21) they will be only briefly referred to here. They are best developed as models of cross-modality single-word processing, originally as models of the processes which intervene between seeing a printed word and reading it aloud but with later incorporation of auditory and graphic processes. Nevertheless they are still agreed to be seriously underspecified (Ellis/ Young 1988), and have faced more radical criticisms (e. g. Seidenberg 1988). This applies both to models of single word processing and sentence processing. Nevertheless they act as working hy potheses as to how the mind processes these restricted aspects of language and offer a framework through which to test a rationale for direct therapy. What these models provide is not a prescription for aphasia therapy , but a method of examining an individual patient’s disturbances in language processing in such a way as to be able to select from existing therapeutic tasks those ones which, at a first pass, would seem to have some prospect of ameliorating or circumventing the condition. These tasks may be drawn from any of the methods previously described, and from the trial and error techniques which have been built up through the intuitive approach to aphasia therapy . What is different in the psy cholinguistically based approach is the individual selection of specific techniques based on a hy pothesis about the nature of the cognitive changes the patient has undergone. The approach used may be reteaching, reactivatory , reorganisational or substitutory , depending on what aspects of the language processing sy stem are considered to be malfunctioning. Since one of the tenets of cognitive neuropsy chology is the modularity of mental processing, the dominant approaches are reorganisational and substitutory , in which the aim is to by pass a malfunctioning module by
drawing on alternative routes. With reorganisation, as in the Lurian philosophy , the substitution becomes internalized, and is absorbed into the new functioning sy stem. Some substitutions require the continuing use of an external prosthesis, for example, the use of computers as a word-finding prompt (Colby / Christinaz/Parkison et al. 1981; Bruce/Howard 1987). Nevertheless, other approaches besides the reorganisational and substitutory may be justified, and remain consistent with the theory of mental modularity . For example, if the patient appears to have a specific impairment of some semantic categories (as has been reported by a number of investigators, notably Warrington/McCarthy 1987), an appropriate approach for the therapist to consider may be reteaching of items in these categories. If, as may be more comon, the semantic disorder seems to be a more general blurring of fine semantic distinctions, a reactivatory approach, using exercises which stimulate the patient’s residual awareness of word meanings, may be attempted. This method was used yb Howard/Patterson/ Franklin et al. (1985) and shown to be effective in improving patients’ naming abilities, and to have an influence which lasted at least 24 hours, in contrast to facilitating naming by phonemic cuing. The improvement was achieved, moreover, without the patients themselves having any practice in producing spoken names, a result consistent with the proposed psy cholinguistic model, in which the semantic sy stem is conceived of as a module essentially independent of word form. The model also implies that different ty pes of therapeutic exercises should be appropriate for different ty pes of anomic difficulties: semantic exercises may be effective with patients with semantic degradation, while exercises which emphasise word-form may be effective for patients whose impairment is not essentially semantic, but is in retrieving lexical form (Lesser 1989). This hy pothesis has been tested in a therapy study by Nettleton/Lesser (1991), and received some support. Since the application of psy cholinguistic modelling in neuropsy chology was first made in reading, it is not suprising that the first detailed applications of cognitive neuropsy chologically based rehabilitation in aphasia were directed at the same behavior, with writing not far behind. In what was probably the first paper to review specifically the relationship between (cognitive) neuropsy chology and therapy , Beauvois/Derouesné (1982) de-
31. Aphasia Therapy
scribe the model-based therapy they used with four aphasic patients. With one (with an aphasia categorised as d y n a m i c in Luria’s classification) therapy was directed at elaboration of ideas rather than at language. With another (with tactile aphasia), help was given in the form of encouragement to visualise held objects which he could not name. But the most detailed programmes described were devised for two patients with reading disorders, one with a pure alexia and o p t i c a p h a s i a for colours, one with phonological alexia. Assessment indicated in the first patient, M. P., that the traditional therapy for such an alexia — retraining in reading through using the intact writing sy stem by tracing letters during reading — would not be successful. M. P. appeared to have a visuo-verbal dissociation such that any direct association of what she saw with language was not possible. Accordingly she was trained to use a roundabout strategy to link seen letters with their names; the seen letter was associated with an arbitrary gesture, the seen gesture was then identified with a verbal code, and this verbal code was then translated into the name of the letter. After five months of this therapy (begun two y ears after her stroke) there were highly significant improvements in her ability to read letters and words. Four y ears later she was reading novels, slowly , but as her main relaxation. The other patient, R. G., with phonological alexia, was unable to read nonwords alound, and made errors on reading aloud sentences which suggested he was snatching at their gist rather than reading them exactly . His errors were particularly noticeable on function words. The therapists interpreted this pattern of reading as an inability to override contextual expectations, and encouraged him to read sentences as a series of isolated words. After a month of practice in this programme R. G. ’s reading of words in sentence contexts, and particularly of function words, had improved highly significantly. At about the same time, Hatfield (1983) was also apply ing to therapy for agraphia the insights from the then current two-route models which Beauvois and Derouesné had applied to alexia (the two routes being the lexical-semantic and the phonological-graphemic). Hatfield reports her application of the two-route model of writing to four aphasic patients. Three of them were diagnosed as having deep agraphia (i. e. they could write to dictation only by means of the lexicalsemantic route, and made more errors on
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function words than on content words). Therapy drew on their superior ability to write the content word rather than the function word member of a pair of homophonic words. The patients learned to associate such homophonic pairs as bean/been and hymn/him, with the function word alway s being associated with a content word which they could already spell. By use of this strategy all three patients showed some improvement in the ability to spell the targeted function words. The fourth patient was diagnosed as having a surface agraphia and as spelling to dictation by using a simple phoneme-to grapheme translation, with loss of the lexical memory of the written form of many words. The therapy programme devised for her was to teach her some of the rules of spelling in English, so as to compensate for her lack of knowledge of lexical form by the ability to reconstitute words by rule. This was an overtly didactic approach. A similar approach has been used in Italian by Carlomagno/Parlato (1989) with a patient in whom both the lexical and the nonlexical routes to writing were considered to be seriously damaged. Reading disorders have similarly been treated by the use of an overtly didactic approach. De Partz (1986; Bachy Languedock/de Partz 1989) found that the teaching of the grapheme-to-phoneme correspondence rules of French to a patient with deep dy slexia was so effective that his much improved reading, after nine months, showed the features of surface dy slexia in its reliance on pronunciation rules. A therapy for surface dy slexia, using memonic by -pass strategies like those effective with Hatfield’s deep dy sgraphic patients, is reported by Coltheart/ By ng (1989). A head-injured postal-worker, E. E., showed the subty pe of surface dy slexia that indicates that meaning is accessed only through the sound of misread words, and not directly from visual input through a lexicalsemantic route. In therapy he learned to read correctly 24 words, all ending in -ough, by practising associating them with pictures of the words. A similar strategy of pairing other written words with sy mbols helped him to learn further sets of high frequency words. In all these studies it is notable that conventional clinic techniques are used. The extent to which the actual techniques selected are dependent on interpretation of the patient’s disorder through a psy cholinguistic model has also been questioned (Caramazza 1989; Basso 1989). For example the use of analogy with homophonic content words for
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the spelling of function words is a technique which originated in clinics long before psy cholinguistic models were fashioned in their present form. The value of the cognitive neuropsy chological approach to aphasia therapy , therefore, does not lie (at least at present) in its proposing innovative techniques of intervention. The question is whether it can be demonstrated that it has contributed guidance of the selection of a particular technique bey ond that of an experienced clinician’s observation. This could be as much in indicating which techniques would not be expected to address the deficit, as in indicating which would. For example the ty pe of remediation used with a nurse with a surface dy slexia by Scott/By ng (1989), i. e. judging the correctness of homophones presented in sentences on a computer, would not be appropriate for a patient in whom the surface dy slexic sy mtoms are due to an impairment in the lexical route which occurs after semantic access rather than before it. Psy cholinguistic models have the advantage of providing a coherent framework, which is so far supported by experimental studies, through which aphasia therapists can understand some aspects of their patients’ disorders (not least by keeping track of them through a visual diagram). They also provide justifications for not using certain enshrined clinical practices unselectively , for example in not endorsing spoken naming drills for those anomic patients whose disorder is predominantly semantic. They are also of potential help with other levels of language than single words, in particular, with sentence grammar, although psy cholinguistic models at the sentence level (and at the higher level of discourse) are at present even less well specified than lexical models. The sentence level model which has so far been applied in aphasia therapy is based on an adaptation of Garrett’s model by Schwartz (1987), with a particular emphasis on mapping between sy ntactic and semantic representations through the establishment of thematic roles in sentences. Linebarger (1990) has proposed that the difficulties some agrammatic speakers have is in this mapping between sy ntax and semantics. Two studies of therapy have reported the application of this notion to treatment (Jones 1986; By ng/ Coltheart 1986; By ng 1988). Both employ ed not only a teaching method but one that was overtly metalinguistic, in that the two patients concerned were taught about thematic roles and their relationship to word order in Eng-
lish. By ng/Coltheart used sentences incorporating locative prepositional phrases (e. g. the pan is in the jug), which had to be distinguished from those where the lexical items were in reversed roles, as illustrated in pictures. Jones used a more varied approach, getting her patient first to identify the verb in sentences, and then to distinguish various thematic roles, such as w h o or w h a t was the doer, w h o m or w h a t the theme, w h e r e the setting was and so on. This therapy , conducted with a patient with Broca’s aphasia who had failed to improve after some y ears of therapy on spoken language, specifically discouraged attempts at sentence production, to the patient’s relief. The theoretical account offered for his disorder is that his mapping disorder was bidirectional, and that work on comprehension should therefore result in improvement in speech. The outcome supported this account. Both with Jones’ and with By ng/ Coltheart’s patients, after the therapy aimed at improving comprehension of thematic roles, agrammatic speech was ameliorated. This is not, of course, a prescription for all ty pes of agrammatism, and Garrett’s model would indeed imply that disturbances could apply at other levels of sentence production, for which direct work on speech (such as generating sy ntactic trees and lexical insertion) might be appropriate. It is germane to the cognitive neuropsy chological approach to aphasia therapy that a prerequiste is the detailed analy sis of the patient’s discorder, and the specification of in what module or process the deficits appear to lie. The emphasis in cognitive neuropsy chology on individual assessment and individual variability is so strong that many of its practitioners advocate the abandonment of sy ndromes, and even subdivisions of the classical sy ndromes as in agrammatism (Badecker/ Caramazza 1985; Ellis 1987; Howard/Patterson 1987). They are bolstered in this by the independence of ps y cholinguistic models from theories of localization, such as dominate the approaches we described in the last two sections. So far only limited attempts have been made to map the abstract level of psy cholinguistic modelling onto areas of the brain (for an example of this, see Petersen/ Fox//Posner et al. 1988), though as neuroscience comes closer to neuropsy chology we may expect the development of an interdisciplinary field. Not only this, but clinical convenience, implies the use of grouped patients identified by some convenient label. Thera-
31. Aphasia Therapy
pies are therefore becoming identified with what have been described as s y m p t o mc o m p l exe s rather than sy ndromes. This characterizes the therapy as directed at specific sy mptoms related to a model, without the implication that the patient shows all the other features that can be associated with a sy ndrome. Replication of therapy studies may thus be undertaken on other individuals who share the same critical sy mptoms for that procedure to be proposed as appropriate.
4.
Communication Therapy
Emphasis on the needs of the individual is also paramount in the final approach to aphasia therapy that we shall discuss, though here the individuals are assessed as members of their social network. If the cognitive neuropsy chological approach to therapy has independence from a medical model, so even more emphatically does this one, drawing primarily on sociolinguistic ethnomethodolog y , the study of language and communication in their every day settings. Functional communication therapy has sometimes been contrasted with the cognitive neuropsy chological approach in that it focusses on the patients’ use of their assets, whereas the latter tends to be directed towards remedy ing deficits. This contrast is somewhat artificial in that, as we have seen, the logic of the reorganisation and substitution methods in apply ing a psy cholinguistic model is to capitalise on retained routes. In a more global way , however, functional communication therapy aims to develop the patients’ communicative assets. This ty pe of approach to therapy is two-pronged. One prong relates to direct intervention with patients, generally in clinical settings (as with the other approaches to therapy we have described). The other is indirect, following the logic that, if communication is necessarily an activity involving at least two people, aphasic patients’ communication can be improved by directing intervention at their partners. 4.1. Direct Intervention In 1972, Wepman, a respected American speech pathologist who had play ed a major role in the development of stimulation therapy , published a paper advocating the cessation of formalised work on language exercises, with switching of both the therapist’s and the patient’s attention to the meaning of the message rather than the medium. He cited
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the case of a lawy er who had failed to respond to formal clinical exercises, but whose communication was transformed when the therapist discussed with him the legal briefs that he had been engaged on at work. To some extent this may seem to be simply an extension of the classical clinical principle of using materials which are pertinent and motivating to the patient. Wepman, however, went bey ond such an interpretation. He proposed that aphasic patients’ language difficulties may be due to an impairment in thought (a notion which also has a long history e. g. Marie 1906), and that “thought-centred therapy ” is therefore a logical way to approach their problem. As Howard/Hatfield (1987, 71) comment “This proposal at first sight is so vague that it seems to be a recipe for almost total non-therapy ; y ou could do almost any thing and maintain that this was thought stimulation”. We come back again to the question raised at the beginning of this chapter, whether there are any reasons to expect the therapist’s intervention to be more beneficial than that of volunteers or family members. As Howard/Hatfield point out, however, there is a cognitive neuropsy chological justification for Wepman’s claim that this form of therapy could be successful for some patients: this conception of the aphasic disorder comes close to the interpretation of agrammatic comprehension as a failure to map the sy ntactic operation of word order onto meaning, the ‘mapping hy pothesis’ of agrammatism. In such a case, at the very least the therapist’s assessment of whether this would be an appropriate regime for an individual patient at a particular time is critical. A more general reaction to statements such as Wepman’s was one encouraged by the development of interest in pragmatics by linguistics in the 1970s (see Levinson 1983, for a review). The formalizing of notions about pragmatics offered a way of structuring clinical programmes so as to maximize communicative effectiveness (including nonverbal communication, and verbal communication by other means than speech). Two of the first ideas to be adopted were the notion from conversational analy sis of turn-taking, and, from a then currently popular notion in linguistics, of ‘speech acts’. The latter drew attention to the way in which spoken or written language in itself can perform behavioral acts (e. g. Ipromise) rather than reporting on them. Most importantly it emphazied the variety of speech acts — not only performatives, but requests, questions, commands and so on
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— and the frequent discrepancy between the literal form of words and the speaker’s intent. We have already described Doy le/Goldstein/ Bourgeois et al.’s (1989) therapy programme for aphasic patients, aimed at eliciting requests for information. Another well-established clinical procedure is aimed at facilitating patients’ convey ing of information, in a situation which mimics the turn-taking of natural conversation. In Promoting Aphasics’ Communicative Efficiency (PACE) (Davis/ Wilcox 1985), therapist and patient take turns at convey ing (through any means, verbal or non-verbal) what is represented on a stack of cards. The therapist models what is expected to be productive for the patient, but there is no direct instruction, so as not to spoil what is implied to be the ‘naturalness’ of the reciprocal communication. This procedure may be useful as practice for the patient in apply ing strategies which have already been drilled, such as the use of sy mbolic gesture, but this is different from what the authors claim to be one of the principles of PACE — that there should be a free choice of channels of communication. The extent to which ‘new’ information is being convey ed in such a situation is questionable, since therapists may feel the need to prime themselves with some knowledge of the set of cards to be used. The emphasis on turn-taking may also be unnecessary, since the only ty pe of aphasia in which this seems to be in question is fluent aphasia with p r e s s- o f- s p e e ch, and there is no reason to expect a disruption of awareness of turn-taking in aphasia in general. The theory base of such an approach is therefore slender, and the extent to which it reproduces a natural situation is questionable. An overtly instructional method is used in Holland’s sy stem of Conversational Coaching (Holland 1991). This aims to maximize communicative effectiveness by analy sing, in cooperation with the patients, their most productive strategies, and rehearsing the use of these through individually prepared scripts appropriate to their interests and abilities. The scripts could convey some item of news or gossip. After rehearsal with the therapist, a relative or helper is brought into the room, so that the patient can relay the information in the script. This meeting is usually videotaped, for later analy sis by the therapist, relative and patient of the means by which effective communication was or could be achieved (this brings in the further dimension of communication therapy — indirect inter-
vention — which we shall discuss in the next section). The Conversational Coaching programme is then extended by calling in a stranger to the patient, to whom the script’s message can also be convey ed. This is a promising approach in communication therapy , but its value rests upon the skilled analy sis of strategies. At present this is in the very early stages of sy stematic investigation, and so far predominantly only in respect of the analy sis of the spoken elements of conversation. In present clinical practice, therefore, the analy sis of communication strategies remains largely unformalized, although advice on it is plentiful (see, for example, Aten 1986) as we describe shortly. What we have described so far is predominantly one-to-one direct therapy between patient and therapist. There is an inherent contradiction in apply ing this to functional communication, in that the patient’s communicative needs with this one partner in a clinical setting are limited. The situation is one in which therapist and patient have inherently different roles, however much the therapist may be motivated to engage the patient as a principal in sharing ideas. Advocates of functional communication therapy , therefore, frequently utilise groups. There are two main ty pes of this therapy , game-play ing and roleplay ing. Stroke groups run by volunteers or social workers generally involve the patients in language-related games, as well as social outings, and the use of games has also been proposed as a part of therapist-directed treatment (Davis/Wilcox 1985). The effectiveness of such an approach in improving communication is difficult to evaluate, although patients and their relatives may derive other benefits (Lesser/Watt 1978). Aten/Caligiuri/ Holland (1982), however, have demonstrated positive benefits on communication through role play in group activities, in which patients discussed and applied strategies they could use in a variety of situations such as shopping. This approach has also been claimed to improve self-confidence and motivation as well as the specific use of language itself (Tsvetkova 1980). 4.2. Indirect (Communication) A more radical divergence in communication therapy is the focussing of therapy on the aphasic person’s communicative partners, rather than on the patient. This is an application of the principle that communication is a social activity and that the enhancement of
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communication can be achieved by improving the partner’s own use of co-operative strategies with the patient. This is different from the psy chotherapeutic counselling of the patients’ relatives, to which we shall refer in the next section. It was first explicitly advocated in aphasia in respect of a form usually neglected by the more classical treatments, jargonaphasia (Martin 1981). Amongst Martin’s recommendations are to provide the partner with as much information about the patient’s disorder as possible, perhaps by inclusion in therapy sessions, to demonstrate that it is possible to understand the patient as well as to be understood, and to train in specific techniques of modelling and encouraging monitoring. Like most other advocates of communication therapy , Martin saw this kind of approach as complementary to direct help from the therapist on communication and language. Holland (1991) makes the same point in discussing communication therapy , that it does not need to exclude direct work on language where this is indicated. By analogy with practice in the education of the deaf, this combined approach has sometimes been referred to as Total Communication. Other therapists have focussed more on naturalistic communication in every day settings. Green (1984, 41) states that “management programmes should place a greater emphasis upon the u s a ge of language within naturalistic contexts”. She describes an interactional approach to aphasia therapy based on detailed observation of family conversations. Ideally , given that utterances are alway s dependent on the contexts in which they are uttered, this should be within the patient’s own environment, although she admits that home-like conditions may need to be simulated in clinic settings, for practical reasons. She cites examples of productive strategies which have been observed and which can be utilized by aphasic people’s partners: slowing of rate, pausing, use of less ambiguous sentences, construction of sentences so that key words are at the end, changes of topic, use of alerters, stress and gesture and rephrasing. Green’s and Marshall’s (1987) recommendations concern strategies to improve the patient’s comprehension. But this kind of approach has also led to a burgeoning interest in the application to aphasia of techniques of conversational analy sis derived from sociolinguistics, such as study of the collaborative use of repair in word-finding difficulties (Lesser/
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Milroy 1993). This development holds the promise of tailoring recommendations for management to the individual’s communicative needs, in the same way that the cognitive neuropsy chological approach provides specification of the individual’s psy cholinguistic characteristics as a basis for selection of appropriate direct therapies for improving lexical and sentence skills. 4.3. Indirect (Psychotherapeutic) The approaches described in the last two sections come clearly within the province of the aphasia therapist’s work, in that they draw upon the specialized applications of linguistics which form part of this profession’s training. Aphasia therapists normally also include a limited element of counselling in their responsibilities, aware of the needs of both the patient and the family members for support for the psy chological and psy chosocial consequences of brain damage (Brumfitt/Clarke 1983). Indeed one study (Hartman/Landau 1987) suggests that counselling therapy provided by speech therapists may be as effective as ‘conventional’ aphasia therapy , at least during the period of recovery between one and seven months post onset of aphasia. ‘Family therapy ’ for aphasia, however, as formulated by Wahrborg (1989) is seen as an outgrowth of psy chotherapy which requires a specialized training. Although it shares with the therapy we have just been describing the aim of improving the families’ communication skills, it also has the aim of avoiding emotional disorders and psy chological deterioration. This deals, therefore, with communication skills in a different sense from that with which linguistics is concerned, but includes family dy namics and the emotional contexts of communication. Wahrborg/Borenstein (1990, 374) conclude that there is evidence to support the “assumption that families and family life have an impact on the rehabilitation outcome”, and that what happens psy chologically and communicatively within aphasia families needs to be analy sed. One such sy stem for undertaking this has been proposed by Mulhall (1988). This is a computerized, questionnaire-based anal y sis of the dy namics of spouse-aphasic relationships. It can be used in rehabilitation, in providing the partners with insight into these dy namics, with a later re-assessment of the effects of achieving this insight.
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5.
Evaluation
Although the use of many of these approaches to therapy has not been evaluated in way s which stand up to close inspection, the paradigm shift we referred to earlier as having taken place since the 1980s has led to much closer attention being paid to methodologicall y -sound experimental designs for evaluating the effects of intervention. Group designs have continued to have their practitioners (e. g. Wertz/Weiss/Aten et al. 1986; Shewan/Bandur 1986), but the majority of efforts have been directed at single-case studies. Group designs may be necessary at some stage for confirming hy potheses about the nature of aphasia itself (Zurif/Gardner/Brownell 1989; Fitz-Gibbon 1986), but since therapy should be based on a detailed analy sis of an individual’s disorder, and the predominant form of intervention used is one-to-one, it is single-case studies that now dominate the approach to research into aphasia therapy. There are several descriptions of appropriate designs in single-case studies of aphasia therapy (see for example Coltheart 1983; Pring 1986; Howard/Hatfield 1987; Willmes 1990). An important question is the extent to which these can be applied in routine clinical practice, or are suitable only for researchers into aphasia therapy . Designs which require more time than the working practitioner can spare, and can therefore only be used by researchers, still have their value; they can indicate what the results of therapy can be expected to be for specific ty pes of patients, provided that the study identifies their characteristics in sufficient detail for them to be applied to other cases. As we have seen, also, one previous obstacle to apply ing the results of earlier (group) studies, that of underspecification of the actual treatments used, need no longer apply . But, given the present weakness of knowledge of brain-behavior relationship, there is still a pressing need for the practising therapist to be able to evaluate the actual (as opposed to the predicted) consequences of interventions undertaken with individual patients. Without this the therapist remains uncertain as to whether any good is actually being done and whether the patient has reached, even temporarily , a plateau in recovery. Lapointe (1977) proposed a method, Base10, specifically for use in routine clinical work. This is a framework which can be used with a variety of contents, and therefore
matched to what are thought to be the patients’ specific needs. It proposes that 10 items should be identified in respect of a particular therapeutic task, measured over about three occasions to establish a baseline, and then worked upon in therapy for 10 sessions, so that progress, if any , can be graphed. Progress on 10 items drilled in such a format is commonly shown to occur, and the graph can often be used in motivating the patient. Such a formula, however, provides no real evidence that the therapy is effective in itself. The patient may be improving spontaneously , and a three-point baseline is not sufficient to test this. Nor is there any evidence to show that the change is not due to friendly support and the feeling that someone is now interested in alleviating the aphasia (the ‘placebo effect’). Two precautions have been suggested to overcome the first criticism, i. e. the taking of a longer base-line measurement (Pring 1986), and the use of this design only with patients past the period of spontaneous recovery . Sarno (1981) comments on the lack of consensus as to what this period is; the greatest recovery is likely to take place during the first three months, but studies of evaluation generally take at least six months as the period over which spontaneous recovery could significantly influence the results. Neither of these precautions is helpful to the practizing aphasia therapist. The criticism that the effect of the intervention may be a nonspecific one due to the feeling that someone is taking an interest has been tackled in a different way . Designs have been suggested which are aimed at controlling for this. One is to use a crossover design (Coltheart 1983). For this two tasks need to be identified, to which the patient is expected to respond differently . Performance on both tasks is re-measured after a period of therapy on one. Attention in therapy is then switched to the second task, with performance on both tasks measured again at the end of this period. Getting clear results from such a design does indeed depend on the theoretical distinctiveness of the two tasks; despite the postulated modularity of language processes, it is not infrequent to find improvement on both tasks when only one has been treated (consistent with the unitary nature of aphasia proposed by Schuell). A second design, which can be used where effects are expected to be specific to items, is to split the list of items into two matched or random sets, and to work only on one (Howard/Patterson/Franklin et al. 1985). If, as pre-
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dicted, the improvement occurs only on the treated set, it can be claimed that the intervention was not due to a placebo effect or to spontaneous recovery . Again it is more common to find some effects on the untreated list; in addition to the other two possible reasons for this (placebo or spontaneous recovery ), it may be due to generalization — a desirable consequence for the patient, but ambiguous for proving that the result was due to the therapy itself. Nevertheless it is essential to have some comparison of the effect of treatment with non-treatment (even when initially non-treated items or tasks are to be the subject of later therapy ). If the effect is shown only to occur with treatment, this is real evidence of its effectiveness, and the absence of generalization can be supportive of the model of psy cholinguistic processing applied (By ng/ Coltheart 1986). Assessing the value of the intervention to the patient also requires the measurement of how long the effects of treatment last, and many designs incorporate remeasurement after a period without treatment to test their stability . Howard/Patterson/Franklin et al. (1985) indeed refer to effects on naming which last less than 24 hours as being due only to facilitation, which they distinguish from therapy . It is also often desirable to include a measure of functional communication to examine whether or not the hoped-for extension of clinical work into something useful in every day life has occurred. Such measures range from formal assessment of communication using a standardized test (such as Holland’s Communicative Activities in Daily Living 1980), through a detailed conversational analy sis (Lesser/Milroy 1993) to a rapid questionnaire for use by carers (such as the Communicative Effectiveness Index of Lomas/Pickard/Bester et al. 1989). In routine clinical work it may be possible to incorporate some of these designs. Given that it is generally good practice to work on more than one aspect of language at a time, and to use more than one method of intervention in order to maintain the patient’s interest and reduce fatigue, it should be possible to use cross-over designs, both in comparing tasks and in comparing methods. As Howard/Hatfield (1987, 121) comment, use of these designs is “a potential and largely unexploited source of sound empirical data on the effectiveness of therapeutic techniques”.
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6.
Delivery of Services
No review of aphasia therapy could claim adequate coverage without some comment on the actual delivery of the interventions described in earlier sections of this chapter. Aphasia therapy takes place in many settings: hospital for in-patients and out-patients, specialized units for different ty pes of aetiologies such as head-injury and stroke, rehabilitation units specialized for y oung or old age-groups, patients’ own homes, health clinics, adult literacy centres (Parr 1985), and residential colleges (Borenstein/Wahrborg/Linell et al. 1987). In some countries volunteer-run clubs also provide substantial help for aphasic and other stroke patients (Griffith/Miller 1980; Lesser/Watt 1978), though this is not alway s integrated with the speech therapy service, and may not provide ‘aphasia therapy ’ in the sense that we have been using this term in this chapter. The provision of professional therapy for aphasic people varies widely around the world, and, even in countries where it is well established although the supply of therapists is limited, therapy for aphasic adults tends to take second place to the more pressing demands of children with developmental speech and language disorders (Rossiter/McInally 1989). With increasing interest in cost-effectiveness in public health services, there has therefore been considerable discussion of three issues. The first is whether or not certain ty pes of aphasic patients should be given priority of treatment over others. Another is whether the pattern of delivery of therapy as intensive or distributed, or as group or one-to-one, influences its effectiveness. The third is the one we referred to at the beginning of this chapter i. e. the extent to which unpaid volunteers or modestly -paid assistants can be used as supplements (or alternatives) to qualified therapists. 6.1. Priorities in Treatment Enderby /Davies (1989) have suggested that aphasic patients can be divided into three groups according to the severity of the disorder. They propose that maximum therapeutic effort should be directed at the middle group, which, they argue, is the most likely to benefit. Severely impaired chronic aphasic people have been reported as having an “irreversible ys ndrome” (Schuell/Jenkins/Jiménez-Pabón 1964; Sarno/Silverman/Sands 1970), and, in times of stringency , it has been argued that therapists’ time with them may
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not be well spent. This, however, is based on a notion of aphasia therapy as being concerned only with the restoration of spoken language. If functional communication is the target of therapy , achieving some improvement in global aphasia may make the difference between adequate coping in every day life or not, reducing the stress on the family and perhaps avoiding more serious breakdowns (Edelman 1987). Similarly there have been arguments for concentrating more therapeutic effort on the mildly impaired, on the grounds that these are the people who may be able to return to work, if given a relatively modest amount of therapy (Marshall 1987). Since there is no consensus of opinion on this matter, and little research, in practice aphasia therapists tend to make their own decisions based on such parameters as estimated motivation of the patient, availability of supportive family members to assist with home assignments, ability to travel to the clinic and so on. 6.2. Pattern of Delivery It has been proposed that aphasia therapy has to be intensive for it to be effective. David (1983, 22), for example, concludes from a review of several studies that “Very intensive therapy (18—25 hours per week) seems to be more effective than a more intermittent exposure”. It has also been noted that, in the British studies which reported that therapy from speech therapists was no more effective than either no therapy or the help given by volunteers, the amount of contact the patients had with their speech therapists was only about two hours a week. The ty pical pattern of therapy in some countries is more intensive than this, perhaps due to limits on time for insurance cover, or the greater use of residential centres. Hagen’s (1973) and Wertz/Weiss/ Aten et al.’s (1986) reports on successful therapy in the USA, for example, refer to between 8 and 18 hours of therapy per week. The claim that intensive therapy is superior to non-intensive therapy was examined in a study by Brindley /Copeland/Demain/Marty n (1989). Five men and five women with a Broca’s aphasia of between 18 and 130 months duration were given three months of intensive residential therapy (25 hours a week, given by a team of therapists, helped by a volunteer) sandwiched between three-month periods of non-intensive therap y . The measures of change were a Functional Communication Profile (FCP), grammatical analy sis and a
questionnaire to relatives. Although the patients’ group results showed a significant inprovement in speech rating on the FCP and on the grammatical analy sis after the period of intensive therapy , compared to ratings made after the first period of non-intensive therapy , the conclusion that intensive therapy is superior may not be justified. The number of hours of treatment in the two conditions differed by a factor of more than 10. Moreover the non-intensive treatment consisted of ‘conventional therapy ’ by various therapists, while the intensive therapy followed specific programmes and was conducted by a team. The appropriateness of intensive therapy may also depend on the duration and severity of aphasia. Except when the disability is mild, the therapist’s intervention immediately post onset may need to be primarily in counselling and assessing rather than in direct treatment. One study has compared group treatment with individual treatment. Wertz/Collins/ Weiss et al. (1981) compared two sets of patients who received eight hours of treatment a week between four and 48 weeks post onset. Taking the results of patients who were at least six months post onset (and arguably past the period of significant spontaneous recovery ) Wertz and his colleagues indicate that both group and individual therapy were effective. Fawcus (1983, 118) concluded that “at present there are no data to support the claim that group work is potentially a more successful learning situation than the individual treatment session”, and warns that, when provision of speech therapy services is inadequate, groups may be used as a substitute for individual treatment rather than a complement to it. Kearns’ (1986) review of group therapy for aphasia also complains of the lack of research into the efficacy of such an approach; he comments that it evolved as a practical response to the large influx of headinjured soldiers after the second World War, and that about three quarters of therapists who use group therapy have no specialist training in this method. 6.3. Stretching the Service Other way s of stretching the service are to extend the amount of the patient’s therapy time which does not require the direct supervision of a therapist. We have already referred to the use of microcomputers in therapy . An example of the use of microcomputers supplied for home use to work through standard programmes is in the work of Petherham
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(1991). The use of computers to provide an expert sy stem to aid therapists in assessment and selection of therapeutic exercises has also been proposed (Gu y ard/Masson/Quinious 1990), although this has been suggested as premature in the light of our current understanding of aphasia (Hirson/Chiat 1990). Videodiscs have also begun to be used in therapy (Bruckert/Gonon/Michel/Bez 1989). Other technical innovations have been pioneered by Vaughn in Birmingham, Alabama. She first developed a sy stem of therapy delivery by telephone, including remote control of writing, later adding telecomputer treatment (Fitch/Cross 1983). This is offered as a way of geographically stretching the service to rural areas. At first glance the use of assistants (and even more economically volunteers) may seem to be another way of making speech therapists’ work more effective in an understaffed service. Wade (1983) has pointed out, however, that engaging, training and supervising volunteers may be very demanding on therapists. Marshall/Wertz/Weiss et al.’s (1989) analy sis of the Wertz/Weiss/Aten et al. (1986) study in which “home therapists” (predominantly relatives) were used emphasizes the considerable amount of time and effort which the professional speech therapists spent in training them and in monitoring their efforts. A study by Quinteros/Williams/White/ Pickering (1984) examined the costs of using volunteers as part of an aphasia therapy service. Twenty four patients were allocated to either hospital or community speech therapy , and as part of the latter each was paired with a volunteer. The community group received monthly speech therapy at home, together with monthly practice sessions at home with the volunteer and fortnightly attendance at a speech therapy group. This proved one and a half times more costly than the hospital treatment, which comprised only monthly sessions. There were signs, however, that the community programme resulted in more improvement in the patients than did the hospital programme. Moreover the difference in costs would be reversed if the number of patients were to be somewhat larger, and the amount of hospital-based therapy increased to match the contact experienced by the community programme. Some of the cost was in training the volunteers — a recurrent cost, given the high turn-over to be expected of volunteer helpers. This suggests that the use of already trained and paid assistants might be beneficial. This notion has been taken up by the Health Service in England and Wales,
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with a proposal to develop training for therapy assistants, ranging from generic helpers to assistants with specific training relevant to different paramedical therapies. Such assistants would not be substitutes for volunteers, in that their relationships with patients would differ from that of ‘equal friends’ by virtue of their semi-professional role; nor is it likely that they would be employ ed as home-sitters to give relatives relief, a useful role for volunteers. They could, however, relieve therapists of some ancillary duties, such as taking care of the patients’ welfare outside the therapy session and assisting in therapy exercises under supervision. The distinction between a high-grade assistant and a qualified therapist will give cause for some close scrutiny . One essential difference will lie in the therapist’s capacity to initiate and undertake research — not only in studies for publication, but in the day -to-day interaction with the patient. If aphasia therapy is seen as a continuing process of forming hy potheses about a patient’s disorder, testing these through therapy and making adjustments to provide more effective therapy (Jones/By ng 1989), research is an inherent component of the day -to-day treatment and management of aphasia. With the extension of numbers of speech therapy assistants, it will be important for therapists not to see themselves as predominantly directing their expertise to assessment, preparation of programmes, supervision of therapy -implementing assistants and counselling. In order to understand aphasia and the aphasic individuals to whom they are committed, and in order to learn more about the therapeutic process itself, they will need to maintain direct and continuing contact with the patients themselves. As the other chapters on aphasia in this volume testify , the study of acquired language disorders is ever-increasing in its range, depth and complexity . The application of this knowledge to therapy needs the expertise of specialist therapists, who can not only understand and contribute to theories but extrapolate from them to practice. But no theory of aphasia is y et fully justified, and it is also important that therapists maintain their close contact with patients as a source of data and further insights through which to moderate both theory and practice.
7.
Conclusion
Very often the tasks which aphasia therapists undertake with patients seem simple. As this review has tried to indicate, the simplicity is
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illusory . The essence of the therapist’s skill is in the selection of the right task for the right patient at the right time, the sensitive interaction with the patient during its execution, and the delicate interpretation of its outcome. Despite the theoretical weakness of many approaches to therapy , the still y awning gap between psy cholinguistic models and neuroscience, and the infancy of the sy stematic application of sociolinguistic principles to our understanding of aphasic language, the practice of aphasia therapy has been transformed over the last decade in those areas where an enlightened service has made this possible. As the theory base of aphasiology extends, it is important that services for patients follow suit in applying these insights to their welfare.
8.
References
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Holland, A. L. (1970). Case studies in aphasia rehabilitation using programmed instruction. Journal of Speech and Hearning Disorders, 35, 11—16. Holland, A. L. (1980). Communicative abilities in daily living. Baltimore: University Park Press. Holland, A. L. (1991). Pragmatic aspects of intervention in aphasia. Journal of Neurolinguistics, 6, 197—211. Howard, D. (1986). Bey ond randomised controlled trials: the case for effective case studies of the effects of treatment in aphasia. British Journal of Disorders of Communication, 21, 89—102. Howard, D. & Hatfield, F. M. (1987). Aphasia therapy: historical and contemporary issues. Hove: Lawrence Erlbaum Associates. Howard, D. & Patterson, K. (1987). Models for therapy . In X. Seron & G. Deloche (Eds.), Cognitive approaches in neuropsychological rehabilitation. 39—64. Hove: Lawrence Erlbaum Associates. Howard, D., Patterson, K., Franklin, S., OrchardLisle, V. M., & Morton, J. (1985). The treatment of word-retrieval deficits in aphasia: a comparison of two therapy methods. Brain, 108, 817—829. Ince, L. P. (1968). Desensitization with an aphasic patient. Behavior Research and Therapy, 6, 235— 237. Jones, E. V. (1986). Building the foundations for sentence production in a non-fluent aphasia. British Journal of Disorders of Communication, 21, 63—82. Jones, E. V. & By ng, S. (1989). The practice of aphasia therapy : an opinion. Bulletin of the College of Speech Therapists, September 1989, 2—4. Kearns, K. P. (1986). Group therapy for aphasia: theoretical and practical considerations. In R. Chapey (Ed.), Language intervention strategies in adult aphasia. 304—318. Baltimore: Williams and Wilkins. Kohn, S. E., Smith, K. L., & Arsenault, J. K. (1990). The remediation of conduction aphasia via sentence repetition: a case study . British Journal of Disorders of Communication, 25, 45—60. Kraat, A. W. (1990). Augmentative and alternative communication: does it have a future in aphasia rehabilitation? Aphasiology, 4, 321—338. Lapointe, L. L. (1977). Base-10 programmed stimulation: task specification, scoring and plotting performance in aphasia therapy . Journal of Speech and Hearing Disorders, 42, 90—105. Lesser, R. (1987). Cognitive neuropsy chological influences on aphasia therapy . Aphasiology, 1, 189— 200. Lesser, R. (1989). Some issues in the neuropsy chological rehabilitation of anomia. In X. Seron & G. Deloche (Eds.), Cognitive approaches in neuropsychological rehabilitation. 65—104. Hove: Lawrence Erlbaum Associates.
Lesser, R. & Milroy , A. L. (1993). Linguistics and aphasia: psycholinguistic and pragmatic aspects of intervention. London: Longman. Lesser, R. & Watt, M. (1978). Untrained community help in the rehabilitation of stroke sufferers with language disorders. British Medical Journal, 2, 1045—1048. Levinson, S. C. (1983). Pragmatics. Cambridge: Cambridge University Press. Lincoln, N. B., McGuirk, E., Mulley , G. P., Lendrem, W., Jones, A. G., & Mitchell, J. R. A. (1984). Effectiveness of speech therapy for aphasic stroke patients: a randomised controlled trial. Lancet, 1, 1197—1200. Linebarger, M. C. (1990). Neuropsy chology of sentence parsing. In A. Caramazza (Ed.), Cognitive neuropsychology and neurolinguistics: advances in models of cognitive function and impairment. 55—122. Hillsdale: Lawrence Erlbaum Associates. Lomas, J., Pickard, L., Bester, S., Elbard, H., Finlay son, A., & Zoghaib, C. (1989). The communicative effectiveness index: development and psy chometric evaluation of a functional communication measure for adult aphasia. Journal of Speech and Hearing Disorders, 54, 113—124. Luria, A. R. (1963). Restoration of function after brain injury. Oxford: Pergamon. Luria, A. R. (1966). Higher cortical functions in man. London: Tavistock. Luria, A. R. (1970). Traumatic aphasia. Le Hague: Mouton. Marie, P. (1906). The third left frontal convolution play s no special role in the function of language. In M. F. Cole & M. Cole (Eds.), (1971), Piere Marie’s papers on speech disorders. New York: Hafner. Marshall, R. C. (1987). Reapportioning time for aphasia rehabilitation: a point of view. Aphasiology, 1, 59—73. Marshall, R. C. & Watts, M. (1976). Relaxation training: effects on the communicative ability of aphasic adults. Archives of Physical Medicine and Rehabilitation, 57, 464—467. Marshall, R. C., Wertz, R. T., Weiss, D. et al. (1989). Home treatment for aphasic patients by trained nonprofessionals. Journal of Speech and Hearing Disorders, 54, 462—470. Martin, A. D. (1981). Therapy with the jargonaphasic. In J. W. Brown (Ed.), Jargonaphasia. 305—326. New York: Academic Press. Meikle, M., Wechsler, E., Tupper, A., Benenson, M., Butler, J., Mulhall, D., & Stern, G. (1979). Comparative trial of volunteer and professional treatments of dy sphasia after stroke. British Medical Journal, 2, 87—89. Mulhall, D. J. (1988). The management of the aphasic patient. In F. C. Rose, R. Whurr & M. A. Wyke (Eds.), Aphasia. 489—517. London: Whurr.
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Ruth Lesser, Newcastle upon Tyne (UK)
32. Psychosocial Aspects of Aphasia 1. 2. 3. 4. 5.
1.
A Framework for Psychosocial Studies Adjusting to the Social Context Intervention and Rehabilitation Future Perspectives References
A Framework for Psychosocial Studies
1.1. The Background The origins of research into the psy chological and psy chiatric rehabilitation of aphasic individuals stems from the pioneering work of Goldstein (1942). His work with individuals with brain injuries resulting from combat, highlighted both the cognitive and personality changes resulting from such damage. The therapeutic implications of this work were emphasized by Wepman (1951). The focus of much of the earlier research in this field was on the social and emotional changes resulting from aphasia (e. g. Biorn-Hansen 1957). This led to a series of studies on the psy chiatric aspects of aphasia. The results of much of this research have been drawn together in a major review by Starkstein/Robinson (1988) which concludes that depressed aphasic individuals show a lower rate of recovery and significantly higher levels of cognitive impairment than non-depressed patients. It is however, only relatively recently that consideration has been given to the relationship between individual changes in the emotional behavior of aphasic individuals and their subsequent adjustment to their families and the wider social context (Buck 1968). It is now critical that the study of psy chosocial adjust-
ment to aphasia is seen as a distinctive research area in it own right in which the focus is on rehabilitation rather than the emotional responses of aphasic individuals. The aim of this review is to help define this distinctive area, to review significant research in this field and to highlight areas requiring further investigation. 1.2. Psychosocial Aspects The study of psy chosocial aspects is concerned with rehabilitation and adjustment to the disability rather than investigation into the nature of the impairment itself. As Code/ Müller (1983) have noted, the psy chosocial perspective in aphasia therapy remains the most underdeveloped and y et is fundamental in the rehabilitation process. Psy chosocial adjustment concerns not only coming to terms with a totally new set of circumstances for the individual experiencing aphasia, but has wider implications within the social network in which the individual lives, and in particular on the family . The prime focus of research into psy chosocial adjustment is to understand better how to facilitate psy chological well being in aphasic individuals; the effects an aphasic individual has on significant others and implications for the family and the broader social network; and the extent to which society in its broadest sense is able to respond and accommodate these changes in a positive manner. From the perspective of the individual aphasic person, it is the study of the extent to which the loss of communication, and hence personhood, can be compensated through coping strategies which lead to a
32. Psychosocial Aspects of Aphasia
regaining of control over the environment and adjustment to the disability . This directs study to the rehabilitation process and hence incorporates those factors which affect psy chosocial adjustment.
2.
Adjusting to the Social Context
2.1. The Effects on the Family Network It is now well established that aphasia is a family problem. Spouses of aphasic people have been shown to suffer marked changes in their well being both phy sical and psy chological. Early studies by Malone/Ptacek/Malone (1970) and Artes/Hoops (1976) have all shown the difficulties faced by spouses. As well as more predictable disturbances such as lack of sleep and tiredness through having to provide constant care, there is also some indication that children within the family situation receive less time and therefore find it difficult to adjust to the new situation. A study by Biorn-Hansen (1957) has suggested that spouses may at times reject their aphasic partners and indeed show some distaste towards them. There is also evidence to suggest that spouses may be overprotective (Malone/ Ptacek/Malone 1970). The cy clic nature of the familial relationship has been demonstrated by Mulhall (1978) who has shown how frustration in the aphasic person can lead to anger in the spouse which in turn leads to rejection and a subsequent break-down in communication. The work of Kinsella/Duffy (1979) has highlighted a range of difficulties in adjustment. They found that from a sample of 79 couples, 42% of the spouses were suffering from clinical depression and that 78% of them were either taking tranquilisers or sleeping pills. Furthermore, 83% of the couples had ceased to have sexual intercourse although it was judged there was no phy sical disability preventing it. Taken together these studies demonstrate that marital relationships between aphasic individuals and their partners are characterised by problems of interpersonal communication, diminished sexual satisfaction and loss of partnership, as well as individual responses including isolation, anxiety and susceptibility to minor psy chiatric disorders. More recent studies have confirmed these findings (e. g. Christensen/Anderson 1989) and highlighted the difficulties posed by role changes that often involve making medical and financial descisions as well as offering personal care. As Woodhouse/
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Müller have shown (1987), the majority of those providing care are female and are normally spouses or daughters of the aphasic person. A study by Oranen/Sihvonen/Äy stö/ Hagfors (1987) identified five patterns of coping and showed that the best adjusted families were characterised by an optimistic coping approach and the least well adjusted through depressive or nervous coping patterns. Similar results have been found in studies of brain injured individuals suffering from aphasia which is indicative that aphasia is a causal factor in adjustment by spouses and partners (Rosenbaum/Majenson 1976). In a recent review Wahrborg (1991) has concluded that family members of aphasic individuals are prone to developing minor psy chiatric disorders; that this alters the nature and quality of the interaction between the spouse and the aphasic partner; and that in general a lack of knowledge about the disability further accentuates the problem. These important conclusions reflect significant research efforts during the last two decades which have provided clear evidence of the detrimental effects on the aphasic individual and the family network. 2.2. Interpersonal and Professional Perceptions There have been relatively few studies of differences in the perception of disability and prognosis by the individual aphasic persons themselves, their family members and the professional concerned. Skelly (1975) has shown that aphasic people are often approached by nursing and medical personnel in a way that they perceive as insulting or degrading which can lead to a loss of interest in the rehabilitation process. A series of studies has investigated how relatives and aphasia therapists perceive the individual aphasic person’s communication skills. Helmick/Watamori/Palmer (1976) in comparing test results with the judgments made by spouses as regards the language disability , concluded that spouses of aphasic persons view communication to be less impaired than it actually is. It was suggested that spouses may have unrealistic expectations of future improvements. However, Holland (1970), in discussing the study by Helmick and colleagues, argued that the spouse is better able to make use of contextual cues and might in fact be in a better position to assess the communicative abilities of the aphasic person. As Helmick/Watamori/Palmer (1977) re-affirm there is often a discrep-
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ancy between the spouses and the clinician perception. A study by Müller/Code/Mugford (1983) using the Code-Müller psy chosocial scale of adjustment (Müller/Code 1983; Code/Müller 1992) showed that relatives and indeed aphasic persons themselves, view psy chosocial adjustment more optimisticall y than the clinicians involved. Herrmann/Wallesch (1989) using a more sophisticated version of the Code/Müller scale of psy chosocial adjustment, demonstrated that patients and relatives suffer considerable ps y chosocial strain and that they rated the probability of an improvement in psy chosocial adjustment as being significantly higher than did clinicians. Shewan/Cameron (1984) have shown that there is limited agreement between aphasic individuals and their spouses as regards communication and related problems. Herrmann/Wallesch found considerable psy chosocial changes in aphasic individuals including differences in job opportunities, household work and the administration of income and property, as well as social changes affecting in particular recreational activities and holiday s. Using this same scale Herrmann/Wallesch (1990) investigated the perception of different professional groups using a Multiattribute Utility Technique in the investigation of phy siosocial factors. Little agreement was found between a wide range of professional groups including occupational therapists, ps y chotherapists, neurops y chologists, neurologists and speech therapists. This highlights the importance of undertaking individual assessment and therapy within a specific rehabilitative context in order to provide effective intervention for aphasic individuals.
3.
Intervention and Rehabilitation
3.1. Counselling and Social Perspectives There have been few evaluative studies on the effectiveness of intervention directed specifically at psy chosocial adjustment. This research has been hampered to some extent by there being only a limited range of appropriate assessment procedures available. This remains an important research field. There have however, been a number of approaches to the use of groups as a means of improving psy chosocial behaviour. Fawcus (1983) and Pachalska (1991) have strongly advocated the use of groups and have developed a wide range of clinical techniques to provide a supportive environment for aphasic individuals. The difficulties of providing empirical data
on the effectiveness of group therapy have been noted by Kearns (1986). As y et there is no definitive answer to this question. Brumfitt/Clarke (1983) initiated the application of psy chotherapeutic techniques derived broadly from psy chotherapy to the management of aphasia. Wiig (1973) has offered guidelines on sexual counselling and in terms of integrating aphasic individuals more widely into societ y , Borenstein/Linell/Wahrborg (1987) have evaluated the effectiveness of a structured one week course involving social contact outside of the hospital environment. This was shown to be beneficial and was followed up by a study integrating y ounger aphasic people into a ‚Folk High School’ which resulted in evidence to show an improvement in psy chosocial and linguistic functioning (Borenstein/Wahrborg/Linell et al. 1987). There remains however difficulties in evaluating studies of naturalistic approaches to therapy. 3.2. Family Support and Involvement There is tentative evidence to suggest that the spouse exerts influence on the recovery and rehabilitation pattern of aphasic people (Buxbaum 1967). Rollin (1987) has brought together a diverse literature in promoting the involvement of families in aphasia rehabilitation and in particular the introduction of family therapy . He advocates that trained family therapists with a knowledge of aphasia or speech-language pathologists trained in family therapy can positively influence the rehabilitation process by undertaking sy stematic family therapy involving all significant others as well as the individual aphasic person. A great deal of this work is derived from his own experience as a family therapist. A short empirical report by Wahrborg/Borenstein (1989) tentatively suggests that family therapy relieves depression and provides social and emotional support. In a more wide ranging debate concerning the benefits of family therapy , Wahrborg (1991) argues that training programmes in famil y therap y should be provided for those professionals involved in aphasia rehabilitation. There are however reservations as regards the efficacy of family therapy and the extent to which speech and language therapists should be trained as counsellors. There is increasing recognition of the importance of family members in the rehabilitation process but a need to ascertain more precisely how best to utilise their skills.
32. Psychosocial Aspects of Aphasia
3.3. Spouse and Carer Adjustment The need to provide support for the spouses and partners of aphasic individuals is clearly supported by the studies set out above. In particular the deterioration in general health and psy chological wellbeing can be seen as likely to further disrupt the family relationship. It has been argued that it is appropriate for speech and language pathologists to initiate intervention on the grounds that they have a specialist knowledge not only of the language impairment and methods of rehabilitation but of those problems faced by aphasic individuals. Bowling (1977) offered unstructured social support to individuals to attend a group as and when they felt fit. Although attendance was spasmodic, a third of the subjects did indicate that the group had been beneficial to them, although the evidence presented is incomplete. A study by Bevington (1985) offered a structured programme of a specific educational nature. Again there is some evidence to suggest an improvement in knowledge for those regularly attending the group. A non-directive, open-ended group programme offered by Bernstein (1979), was in the end rather poorly attended and no sy stematic measures of the psy chosocial benefits gained were taken. Nevertheless, there was sufficient evidence from the studies to encourage Rice/Paull/Müller (1987) to carry out an evaluation study of a social support group for spouses of aphasic partners. The group offered both emotional support and structured educational activities. Comparison between good and poor attenders on measures of psy chosocial adjustment showed significant improvement on tests of social dy sfunction, somatic sy mptoms, anxiety and psy chological well being for those attending. There is a need for work of this kind to be followed up and for a wider variety of intervention techniques to be evaluated.
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between four and seven. There remain however significant gaps in our knowledge of how children experience and adjust to adult aphasia. This is an important area for future research to inform the rehabilitation process. 4.1.2. Measurements of Psychosocial Change There is a recognised need to develop more sophisticated and sensitive measures of psy chosocial adjustment which can determine change over time. It may prove beneficial to extend single case study methodology to include psychosocial factors. 4.1.3. Psychosocial Adjustment and Linguistic Performance There is a need to determine the extent to which a high level of psy chosocial adjustment is a causal factor in linguistic improvement in aphasic individuals. There is as y et no clear evidence from those research studies which have begun to address this issue (e. g. Buxbaum 1967). 4.1.4. Efficacy of Intervention with Aphasic Individuals There is a need to undertake a series of efficacy studies to determine the extent to which psy chosocial adjustment can be facilitated. There is some evidence to suggest that clinically orientated approaches are not effective (Lincoln/Jones/Mulley 1985), and future researchers need to evaluate the extent to which family members and other social networks can have psychologically beneficial effects. 4.1.5. Effective Provision of Spouse and Family Support
4.1. Research Issues
In recognising the psy chosocial consequences for spouses, partners, and other family members, it is necessary to undertake research reviewing how best to support them. Currently , there are very few studies addressing this issue and insufficient resource prioritisation for this group.
4.1.1. The Perceptions of Children
4.1.6. Integration into Society
Although there has been some mention of children in the research literature (Kinsella/ Duffy 1979) there has been little sy stematic research of the effects on children of there being an aphasic individual in the family . Starch (1990) has evaluated an educational programme targeted at y oung children aged
There is little information available concerning the extent to which aphasic individuals and their families are fully integrated into society . It is difficult to obtain information of how many aphasic individuals could be helped to return to work and how best to support them (Ramsing/Blomstrand/Sullivan 1991).
4.
Future Perspectives
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4.1.7. Policy Implications The extent to which aphasic individuals and their families adjust to society has wider implications for government policy and the long term provision of health care (Frattali 1992). Although rehabilitation is managed differently on an international basis there is a need to develop and evaluate good practice in the provision of health care. This might best be facilitated by developing measures of the quality of life derived from aphasic individuals themselves (Lomas/Pickard/Mohide 1987). 4.2. Longitudinal Studies In order to fully resolve a number of the research issues highlighted above it would prove to be of enormous benefit to undertake longitudinal studies. The field of aphasia research has rarely attracted sufficient funding to enable work of this kind to be carried out and there are very few studies which have assessed changes for a period of longer than one y ear. Those studies which have been published have focused on the assessment of language function rather than psy chosocial factors (Hanson/Metter/Riege 1989). There is good evidence to show that aphasia results in long term family problems and therefore the extended rehabilitation process extends over a considerable period. Longitudinal interdisciplinar y and multi-international research into the most effective models of rehabilitation for aphasic individuals and their families, is the next important stage in furthering our understanding of psy chosocial adjustment in aphasia.
5.
References
Artes, R. & Hoops, R. (1976). Problems of aphasic and non-aphasic stroke patients as identified and evaluated by patients’ wives. In Y. Lebrun & R. Hoops (Eds.), Recovery in Aphasics. 31—45. Amsterdam: Swets and Zeitlinger. Bernstein, J. C. (1979). A supportive group for spouses of stroke patients. Aphasia, Apraxia, Agnosia, 1, 30—35. Bevington, L. J. (1985). The effect of a structured education programme on relatives’ knowledge of communication with stroke patients. Australian Journal of Communication Disorders, 5, 29—41. Biorn-Hansen, V. (1957). Social and emotional aspects of aphasia. Journal of Speech and Hearing Research, 22, 53—59. Borenstein, P., Linell, S., & Wahrborg, P. (1987).
An innovative therapeutic program for aphasic patients and their relatives. Scandinavian Journal of Rehabilitation Medicine, 19, 51—56. Borenstein, P., Wahrborg, P., Linell S., Hedberg, E., Asking, M., & Ahlsen, E. (1987). Education in Folk High School for y ounger aphasic people. Aphasiology, 1, 263—266. Bowling, J. H. (1977). Emotional problems of relatives of dy sphasic patients. Australian Journal of Communication Disorders, 5, 29—41. Brumfitt, S. & Clarke, P. (1983). In C. Code & D. J. Müller (Eds.), Aphasia Therapy. An application of psy chotherapeutic techniques to the management of aphasia. 89—100. London: Edward Arnold. Buck, M. (1968). Dysphasia: Professional Guidance for Family and Patient. Englewood Cliffs, New Jersey: Prentice-Hall. Buxbaum, J. (1967). Effect of nurturance on wives’ appraisals of their marital satisfaction and the degree of their husbands’ aphasia. Journal of Consulting Psychology, 31, 240—243. Christensen, J. M. & Anderson, J. D. (1989). Spouse adjustment to stroke: aphasic versus non aphasic partners. Journal of Communication Disorders, 22, 225—231. Code, C. & Müller, D. J. (1983). Perspectives in aphasia therapy : an overview. In C. Code & D. J. Müller (Eds.), Aphasia Therapy. 3—13. London: Edward Arnold. Code, C. & Müller, D. J. (1992). The Code-Müller Protocols: Assessing Perceptions of Psy chological Adjustment to Aphasia. Kibworth: Far Communications. Fawcus, M. (1983). Group therapy : a learning situation. In C. Code & D. J. Müller (Eds.), Aphasia Therapy. 113—119. London: Edward Arnold. Frattali, C. M. (in press). Functional assessment of communication: merging public policy with clinical views. Aphasiology, 6, 63—83. Goldstein, K. (1942). Aftereffects of Brain Injuries in War. New York: Grune and Stratton. Hanson, W. R., Metter, E. J. & Riege, W. H. (1989). The course of chronic aphasia. Aphasiology, 1, 19—29. Helmick, J. W., Watamori, T. S., & Palmer, J. M., (1976). Spouses’ understanding of the communication disabilities of aphasic patients. Journal of Speech and Hearing Disorders, 41, 238—243. Helmick, J. W., Watamori, T. S., & Palmer, J. M. (1977). Reply to Holland’s comment on ‚Spouses’ understanding of the communication disabilities of aphasic patients’. Journal of Speech and Hearing Disorders, 42, 308—310. Herrmann, M. & Wallesch, C. W. (1989). Psy chosocial changes and psy chosocial adjustment with chronic severe aphasia. Aphasiology, 3, 513—526. Herrmann, M. & Wallesch, C. W. (1990). Expectations of psy chosocial adjustment in aphasia: a
32. Psychosocial Aspects of Aphasia
MAUT study with the Code-Müller Scale of Psy chosocial Adjustment. Aphasiology, 4, 527—538. Holland, A. (1970). Comment on ‚Spouses’ understanding of the communication disabilities of aphasic patients’. Journal of Speech and Hearing Disorders, 42, 307—308. Kearns, K. P. (1986). Group therapy for aphasia: theoretical and practical considerations. In R. Chapey (Ed.), Language Intervention Strategies in Adult Aphasia. 304—318. Baltimore: Williams and Wilkins (2nd Edition). Kinsella, G. & Duffy , F. D. (1979). Psy chosocial readjustment in the spouses of aphasic patients. Scandinavian Journal of Rehabilitation Medicine, 11, 129—132. Lincoln, N. B., Jones, A. C., & Mulley , G. P. (1985). Psy chological effects of speech therapy . Journal of Psychosomatic Research, 29, 467—474. Lomas, J., Pickard, L., & Mohide, A. (1987). Patient versus clinician item generation for quality of-life measures. Medical Care, 25, 764—769. Malone, R., Ptacek, P., & Malone, M. (1970). Attitudes expressed by families of aphasics. British Journal of Disorders of Communication, 5, 174— 179. Mulhall, D. J. (1978). Dy sphasic stroke patients and the influence of their relatives. British Journal of Disorders of Communication, 13, 127—134. Müller, D. J. & Code, C. (1983). Interpersonal perceptions of psy chosocial adjustment to aphasia. In C. Code & D. J. Müller (Eds.), Aphasia Therapy. 101—112. London: Edward Arnold. Müller, D. J., Code, C., & Mugford, J. (1983). Predicting psy chosocial adjustment to aphasia. British Journal of Disorders of Communication, 18, 23—29. Oranen, M., Sihvonen, R., Ay sto, S. & Hagfors, C. (1987). Different coping patterns in the families of aphasic people. Aphasiology, 1, 277—281. Pachalska, M. (1991). Group therapy for aphasic patients. Aphasiology, 5, 541—554. Ramsing, S., Blomstrand, C., & Sullivan, M. (1991). Prognostic factors for return to work in stroke patients with aphasia. Aphasiology, 5, 583— 588.
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Rice, B., Paull, A., & Müller, D. J. (1987). An evaluation of a social support group for spouses and aphasic adults. Aphasiology, 3, 247—256. Rollin, W. J. (1987). The Psychology of Communication Disorders in Individuals and their Families. Englewood Cliffs, New Jersey: Prentice-Hall. Rosenbaum, M. & Majenson, T. (1976). Changes in life patterns and sy mptoms of low mood as reported by wives of severely brain-injured soldiers. Journal of Consulting and Clinical Psychology, 44, 881—888. Shewan, C. M. & Cameron, H. (1984). Communication and related problems as perceived by aphasic individuals and their spouses. Journal of Communication Disorders, 17, 175—187. Skelly , M. (1975). Aphasic patients talk back. American Journal of Hearing, 7, 1140—1142. Starch, S. A. (1990). Increasing y oung children’s understanding of aphasia: a unique educational approach. In T. E. Prescott (Ed.), Clinical Aphasiology, Volume 20. Austin, T. X.: Pro Ed. Starkstein, S. E. & Robinson, R. G. (1988). Aphasia and depression. Aphasiology, 2, 1—20. Wahrborg, P. (1991). Assessment and Management of Emotional and Psychosocial Reactions to Brain Damage and Aphasia. London: Whurr. Wahrborg, P. & Borenstein, P. (1989). Family therapy in families with an aphasic member. Aphasiology, 1, 93—98. Wepman, J. M. (1951). Recovery From Aphasia. New York: Ronald Press. Wiig, E. H. (1973). Counselling the adult aphasic for sexual readjustment. Rehabilitation Counselling Bulletin, 17, 110—119. Williams, S. E. & Freer, C. A. (1986). Aphasia: its effect on marital relationships. Archives Physical Medicine and Rehabilitation, 67, 250—252. Woodhouse, L. & Müller, D. J. (1987). Caring for the carers: support levels for families of dy sphasic adults. Journal of the Royal Society of Health, 107 , 49—50.
Dave Müller, Ipswich, Suffolk (United Kingdom)
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33. Pathology of Nonaphasic Language Behavior after Focal Left Hemispheric Damage 1. 2. 3. 4. 5.
Frontal Lobe Language Disorders ‚Latent Dysphasia’ after Non-perisylvian Cortical Damage Subcortical Language Disorders Conclusion References
In the present chapter I will discuss some language disorders due to focal pathology of the left hemisphere which can be considered nonaphasic for either or both of the following reasons. First, a disorder may be classified as nonaphasic on theoretical grounds, when it does not (at least overtly ) involve the main levels of language organization according to current linguistic descriptions (phonology , morphology , sy ntax, lexical semantics). This definition includes several different varieties of impairment of language use, which are (supposedly ) associated with a ‚normal’ linguistic competence, and which usually appear following damage to frontal regions of the left hemisphere. Second, a language impairment may be grouped as nonaphasic on clinical grounds, if it is not apparent on standard language examination, but some definite impairments are perceived subjectively by the patient, and can be demonstrated with appropriate, in-depth testing. Such disorders usually affect lexical-semantic abilities, nonliteral and creative language use and have been labelled ‚minimal dy sphasia’ in a seminal paper by Macdonald Critchley (1972). A disorder of this ty pe can be observed both in the acute stage after non-perisy lvian lesions and in patients who have recovered from a ‚standard’ aphasia.
1.
Frontal Lobe Language Disorders
A discussion of ‚nonaphasic’ frontal language disorders must include several different conditions, each of which affects the ability of the patient to express him or herself. One such condition, the total suppression of vocalization and speech, known as ‚mutism’, is frequently observed immediately after frontal damage. Mutism has innumerable causes and several different pathophy siological mechanisms (see Table 33.1). Leaving aside peripheral conditions, even in the case of disease to the central nervous sy stem the patient may be unable to speak for various reasons. For
A. Peripheral Laryngeal disease Neuromuscular disorders B. Central Bulbar disorders Motor neuron disease Brainstem infarction, neoplasm, trauma or infection Pseudobulbar disorders Opercular syndrome (Foix-ChavanyMarie) Motor neuron disease Multiple sclerosis Other causes Advanced extrapyramidal disorders Progressive supranuclear palsy Parkinson’s disease Huntington’s disease Dystonia Wilson’s disease Advanced dementing disorders Alzheimer’s disease Pick’s disease Multi-infarct dementia Transient mutism after closed head injury Transient mutism with aphasia Broca’s aphasia Transcortical motor aphasia Dynamic aphasia Global aphasia Subcortical aphasia Aphemia Akinetic mutism Post-callosotomy mutism C. Psychiatric disorders Depression Schizophrenia Hysteria Table 33.1: Differential Diagnosis of Mutism (modified from Cummings/Benson/Houlihan/Gosenfeld 1983)
instance, bilateral damage to the opercular regions is sufficient to give rise to permanent mutism. Detailed testing proves some of these patients to be totally proficient in auditory comprehension and written communication and therefore nonaphasic (Villa/Caltagirone 1984; Cappa/Guidotti/Papagno/Vignolo 1987). Mutism in these cases is probably as-
33. Pathology of Nonaphasic Language Behaviorafter Focal Left Hemispheric Damage
sociated with a pseudobulbar impairment of phonation and articulation (Foix/Chavany / Marie 1926), the responsible lesions being less extensive in the left hemisphere, with partial sparing of the inferior frontal gy rus. In contrast, transient mutism is associated with lesions limited to the left frontal lobe. The outcome of this complete but temporary suppression of speech can take two different directions. First, it may lead to a lasting impairment of speech production, due to articulatory disruption, without any disturbance of language, referred to as ‚aphemia’. Second, it can cause a reduction of spontaneous speech, usually connected to subtle impairment in complex language tasks termed ‚transcortical motor aphasia’. Both ‚aphemia’ and ‚transcortical motor aphasia’ are distinct clinical sy ndromes, which can be observed in relatively pure form and are associated with different lesion locations. A p h e m i a generally coincides with damage to the inferior precentral gy rus with variable extension to the posterior operculum (Schiff/Alexander/ Naeser/Galaburda 1983) and is best considered as a neurophonetic disorder. Therefore, I will now devote my attention to the sy ndrome of t r a n s c o r t i c a l m o t o r a p h a s i a (TMA), which (at least as it is used to indicate a subgroup of patients) probably corresponds to the theoretical criteria for a nonaphasic language disorder indicated in the introduction. This time-honored taxonomical label, originally introduced by Lichtheim (1885), is generally used to indicate a clinical picture characterized by two distinguishing features, namely , a severe quantitative reduction of spontaneous speech in combination with a preserved ability to repeat. Other names have also been used to designate this sy ndrome (dy namic aphasia, verbal akinesia, verbal ady namia, and so on). As is usually the case, however, all of these terms are used to refer to an extremely diverse clinical picture. This diversity is reflected by the proposal, starting from Kleist (1934) through Goldstein (1948) to de Lacy Costello/Warrington (1989), to distinguish ‚subty pes’ of TMA. A basic distinction, which respects differences in lesion location and (possibly ) in pathophy siological mechanisms, is between the relatively seldom ‚pure’ form, and other more common cases involving more widespread linguistic impairment. In the ‚pure’ form of TMA, only monologic speech is impaired, while confrontation naming, repetition and auditory comprehen-
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sion are preserved. One major problem in the assessment of these patients is that spontaneous speech or naming are sometimes only as unimpaired as one is able to judge from their very limited production. The ‚pure’ form of TMA has been connected to lesions of the medial frontal lobe, which, after a transient period of mutism, leave the patient with severely reduced spontaneous speech but normal naming and reading aloud (Masdeu/ Schoene/Funkenstein 1978). An extension to the cingulate regions is usually associated with a severe reduction of all motor activity , including spontaneous speech, which is called akinetic mutism (Buge/Escourolle/Rancurel/ Poisson 1975). In contrast, in the more common cases of TMA, disorders in naming as well as at the phonologic and/or the morphosy ntactic level of production are evident. Such clinical pictures usually coincide with other lesion sites, which share the characteristic of sparing the perisy lvian language area. For example, in the left frontal lobe, the lesion usually involves the dorsolateral cortex in front of Broca’s area or the dorsomedial cortex, including the supplementary motor area (see Freedman/Alexander/Naeser 1984 for a review); articulatory disturbances or mild disorders of auditory comprehension are present if the damage encroaches on the perisy lvian language areas. Another cause of TMA-ty pe impairments can be subcortical lesions, involving deep grey structures and white matter: they will be discusses later on. — Several interpretations have been proposed for the pathophy siology of TMA. Kleist (1934) propagated that the sy ndrome is the result of an ‚Antriebsmangel der Sprache’ (loss of the impulse to communicate) which fits well with the later proposal of a ‚fronto-limbic’ disconnection (Rubens/Kertesz 1983). Recently , a variant of this interpretation has been offered in neurochemical terms, suggesting that an interruption of the mesofrontal dopaminergic projections could be responsible for this sy ndrome (Albert/Bachman/Morgan/Helm-Estabrooks 1988). Another closely related interpretation was originally proposed by Botez/ Barbeau (1971). They ascribed the suppression or quantitative reduction of spontaneous speech to a lesion in a complex network of subcortical and frontal structures which constituted the “starting mechanism of speech”. Several psy cholinguistic theories have been proposed to account for the sy ndrome. Their origin too can be traced back to Lichtheim’s original postulation of such a clinical picture
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(1885). Rephrased in present day terminology (McCarthy /Warrington 1984), the sy ndrome may be interpreted as the result of the interruption of the direct connection between semantic analy sis and speech production, with preservation of the phonological route. In a ver y influential account Luria/Tsvetkova (1967) provided experimental evidence for an impairment in propositionalizing. They attributed the impairment to defective formation of the linear scheme of the sentence, which the patient could correct when external cues were available. For example, the patient was given a linear array of pieces of paper corresponding in number to the units he or she had to arrange in the sentence in order to produce a coherent narrative. Unable to duplicate Luria and Tsvetkova’s results, de Lacy Costello/Warrington (1989) have suggested a more ‚central’ defect in the process of sentence production, at the level of verbal planning. These two interpretations can be mapped to two different levels of Garrett’s model of sentence production (1984). Luria and Tsvetkova’s findings suggest a defect in the stage of verbal planning where the sy ntactic form of the sentence is produced (positional level representation). On the other hand according to De Lacy Costello and Warrington the impairment in TMA is at the stage where lexical-semantic representations of words are accessed and the argument structure of verbs is specified (functional level representation). The relatively well defined picture of TMA should be kept distinct from other disorders of verbal communication, which can be observed in patients with extensive damage to the frontal lobes (Stuss/Benson 1986). In the latter cases, the disorder is not specific for language, but it may include not only features of TMA (quantitative reduction, perseverations) but also disorders of contextual language utilization (which may be more fruitfully described at the pragmatic level, such as appropriateness of response to the interlocutor, narrative coherence, sensitivity to the social context). A general impairment of goaldirected behavior is a crucial feature of the so called frontal sy ndrome, and, as originally proposed by Luria (1966), language play s a basic role in the regulation of human activity. Even if a full-fledged frontal sy ndrome is not present, patients with left frontal damage, in comparison to those with right frontal damage and normals, show a definite impairment on complex verbal reasoning and verbal
memory tasks (Novoa/Ardila 1987). This impairment is qualitatively similar to the latent dy sphasia of nonaphasic left hemisphere patients, which will be discussed below.
2.
‚Latent Dysphasia’ after Non-perisylvian Cortical Damage
Originally , ‚minimal aphasia’ was defined by Critchley (1972) on strictly semeiological grounds, as a sy ndrome characterized by poverty of spontaneous speech, difficulty in the comprehension of complex sentences or nonliteral language (metaphors, idioms) and impairment of creative language usage. At this time, no one attempted to specify underly ing phy siopathological mechanisms. The disorder thus referred to several different conditions: patients who had recovered from severe aphasia, individuals with highly developed language skills and mild language disturbances, subtle language disorders due to increased intracranial pressure or slowly progressive degenerative pathology . In the present context, I will focus on a more restricted aspect, i. e. on the subtle language disorders which can be observed, on appropriate testing, in individuals with a recent acute vascular lesion of the left hemisphere. In a recent study (Vallar/ Cappa/Papagno 1988) we selected a group of patients with a recent left hemispheric stroke who had no signs of aphasia on a ‚standard’ language assessment test (Basso/Capitani/ Vignolo 1979) and scored within normal limits on two sensitive language tasks (Token test by De Renzi/Vignolo 1962, in the reduced version by De Renzi/Faglioni 1978, and Reporter test by De Renzi/Ferrari 1978). They were submitted to a further extensive assessment of language, including measures of phonological, lexical-semantic and sy ntactic abilities, and of verbal memory , and their performance was compared with right hemisphere-damaged subjects and normal controls. The ‚nonaphasic’ patients showed a mild, but clear-cut impairment in word comprehension and word retrieval, associated with a defect in verbal long-term memory . It is noteworthy that in a subsequent study of a larger sample of right hemisphere-damaged subjects (Cappa/Papagno/Vallar 1990), a similar pattern of mild lexical-semantic impairment was found only in a minority of subjects. An analy sis of lesion site, as shown by CT scan, in left hemisphere-damaged subjects showed two possible anatomical patterns: ei-
33. Pathology of Nonaphasic Language Behaviorafter Focal Left Hemispheric Damage
ther a) cortical lesions, confined to the medial temporal lobe and occipital regions, or b) small subcortical lesions involving the thalamus, the basal ganglia or the white matter (see below). None of the lesions involved the perisy lvian language areas, associated with ‚standard’ aphasic sy ndromes, or the anterior frontal lobe, the involvement of which produces the patterns of language impairment described in the previous section. Patients with lesions of the posterior cerebral artery territory were particularly represented in the cortical group. This lesion site is often associated not only with the well-known sy ndrome of alexia without agraphia (Dejerine 1892) and with verbal long-term memory impairment (Benson/Marsden/Meadows 1974) but, as shown recently in a sy stematic study by De Renzi/Zambolin/Crisi (1987), with failure on naming tasks, independent of modality of presentation and of presence of alexia.
3.
Subcortical Language Disorders
While there is a lively debate about the phy siopathological mechanisms underly ing subcortical aphasia (see Perani/Vallar/Cappa et al. 1987 for a discussion), it is generally accepted nowaday s that clear-cut aphasic sy ndromes can be observed after lesions confined to the thalamus, the basal ganglia and/or the neighboring white matter tracts (see Wallesch/ Papagno 1988, for a review). On the other hand, it has been observed that in subcortical lesions it is quite difficult to predict the presence and characteristics of aphasia after damage to a given location (Cappa/Cavallotti/ Guidotti et al. 1982). A key factor for the appearance of aphasia is lesion size. In a recent study (Perani/Vallar/Cappa et al. 1987) the lesions associated with both severe hy poperfusion in the ipsilateral cortex and clinical evidence of aphasia were of a significantly larger size than those associated with negative cases. However, small lesions in some critical locations are concomitant with aphasia. A ty pical example is the TMA observed after infarction in the anterior choroidal artery territory (Wallesch 1985; Cappa/Sterzi 1990), though it is probably a transient disorder with rapid recovery . Moreover, there is some evidence that, within the thalamus, anterior lesions are more commonly associated with aphasia, while posterior lesions are not (Graff Radford/Damasio/Yamada et al. 1985; Cappa/Papagno/Vallar/Vignolo 1986). However, evidence also exists that in patients with
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subcortical lesions, who are not clinically aphasic, there are some subtle language impairments apparent on detailed testing. In the previously described series of recent left hemisphere lesions without aphasia, (Vallar/Papagno/Cappa 1988) five out of eleven patients had a subcortical lesion. In the chronic stage Wallesch and his coworkers (Wallesch/Kornhuber/Brunner et al. 1983; Wallesch/Kornhuber/Kunz/Brunner 1983) have shown mild language defects in patients with basal ganglia, but not with thalamic lesions.
4.
Conclusion
In this article, several aspects of language impairment after focal left hemisphere pathology which could not fit in a standard definition of aphasia have been reviewed. The only conclusion which can be drawn is that incursions in this ‚no man’s land’ between language modules and the ‚cognitive cloud’ have been fragmentary and have often lacked any sound theoretical framework. Concepts from neurological aphasiology and descriptive linguistics appear to be of limited usefulness in this area. A better understanding of the disorders of language described in this chapter is extremely important not only for theoretical considerations, but also from the practical standpoint of rehabilitation. Indeed, it is a common experience that traditional methods of aphasia therapy are ineffective in the treatment of the so-called ‚inertia’ of TMA (Huntley /Gonzalez Rothi 1988) and in dealing with the subjective complaints of those patients classified as nonaphasic after conventional testing. Acknowledgement: I wish to thank Prof. Luigi A. Vignolo for his helpful reading of this chapter and Dr. Giuseppe Vallar for many fruitful discussions.
5.
References
Albert, M. L., Bachman, D. L., Morgan, A., & Helm-Estabrooks, N. (1988). Pharmacotherapy of aphasia. Neurology, 38, 877—879. Basso, A., Capitani, E., & Vignolo, L. A. (1979). Influence of rehabilitation on language skills in aphasic patients. Archives of Neurology, 36, 190—196. Benson, D. F., Marsden, C. D., & Meadows, J. C. (1974). The amnesic sy ndrome of posterior cerebral artery occlusion. Acta Neurologica Scandinavica, 50, 133—145.
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Botez, M. I. & Barbeau, A. (1971). Role of subcortical structures and particularly of the thalamus in the mechanisms of speech and language. International Journal of Neurology, 8, 300—320. Buge, A., Escourolle, R., Rancurel, G., & Poisson, M. (1975). “Mutisme akinétique” et ramollissement bicingulaire. Trois observations anatomo-cliniques. Revue Neurologique, 131, 121—137. Cappa, S. F., Cavallotti, G., Guidotti, M., Papagno, C., & Vignolo, L. A. (1982). Subcortical aphasia: two clinical-CT scan correlation studies. Cortex, 19, 227—242. Cappa, S. F., Guidotti, M., Papagno, C., & Vignolo, L. A. (1987). Speechlessness with occasional vocalizations after bilateral opercular damage. Aphasiology, 1, 35—39. Cappa, S. F., Papagno, C., & Vallar, G. (1990). Language and verbal memory after right hemispheric stroke. A clinical-CT study . Neuropsychologia, 28, 503—509. Cappa, S. F., Papagno, C., Vallar, G., & Vignolo, L. A. (1986). Aphasia does not alway s follow left thalamic hemorrhage: a study of five negative cases. Cortex, 22, 639—647. Cappa, S. F. & Sterzi, R. (1990). Infarction in the territory of the anterior choroidal artery : a cause of transcortical motor aphasia. Aphasiology, 4, 213—217. Critchley , M. (1972). Communication: recognition of its minimal impairment. In M. Critchley , J. L. O’Leary , & B. Jennet (Eds.), Scientific foundations of neurology. 221—227. London: Heinemann. Cummings, J. L., Benson, F. D., Houlihan, J. P., & Gosenfeld, L. F. (1983). Mutism: loss of neocortical and limbic vocalization. Journal of Nervous and Mental Diseases, 171, 255—259. Dejerine, J. (1892). Contributions à l’étude anatomopathologique et clinique des différentes variétés de cécité verbale. Mémoires de la Société de Biologie, 4, 61—90. de Lacy Costello, A. & Warrington, E. K. (1989). Dy namic aphasia: the selective impairment of verbal planning. Cortex, 25, 103—114. De Renzi, E. & Faglioni, P. (1978). Normative data and screening power of a shortened version of the token test. Cortex, 14, 41—49. De Renzi, E. & Ferrari, C. (1978). The reporter’s test — a sensitive test to detect expressive disturbances in aphasics. Cortex, 14, 279—293. De Renzi, E. & Vignolo, L. A. (1962). The token test: a sensitive test to detect receptive disturbances in aphasics. Brain, 85, 665—678. De Renzi, E., Zambolin, A., & Crisi, G. (1987). The pattern of neuropsy chological impairment associated with left posterior cerebral artery infarcts. Brain, 110, 1099—1116. Foix, C., Chavany , J. A., & Marie, P. (1926). Diplegie facio-linguo-masticatrice d’origin cortico-
souscortical sans paraly se des membres. Revue Neurologique, 33, 214—219. Freedman, M., Alexander, M. P., & Naeser, M. A. (1984). Anatomical basis of transcortical motor aphasia. Neurology, 34, 409—417. Garret, M. F. (1984). The organization of processing structure for language production. Applications to aphasic speech. In D. Caplan, A. R. Lecours, & A. Smith (Eds.), Biological perspectives on language. 172—193. Cambridge MA: MIT Press. Goldstein, K. (1948). Language and language disturbances. New York: Grune and Stratton. Graff Radford, N. R., Damasio, H., Yamada, T., Eslinger, P. J., & Damasio, A. R. (1985). Nonhemorrhagic thalamic infarction: clinical, neuropsy chological and electrophy siological findings in four anatomical groups defined by computerized tomography. Brain, 108, 485—516. Huntley , R. A. & Gonzalez Rothi, L. J. (1988). Treatment of verbal akinesia in a case of transcortical motor aphasia. Aphasiology, 2, 55—66. Kleist, K. (1934). Gehirnpathologie. Berlin: Springer. Lichtheim, L. (1885). On aphasia. Brain, 7 , 433—484. Luria, A. R. (1966). Higher cortical functions in man. New York: Basic Books. Luria, A. R. & Tsvetkova, L. (1967). The mechanism of “dy namic aphasia”. Foundations of Language 4, 296—307. Masdeu, J. C., Schoene, W. C., & Funkenstein, H. (1978). Aphasia following infarction of the supplementary motor area. A clinicopathologic study . Neurology, 28, 1220—1223. McCarthy , R. & Warrington, E. K. (1984). A tworoute model of speech production. Evidence from aphasia. Brain, 107, 463—485. Novoa, O. P. & Ardila, A. (1987). Linguistic abilities in patients with prefrontal damage. Brain and Language, 30, 206—225. Perani, D., Vallar, G., Cappa, S. F., Messa, C., & Fazio, F. (1987). Aphasia and neglect after subcortical stroke. Brain, 110, 1211—1229. Rubens, A. B. & Kertesz, A. (1983). The localization of lesions in transcortical aphasias. In A. Kertesz (Ed.), Localization in neuropsychology. 245—268. New York: Academic Press. Schiff, H. B., Alexander, M. P., Naeser, M. A., & Galaburda, A. M. (1983). Aphemia. Clinical-anatomic correlations. Archives of Neurology, 40, 720—727. Stuss, D. T. & Benson, D. F. (1986). The frontal lobes. New York: Raven Press. Vallar, G., Papagno, C., & Cappa, S. F. (1988). Latent dy sphasia after left hemisphere lesions: a lexical-semantic and verbal memory defect. Aphasiology, 2, 463—478.
34. Verbal Communication Deficitsafter Right-Hemisphere Damage
Villa, G. P. & Caltagirone, C. (1984). Speech suppression without aphasia after bilateral perisy lvian softenings (bilateral rolandic operculum damage). Italian Journal of Neurological Science, 5, 77—83. Wallesch, C. W. (1985). Two sy ndromes of aphasia occurring with ischemic lesions involving the left basal ganglia. Brain and Language, 25, 357—361. Wallesch, C. W., Kornhuber, H. H., Brunner, R. J., Kunz, T., Hollerbach, B., & Suger, G. (1983). Lesions of the basal ganglia, thalamus and deep white matter: differential effects on language functions.
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Brain and Language, 20, 286—304. Wallesch, C. W., Kornhuber, H. H., Kunz, T., & Brunner, R. J. (1983). Neuropsy chological deficits associated with small unilateral thalamic lesions. Brain, 106, 141—152. Wallesch, C. W. & Papagno. C. (1988). Subcortical aphasia. In F. C. Rose, R. Whurr, & M. A. Wy ke (Eds.), Aphasia. 256—287 . London: Whurr Publishers.
Stefano F. Cappa, Brescia (Italy)
34. Verbal Communication Deficits after Right-Hemisphere Damage 1. 2. 3. 4. 5. 6.
Prosody Lexical Semantics Text and Pragmatics Specificity of the Verbal Communication Disorders Incidence of Verbal Communication Deficits References
Apart from exceptional cases of crossed aphasia, right-hemisphere lesions can result in verbal communication problems that do not compose an aphasia proper, but that can nevertheless affect the individual’s relations with others. Since these disorders only rarely affect phonological, morphological or sy ntactical components of language, the present chapter will focus instead on impairments of prosody , lexical-semantics, text-level performance and pragmatic ability . Finally , the specificity and the incidence of these impairments will be considered.
1.
Prosody
Linguistic prosody refers to the use of intonation to realize lexical and emphatic stress and to express different modalities such as exclamation. In contrast, emotional prosody denotes emotional states, such as happiness. Both ty pes of prosody can be disturbed in right-brain damaged patients (RBDs). Lefthemisphere lesions can also affect prosody . However, RBDs exhibit more difficulties with the processing of emotional prosody than leftbrain-damaged patients (LBDs) do. As far as the more basic acoustic parameters of prosody are concerned, either for linguistic or for emotional prosody , a left-hemisphere lesion
interferes more with the local and rapid processing of acoustic information, whereas a right-hemisphere lesion impairs processing of acoustic events distributed over longer periods of time (Perecman/Kellar 1981). One of the strongest assumptions with regard to RBDs is that the taxonomy of prosodic deficits parallels that of aphasic deficiencies. Looking at the ability to produce, understand, and repeat emotionally -loaded prosodic patterns, Elliot Ross (1981) attempted to identify sy ndromes such as m o t o r aprosodia, sensory aprosodia, t r a n sc o r t i c a l- s e n s o r y aprosodia, g l o b a l aprosodia and other aphasia-like clinical manifestations. However, Ross’ proposal bears some problems: (a) the subjectivity of the examination protocol used, (b) the postulate that aphasia taxonomy in itself is well-ascertained and unanimously accepted, (c) the fact that the disorders reported were mostly present in the first three day s following the insult, thus possibly confused with the patients initial reaction to the disease, and (d) the overly optimistic attitude of Ross who even states that he had never seen a perisy lvian RBD patient without a prosodic deficit. Despite the fact that emotional prosody appears to be quite regularly affected in RBD patients as a group, there is still no clear global taxonomical conceptualization of those deficits. Among the problems encountered, are the methodological difficulties of evaluating the emotional component of prosody. RBDs show deficits in comprehension of emotional prosody even when the basic linguistic components of the message have been removed through filtering (Heilman/Bowers/
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Speedie/Coslett 1984). A left-hemisphere damage also results in such deficits. However, right-hemisphere lesions affect the processing of the prosodic cues themselves whereas deficits caused by left-hemisphere-lesions essentially reflect the complexity of the task (Tompkins/Flowers 1985). These facts suggest that the deficits RBDs have in understanding emotional prosody originate more from disturbances in the processing of prosody itself than from disturbances in the processing of its emotional component. Concerning the production of emotional prosody , no satisfactory study of the ability of RBDs to spontaneously produce emotion through prosody have been conducted so far. There exists only a strong clinical impression that some RBDs exhibit flattened monotonous speech. To what extent this characteristic reflects a prosodic impairment per se or a more global indifference remains to be seen. Deficits for the comprehension of lexical stress can occur in RBDs, but also in leftbrain-damaged aphasics. RBDs also show deficits in understanding emphatic stress as well as in processing intonation-based modalities. However, in the latter case, RBDs are significantly more impaired than aphasics, who are in turn more impaired compared to controls (Grant/Dingwall 1985). Most studies examining the expression of linguistic prosody have aimed at identify ing the most relevant acoustic parameter involved in such a production. An important finding is the striking discrepancy between the subjective and the instrumental analy sis of expressed linguistic prosody (Dordain/Degos/ Dordain 1971). These results emphasize both the limits of a subjective approach and the difficulties of obtaining relevant acoustical parameters.
2.
Lexical Semantics
RBDs can have difficulties completing sentences, providing word definitions (Eisenson 1973), and naming objects which are related to their hospitalization or incapacities (Weinstein 1964). They also have difficulties selecting the object corresponding to an orally presented word from an array of associated responses. However, according to Gainotti/ Caltagirone/Miceli (1983) and Bishop/By ng (1984) these impairments might be attributed to a nonspecific mental deterioration or to visuoperceptual disorders. According to Gainotti/Caltagirone/Miceli (1983), RBDs make
many more visuosemantic errors than normal controls on picture-naming tasks. However, Coughlan/Warrington (1978) reported that RBDs performed normally on a visual objectnaming task and on a naming task involving orally-described objects. RBDs have problems in judging antony mic relationships (Gardner/Silverman/Wapner/ Zurif 1978) but not in processing sy nony my (Goulet/Joanette 1988). They score poorly , when they have to process the connotative or the metaphorical meanings of words presented in a triad including a target word associated literally with one word of the triad and metaphorically with the other word (Brownell 1988). However, it is not clear if the poorer performance is due to the incapacity to process the nonliteral meaning of words, or to a greater attraction of the literal meanings of words. RBDs have been said to be sensitive to cohy pony mic relationships and to be able (Goulet/Joanette/Gagnon/Sabourin 1989; Wilkins/Moscovitch 1978) to judge whether drawings or words represent natural or man-made objects. But below average sensitivity to cohy pony mic relationships has also been reported (Chiarello/ Church 1986; Gagnon/Goulet/Joanette 1989). When they occur, lexical-semantic errors made by RBDs reflect disruptions in effortful activation or processing of the lexical-semantic information rather than in impairments of this lexical-semantic knowledge. Indeed, RBDs have been shown to be impaired for the controlled processing of the connotative meaning of words and cohy pony mic relationships but not in an automatic priming experiment involving these two ty pes of material (Gagnon/Goulet/Joanette 1989; Tompkins 1990). The contradictory results mentioned above demonstrate that the presence as well as the nature of the lexical-semantic impairments in RBDs is debatable. This contradiction is also evident in RBDs performance on verbal fluency tasks. The use of formal criteria (words beginning with a predetermined letter) revealed that RBDs performed normally in some studies but not in others (Joanette/Goulet/Hannequin 1990). Generally , reduced verbal fluency scores are either attributed to a frontal sy drome or to a nonspecific lesion effect. They have also been related to a reduced I. Q. Testing for semantic criteria (e. g., animal names), also brought about opposing results. For example, Newcombe (1974, 314) reported that RBDs produce as many words
34. Verbal Communication Deficitsafter Right-Hemisphere Damage
as normals, whereas Boller (1968) attributed the reduction of verbal fluency performance of the RBDs to a nonspecific lesion effect. Grossman (1981) failed to find that RBDs produce a smaller number of words but reported that RBDs employ ed word-finding strategies that differed from those used by LBDs and normals. Interestingly , Lifrak/ Novelly (1984) showed that RBDs were impaired when they had to supply words respecting semantic criteria but not when no criteria were used (free production). In the same vein, it has been reported that RBDs performed less well than normals when semantic criteria were used but not when formal criteria were used (Joanette/Goulet 1986; Laine/Niemi 1988). This finding has been interpreted as an indication that word-finding problems observed in RBDs are of a semantic nature. In contrast, Cappa/Papagno/Vallar (1987) found that a right-hemisphere lesion did not alter verbal-fluency performance based on either formal or semantic criteria. Controlling for the degree of productivity associated with each ty pe of criteria, Sabourin/ Goulet/Joanette (1988) showed that RBDs were impaired when highly productive criteria were used, be it semantic or formal.
3.
Text and Pragmatics
RBDs may also exhibit deficits in understanding or producing a text. Furthermore, disturbances in the processing of the pragmatic aspects of verbal communication are among the most ty pical sy mptoms after a right-hemisphere lesion. Processing of the emotional and spatial information integrated in stories is impaired in RBDs (Wapner/Hamby /Gardner 1981). In addition, they have difficulty rejecting minimally plausible incongruous events by reference to a given story , a finding which borders on pragmatics. These patients also have difficulties in the re-organization of sentences into a coherent story despite the presence of temporal or spatial clues (Delis/Wapner/ Gardner/Moses 1983; Huber/Gleber 1982). When RBDs have to match sentences or pictures on the basis of their emotional meaning, their errors seem to result more from difficulties to establish unexpected links between the pictures or the sentences, than from an erroneous processing of emotional content itself (Cicone/Wapner/Gardner 1980). Moreover, RBDs have also been shown to have problems in sy nthesizing and interpreting the
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information explicitly or implicitly contained in a text in order to find the moral of a fable (Gardner/Brownell/Wapner/Michelow 1983). According to Joanette/Goulet (1990), RBDs, as a group, produce narratives which are comparable to those of non-brain-damaged individuals in the number of words as well as lexical and sy ntactic cues, but they do show some difficulties with cohesion and coherence of narratives. 50% of the RBDs in this study produced narratives containing a smaller amount of information as compared to those of controls. RBDs are impaired by comparison to normals when they have to process some very specific texts whose understanding is context-dependant such as humorous, sarcastic and ironic texts (Joanette/Goulet/Hannequin 1990). However, whether this impairment is primarily directed towards the processing of humor, sarcasm or irony per se or whether it reflects RBDs’ difficulties in accessing nonliteral information, or being able to reject minimally plausible choices in a multiplechoice task is a matter for further research. In addition, RBDs exhibit problems in their ability to understand indirect speech acts y (We lman/Brownell/Roman/Gardner 1989). Some RBDs have difficulties in accessing the non-literal meaning of an indirect request, even though there might be differences according to the nature of indirect requests. However, it is not clear if this impairment is to be attributed to a lowered sensitivity to context-induced constraints or to a difficulty in accessing second-level meaning of the message given these constraints. RBDs also perform poorly when asked to interpret metaphoric texts or phrases. They tend to choose the literal meaning of metaphors more often than normal controls. However, these results cannot y et be isolated from a possible impairment of RBDs in rejecting minimally plausible events. Moreover, the distinctive nature of the metaphors such as their degree of frozeness, has y et to be taken into consideration. Only then will it be possible to know if the problem lies with the nature of the tasks used in the past or if there is a real deficit in metaphorisation abilities. Many of the above-mentioned deficits among RBDs have indicated the possibility that these patients might have inferencing difficulties (Brownell/Potter/Bihrle/Gardner 1986). However, such difficulties have not been clearly demonstrated. Some studies have shown that RBDs have problems with logical
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inferencing or sy llogistic reasoning (e. g. Read 1981) while another failed to demonstrate such problems (Joanette/Goulet 1987). Problems found have been attributed to impairments of spatial abilities, but the tasks used never allowed a clear distinction between linguistic and spatial problems. The literature is also incongruent concerning RBDs’ capacities to make inferences based upon short narrations. For instance, inferencing deficits have been reported in three studies (Brownell/ Potter/Bihrle/Gardner 1986; GoodenoughTrépanier/Powelson/Zurif 1982; Tompkins/ Mateer 1985) while no such deficits have been reported in three other studies (Brookshire/Nicholas 1984; Joanette/Goulet 1987; McDonald/Wales 1986). Interestingly in one study reporting inferencing deficits (Brownell/Potter/Bihrle/Gardner 1986) and in one study failing to find such deficits (McDonald/ Wales 1986), the main problem of RBDs was rejecting false statements.
4.
Specificity of the Verbal Communication Disorders
None of the impairments mentioned here have been clearly established as being specific to a right-hemisphere lesion. Another aspect of the specificity of these impairments lies in their linguistic nature. Impairments of many cognitive processes, other than linguistic ones, could contribute to these deficits.
5.
Incidence of Verbal Communication Deficits
Only half of the studies examining similar aspects of verbal communication with similar tasks reported an impairment of RBDs (Joanette/Goulet/Daoust 1991). The sole exceptions are those studies evaluating emotional prosody ; all of them reported such an impairment. Moreover, many studies reported a breakdown of their patients into those with and those without an impairment. In those studies, approximately half of the RBDs exhibit a deficit. Among impaired RBDs, there can be different contrastive patterns leading to double dissociations: for example, some are impaired in a verbal-fluency task but not in a narrative task, and vice-versa. The frequency of such impairments might be linked to how much a given individual’s right hemisphere contributed to verbal communication before the insult. For example, a focal right hemisphere lesion has been shown to result
in more verbal communication deficits when the individual right hander has a familial history of left-handedness and when he or she is less educated (Joanette/Lecours/Lepage/ Lamoureux 1983). Such factors are in line with the notion of a less-marked lateralization to the left in right-handers in the presence of a familial sinistrality or a lower level of education. Another explanation would be the localization of the lesion as suggested by Joanette/Lecours/Lepage/Lamoureux (1983).
6.
References
Bishop, D. & By ng, S. (1984). Assessing semantic comprehension: Methodological considerations, and a new clinical test. Cognitive Neuropsychology, 1, 233—243. Boller, F. (1968). Latent aphasia: right and left “non aphasic” brain-damaged-patients compared. Cortex, 4, 245—256. Brookshire, R. H. & Nicholas, L. E. (1984). Comprehension of directly and indirectly stated main ideas and details in discourse by brain-damaged and non-brain-damaged listeners. Brain and Language, 21, 21—36. Brownell, H. H. (1988). Appreciation of metaphoric and connotative word meaning by braindamaged patients. In C. Chiarello (Ed.), Right hemisphere contributions to lexical semantics. 19—32. New York: Springer-Verlag. Brownell, H. H., Potter, H. H., Bihrle, A. M., & Gardner, H. (1986). Inference deficits in right brain-damaged patients. Brain and Language, 27 , 310—321. Cappa, S. F., Papagno, C., & Vallar, G. (1987). Language and verbal memory in right-brain-damaged patients (RBD): a comparison with left-braindamaged (LBD) with aphasia. Journal of Clinical and Experimental Neuropsychology, 9, 263. Chiarello, C. & Church, K. L. (1986). Lexical judgements after right- or left-hemisphere injury . Neuropsychologia, 24, 623—630. Cicone, M., Wapner, W., & Gardner, H. (1980). Sensitivity to emotional expressions and situations in organic patients. Cortex, 16, 145—158. Coughlan, A. K. & Warrington, E. K. (1978). Word-comprehension and word-retrieval in patients with localized cerebral lesions. Brain, 10, 163—185. Delis, D. C., Wapner, W., Gardner, H., & Moses, J. A. (1983). The contribution of the right hemisphere to the organization of paragraphs. Cortex, 19, 43—50. Dordain, M., Degos, J. D., & Dordain, G. (1971). Troubles de la voix dans les hémiplégies gauches. Revue de Laryngologie, 3—4, 178—187.
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Eisenson, J. (1973). Right-brain damage and higher intellectual functions. In J. Eisenson (Ed.), Adult aphasia. 38—41. Prentice-Hall: Appleton-Century Crofts. Gagnon, J., Goulet, P., & Joanette, Y. (1969). Activation automatique et contrôlée du savoir lexicosémantique chez les cérébrolésés droits. Langages, 96, 95—111. Gainotti, G., Caltagirone, C., & Miceli, G. (1983). Selective impairment of semantic-lexical discrimination in right-brain-damaged patients. In E. Perecman (Ed.), Cognitive Processing in the right hemisphere. 149—167. New York: Academic Press. Gardner, H., Brownell, H. H., Wapner, W., & Michelow, D. (1983). Missing the point: The role of the right hemisphere in the processing of complex linguistic materials. In E. Perecman (Ed.), Cognitive Processing in the right hemisphere. 169—191. New York: Academic Press. Gardner, H., Silvermann, J., Wapner, W., & Zurif, E. (1978). The appreciation of antonomic contrasts in aphasia. Brain and Language, 6, 301—317. Goodenough-Trépanier, C., Powelson, J., & Zurif, E. (1982). Bridging in right hemisphere patients. Presented at the Academy of Aphasia Annual Meeting, Lake Mohonk, New York. Goulet, P. & Joanette, Y. (1988). Semantic processing of abstract words in right brain-damaged patient. Journal of Clinical and Experimental Neuropsychology, 10, 312. Goulet, P., Joanette, Y., Gagnon, J., & Sabourin, L. (1989). Semantics in right-brain-damaged righthanders. Journal of Clinical and Experimental Neuropsychology, 11, 353. Grant, S. R. & Dingwall, W. O. (1985). The role of the right hemisphere in processing linguistic prosody. Presented at the 13th Annual Meeting of the International Neuropsy chological Society , San Diego. Grossman, M. (1981). A bird is a bird: Making reference within and without superordinate categories. Brain and Language, 12, 313—331. Heilman, K. M., Bowers, D., Speedie, L., & Coslett, H. B. (1984). Comprehension of affective and nonaffective prosody. Neurology, 34, 917—921. Huber, W. & Gleber, J. (1982). Linguistic and nonlinguistic processing of narratives in aphasia. Brain and Language, 16, 1—18. Joanette, Y. & Goulet, P. (1986). Criterion-specific reduction of verbal fluency in right brain-damaged right-handers. Neuropsychologia, 24, 875—879. Joanette, Y. & Goulet, P. (1987). Inferencing deficit in right brain-damaged: absence of evidence. Presented at the 10th European Conference of the International neurops y chological Societ y , Barcelona. Joanette, Y. & Goulet, P. (1990). Narrative discourse in right-brain-damaged right-handers. In
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Y. Joanette & H. H. Brownell (Eds.), Discourse ability and brain damage. 131—153. New York: Springer-Verlag. Joanette, Y., Goulet, P., & Daoust, H. (1991). Incidence et profils des troubles de la communication verbale chez les cérébrolésés droits. Revue de Neuropsychologie, 1, 3—27. Joanette, Y., Goulet, P., & Hannequin, D. (1990). Right hemisphere and verbal communication. New York: Springer-Verlag. Joanette, Y., Lecours, A. R., Lepage, Y., & Lamoureux, M. (1983). Language in right-handers with right-hemisphere lesions: a preliminary study including anatomical, genetic, and social factors. Brain and Language, 20, 217—248. Laine, M. & Niemi, J. (1988). Word fluency production strategies of neurological patterns: semantic and phonological clustering. Journal of Clinical and Experimental Neuropsychology, 10, 28. Lifrak, M. D. & Novelly , R. A. (1984). Language deficits in patients with temporal lobectomy for complex-partial epilepsy. Presented at the 12th annual meeting of the International Neuropsy chological Society, Houston. McDonald, S. & Wales, R. (1986). An investigation of the ability to process inferences in language following right hemisphere brain damage. Brain and Language, 29, 68—80. Newcombe, F. (1974). Selective deficits after focal cerebral injury . In S. J. Dimond & J. G. Beaumont (Eds.), Hemisphere function in the human brain. 311—334. New York: J. Wiley. Perecman, E. & Kellar, P. (1981). The effect of voice and place among aphasics, non aphasic right-damaged, and normal subjects on a metalinguistic task. Brain and Language, 12, 213—223. Read, D. E. (1981). Solving deductive reasoning problems after unilateral temporal lobectom y . Brain and Language, 12, 92—100. Ross, E. (1981). The aprosodias: Functional-anatomical organization of the affective components of language in the right hemisphere. Archives of Neurology, 38, 561—569. Sabourin, L., Goulet, P., & Joanette, Y. (1988). La disponibilité lexicale chez les cérébrolésés droits. Canadian Psychology, 29, 2 a. Tompkins, C. & Mateer, C. A. (1985). Right hemisphere appreciation of prosodic and linguistic indications of implicit attitude. Brain and Language, 24, 185—203. Tompkins, C. A. & Flowers, C. R. (1985). Perception of emotional intonation by brain-damaged adults: the influence of task processing levels. Journal of Speech and Hearing Research, 28, 527—538. Tompkins, C. A. (1990).- Knowledge and strategies for processing lexical metaphor after right or left hemisphere brain damage. Journal of speech and hearing research, 33, 307—316.
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quest by left and right-brain-damaged patients: The effects of verbal context and conventionality of wording. Brain and Language, 36, 580—591. Wilkins, A. & Moscovitch, M. (1978). Selective impairment of semantic memory after temporal lobectomy. Neuropsychologia, 16, 73—79.
Yves Joanette/Pierre Goulet, Lab. Th.Alajouanine, Montréal, Québec (Canada) Didier Hannequin, C. H. U. de Rouen (France)
35. Pathology of Language Behavior in Dementia 1. 2. 3. 4. 5. 6. 7.
1.
Introduction Alzheimer’s Disease Parkinson’s Disease Huntington’s Disease Pick’s Disease Progressive Aphasia and Dementia References
Introduction
The sy ndrome of dementia produces deterioration of intellect, memory , communicative function, and personality , sufficient to interfere with social and occupational responsibilities (American Psy chiatric Association 1987). It is associated with my riad diseases and conditions, some of which are reversible. The most common cause of dementia is Alzheimer’s disease (AD), an irreversible neurodegenerative disease which accounts for approximately 50% of dementia cases. The incidence of AD is greatest in senescence, with a steep increase from 60 to 89 y ears (Rorsman/Hagnell/Lanke 1986), and because of the ‚gray ing’ of the earth’s population, the number of AD patients is rising dramatically. Throughout the world, health professionals are challenged by the needs of dementia patients and their families. Vital to their care is understanding disease effects on language and the ability to communicate, a need which has motivated much research in the last decade. Before reviewing this research, it is appropriate to define the term language, however defining language is not necessarily a straight forward enterprise. Consider that individuals, who have trouble naming, are diagnosed as having a ‚language problem’. If the words for the to-be-named objects have
been lost from the mind of the anomic individual, then it is a language problem. However, if the individual has knowledge of the object and its name, but cannot access the name, some would describe this as a memory problem. What has sometimes been called a language problem can be explained as a deficit in attention or other nonlinguistic cognitive sy stem. Certainly the expression of linguistic knowledge is affected by other nonlinguistic functions such as perception, attention, and memory , but these deficits differ from those caused by a loss of linguistic knowledge. Linguists distinguish between loss of language knowledge and errors in the application of language knowledge, referring to the former as a competency problem and the latter a performance problem (Slobin 1971). They emphasize that impaired linguistic performance does not necessarily mean that the individual lacks linguistic competence because linguistic performance is an amalgam of many functions, some of which are nonlinguistic. For the purpose of this chapter, language refers to (a) linguistic knowledge comprising phonologic, sy ntactic, semantic, and pragmatic rules, and (b) the use of these rules in the production and comprehension of meaningful expressions. The different ty pes of linguistic knowledge appear to be represented brain areas and the processes by which they are manipulated appear to be subserved by different neuronal sy stems. Whereas the production and comprehension of phonologic and sy ntactic information are likely carried out within a modular sy stem (see Fodor 1983 for criteria for modularity ), semantic and pragmatic analy ses likely are not. The distri-
35. Pathology of Language Behavior in Dementia
bution of neuropathology of the etiologically different dementing diseases may affect the neuroanatomical substrates important for certain ty pes of linguistic knowledge and processes and spare others. Knowledge of the brain areas affected in the various dementing diseases and disease effects on neuropsy chological function are requisite to understanding the communication abilities of dementia patients. Thus, in the ensuing text, specification will be made of the neuropathology and neuropsy chology of Alzheimer’s, Pick’s, Parkinson’s, and Huntington’s diseases, AD, PKD, PD, and HD respectively to provide a foundation for appreciating the communication disorders.
2.
Alzheimer’s Disease
2.1. Neuropathology The diagnosis of AD requires the presence of characteristic morphological changes in the brain, notably , neurofibrillary tangles (NFTs), neuritic plaques, granulovacuolar degeneration (GVD), Hirano Bodies, and amy loid deposits in leptomeningeal and cortical blood vessels (Henderson/Finch 1989). These cellular changes, together with cell loss, occur within the neocortex, hippocampi, basal forebrain, amy gdalae, nucleus locus ceruleus, and the brainstem raphe nuclei. Of these morphological changes, the NFT is the most characteristic. NFTs are intraneural fibrillary structures that appear as clusters of unbranched fibrillary structures twisted into a helix (Kidd/Allsop/Landon 1985). Within the medial temporal lobe NFTs tend to proliferate in entorhinal neurons (Hooper/Vogel 1976). Within the neocortex, NFTs have a predilection for py ramidal cells within lay ers II and V of multimodal associations areas that are reciprocally related to the limbic cortex and hippocampus. Primary motor and sensory areas are ty pically spared (Lewis/Campbell/Terry /Morrison 1987). PET studies show decreased glucose metabolism within association cortex, more so in temporoparietal than frontal regions (Duara/ Grady /Haxby et al. 1986). In some individuals the degree of hy pometabolism is more severe in one of the hemispheres, a fact that has neuropsy chological consequences (Grady/Haxby/Schlageter et al. 1986). Occurring in the same neural structures as NFTs are neuritic plaques, sometimes called senile plaques. They are clumps of degener-
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ating neurons which surround a core containing deposits of amy loid (Kidd 1964) and aluminosilicates (Cand y /Oakle y /Klinowski et al. 1986). The clumps occur within neuropil and contain abnormal, distended, unmy elinated neurites. GVD is a descriptive term referring to the existence of one or more clear spherical vacuoles that contains granular debris. GVD is most commonly observed in hippocampal py ramidal neurons. Hirano bodies are rod-shaped structures occurring within neurites and perikary a of hippocampal neurons. They were originally reported in patients with the parkinsonian dementia/amy otrophic lateral sclerosis complex of Guam (Hirano/Dembitzer/Kurland/ Zimmerman 1968). Concerning biochemical alterations, decrements in brain concentrations of many neurotransmitters and related enzy mes occur in individuals with AD. Best known of the neurotransmitter decrements is the cholinergic deficit in cells within the basal nucleus that project to the cortex. Also affected are the noradrenergic neurons of the brain-stem locus ceruleus, and the serotonergic cells of the raphe nucleus. Of the neuropeptides, somatostatin has been reported to dramatically decline (Davies/Wolozin 1987). As pointed out by Henderson/Finch (1989), deficits in such widely projecting subcortical nuclear areas can be expected to have far-reaching effects on a variety of cognitive functions. For example, the noradrenergic sy stem has been linked to vigilance and selective attention, and the cholinergic system to memory. 2.2. Neuropsychology Neuropsy chologically , AD patients exhibit progressive deterioration in memory , intellect, and personality . Most studied are disease effects on memory . Using terminology popularized by Baddeley (1987), Squire (1987), Mishkin/Appenzeller (1987) and others, Alzheimer’s disease can be said to particularly impair working and declarative memory sy stems (the latter comprising episodic and semantic memory ) while sparing procedural memory (memory for learned skills). The most common early sy mptom is episodic memory deficit in the form of an inability to remember a recent episode such as where the car was parked, or what was eaten for dinner the previous night (Bay les/Kaszniak 1987). Less obvious to casual observers are concomitant changes in working memory ,
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notably the attenuation of span and the diminished efficiency of the central executive sy stems. Deficits in span and attention result in poor encoding of new information and therefore difficulty in developing new longterm memory for episodes and facts. As the disease progresses, individuals appear to lose their knowledge of the world (declarative memory ) and the ability to manipulate it. In sharp contrast, they retain the ability to perform procedures such as hitting a golf ball or driving a car. An explanation for this apparent dissociation is the distribution of neuropathology in the disease. Declarative memory is impaired because of its reliance upon the preservation of cortical association areas in which neuropathological changes are prominent; procedural memory is spared because of its putative reliance upon the preservation of basal ganglia and its connections. The progressively poor performance of AD patients on mental status tests reflects their growing memory deficits. Early in the disease, the affected individual is disoriented for time, later for place, finally , for person. In the late stages, patients may no longer recognize their faces in the mirror. Although deficits in visuoperceptual and visuospatial abilities have been reported (Pirozzolo/Hansch/Mortimer et al. 1982), these abilities are less studied than memory . Abnormalities have been noted with visuoconstructional tasks, maze tests, map reading, and the performance subtests of the Wechsler Adult Intelligence Scale (Becker/Huff/Nebes et al. 1988; Storandt/Botwinick/Danziger et al. 1984). Visuoperceptual discrimination for meaningful and nonmeaningful stimuli has been demonstrated to decline in AD patients (Brouwers/Cox/Martin et al. 1984; Eslinger/ Benton 1983), as has the ability to identify the spatial orientation of lines in relation to a model. Finally , AD patients have difficulty drawing and copying. AD profoundly affects personality . Thal (1988) observed that the sy mptoms often include easy distractibility , difficulties with work, problems with directions or taking trips. According to primary caregivers, the most common early sy mptoms were difficulty handling finances, forgetting the location of objects, and becoming less aware of recent events(Bay les 1991 b). Rubin/Morris/Storandt/ Berg (1987) reported the common occurrence of agitation, apath y , and self-centeredness. Petry /Cummings/Hill/Shapira (1988) re-
ported that AD patients are less reasonable, energetic, happy , affectionate, and easy going. Drevets/Rubin (1989) observed the frequent occurrence of delusions, misidentifications, and hallucinations throughout the disease course. In this study , rates of psy chosis ranged from 42% to 84% among moderate and severely demented subjects. These authors state that at least half the individuals with AD will display psy chosis at some point during the disease. 2.3. Effects on Language By definition, the aforementioned neuropsy chological and personality changes affect communicative function and language performance. At issue in this section is whether AD affects language knowledge. When summarizing the effects of AD on language, it is important to consider whether distinct clinical subgroups of AD patients exist in whom language is differently affected. Subgroups for whom disease effects on language may differ are defined by : age at onset; family history of disease; presence of extrapy ramidal sy mptomatology ; and distribution of neuropathology. Age- a t- o n s e t: The presenile form of AD has been associated with more severe cognitive deficits (Capitani/Della Sala/Spinnler 1990), among them language deficit. Many investigators report such a relation (Seltzer/ Sherwin 1983; Faber-Langendoen/Morris et al. 1988; Filley /Kelley /Heaton 1986; Chui/ Teng/Henderson/Moy 1985). However, these reports have been debated by other investigators. Selnes/Carson/Rovner/Gordon (1988) did not find a significant relation between age-at-onset and language deficit. Nor did Cummings/Benson/Hill/Read (1985), who observed language impairment in AD patients to be proportional to dementia severity. Bay les (1991a) observed that investigators of the relation of age-at-onset to degree of language deficit failed to use methodology whereby the AD subjects’ language score(s) were controlled for the effects of dementia severity . This is a necessary control because of the well established relation between dementia severity and language performance scores (Selnes/Carson/Rovner/Gordon 1988; Cummings/Benson/Hill/Read 1985). Ba y les controlled for disease severity effects in a study of 86 Alzheimer’s patients and found age-at-onset to be related to degree of language deficit, but in such a way that the older
35. Pathology of Language Behavior in Dementia
the age-at-onset the greater the language deficit. Bay les constructed a general linear model to assess the extent to which performance on the Global Deterioration Scale (Reisberg/ Ferris/De Leon/Crook 1982), Mini-Mental State Examination (Folstein/Folstein/McHugh 1975) place and time questions and figure copy ing task predicted language performance. By first considering the severity variables, the effects of disease duration and age-at-onset on language were evaluated after effects of disease severity were removed. To assess the possibility that the observed relation between age-at-onset and language performance was caused by the effects of normal aging, the language tests were administered to normal subjects of similar ages who scored perfectly on dementia severity measures. Bay les failed to find convincing evidence that performance on the four linguistically oriented tasks declines with normal aging. Fa m i ly h i st o r y . Family history has also been linked with special clinical characteristics. Folstein/Breitner (1981) determined that the presence of aphasia or agraphia in AD patients was highly predictive of dementia in first-degree relatives. In 1984 Breitner/Folstein reported language disturbance and apraxia in 78% of their familial cases and a sevenfold increase in lifetime dementia risk for relative of language disordered AD probands versus control subjects. In a study published in the same y ear, Hey man/Wilkinson/ Stafford et al. (1984) reported a failure to document a relation between family history and language performance. Further, they reported that the frequency and severity of linguistic deficits in AD patients was associated to duration of illness. Chui/Teng/Henderson/ Moy (1985) found no association between family history of AD and aphasia, and Knesevich/Toro/Morris/La Barge (1985) observed that a lack of aphasia was associated with a higher prevalence of familial cases. P r e s e n c e o f ex t r a py r a m i d a l sy m pt o m a t o l o g y: The clinical heterogeneity of AD with regard to the presence of extrapy ramidal features, primarily rigidity and hy pokinesia has been noted (Pearce 1974; Sulkava 1982; Molsa/Martilla/Rinne 1984; Chui/ Teng/Henderson/Mo y 1985; Ma y eux/Stern/ Spanton 1985). However, as y et, it is unclear whether the coexistence of extrapy ramidal sy mptomatology has consequences for either linguistic competence or performance.
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D i st r i b u t i o n o f n e u r o p a t h o l o g y : As previously noted, the neuropathology of AD may be greater in one cerebral hemisphere. In fact, the possibility has been raised that the left hemisphere is particularly vulnerable to disease effects (Sourander/Sjogren 1970; Seltzer/Sherwin 1983; Seltzer/Burres/Sherwin 1984). Using PET, several investigators have found that individuals with AD vary in the degree of hy pometabolism in homologous regions of the cerebral hemispheres (Chase/ Fedio/Foster et al. 1984; Friedland/Budinger/ Ganz et al. 1983; Haxby /Duara/Grady et al. 1985). Individuals with greater left than right hy pometabolism had greater language deficits (Haxby /Duara/Grady et al. 1985). Chase/Fedio/Foster et al. (1984) noted a close association between WAIS verbal IQ scores and cortical metabolism in the left cerebral hemisphere, especially in the left temporal lobe. Martin/Cox/Brouwers/Fedio (1985) observed that whereas the majority of their 43 AD subjects were proportionately impaired in retrieval and use of semantic knowledge and visuoconstructional skill, a subset of patients presented with deficits limited to one of these domains of functioning. Nine AD subjects had severely impaired naming and verbal fluency skills relative to visuo-constructional skills. Subsequentl y , Martin/Brouwers/Lalonde et al. (1986) reported results of principal component and cluster analy ses of the performance data of 42 of the 43 AD patients described in the 1985 study. Five subject clusters were identified, one of which contained the nine patients in whom dy snomia was disproportionate to severity of dementia. These subjects were described as having poor wordfinding skills concurrent with intact visual perceptual and construction skills. A second cluster of eight individuals exhibited the opposite pattern, disproportionately poor visual perceptual and constructional skills compared to word-finding. Individuals in the three other clusters exhibited relatively equal deficits on all measures. Becker/Huff/Nebes et al. (1988) attempted replication of the findings of Martin and associates. The performance data of their 86 probable AD patients were analy zed and similar results obtained. Eleven patients in the sample were described as having focal ‚lexical/ semantic impairments’ and four had focal ‚visuoconstructional impairments.’ The results of these investigators call into question the appropriateness of the stage
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model as a basis for predicting language performance. Therefore, Bay les/Trosset (1991) attempted to evaluate its efficacy for predicting naming disorder. Their data were interpreted as demonstrating the inadequacy of dementia severity for predicting naming performance in many AD patients, but, nonetheless, failed to offer support for defining these patients as comprising statistically distinct subgroups. Bay les/Trosset (1992) analy zed the confrontation naming performance data of 102 probable AD patients. Severity of dementia was defined by rating on the Global Deterioration Scale (GDS) (Reisberg/Ferris/de Leon/Crook 1982) and performance on the Mini-Mental State Examination (Folstein/ Folstein/McHugh 1975) questions related to time and place orientation and ability to copy a figure. The GDS was chosen because language ability does not prominently influence judgments of dementia severity . Using a hierarchical general linear model to predict naming performance on the basis of perceived dementia severity , dementia severity was found to account for approximately one-third of performance variability . Additional contributions due to age-at-onset, duration, and family history were negligible. Less than onequarter of the unexplained variation could be attributed to measurement error. Therefore, naming ability can be argued to have a subcomponent not subsumed by overall cognitive ability . Nonetheless, no statistical evidence was found to suggest that this subcomponent decomposes the AD population into clinically distinct subgroups. The picture that emerged was of a single population characterized by considerable variability . With the caveat in mind that within the population of AD patients clinical subgroups may exist, the literature about the effects of AD on language will be reviewed. 2.3.1. Form Until the late stages, the form of language is relatively intact in individuals with AD. Their verbal and written constructions are grammatical though sometimes simplified (Hier/ Hagenlocker/Shindler 1985). This is in vivid constrast to the progressive loss of content. Preservation of grammar has been frequently observed (Kempler/Curtiss/Jackson 1987; Schwartz/Marin/Saffran 1979; Appell/Kertesz/Fisman 1982) and was memorably described by Whitaker (1976) whose severely demented patient spontaneously corrected
sy ntactic and phonologic errors in sentences she repeated. In no case did she correct a semantic error. Bay les/Boone (1982) documented that the ability of spontaneously correct grammar and phonology was not idiosy ncratic to Whitaker’s patient but a common phenomenon in moderately and severely demented AD patients. 2.3.2. Content Production Glaringly affected in AD is the ability to produce meaningful content. Consider the following discourse samples of patients in different stages of the disease who were asked to describe a common object. Subject # 1. Moderately severe AD patient describing an orange pencil. “We have a pencil here to use. One that I have selected to use is one that is involved with the color of orange, and we have used this so much that it’s been cut again by the cutter. Have to get another pen that will match the color so that every body that has used one of our pencils.” Subject # 2. Severe AD patient describing an orange pencil. “Yeah, up. Safe together and trot around so we could get same short thing that we have for the small short thing but still by making the various corrections as we’re going along. We can alway s make corrections that vary in there, too. And they can be a correction y ou all have plenty of time for that.” The deficits observed by many investigators in the connected speech of AD patients can be seen in these samples. For example, numerous investigators have described the discourse of AD patients to be impoverished in content (Hart 1985; Hier/Hagenlocker/ Shindler 1985; Nicholas/Obler/Albert/HelmEstabrooks 1985; Bay les/Tomoeda/Kaszniak et al. 1985; Appell et al. 1982). Miller/Hague (1975) observed, however, that the free speech of AD patients did not indicate selective loss of rare words. The aforementioned preservation of the grammatical form of language is apparent in these discourse samples, a phenomenon observed by Ulatowska/Allard/Donnell et al. (1988) who studied the discourse performance of AD patients. Ulatowska/Allard/Donnell et al.’s (1988, 122) ten AD patients revealed “preservation of sentential level and discourse level linguistic structures, as evidenced by the absence of significant differences between DAT [AD] and normal subjects either in the amount of complexity of language, or in the manipulation of narrative superstructure.”
35. Pathology of Language Behavior in Dementia
However, they were impaired in ability to provide a summary and moral for a story , exhibited deficits in content and reference, and provided more irrelevant information. In the next series of examples, the same patient is describing the Normal Rockwell Easter Morning Picture two years apart. F i r st Te st i n g: “This appears to be a family picture with uh three women that are involved in the picture and the y oung boy plus what looks to be the father of the rest of the family . The father, the mother, the daughter, the son and all are dressed up neatly for a Sunday program at church. And um the father is taking the time to read the Sunday morning paper and the first thing he looks at in it is the section of comics which are now spread around the floor and uh there daddy is there with his cup of coffee for Sunday . The father is taking life very easy with a uh robe and keeping his ey es closely on what might happen next here before he gets ready for church. Daddy sits in a very comfortable chair waiting for every body may be to go on to church without him.” S e c o n d Te st i n g: “That’s what I was try ing to figure, and I was thinking because they were telling me how much these were worth and what they can do for y ou. And they had a little bitty , what looks like a very small clearance area, and, that’s how much he picked up on this way last night home and the rest of it’s back there at the back end, pretty much so that it came back home.” These samples were obtained in a study by Tomoeda/Bay les (1992) in which descriptive discourse was elicited once a y ear for five y ears from 3 AD patients and 3 age- and education-matched control subjects by having them describe a Norman Rockwell picture. The discourse samples were analy zed in terms of total number of words, information units, conciseness, circumlocutions, frustrations, revisions, aborted phrases, and ideational repetitions. Of these, total number of words, conciseness, and information units significantly decreased over the five y ear period. Thus, whether the discourse data are examined cross-sectionally or longitudinally , the production of meaningful content can be seen to diminish. 2.3.3. Content Comprehension Hart (1985) reported decrements in the ability of AD patients to respond to the auditory commands of the Token Test (De Renzi/Faglioni 1978) which gradually increase in com-
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plexity . Hart’s data indicated that the performance of AD patients on a 36-item version of the Token Test correlated significantly with that on the Wechsler Memory Scale and the Wechsler Adult Intelligence Scale (WAIS). Hart acknowledges that because correlation does not necessarily imply causation, the relation between memory and language impairment remains to be determined. It was noted that subjects in this study sometimes failed items in the final segment of the test which, although linguistically more complex, are of shorter verbal span and require less complex motor programming than commands in the penultimate section. Reading comprehension is affected relatively early but the mechanics of reading are retained until the advanced stages of the disease (Hart/Smith/Swash 1986; Vance/Bay les 1990). Vance/Bay les observed that the mechanics of reading were among the last skills to be retained in severely demented individuals and persisted long after loss of the ability to comprehend the written material. According to Hart (1988), the preservation of reading, particularly the ability to read irregularly spelled words suggests that the lexicon remains relatively intact. Benson/Cummings/Tsai (1982) suggest that the dissociation between the ability to read aloud and read for meaning in AD patients distinguishes them from individuals with angular gy rus sy ndrome in whom reading aloud and reading for meaning are affected. Many investigators have explored the question of whether lexical-semantic information is lost or inaccessible in AD patients by study ing the effects of manipulating semantic context on the ability of patients to make decisions about words. The assumption in such studies is that semantic memory is an associative network and the activation of an item results in the spreading of activation to related items. For example, it can be shown that prior exposure to a related item, for example the word lemon, causes subjects to respond faster to the word lime in a paradigm in which subjects are asked to decide whether two stimuli are both real words. This effect is called semantic priming and occurs if the first word is presented simultaneously or precedes the second word (Fischler 1977 a) and can occur if the two stimulus words are semantically related or associated (Fischler 1977 b). Activation of semantically related items within the network occurs automatically and without an individual’s conscious awareness. If, in AD, semantic memory has
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deteriorated and lexical-semantic knowledge is lost, one would expect to see a loss of the semantic priming effect. The results of semantic priming studies are mixed. Some investigators report that AD patients are as sensitive to semantic context as normals (Nebes/Martin/Horn 1984; Nebes/Boller/ Holland 1986; Hartman 1987; Margolin 1987; Albert/Milberg 1989; Nebes/Brad y /Huff 1989). Other investigators report the lack of semantic priming in a lexical decision task (Ober/Shenaut 1988), and the lack of associative priming (Huff/Mack/Mahlmann/Greenberg 1988; Salmon/Shimamura/Butters/ Smith 1988). Yet others report hy perpriming, or greater response from the prior exposure to a semantically related item (Chertkow/ Bub/Seidenberg 1989; Chertkow/Bub 1990). The variability in the results of these priming studies has y et to be fully appreciated but may occur because of differences in the strength of association or semantic relation between stimuli, the length of interval between the prime and target, the task the subject was asked to perform (lexical decision, stem completion, word reading, etc.), and the subject’s stage of dementia. Early stage AD patients, in whom semantic memory is mildly affected, may be primeable. Late-stage patients, in whom semantic memory is likely to be severely affected, may not be benefitted by primes. 2.3.4. Use of Language The effects of AD on the use of language in conversation are well-recognized though few investigators have undertaken the difficult task of quantify ing these effects. Critchley (1964) observed that AD patients seem to form appropriate semantic intentions, but as their episodic memory worsens, these intentions are forgotten, hence they stop midway in their utterances. Slauson/Bay les/Tomoeda (1987) noted that AD patients have difficulty sustaining conversation and severely demented individuals fail to greet, respond to compliments, correct statements made by their conversational partners, and appropriately close conversations. Golder (1988) studied the ability of two AD patients to engage in conversation and observed turn-taking violations, interruptions, inappropriate silences, and topic shifts. Results of a longitudinal study of the effects of AD on linguistic communication by Bay les/Tomoeda/Kazniak/Trosset (1991) suggest that how language is used play s a crucial
part in lexical/semantic access and retrieval. The central question in this longitudinal study was whether conceptual knowledge is lost or the ability to use conceptual knowledge. The investigators reasoned that if AD patients lost conceptual knowledge, they should miss the same concepts across tasks. And, indeed other investigators have reported error consistency across tasks (Henderson/Mack/Freed et al. in press; Warrington 1975; Huff/Corkin/Growdon 1986; Flicker/Ferris/Crook/Bartus 1987; Gainotti/Daniele/Nocentini/Silveri in press; Chertkow/Bub 1990). To test their hy pothesis, Bay les/Tomoeda/Kaszniak/Trosset (1991) devised a paradigm in which 69 AD subjects were administered the following 11 tasks, each using the same 13 concepts: confrontation naming, auditory comprehension, dictation, oral reading, definition, reading comprehension, coordinate naming, superordinate naming, superordinate identification, pantomime expression, and pantomime recognition. Thus, the paradigm generated data about the ability to use language in these myriad ways. Data analy sis revealed only a few instances in which a concept was missed across all 11 tasks. When performance on the oral reading and dictation tasks were removed from analy sis, because of their questionable reliance on semantic memory , the number of missed concepts rose only modestly . A substantial rise in the number of missed concepts occurred, however, when performances on the four multiple choice tasks were removed. Bay les and associates argue that interpreting the larger number of missed concepts on the five remaining semantic tasks as evidence of itemspecific loss in semantic memory is problematic, nonetheless, because these generative semantic tasks were among the hardest in the battery and the frequency with which an individual subject missed a concept across all tasks accorded with the subject’s dementia severity level. Results demonstrate that task difficulty , more than concept specificity , predict whether a concept is missed. Overall, results suggest that a concept will “disappear” when all of the tasks in which it is a stimulus become too hard for the patient to perform. These data indict the practice of addressing the question of loss of knowledge or loss of access by using batteries of effortful, attention-demanding tasks. Working on the assumption that for each concept, the abilities to perform a fixed set of tasks deteriorate in the same fixed order,
35. Pathology of Language Behavior in Dementia
and that this order defines relative task difficulty , Bay les and colleagues analy zed the data. Because the sample was of insufficient size to consider the order of deterioration of all tasks simultaneously , subsets were considered and the following observation made: (a) Auditory comprehension and reading comprehension are almost identically difficult; (b) dictation is almost invariably more difficult than oral reading; (c) confrontation naming is decisively easier than either coordinate or subordinate naming; (d) definitions, pantomime expression, and pantomime recognition are of roughly comparable difficulty. Summary : Communication and language performance problems are omnipresent in individuals with AD. Deficits in linguistic knowledge occur primarily in semantics and pragmatics with sparing of sy ntax and phonology. 2.4. Gaps in the Literature The primary gap in the literature is the dearth of longitudinal data on the effects of AD on linguistic communication. However, the Arizona study and others are nearing conclusion and data will soon be forthcoming. The issue of whether AD comprises subgroups of patients who are linguistically unique continues to be debated. Then too, the debate continues as to whether the disease affects linguistic competence as well as performance. Among those who believe that AD eventuates in a loss of lexical-semantic knowledge, disagreement exists as to whether the loss is from the bottom up or top down. Bottom-up theorists argue that AD patients lose knowledge of attributes of objects before categorical knowledge of objects. Finally , virtually no one has been able to relate changes in linguistic communication seen in life to distribution of pathology at post-mortem. For example, do late-stage patients who are mute differ in distribution of pathology from those who are echolalic?
3.
Parkinson’s Disease
3.1. Neuropathology Parkinson’s disease is a cluster of signs associated with a variety of causes. Four variants of the parkinsonian sy ndrome account for the majority of cases: idiopathic, drug-
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induced, post-encephalitic, and arteriosclerotic. By far the most common variant is idiopathic meaning that the etiology is unknown. Degenerative changes in the basal ganglia, basal nucleus, neocortex, and nucleus locus ceruleus cause the classic sy mptomatology of tremor at rest, muscular rigidity , and brady kinesia. The most conspicuous neuropathologic alteration is depigmentation of the substantia nigra in the basal ganglia and loss of the neurotransmitter dopamine. Lewy bodies, which are dense spherical intracy toplasmic inclusion bodies, are diagnostic of the disease. Associated with these degenerative changes is diffuse cortical atrophy occurring in approximately 60% of PD patients (Alvord/Forno/ Kusske et al. 1974; Becker/Grau/Schneider et al. 1976; Selby 1968). A result of these degenerative changes is a significant reduction in cerebral blood flow (Lavy /Melamed/Cooper et al. 1979). 3.2. Neuropsychology Considerable variation exists in the neuropsy chological status of PD patients. Whereas some individuals experience little, if any , cognitive deficits, others develop dementia. Estimates of the incidence of dementia in PD in the literature vary dramatically from 2% to 77% (Celesia/Wanamaker 1972). More recently , Lees/Smith (1983) reviewed the early literature to determine the incidence of dementia if DSM-III criteria were used to define its existence. They reported approximately 15% of PD patients to have dementia. Although the majority of PD patients do not appear to develop dementia, they experience some intellectual deficit (Pirozzolo 1982). The cause of dementia in PD patients is unknown. Some theoreticians argue that it is caused by the coexistence of AD, and indeed, AD-like neuropathology has been reported in many demented PD patients (Hakim/Mathieson 1979; Boller/Mizutani/Roessmann/Gambetti 1980). Other theoreticians assert that basal ganglia and other subcortical structures are sufficiently important to normal cognitive function that damage to them results in dementia even when the cortex is spared (de la Monte/Wells/Hedle y -Wh y te/Growdon 1989; Cools/van den Bercken/Horstink et al. 1984; Lees/Smith 1983; Stern 1983; Mortimer/ Pirozzolo/Maletta 1982). For dementia to be diagnosed, the PD patient must exhibit memory and intellectual deterioration sufficient to interfere with oc-
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cupational and social functioning, thus meeting the DSM-III criteria for dementia. Some clinicians report that the dementia in PD patients is qualitatively similar to that observed in AD patients (Boller 1980; Pirozzolo/ Hansch/Mortimer et al. 1982). Others, like Alexander/Geschwind (1984), Cummings/ Darkins/Mendez et al. (1988), and Albert (1978) argue that they differ qualitatively. C o g n i t i ve d e f i c i t s o f P D p a t i e n t s: According to Brown/Marsden (1990) consensus is developing that PD patients have difficulty with: shifting mental sets, recall memory (Alexander/Geschwind 1984; Boller 1980; El-Awar/Becker/Hammond et al. 1987; Albert 1978; Wilson/Kaszniak/Klawans/Garron 1980; Pirozzolo/Hansch/Mortimer et al. 1982; Huber/Shuttleworth/Paulson 1986), internal control of attention (Brown/Marsden 1988), sequencing, temporal ordering and recency discrimination (Sagar/Sullivan/Gabrieli et al. 1988; Sullivan/Sagar/Gabrieli et al. 1985), and effort-demanding tasks (Weingartner/ Burns/Diebel/Le Witt 1984). An intriguing potential difference between the memory impairment in PD and AD may be in the degree to which procedural memory is affected. Recall that the neuropathology of AD yt pically spares procedural memory which is reliant upon the integrity of the basal ganglia. Because the neuropathology of PD primarily affects the basal ganglia, procedural memory is thought to be particularly vulnerable (Saint-Cyr/Taylor/Lang 1988). Another differentiating characteristic of PD may be slowness in thinking (brady phrenia) (Naville 1922) and motor function (brady kinesia). Both may contribute to a diminished performance in the PD patients. Depression is a common part of the disease, the incidence of which has been estimated to range from 30% (Lieberman/Dziatolowski/Kupersmith et al. 1979) to 76% (Alexander/Geschwind 1984). As y et it is unclear to what degree the depression is exogenous, endogenous, or both. 3.3. Effects on Language As is clear from the literature reviewed in the previous section, PD patients are not a homogenous group. Some develop dementia, the majority appear to have some ty pe of intellectual deficit, and a subset remains intellectually normal. Those individuals who develop dementia alway s have communication deficits. The intellectual deterioration that defines the dementia substantially diminishes the
ability to meaningfully communicate. However, whether these individuals also lose linguistic knowledge is unclear because deficits in perception, attention, executive function and memory counfound the evaluation of linguistic competency. In the nondemented but intellectually diminished PD patient, evaluating linguistic competence may be somewhat easier. However, linguistic incompetence and nonlinguistic intellectual deficit also can be confounded. To date, few investigators have studied language competence and performance in either group of PD patients. The studies that have been done are subclassified according to whether they provide information about disease effects on language form, content (semantics), and use. 3.3.1. Form No deficits in phonologic knowledge have been reported in either demented or nondemented patients. Neither are there reports of loss of sy ntactic knowledge. However, two reports exist of simplification of grammar in PD patients. Cummings/Darkins/Mendez et al. (1988) used the Boston Diagnostic Aphasia Examination (Goodglass/Kaplan 1976) to evaluate the grammatical form of phrases in a discourse sample from demented and nondemented PD patients. Nondemented and demented PD patients were observed to produce simpler constructions compared to normal control subjects and Alzheimer’s patients respectively . Illes/Metter/Hanson/Iritani (1988) also noted a decrease in the sy ntactic complexity in the spontaneous utterances of patients with mild compared to moderate PD. 3.3.2. Content Conceptual or semantic knowledge has been evaluated with naming, vocabulary , and auditory comprehension tests. Freedman/Rivoria/Butters et al. (1984) and Levin/Llabre/ Weiner (1989) reported normal naming in nondemented PD patients on the Boston Naming Test (Kaplan/Goodglass/Weintraub 1983). However, Matison/Ma y eux/Rosen/ Fahn (1982) did not. In the Matison study , nondemented PD subjects scored one standard deviation below normal subjects. Globus/Mildworf/Melamed (1985) noted only mild deterioration in naming. More consistency exists in the reports of PD patients on generative naming or verbal fluency tasks. In these tasks, individuals are instructed to generate exemplars of items in
35. Pathology of Language Behavior in Dementia
a category , such as modes of transportation, names of animals, or words beginning with a particular letter. Most, but not all, researchers report significant impairments in nondemented PD patients (Matison/May eux/Rosen/Fahn 1982). Lees/Smith (1983) observed a significant decrement in only one of three stimulus categories, specifically , words beginning with the letter M but not with D or B. Miller (1985) discerned no difference in naming words beginning with the letters F, A, and S between PD patients and age-matched controls. Levin/Llabre/Weiner (1989) administered three generative naming tasks to 41 PD patients who were impaired only in the ability to generate names of food. Another approach to the study of semantic knowledge is having subjects decide, as quickly as possible, whether a string of letters shown on a television screen is a real word. The reactions can be biased by the prior presentation of semantically related words. Hines/ Volpe (1985) administered such a task to 15 PD patients. Although PD patients were slower than normal subjects, their reaction times were faster when the target was preceded by a semantically associated word, leading Hines and Volpe to conclude that “Parkinson’s disease seems to have no effect on the final level of activation in semantic memory” (Hines/Volpe 1985, 106). Some evidence has been published that suggests semantic deficits. Tweedy /Langer/ McDowell (1982) observed impairment in the recall and recognition of verbal information in 35 nondemented PD patients. Further, the PD patients benefitted less from semantic recall cues than normals and right-brain damaged individuals. The PD patients also were noted to have difficulty identify ing sy nony ms of previously seen words. Scholtz/Sastry (1985) described disturbance in the ability of PD patients to cluster verbal material to facilitate recall. Levin/Llabre/Weiner (1989) evaluated immediate and delay ed recall of discourse material using the Logical Memory Passages of the Wechsler Memory Scale. PD subjects performed significantly below normals in both recall conditions. Several investigators have tested semantic knowledge using vocabulary tests, but none report decrements in nondemented PD patients (Matison/Ma y eux/Rosen/Fahn 1982; Huber/Shuttleworth/Paulson 1986; Pirozzolo/Hansch/Mortimer et al. 1982). To the contrary , Matison and colleagues using the Vocabulary Subtest of the Wechsler Adult Intel-
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ligence Scale (WAIS) (Wechsler 1955) reported a mean performance that was above the average of the national and old-aged samples. A report of the auditory comprehension ability of PD patients was published by Cummings/Darkins/Mendez et al. (1988). Using subtests from the BDAE, deficits were observed in the comprehension of complex commands in nondemented PD patients which were more severe in demented PD patients. When comparison was made of the performance of demented PD and AD patients, the groups were “... not distinguished by auditory comprehension ... reading comprehension, [or] repetition ...” (Cummings/Darkins/ Mendez, C 682). Bay les (1990) studied the performance of 12 nondemented PD patients on four linguistically oriented tasks: the Peabody Picture Vocabulary Test (Dunn 1959); an oral object description task (Bay les 1982); the Similarities subtest of the WAIS (Wechsler 1955); and a story -retelling task (Bay les 1982). A composite score was formed to reflect performance on the four tasks. After controlling for the effects of disease severity , a significant effect was observed for the presence of PD suggesting that PD does affect linguistic competence and/or performance. However, when the additional effects of performance on the Block Design subtest of the WAIS were controlled, the PD effect was of borderline significance. These results are reminiscent of those in the literature. Whereas nondemented PD patients can be demonstrated to perform significantly more poorly on linguistically oriented tasks, the performance deficit cannot be conclusively demonstrated to result from a language deficit per se. D i s c o u r s e s a m p l e: The following is a sample of discourse from a mildly demented PD patient who was asked first to describe a safety pin and then a match. Sample # 1: Stimulus: Safety Pin “This is a metallic object. It’s compressible. It is one of the two lengths of the object which are, which are parallel to each other. It is compressible into these lengths, and it’s compressible. And, uh, it is available to be compressed and kept in a catch ...” Sample # 2: Stimulus: Matches “This is a light cardboard folder which encl-, encloses a dozen or more longitudinal bodies tipped each one tipped with a red, chalky material substance. The rest of the each of the bodies is made apparently of cardboard and is col-
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ored dark, faded blue ... On the opposite side the folded bodies uh folded match case is a black band of uh safety matches phosphorus for illumination purposes.” As was the case with AD patients, the discourse of the demented PD patients is disordered primarily in content and not form. The discourse of nondemented PD patients appears to be normal. Bay les (1991) analy zed the oral discourse of 36 nondemented PD patients and 27 normal control subjects and found no significant differences in total number of words, information units, revisions, aborted phrases, ideational repetitions, and conciseness. 3.3.3. Use As y et, there are no published reports of possible disease effects on standardized tests of pragmatic knowledge. However, the ability to use language for various purposes can be studied by observing patients in every day situations. Although a subtle deficit cannot be ruled out by this less rigorous approach, observation of 60 PD patients in the Arizona longitudinal study has not revealed impairment in their ability to use language purposefully in everyday life. S u m m a r y : The evidence for a language deficit per se comes from reports of diminished performance on generative naming tasks and the recall of verbal information. In the former, what appears to be a language deficit may be a decrement in the cognitive processes that influence language production, such as executive function or mental flexibility . In the latter, what appears to be a linguistic deficit may be a problem in the memory processes of retrieval and encoding and unrelated to the fact that the information being remembered is linguistic. Before it can be concluded that an individual has a linguistic competency problem, it must be established that the apparent deficit is not a linguistic performance problem. To conclude that PD patients have a deficit in linguistic performance, it must be established that the apparent deficit is not being caused by a deficit in a more elemental nonlinguistic function that influences linguistic performance. 3.4. Gaps in the Literature Yet to be determined are the consequences, if any , of the circumscribed intellectual deficits experienced by nondemented PD patients on linguistic communication. Hand-in-hand with this issue is whether the disease affects lan-
guage as well as nonlinguistic functions. As was the cause with AD, no data are published on the longitudinal effects of PD on language in either demented or nondemented PD. Finally, as y et it is unclear whether the dementia of PD affects linguistic communication differently from the dementia of AD.
4.
Huntington’s Disease
4.1. Neuropathology The neostriatum and frontal lobes are the site of pathology in early HD, an autosomal dominant genetic disorder that alway s causes dementia. The brain atrophy and neurochemical deficiencies that characterize the disease cause chorea and dementia. Atrophy is prominent in the caudate nucleus and putamen of the basal ganglia, the cortex, and the substantia nigra. Early in the disease degeneration occurs in the small Golgi ty pe II neurons within the caudate and putamen. These cells function to inhibit movement. Later in the disease, larger neurons in these areas are affected (Vonsattel/Mey ers/Stevens et al. 1985; Lange 1981; Lange/Thorner/Hopf/Schroder 1976). In the cortex, most notably in frontal and occipital areas, diffuse neuronal loss occurs. In conjunction with these abnormalities are neurochemical depletions, specificall y of gamma-aminobuty ric acid and acety lcholine and their respective sy nthesizing enzy mes within the caudate nucleus. Neuronal degeneration is detected by radiographic changes in striatal glucose metabolism on PET (Kuhl/Metter/Riege/Markham 1984; Hay den/Martin/Stoessl et al. 1986; Young/Penne y /Starosta-Rubinstein et al. 1986). Later disease effects are apparent by computed tomograph y (Terrance/DeLane y / Alberts 1977; Barr/Heinze/Dobben et al. 1978; Neoph y tides/Di Chiro/Barron/Chase 1979). 4.2. Neuropsychology Chorea precedes dementia in HD, though there are exceptions. The motor dy sfunction begins as unsteadiness, and fidgeting in the extremities, face, and neck. Ultimately the irregular, jerky , and stretching movements of the full blown chorea affect the whole body . Patients are described as having a shuffling, jerky gait in which the upper body seems to move ahead of the hips and legs. A variety of affective changes have been observed including depression, mania, irrita-
35. Pathology of Language Behavior in Dementia
bility , impulsivity , apathy , and in many patients psy chosis develops (Caine/Hunt/Weingartner/Ebert 1978). Suicide is high, approximately 7%, among those recently diagnosed (Reed/Chandler 1958). HD patients alway s become demented. The dementia is characterized by deficits in attention, memory , visuospatial processing, and planning. HD patients have difficulty sustaining performance on motor and cognitive tasks (Fedio/Cox/Neophy tides et al. 1979; Fisher/ Kennedy /Caine/Shoulson 1983). Subtle declines in intellectual functioning begin y ears before the occurrence of motor sy mptoms (Ly le/Gottesman 1977). When motor sy mptoms are evident, so also are deficits in memory , attention, and the ability to organize and sequence information (Josiassen/Curry /Roemer et al. 1982). Later, when the dementia is florid, HD patients perform inferiorly to normals on all subtests of intellectual tests (Butters/Sax/Montgomer y /Tarlow 1978; Josiassen/Curry/Roemer et al. 1982). Butters/Sax/Montgomer y /Tarlow (1978) describe early anterograde memory impairment and report that poor performance on short-term memory tasks is more the result of impaired retrieval than faulty encoding. Evidence for this view is that HD patients perform disproportionately better on recognition than free-recall tasks (Butters 1984; Butters/Wolfe/Granholm/Martone 1986). Further, HD patients have been reported to successfully employ verbal mediators to improve memory for pictorial materials (Butters/Albert/Sax 1983). Nonetheless, HD patients are recognized to ultimately suffer deficits in their ability to encode and elaborate information (Caine/Ebert/Weingartner 1977; Weingartner/Caine/Ebert 1979). Unlike AD patients, HD patients are reported to be impaired in the acquisition of new procedures, a phenomenon explained by disease effects of the basal ganglia. Performance deficits of HD patients on WAIS subtests measuring visuoconstructional and visuomotor abilities have been reported early (Josiassen/Curry /Mancall 1983; Moses/Golden/Berger/Wisniewski 1981; Fedio/Cox/Neophy tides et al. 1979). According to Potegal (1971), HD patients also have difficulty defining their position in space related to a fixed point. Fedio/Cox/Neophy tides et al. (1979) observed difficulty on tasks requiring right-left discrimination. Because connections between prefrontal cortex and the caudate nucleus form a circuit, disease in the caudate could be expected to
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affect frontal lobe function, specifically executive function and indeed several reports exist of executive dy sfunction. These deficits take the form of difficulty planning (Caine/ Hunt/Weingartner/Ebert 1978; Fedio/Cox/ Neophy tides et al. 1979), loss of mental flexibility , and increased perseveration (Josiassen/ Curry /Roemer et al. 1982), and impairment in set shifting (Fedio/Cox/Neophy tides et al. 1979). Tests that assess planning and sequencing and visuospatial functions were those with greatest discriminative power in distinguishing between patients with stage I and II HD, according to Shoulson (1986). Further, the Stroop and Trails B tests were the most powerful correlates of the indexes of caudate atrophy. 4.3. Effects on Language HD patients have generally been characterized as having intact language. Folstein/ Brandt/Folstein (1990, 97) note, “Patients with HD do not have clinically significant language disorders such as would be seen in patients with cortical lesions of the dominant hemisphere or those with cortical dementias (e. g., DAT).” Certainly HD patients have speech problems secondary to striatal degeneration (Ludlow/Connor/Bassich 1987). 4.3.1. Form The form of language is appropriate throughout most of the course of the disease, though it may be simplified (Podoll/Caspary /Lange/ Noth 1988; Wallesch/Fehrenbach 1988; Gordon/Illes 1987). Only in severely demented individuals is form arguably affected, but in their case, the decimation of the ability to think and the lack of content may make discourse appear to be disordered in form. Wallesch/Fehrenbach (1988) analy zed spontaneous discourse of 18 HD patients and observed “few if any linguistic errors,” no semantic paraphasias and few agrammatical and paragrammatical errors. Podoll/Caspary /Lange/ Noth (1988) noted that sy ntactic structures of spontaneous speech were ty pically reduced to short, simple sentence constructions. Verbal stereotypes were rare and occurred late. 4.3.2. Content and Use When reviewed, the performance of HD patients on linguistically oriented tasks seem more appropriately interpreted as indicative of a deficit in linguistic performance than competence, at least in the early and middle
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stages of the disease. For example, the impairment seen on generative naming, or verbal fluency tasks, has been attributed to lexical access problems (Folstein/Brandt/Folstein 1990; Wexler 1979; Smith/Butters/White et al. 1988). Results of a study by Bay les (1985) document performance deficits but resist interpretation as evidence of loss of linguistic knowledge. Twenty -one HD patients were administered a variety of linguistically oriented tests (naming, PPVT, Similarities subtest of WAIS, FAS verbal fluency test, a sentence judgment and correction task, verbal description, story retelling, sentence disambiguation, and a pragmatics task.) Performance of HD subjects was compared to those of AD and PD patients with dementia (Ba y les/Kaszniak 1987). Comparably demented mild HD and AD patients differed on only a sentence disambiguation task with the HD patients performing more poorly . When moderately demented groups were compared, no significant differences were obtained between moderate AD and PD patients and moderate PD and HD patients. As was the case with the comparison of mildly demented individuals, the only significant differences were between AD and HD patients, in this case, on the verbal description and confrontation naming. On both tasks, AD patients performed more poorly. Smith/Butters/Granholm (1988) administered naming, verbal fluency , and vocabulary tests to HD subjects and a significantly poorer performance was observed in mild HD patients compared with normal control subjects on all measures, results similar to those in the Bay les study . Smith/Butters/Granholm (1988) caution that although these data suggest that HD may involve a breakdown in the organization of the lexical-semantic representation sy stem, it is impossible to rule out possible influences of general performance factors, such as active retrieval ability . Thus, it seems clear that HD affects the ability to communicate but may not cause a loss of linguistic knowledge per se. According to Butters/Wolfe/Granholm/ Martone (1986), HD patients have a preserved capacity to store new verbal information but are extremely deficient in initiating sy stematic retrieval strategies when asked to recall information from either episodic or semantic memory. Certain of the data have been interpreted as evidence of a loss in the sy stem of activa-
tion of semantic knowledge but not loss of semantic knowledge. Smith/Butters/White et al. (1988) studied the integrity of semantic or conceptual knowledge in HD patients and attempted to minimize the influence of performance factors. They used a free association paradigm in which target responses to particular stimulus items were primed. Both free association and priming activities are considered largely automatic and do not require active manipulation of knowledge (Posner/Sny der 1975; Hasher/Zacks 1979). A positive priming effect was found for mild HD, moderate HD, and normal subjects regardless of the strength of association or ty pe of relation. However, whereas HD subjects showed no impairment in the ability to prime, there was a progressive decline in the degree to which association strengths of word pairs affected priming of semantic relations. This change represents a qualitative difference between subjects in the way activation of semantic relations is established and maintained over time. Smith/Butters/White et al. (1988, 274) write, “Although these results do not support the view that HD involves an actual loss of representation of concepts in semantic networks, they are consistent with the notion that the dementia of HD involves a deterioration in the sy stem of activation of concepts and relations in a network.” D i s c o u r s e s a m p l e s: The following samples are from a moderately demented HD patient who was asked to describe common objects. Sample # 1: Stimulus: Nail “Nail, that’s a nail. Boxing, five penny boxer. It’s a quart less than a five penny. That’s a quarter long.” Sample # 2: stimulus: Button “That’s a button. Has holes in it. Has a ...” Sample # 3: stimulus: Envelope “Envelope. It’s bent. It’s a sending for a letter. It’s for letter.” The lack of “productivity ” and “generativy it ” that Rosselli/Rosselli/Penagos/Ardila (1987) describe in later stage HD is apparent. The individuals have difficulty generating a set of meaningful descriptors. As noted by Gordon/Illes (1987), there is diminished phrase length and a reduction in the number of words that would be expected in a normal description. Linguistic communication patter n by st a ge o f d i s e a s e: Several investigators report less deterioration in language abilities than other aspects of cognitive function (Tay lor/Hansotia 1983; Josiassen/Curr y /Mancall
35. Pathology of Language Behavior in Dementia
1983). Josiassen/Curry /Mancall (1983) administered 36 measures to seven recently diagnosed HD patients, nine moderately advanced HD patients, and 48 individuals at risk but asy mtomatic. Verbal performance scores on the WAIS did not discriminate between the groups. Tay lor/Hansotia (1983) did observe markedly lower verbal IQ scores in a sample of 16 HD patients, but they were not as low as performance IQ. 4.4. Gaps in the Literature As was the case with AD and PD, it is unclear whether HD affects linguistic competence as well as performance. If linguistic competence is compromised, is it a bottom-up deterioration phenomenon as AD has been theorized to be? Then too, as with AD and PD, longitudinal data of disease effects on language are nonexistant.
5.
Pick’s Disease
5.1. Neuropathology Pick’s disease is a relatively rare neurodegenerative disease that affects women twice as often as men (Sjogren/Sjogren/Lindgren 1952). Onset is ty pically between the ages of 50 and 60 (Mahendra 1987). It is characterized by severe cell loss and subsequent atrophy primarily in the frontal lobes and anterior portions of the temporal lobes but also in the amy gdala, basal ganglia, and thalamus. Relatively spared are the pre- and post-central gy ri and the posterior superior temporal gy rus (Cummings/Duchen 1981; Uhl/Hilt/ Whitehouse/Price 1983). Occasional reports exist of severe degeneration in the basal nucleus (Uhl/Hilt/Whitehouse/Price 1983). Gustafson/Brun/Risberg (1990) published results of a longitudinal study of four Pick’s patients whose brains came to postmortem examination. Three of the four had frontotemporal atrophy with slight predominance in the temporal lobes in two. One case had atrophy only in the frontal lobes. Degeneration was somewhat asy mmetric in three cases. The central lobes were slightly affected in all cases and the parietal lobes in three. All cases had inflated cells and inclusions. A few neuritic plaques and neurofibrillary tangles were found in one elder individual, but none in the others. 5.2. Neuropsychology The early involvement of the frontal lobes is
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associated with early changes in personality and aberrant social behavior. Affected individuals may be disinhibited, tactless, and insensitive. Ty pically there is a loss of insight. Kluver-Bucy sy ndrome tends to occur early . Severe dy spraxia develops later in the disease (Gustafson/Brun/Risberg 1990). Although Pick’s disease is often confused with AD, memory dy sfunction ty pically is observed at a later stage as are visuospatial and constructional deficits (Cummings/ Duchen 1981; Wechsler/Verity /Rosenschein et al. 1982). Then too, Kluver-Bucy sy ndrome is more prominant in Pick’s patients. 5.3. Effects on Language Feher/Inbod y /Nolan/Pirozzolo (1988) write that language deficits are likely to be greater in Pick’s disease patients than in AD. Cummings (1988) notes that transcortical sensory aphasia occurs in both AD and Pick’s disease. However, Cummings (1988, 99) notes, the anomia of Pick’s is often of the semantic ty pe with “inability to recall the correct name and concomitant inability to recognize the target word when supplied by the examiner.” Cummings goes on to say that Pick’s patients are more repetitive, have a greater tendency to use verbal stereoty pes, and become echolalic or mute in late stage. Gustafson/Brun/Risberg (1990) compared Pick’s and AD patients in a longitudinal study and observed logoclonia to be uncommon. Then too, the combination of mutism and preserved receptive language was more common in Pick’s and severe comprehension deficits with paraphasias and jargon were more common in AD patients. Holland / McBurney / Moossy / Reinmuth (1985) provide the most in-depth description of the deterioration of language in Pick’s patient, a man known as Mr. E. They conducted a retrospective study of his language ability from the time of his first speaking difficulty in 1967 until his death 12 y ears later. Early in the disease his speech slowed, becoming more deliberate. He substituted lower for higher frequency words, a tendency that continued through the language deterioration period. In 1971 he was known to have language formulation and word finding problems though his responses were clear and concise. He exhibited an auditory agnosia and after 1971 became progressively more reluctant to talk. He preferred to write notes to communicate. His notes reveal that he retained memory for names of many friends and places he had been. In the final two y ears
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of life, Mr. E. had marked personality changes. He was passive, impulsive, and exhibited poor judgment. 5.3.1. Form Whereas the AD patient had preserved form, Mr. E’s form deteriorated. He lost the formal sy ntactic elements of language but retained access to the semantic store throughout the disease course. 5.3.2. Content and Use Although no investigators have studied the effects of Pick’s disease on the content and use of language per se, it is possible to infer effects from the anecdotal literature and our knowledge of the distribution of neuropathology . The performance of Mr. E suggests that content is less affected than in AD, and indeed, Pick’s disease tends to spare the posterior portions of the temporal lobes and temporoparietal areas. Use of language likely is affected, however, because of frontal lobe pathology and personality changes. D i s c o u r s e s a m p l e: The following is the last ty pewritten letter from Mr. E. (Holland/ McBurney/Moosy et al. 1985, p. 48). “Dear Ruth and Bob, I cannot compose The letter, not speak, language is good, hearing is good, not sense, noise. Stroke 1970. Note not Mary Jane, and XX Tammy. Envelope none Roger. Sincerely” 5.4. Gaps in Literature Limited data are available about the neurolinguistic effects of Pick’s disease. Most of what is known comes from the anecdotal literature. Diagnosis of this relatively rare disease is problematic making large sample longitudinal investigations difficult.
6.
Progressive Aphasia and Dementia
Progressive aphasia may be the presenting sy mptom of Pick’s disease (Wechsler/Verity / Rosenschein et al. 1982), Alzheimer’s disease (Pogacar/Williams 1984; Green/Morris/Sandson et al. 1990), and Creutzfeldt-Jakob disease (Shuttleworth/Yates/Paltan-Ortiz 1985). It has been reported in individuals ranging in age from the late forties to the mid-seventies. In a study of eight individuals by Green/ Morris/Sandson et al. (1990), the mean age was 62.8 (S.D. = 9.4).
Not all of the progressive aphasia patients reported in the literature have developed dementia; however, not all of these patients have been followed longitudinally . Green et al. did study their eight patients longitudinally and seven developed mild dementia after five y ears. The eight subjects showed deterioration in performance on nonverbal psy chometric measures although it was insufficient to be characterized as dementia. Poeck/Luzzatti (1988) followed three patients longitudinally and demonstrated cognitive decline in all three after five years. In the patients described in the literature (and reviewed by Poeck/Luzzatti 1988), a broad spectrum of language disorders were present from Broca’s aphasia to fluent semantic jargon. Nonetheless, the majority had amnesic aphasia which evolved to severe semantic breakdown. D y snomia, agrammatism, dy sprosody , hesitancy of speech, and other nonfluent characteristics were observed in the eight patients in the study by Green and colleagues. Kirshner/Webb/Kell y /Wells (1984) suggested that there may be a spectrum of disorders associated with progressive aphasia with AD on one end and non-AD-like changes confined to language cortex at the other end. Graff-Radford/Damasio/H y man et al. (1990) described a progressive aphasia patient whose post-mortem examination confirmed Pick’s disease with neuronal loss and glioses in left anterior temporal cortices. The 59-y ear-old man was anomic and had difficulty recalling the names of people that he knew well and difficulty learning the names of new acquaintances. Scheltens/Hazenberg/ Lindeboom et al. (1990) also described a 59y ear-old progressive aphasia patient whose aphasia started with misunderstandings of spoken words and spontaneous paraphasias. Striking atrophy of both temporal lobes was seen on MRI and CT nine y ears after the onset of aphasia. This case was thought to represent a temporal lobe variant of Pick’s disease. Results of Green/Morris/Sandson et al.’s (1990) study of eight patients suggest that progressive aphasia cases more commonly evolve to AD than other disorders. Poeck/ Luzzatti (1988) concur that progressive aphasia patients are most likely a variant of AD.
7.
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Sourander, P. & Sjogren, H. (1970). The concept of Alzheimer’s disease and its clinical implications. In G. E. W. Wolstenholme M. O’Connor (Eds.), Alzheimer’s disease and related conditions. 11—36. London: Churchill Livingstone. Squire, L. R. (1987). Memory and brain. New York: Oxford University Press. Stern, Y. (1983). Behavior and the basal ganglia. In R. May eux & W. G. Rosen (Eds.), The dementias. 195—209. New York: Raven Press. Storandt, M., Botwinick, J., Danziger, W. L., Berg, L., & Hughes, C. P. (1984). Psy chometric differentiation of mild senile dementia of the Alzheimer type. Archives of Neurology, 41, 497—499. Sulkava, R. (1982). Alzheimer’s disease and senile dementia of Alzheimer ty pe: A comparative study . Acta Neurologica Scandinavica, 65, 636—650. Sullivan, E. V., Sagar, H. J., Gabrieli, J. D. E., Corkin, S., & Growdon, J. H. (1985). Different cognitive profiles on standard behavioral tests in Parkinson’s disease and Alzheimer’s disease. Journal of Clinical and Experimental Neuropsychology, 7, 160. Tay lor, H. G. & Hansotia, P. (1983). Neuropsy chological testing of Huntington’s patients: Clues to progression. The Journal of Nervous and Mental Disease, 171, 492—496. Terrence, C. F., De Laney , J. F., & Alberts, M. C. (1977). Computerized tomograph y for Huntington’s disease. Neuroradiology, 13, 173—175. Thal, L. J. (1988). Dementia update: Diagnostic and neuropsy chiatric aspects. Journal of Clinical Psychiatry, 49 (suppl.), 5—7. Tomoeda, C. K. & Bay les, K. A. (1992). Longitudinal effects of Alzheimer’s disease on discourse production. Manuscript submitted for publication. Tweedy , J. R., Langer, K. G., & McDowell, F. H. (1982). The effect of semantic relations on the memory deficit associated with Parkinson’s disease. Journal of Clinical Neuropsychology, 4, 235—237. Uhl, G. R., Hilt, D. C., Whitehouse, P. J., & Price, D. L. (1983). Pick’s disease (lobar sclerosis): Depletion of neurons in the nucleus basalis of Mey nert. Neurology, 33, 1470—1473. Ulatowska, H. K., Allard, L., Donnell, A., Bristow, J., Hay nes, S. M., Flower, A., & North, A. J. (1988). Discourse performance in subjects with dementia of the Alzheimer ty pe. In H. A. Whitaker (Ed.), Neuropsychological studies of nonfocal brain damage. 108—131. New York: Springer-Verlag. Vance, K. T. & Bay les, K. A. (1990). Dissociation of oral reading and semantic information in advanced Alzheimer’s disease patients. Paper presented at the meeting of the Rocky Mountain Psy chological Association, Tucson, AZ. Vonsattel, J. P., Mey ers, R. H., Stevens, T. J., Ferrante, R. J., Bird, E. D., & Richardson, P. (1985). Neuropathological classification of Hun-
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tington’s disease. Journal of Neuropathology and Experimental Neurology, 44, 559—577. Wallesch, C. W. & Fehrenbach, R. A. (1988). On the neurolinguistic nature of language abnormalities in Huntington’s disease. Journal of Neurology, Neurosurgery, and Psychiatry, 51, 367—373. Warrington, E. K. (1975). The selective impairment of semantic memory . Quarterly Journal of Experimental Psychology, 27, 635—657. Wechsler, A. F., Verity , M. A., Rosenschein, S., Fried, I., & Scheibel, A. B. (1982). Pick’s disease: A clinical, computed tomographic, and histological study with Golgi impregnation observations. Archives of Neurology, 39, 287—290. Wechsler, D. (1955). Manual for the Wechsler Adult Intelligence Scale. New York: The Psy chological Corporation. Weingartner, H., Burns, S., Diebel, R., & Le Witt, P. A. (1984). Cognitive impairments in Parkinson’s disease: Distinguishing between effort-demanding and automatic cognitive processes. Psychiatry Research, 11, 223—235. Weingartner, H., Caine, E. D., & Ebert, M. H. (1979). Encoding processes, learning, and recall in
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Huntington’s disease. In T. N. Chase, N. S. Wexler, & A. Barbeau (Eds.), Advances in Neurology, Volume 23: Huntington’s Disease, 215—226. New York: Raven Press. Wexler, N. S. (1979). Perceptual-motor, cognitive, and emotional characteristics of persons at-risk for Huntington’s disease. In T. N. Chase, N. S. Wexler, & A. Barbeau (Eds.), Advances in neurology, Volume 23: Huntington’s disease. 257 —27 1. New York: Raven Press. Whitaker, H. A. (1976). A case of isolation of the language function. In H. Whitaker & H. A. Whitaker (Eds.), Studies in neurolinguistics: Volume 2. 1—58. New York: Academic Press. Wilson, R. S., Kaszniak, A. W, Klawans, H. L., & Garron, D. C. (1980). High speed memory scanning in Parkinsonism. Cortex, 16, 67—72. Young, A. B., Penney , J. P., Starosta-Rubinstein, S., Markel, D. S., Barent, S., Giordan, B., Ehrenkaufer, R., Jewett, D., & Hichwa, R. (1986). PET scan investigations of Huntington’s disease: Metabolic correlates of neurologic features and functional decline. Annals of Neurology, 20, 296—303.
Kathryn A. Bayles, Tucson, Arizona (USA)
36. Language Disorders with Diffuse Brain Disease of Acute Onset 1. 2. 3. 4. 5. 6.
1.
Introduction General Neurological Outcomes Underlying Neurophysiological Mechanisms Language Characteristics of Patients with Diffuse Brain Disease of Acute Onset Conclusions References
Introduction
The study of neurologically -based language impairment in adults has evolved from examination of disorders with focal lesions to research and clinical concerns with disorders of more diffuse neurological substrates. Where aphasia received primary attention in the past, literature now highlights linguistic and communicative deficits in patients suffering closed head trauma, right hemisphere impairment, and dementia. Narrow considerations of purely linguistic phenomena have given way to broader models of behavioral deficit that encompass the full array of neuropsy chological domains and acknowledge
the cognitive underpinnings of some communicative deficits. It is surprising, therefore, to find that almost no language-based research or clinical attention has been paid to one subset of the neurologically -impaired population — individuals who have suffered some form of anoxic encephalopathy with relatively acute onset. Parkin/Miller/Vincent (1987, 655) define anoxic encephalopathy as a diffuse “... deterioration in brain function following disruption or cessation of the brain’s vascular supply”. The causes of anoxic encephalopathy may vary . Relatively unusual incidents such as near-drownings, failed hangings, anesthesia complications or induced hy potension, and carbon monoxide poisoning account for a small percentage of known cases, along with encephalopathy of unknown origin. However, the vast majority of individuals with acute onset anoxic encephalopathy are those who have suffered cardiac arrest followed by cardiopulmonary resuscitation. It is projected
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that between 100,000 and 200,000 out-of-hospital resuscitations are attempted y early in this country (Safar 1986; Krause/White/Aust et al. 1988), with an additional unknown number of resuscitations attempted within the confines of the hospital setting. Although survival-to-discharge rates remain low (between 6% and 35%) for out-of-hospital resuscitations, thousands of individuals survive to be at-risk for disorders of linguistic and cognitive function. Neurological outcome, however continues to be defined in rather broad terms that may obscure deficit. Volpe/Holtzmann/Hirst (1986, 408) state that, “Cognitive abnormalities are often not defined, or defined only as inability to return to former occupation”. Thus, linguistic and communicative quality of life issues for persons with anoxic encephalopathy of acute onset are rarely addressed, and a sy stematic framework for clinical assessment and service delivery is lacking. This chapter briefly reviews general neurological outcomes in patients with anoxic encephalopathies of acute onset, neurophy siological mechanisms presumed to be responsible for deficit, and recent literature concerning language consequences of such encephalopathies. Findings from a six month neuropsy chological follow-up of 39 cardiac arrest patients are summarized.
2.
General Neurological Outcomes
Safar (1988) notes that initial concerns with simple survival and restoration of healthy cardiac function following resuscitation have given way in the last two decades to a preoccupation with quality of survival. Research emphases have shifted to epidemiological analy ses of neurological outcomes, clinical trials of specific treatment regimes designed to improve cerebral status, and exploration of subject or treatment factors influencing neurological outcomes. Neurological outcome data tend to substantiate Krause/White/Aust et al.’s (1988, 714) claim that, “Neurologic injury is the major limitation of cardiac resuscitation”. However, there are marked discrepancies with respect to the proportion of resuscitated individuals who experience return to normal cerebral function, with estimates ranging from 93% (Bedell/Delbanco/Cook/Epstein 1983) to percentages as low as 13% (Bass 1985; BRCT I Study Group 1986).
Differences in sample characteristics may account for some of these discrepancies. However the more fundamental problem concerns a definition of good cerebral recovery . In recent work, measures such as the Glasgow Outcome Performance Scales (BRCT II Study Group 1989) assign “good cerebral performance” to individuals who may still be experiencing minor psy chologic or neurologic deficits, i n c l u d i n g m i l d a p h a s i a or cranial nerve abnormalities. Thus, the scale would classify individuals who have suffered mild cerebral dy sfunction as having made good neurological recovery . It is not surprising that Kotila/Kajaste (1984) plead for greater attention to the identification of neuropsy chological deficits in patients who appear outwardly normal or recovered. To address such deficits, the underly ing neurophy siological mechanisms that might be expected to contribute to impaired functioning must be examined.
3.
Underlying Neurophysiological Mechanisms
Cerebral damage may result from two aspects of the arrest/resuscitation cy cle. The more obvious aspect of the cy cle is that there are finite limits to the amount of time neuronal tissue can withstand sustained lack of oxy genation before irreversible damage or neuronal death occurs (Safar 1988). In addition, the reperfusion and reoxy genation measures necessary to restore metabolism and cell viability initiate a postresuscitation sy ndrome after a period of five minutes without blood flow. Initial anoxia coupled with ensuing resuscitation efforts lead to cell death in predictable regions, including the phy logenetically older regions of the brain in general and particularly the basal ganglia, hippocampus, cerebellum, occipital lobe, and “border zone” or watershed regions of the parietotemporal cortex (c. f., Safar 1988; Parkin/Miller/Vincent 1987; Bigler/Alfano 1988). Reperfusion efforts and failures may also lead to a variety of organ and cell derangements. Neuropsy chological deficits in survivors of anoxic encephalopathy might be predicted to reflect pervasive alterations in basic cognitive processes (e. g., attention and orientation) coupled with more specific deficits in motor functioning (cerebellum, basal ganglia), memory (hippocampus), visual skills (occipital lobe), and perceptual processes and language
36. Language Disorderswith Diffuse Brain Disease of Acute Onset
(temperoparietal regions). These predictions are supported in the linguistic and neuropsychological literature.
4.
Language Characteristics of Patients with Diffuse Brain Disease of Acute Onset
The neuropsy chological literature concerning dy sfunction in patients with anoxic encephalopathies is scattered through a variety of sources and relies heavily upon case studies (for review, see Shadden/Holland 1990). The earliest case study reports tended to focus upon the range of memory impairments in survivors, with particular attention to Korsakoff-like dementia traits. Concern with memory deficits continues to the present day (c. f., Cermak 1976; Cummings/Tomiy asu/ Read/Benson 1984). There appears to be reliable evidence that at least one subgroup of cardiac arrest or anoxic encephalopathic patients is characterized by pronounced impairment of memory skills in the absence of notable deficit in other aspects of cognitive functioning. When neuroradiological or postmortem data are available, amnesic deficits are usually traced to hippocampal lesions (Cermak 1976; Cummings/Tomi y asu/Read/ Benson 1984; Bigler/Alfano 1988). A variety of deficits in visual perception (including cortical blindness) are documented in virtually every study of neuropsy chological consequences of anoxic encephalopathy . Reports of orientation and attentional deficits are common. It is interesting to note that memory and visual perceptual skills underpin many language behaviors, y et the presence of linguistic deficits in a number of these studies is either ignored, controlled for, or denied. For example, Parkin/Miller/Vincent (1987) concluded that language functions were well preserved in the context of pronounced perceptual and memory deficits d e s p i t e their reports of word-finding deficits and acquired dy slexia in the patient they studied. Anomalous treatment of language performance is also evident when one considers that memory measures in a number of studies traditionally include forward and backward digit span. Similar measures of auditory memory span can be found in aphasia tests. In general, reference to speech and language dy sfunction in many studies is inciden-
411
tal or anecdotal. For example, Caronna/Finklestein (1978) noted one subject out of four with motor speech and language comprehension deficits, and Yarnell (1976) indicated that two out of four survivors remaining in a vegetative state retained some ability to comprehend and follow simple commands. Rose/ Sy monds (1960) described their subject’s problems in repeating sentences and in auditory memory span; one of Willanger/Klee/ Lindeneg/Jorgensen’s (1970) y oung patients desplay ed total alexia and severe acalculia. In fact, even early reports examining Korsakofflike sy mptoms of cases with anoxic encephalopathy stressed the presence of confabulation and verbosity. More recent investigations of neuropsy chological sequelae of cardiac arrest and resuscitation have begun to examine a broader range of cognitive functions. In addition to the Parkin/Miller/Vincent (1987), Volpe/Hirst (1983), and Volpe/Holtzmann/Hirst (1986) works, Armengol/Moes (1986) describe neuropsy chological profiles of nine patients with anoxic encephalopathy of vary ing origins. They reported that linguistic and visuospatial skills were impaired in a l l subjects, with deficits in attention, memory , orientation, and task behavior noted in seven of the nine. Similarly , Kotila/Kajaste (1984) identified dy sphasia in four out of ten patients who had suffered out-of-hospital cardiac arrest. The work of Bigler/Alfano (1988) is probably one of the most comprehensive neuropsy chological evaluations to date. They explored profiles of 12 patients who were at least nine months post anoxic brain injury with an initial deep coma and abnormal EEG’s. An extensive neuropsy chological test battery was administered, including languagebased measures such as the Rey Auditory Verbal Learning Task. Only results of WAISR, Wechsler Memory Scale, and HalsteadReitan administrations were discussed in the paper. Experimental subjects were compared with a matched control group of closed head injured patients. Premorbid IQ was estimated. Although the anoxic brain damage group scored within the normal range on the Verbal portion of the Aphasia Screening Exam subtest of the Halstead-Reitan, postmorbid Verbal IQs on the WAIS-R were significantly lower than those of the control group. The anoxic group also performed more poorly on all verbal subtests of the WAIS-R, suggesting that skills such as auditory memory span, vocabulary , and comprehension were im-
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vocabulary , and comprehension were impaired considerably . As in earlier studies, greatest deficits continued to be noted in the memory domain. The authors concluded that, “the clinician assessing the anoxic encephalopathy patient needs to utilize a wide spectrum of neuropsy chological measures along with specific tests of memory function” (Bigler/Alfano 1988, 396). The preceding overview of the neuropsy chological literature concerning linguistic impairment with anoxic encephalopathy is remarkable for its very few comprehensive studies of neuropsy chologic functions and its relative inattention to language. The largest number of subjects considered in any one study was 22 (Bengtsson/Holmberg/Jansson 1969), of whom a much smaller number received the designated psy chologic/psy chiatric battery . Subject selectivity is also apparent. Few studies measure behaviors in an entire sample of survivors. There are a limited number of experimental studies of either the nature of or underly ing processes involved in observed deficits. In general, detailed descriptions of spontaneous naming and verbal expression characteristics of this population are lacking. The word finding deficits mentioned specifically by Bengtsson/Holmberg/Jansson (1969) and Parkin/Miller/Vincent (1987), among others, appear to resemble the tip-of-the-tongue phenomena noted in both aphasia and some forms of dementia. However, impaired wordretrieval processes are not described in any depth. Expressive language disturbances are either labeled aphasia or described relatively consistently as reflecting verbosity , impulsivity , perseveration, and irrelevance. There are no controlled comparisons of naming or broader communicative functions in patients with anoxic encephalopathy , aphasia, and dementia. In response to some of these concerns, a neuropsy chological protocol was developed to provide a mechanism for longitudinal screening of a broad range of deficits and to supplement more traditional outcome measures such as the Glasgow Outcome Performance Scales. Analy sis has recently been completed on neuropsy chological screening examination data gathered from 39 subjects at two weeks and six months post cardiac arrest. These data represent outcomes for the largest body of resuscitated individuals to date that have received a consistent battery of neuropsychological measures in any one study.
The Neuropsy chological Screening Instrument (NPSI) developed for this investigation is a 48 point examination designed for brevity , ease of administration, and capability of translation into different languages. Although brief, it contains tasks well within the normal performance range and samples a range of neuropsy chologic performance areas. The 16 different tasks comprising the instrument sample aspects of orientation, long-term memory , procedural memory , delay ed recall, verbal language comprehension (following commands, answering simple factual questions), verbal expression (picture naming, sentence repetition, word fluency ), reading comprehension, writing, drawing and copy ing, and visuospatial and visuomotor attention and sequencing. For analy sis, items were grouped into three categories: Orientation and Memory , Visuospatial Perception and Attention, and Language. Subjects were drawn from the 516 participants in the Pittsburgh School of Medicine’s multi-site Brain Resuscitation Clinical Trial II (BRCT II) data base (BRCT II Study Group 1989). BRCT II is a randomized, double-masked clinical trial study comparing the effects of lidoflazine with placebo on recovery of cerebral function post cardiac arrest. The Neurops y chological Screening Instrument (NPSI) was administered to all subjects judged able to cooperate at two weeks and six months, with only the 39 subjects tested at both intervals forming the primary data base. A group of 20 control subjects matched for age decade, sex, and gender distribution also completed the NPSI. Data were available with respect to demographics, arrest causes and times, and regular monitoring of coma severity , functional level, and Glasgow Outcome Performance Categories which reflect levels of cerebral and overall performance functioning. In this discussion, only key language-related findings will be highlighted, although visuospatial perception and attentional processes were clearly impaired in the cardiac arrest group as compared with a group of controls. It should be noted, however, that NPSItested subjects received consistently higher ratings than non-tested subjects on the Glasgow Outcome Performance Categories at both two weeks and six months, reflecting their status as the highest functioning component of the survivor group. With respect to language functioning, the following findings are of interest. First, car-
36. Language Disorderswith Diffuse Brain Disease of Acute Onset
diac arrest survivors scored significantly lower than control subjects on the combined Language Cluster at both two and six weeks. In fact, at both intervals, more subjects fell below the one standard deviation cut-off score in the Language Cluster than in any other cluster of subtests. Of the five most consistently discriminating individual subtests, three were in the Language Cluster (word fluency , sentence repetition, and answering questions). Second, on the Language Cluster, 21 out of 39 subjects showed a positive change in performance from two weeks to six months (mean 4.2 points) and only 4 subjects lost 1 or 2 points. However, even at six months, 25 subjects fell below the Language Cluster cut-off score based on one standard deviation below the mean. Third, NPSI scores appeared much more sensitive to cognitive-based neurological dy sfunction than did the Glasgow Outcome Performance Scales. At two weeks, 85% of subjects received the top rating of Good Cerebral Performance, y et only 20% obtained NPSI scores within the normal range. Similarly , at six months, 92% of subjects received top cerebral performance ratings, y et only 39% received normal range scores on the NPSI. It should be noted, however, that the best Cerebral Performance rating obtained by any subject during the first 24 hours post-arrest was highly predictive of Language Cluster performance at six months (r = —.88, p < .001). Fourth, Language Cluster scores at two weeks showed moderate correlation (r = + .50, p < .01) with Language Cluster scores at six months. Finally , when subjects were sorted on the basis of arrest and CPR times, and on the presence or absence of retrograde and anterograde amnesia, Language Cluster performance at two weeks was found to be poorer if CPR times were longer and if anterograde amnesia persisted until six months. Language Cluster performance at six months was found to be poorer if Total Arrest Times were longer, if anterograde amnesia was reported at two weeks, and if retrograde amnesia persisted at six months. Taken together, these findings permit several conclusions. The most important is that, in an anoxic encephalopathic subject population selected only for ability to respond to testing, language deficits are characteristic of the group as a whole. Despite the anticipated scatter of deficits, almost two-thirds of the six months survivors display ed less than op-
413
timal performance in this domain. Particularly sensitive areas appeared to be word fluency , sentence repetition, and answering questions. Since Language Cluster performance on the NPSI continued to improve from two weeks to six months, it is impossible to determine the long-term outcome with respect to language functioning. However, even mild linguistic deficits of six months duration are likely to have a profound impact on quality of life, particularly if coupled with other deficits in cognitive or emotional functioning. Another important conclusion is that global neurological outcome measures frequently overestimated the degree of recovery in resuscitated cardiac arrest patients. Patients described as having normal cerebral functioning on the Glasgow Outcome Performance Scales still evidenced language deficits at six months. This observation does not negate the value of the Glasgow scales, since best Cerebral Performance achieved on this measure during the first 24 hours strongly predicted language performance at six months. Data from this preliminary investigation provide clear support for the presence of language impairment in some resuscitated cardiac arrest patients. Coupled with findings from the work of Armengol/Moes (1986) and Kotila/Kajaste (1984), among others, the need for further focused linguistic research with individuals suffering diffuse brain disease of relatively acute onset is apparent.
5.
Conclusions
Despite growing concerns about quality of life for the survivor of cardiac arrest and other conditions producing diffuse brain damage, it appears that few practitioners are aware of the likelihood that neuropsy chological linguistic deficits in such patients may occur. Of particular concern are the group of individuals whom Kotila/Kajaste (1984) designate as “outwardly normal”. Once the threat to life has been resolved and medical and neurological status is broadly stable, these individuals may return to their homes and families with the understanding that they have overcome their ordeal. Previously undetected deficits in cognitive and linguistic functions, as well as personality and emotional adjustment, may emerge at this time (c. f., Reich/Regestein/ Murawski et al. 1983; Vlay /Fricchione 1985). Unfortunately , these behavioral changes may be sufficiently subtle to escape notice in rou-
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tine medical follow-up. Evaluation and potentially beneficial treatment services for patients and families may be neglected. The preceding brief review of relevant portions of the neuropsy chological literature, coupled with recent data pertaining to postarrest linguistic deficits in the BRCT II clinical trial population, provides sufficiently strong support to conclude that linguistic dy sfunction does occur with some regularity in the anoxic encephalopathy population. The nature and extent of such deficits remains illdefined, and further research concerning linguistic deficits in cardiac arrest survivors is needed. A comprehensive research protocol should include the following: All resuscitated cardiac arrest patients should be administered a neuropsy chological screening examination similar to the NPSI at two weeks, three months, six months, and one y ear. Patients should not be eliminated due to the presence of aphasic deficits or any other selection criteria. This process will provide much-needed basic epidemiological data concerning the frequency of occurrence of neuropsy chological deficits and behavioral change over time. In addition, individuals can be targeted for further testing. Patients identified during the screening process should receive further intensive neuropsy chological testing, including a battery of tasks designed specifically to tap a variety of language functions. Functional communication and discourse assessment must be incorporated into this battery . A common test battery could be identified by a core group of researchers across multiple sites, and a data bank which would include neuroradiological and medical data should be developed. With sufficiently large numbers of subjects, distinct performance profiles could identified for differential diagnostic purposes. Follow-up testing for several y ears would also permit identification of prognostic variables influencing recovery. A separate but parallel series of experimental investigations should probe more closely into the source of linguistic impairment — attempting to identify the contributions of attentional, memory , perceptual and other deficits to observed language dy sfunction. Further, studies of the efficacy of different treatment protocols would shed further light on the underly ing nature and causes of language deficit. Selected cardiac arrest survivors and their families should be followed longitudinally in an attempt to determine the longterm impact
of residual deficits upon quality of life, and the relative contribution of linguistic and communicative breakdown to reduced quality of life. This information would be crucial in counseling with patients and families and in designing family-oriented interventions. In addition to the above-described research efforts, professionals in speech-language patholog y , neurops y cholog y , and neurolog y should work to increase sensitivity to the need for cognitive and linguistic intervention in the cardiac arrest population. Without enhanced sensitivity and awareness, the knowledge base related to language consequences of anoxic encephalopathy will remain inadequate and the individual with diffuse brain damage of acute onset will continue to be underserved. Acknowledgment: This work was supported by a grant (NS/5295) from the Natural Institutes of Health (USA).
6.
References
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Cermak, L. S. (1976). Encoding capacity of a patient with amnesia due to encephalitis. Neuropsychologia, 14, 311—326. Cummings, J. L., Tomiy asu, U., Read, S. & Benson, D. F. (1984). Amnesia with hippo-campal lesions after cardiopulmonar y arrest. Neurology, 34, 679—681. Kotila, M. & Kajaste, S. (1984). Neurological and neuropsy chological sy mptoms after cardiac arrest. 25th Scandinavian Congress of Neurology : Cerebrovascular Diseases (1984, Bergen, Norway ). Acta Neurologica Scandinavica 69 (98), 337—338. Krause, G. S., White, B. C., Aust, S. D., Nay ini, N. R. & Kumar, K. (1988). Brain cell death following ischemia and reperfusion: A proposed biochemical sequence. Critical Care Medicine, 16, 714—726. Parkin, A. J., Miller, J. & Vincent, R. (1987). Multiple neuropsy chological deficits due to anoxic encephalopathy: A case study. Cortex, 23, 655—665. Reich, P., Regestein, Q. R., Murawski, B. J., DeSilva, R. A. & Lown, B. (1983). Unrecognized organic mental disorders in survivors of cardiac arrest. American Journal of Psychiatry, 140, 1194—1197. Rose, F. C. & Sy monds, C. P. (1960). Persistent memory defect following encephalitis. Brain, 83, 199—211. Safar, P. (1988). Resuscitation from clinical death:
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Pathophy siologic limits and therapeutic potentials. Critical Care Medicine, 16, 923—941. Shadden, B. B. & Holland, A. L. (1990). Neuropsy chological outcomes in cardiac arrest survivors: Performance on the Neuropsy chological Screening Instrument (NPSI). Unpublished manuscript. Vlay , S. C. & Fricchione, G. L. (1985). Psy chosocial aspects of surviving sudden cardiac death. Clinical Cardiology, 8, 237—243. Volpe, B. T. & Hirst, W. (1983). The characterization of an amnesic sy ndrome following hy poxic ischemic injur y . Archives of Neurology, 40, 436—440. Volpe, B. T., Holtzman, J. D. & Hirst, W. (1986). Further characterization of patients with amnesia after cardiac arrest: Preserved recognition memory . Neurology, 36, 408—411. Willanger, R., Klee, A., Lindeneg, O. & Jorgensen, E. O. (1970). A neuropsy chological study of cerebral anoxic sequelae of cardiac arrest. Acta Neurologica Scandinavica, Supp 43, 103—104. Varnell, P. R. (1976). Neurological outcome of prolonged coma survivors of out-of-hospital cardiac arrest. Stroke, 7, 279—282.
Audrey L. Holland, Tucson, Arizona (USA)/ Barbara B. Shadden, Fayetteville, Arkansas (USA)
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37. 1. 2. 3. 4. 5.
1.
Dynamical Systems and Speech Introduction and Historical Perspective Functional Constraints on Multiarticulator Coordination Coordination Dynamics of Speech Conclusions References
Introduction and Historical Perspective
The perception of phonological information is remarkably insensitive to acoustic variations introduced, for example, by changes in the rate at which an utterance is produced, the emphatic or sy llabic stress level, or contextual effects. A primary concern of speech science and psy chology from the late 1960’s through most of the 1970’s was to elucidate how the putatively invariant phonological information is encoded in the continuously vary ing acoustic signal. One early hy pothesis was that the motor commands sent to the muscles would stand in one-to-one identity with an individual phonological segment, and that this invariance, although smeared in the acoustic signal, would be observable in electrom y ograms (Liberman/Cooper/Shankweiler/Studdert-Kennedy 1967). However, it was quickly demonstrated that electromy ographic activity was itself strongly context-dependent (e. g., MacNeilage/DeClerk 1969). Shifting the focus of analy sis to articulatory gestures also failed to reveal an invariant relationship between individual motor variables (e. g., displacement, velocity ) and phonological segments (e. g., Butcher/Weiher 1976; Gay /Ushijima/Hirose/Cooper 1974; Kozhevnikov/ Chistovich 1965; Kuehn/Moll 1976; Libery man/Cooper/Shankweiler/Studdert-Kenned 1967; Lindblom 1963). In fact, the variability of individual articulatory gestures as a function of stress, rate, and contextual change is one of the few aspects of speech production on which most investigators agree (but see,
for example, Kelso/Vatikiotis-Bateson/Saltzman/Kay 1985, for evidence of stable kinematic relationships in individual articulators across rate and stress; also Vatikiotis-Bateson 1988). These studies underscore the qualitatively incommensurate nature of phonological segments (ty pically considered as discrete, static, and invariant across contexts) and the changing vocal tract shape which, like the resultant acoustic consequences, is both continuous and context-sensitive. It was thus necessary to postulate a mechanism for minimizing abrupt articulator y changes at segment boundaries. The general form of the proposed mechanism was to spread the individual features among neighboring segments, then translate the resulting feature bundles into commands to articulatory muscles for execution in sequence [see Fowler,Chapter 3; this volume; also Daniloff/Hammarberg 1973 for an example of production models of this type.] The rules governing featural spread were often hotly debated (see Fowler, Chapter 3 this volume, for discussion of feature spreading, coproduction, etc.). Despite their differences, most theories assumed the final stage of translation of feature bundles into muscle commands. Our inadequate understanding of this stage began to be recognized, with a growing appreciation of the complexity of movement control and coordination as exemplified by the Soviet phy siologist Nikolai Bernstein (1967). Although Bernstein’s work was directed largely at understanding coordinated nonspeech limb and body movements, the concepts he identified also motivated empirical and theoretical work in speech production (Fowler/Rubin/Remez/ Turvey 1980). Bernstein’s key insight was that the large number of potential degrees of freedom of the skeletomuscular sy stem precludes the pos-
37. Dynamical Systems and Speech
sibility that each is controlled individually at every point in time. He then proposed a scheme whereby many degrees of freedom could be regulated through the direct, executive control of very few. (Note that “executive” should not be considered here as solely a central or cortical function. For example, brainstem regions could play a putative “executive” role.) In this view, individual variables of the motor sy stem are organized into larger groupings variously called ‚linkages,’ ‚s y nergies,’ ‚collectives,’ or ‚coordinative structures’ (Bo y lls 1975; Easton 1972; Gel’fand/Gurfinkel/Fomin/Tsetlin 1971; Turvey 1977). These groupings are generally thought to be functional, not hardwired, in that the same degrees of freedom may be constrained in different way s to achieve different purposes, and different degrees of freedom may be constrained to achieve the same goal. During a movement, the functional group can be controlled as if it had many fewer degrees of freedom than comprise its parts, thus reducing the number of control decisions required (e. g., Kelso/Southard/ Goodman 1979). In what follows, direct evidence is presented for the speech articulators functioning cooperatively as a flexible taskspecific unit. Also discussed are the stability and flexibility of the units and their actual dy namical description in terms of equations of motion. These dy namics refer to the ‚coordination dy namics’ of the central nervous sy stem, not the phy sical mechanics of moving masses. Finally , the utility of a dy namical description of task-specific units in speech modelling and the relevance to speech disorders are considered.
2.
Functional Constraints on Multiarticulator Coordination
2.1. Spatial Constraints Examples of functional constraints on speech movement, coordinative structures, are evident in speakers’ adjustments to static and dy namic disruptions of articulation. When speakers wear a ‚biteblock,’ a spacer that maintains a constant separation between the upper and lower jaw, they are nonetheless able to produce isolated vowels, and consonant-vowel-consonant ys llables within the normal range of acoustic and kinematic variability (e. g., Lindblom/Sundberg 1971). Significantly , speakers do so even when the availability of acoustic, tactile, or proprioceptive
417
feedback is drastically reduced (e. g., Kelso/ Tuller 1983; Lindblom/Lubker/Gay 1979). A similar outcome is obtained when lip protrusion is impeded during production of rounded vowels. Compensation is achieved even on the first trial by lowering the lary nx to a degree that preserves the vocal tract length characteristic of the vowel and produces acoustically normal vowels (Riordan 1977). Unexpected dy namic pertubation of articulatory motions also fails to disrupt production. In one such experiment, the speaker produces the sy llable/bæb/a number of times. On a few of the productions, the jaw motion is suddenly perturbed while moving toward the final /b/ closure. The upper lip actively compensates for the jaw disruption by increasing displacement so as to produce the bilabial closure for /b/, even on the first occurrence of the perturbation; no concurrent increase in tongue muscle activity is observed. These remote reactions in the upper lip are observed only when the jaw is perturbed during the closing phase of the motion, that is, when the reactions are necessary to preserve the identity of the utterance. When the upward jaw motion is perturbed during the transition to the final /z/ of /bæz/, no compensatory increase in displacement is observed in the lip motions, but the tongue activity increases, an appropriate compensation to achieve the tongue-palate approximation for fricative production. Thus, functionally -specific (phoneticall y -specific) near-immediate compensation to unexpected perturbation is observed in articulators remote from the locus of the perturbation, on the first occurrence of the perturbation. [Abbs/Gracco/Cole 1984; Kelso/Tuller/Vatikiotis-Bateson/Fowler 1984; Shaiman 1989, among many others]. The findings just described are not easily accounted for by traditional motor control models. For example, closed-loop (feedbackdependent) models can account for the accurate production of vowel sounds despite changes in initial position of the jaw (due to the biteblock), but they could not explain why production remains within the normal range when acoustic, tactile, and proprioceptive information is restricted. In theory , open-loop (feedback-independent) models could incorporate the results of restricted afferentation, but have difficulty explaining satisfactorily adjustments to unanticipated perturbations. Considering the degrees of freedom of the vocal tract as a ‚constrained functional group’ means that the sy stem has an intrinsic goal
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which is attainable from any initial configuration by virtue of the sy stem dy namics. That is, the sy stem exhibits ‚equifinality ’ (von Bertalanffy 1973). One very simple example of a dy namical sy stem that display s equifinality , is a massspring sy stem. This sy stem has been used as a model for understanding the adaptive behavior of the articulatory sy stem in perturbed (biteblocks, disruptions of articulator movements) as well as unperturbed speech (variations in stress, speaking rate, contextual variations, etc. See for examples Ostry /Munhall 1985; Kelso/Vatikotis-Bateson/Saltzman/Ka y 1985). A mass-spring system is simply a spring attached at one end to a fixed support and at the other end to a mass (cf. Fowler/Rubin/ Remez/Turvey 1980). When the spring is stretched or compressed and then released, it alway s equilibrates at the same resting length regardless of the amount the mass is initially displaced. In most but not all cases, the massspring description is not meant to be a literal representation of the phy siological speech sy stem with springs and masses representing muscles and articulators. Rather, the massspring sy stem is used as an abstract description of articulatory behavior. A mass-spring sy stem belongs to a generic class of dy namical sy stem with the simplest attractor ty pe, a point attractor (or stable fixed point) to which all neighboring trajectories converge (see Section 3.2.). In an abstract description, the attractor may be conceived of as a limit set in a functionally-defined physiological space. 2.2. Temporal Constraints Speech production depends not only on the spatial relationships among articulator positions but also on their temporal patterning and serial ordering (Lashley 1951). Examples of constraints on timing of multiple articulators are becoming increasingly common (e. g. Kent/Netsell 1971; Kent/Moll 1975; Kozhevnikov/Chistovich 1965; Löfqvist/Yoshioka 1981). Our own work has focussed on the relative timing of vowel-related, V, and consonant-related, C, events across changes in speech rate and sy llable stress. Basically , we reported that across these suprasegmental changes the timing of medial consonant production in CV1 # CV2C utterances (e. g., /ba # wab/) remains stable relative to the interval between events associated with the flanking vowels. The relationship between these articulatory event durations (the interval from V1 to C and from V1 to V2) was
described well by a linear function with a positive slope and nonzero intercept. This occurred whether ‚segment-associated activity ’ was observed at the electrom y ographic (Tuller/Kelso/Harris 1982; 1983) or kinematic levels (Kelso/Saltzman/Tuller 1986; Tuller/ Kelso 1984; Tuller/Kelso/Harris 1983). These ‚relative timing’ results hint at the presence of a functional constraint on movement timing whereby individual sy stem elements are constrained within a particular temporal relationship, while metrical adjustment of the components affords flexibility. The foregoing experiments motivated a flurry of activity among speech scientists, some of whom subsequently corroborated the basic result (Gentil/Harris/Horiguchi/Honda 1984; Linville 1982; Löfqvist 1986; Lubker 1983), and some of whom failed to do so (Munhall 1985; Nittrouer/Munhall/Kelso et al. 1988). In what follows, we argue that the interpretation of relative timing information depends crucially on the experimental paradigm and, more generally , on the distinction between invariance and stability in sy stem behavior. The problem arises because different relative timing stability regimes exist as a function of the independent variable of interest (e. g., speaking rate).
3.
Coordination Dynamics of Speech
3.1. Invariance vs. Stability It is commonplace to assume that if a variable does not change much over a range of parameter values, it is an invariant. Schmidt (1982), for example, argues that the ‚invariance’ of proportions of time spent in various phases of the locomotion step cy cle provides evidence for walking and jogging programs. Criteria for invariance are seldom specified, however, leading to much confusion (cf. Sternberg/Knoll/Turock 1990). One may ask: invariant with respect to what? Or, how much can the mean value of a variable change before one decides that the variable is not invariant? An alternative approach is to show that a variable such as relative timing remains stable, not necessarily strictly invariant, over a range of parameter values, then shifts to a new value as a consequence of loss of temporal stability. Thus, pattern stability and change arise from the same underly ing nonlinear dy namics. Whether loss of stability is observed depends crucially on the range of parameter
37. Dynamical Systems and Speech
values selected for study . An hy pothesized collective variable, such as relative timing, may change little across a wide range of speaking rates. But the fact that relative timing undergoes a phase transition at some critical speaking rate may be more fundamental, undercutting the invariance concept by providing a metric for evaluating fluctuations in the mean value of a variable. Recent observations of phase transitions in speech movement (and perceptual) patterns demonstrates that the dy namical concept of stability (which incorporates stochastic features) is fundamental, it can be tightly coupled to experimental measures, and it better serves the understanding of speech and other forms of motor control than the rather vague use of the term ‚invariance.’ The latter term we reserve for describing sy mmetry under a group of transformations. 3.2. Theoretical Considerations The dy namical approach to speech production originated from the study of bimanual movement coordination and is based upon theories of self organization and pattern formation in nonequilibrium sy stems, particularly Haken’s (1975; 1983) sy nergetics (see for example Kelso/DelColle/Schöner 1990). The aim is to understand coordinated movement as a pattern formation process. In sy nergetics, when a certain parameter or combination of parameters (referred to as ‚controls’) reach a critical point, structure or change in structure occurs spontaneously . At so-called nonequilibrium phase transitions, the emerging patterns may be characterized by collective variables whose dy namics (equations of motion) are low-dimensional. Sy nergetics thus promotes a search for these collective variables (also called order parameters) in experimental model sy stems and the determination of control parameters that move the sy stem through collective states. The dy namics of collective variables may be determined by study ing the stability and loss of stability of movement patterns. Specific empirical phenomena are predicted to occur jointly at transition points. One is the presence of enhanced fluctuations, in which the values of the collective variable undergo large fluctuations with no change in the mean state (cf. earlier remarks on invariance in Section 3.). Another predicted phenomenon is critical slowing down, whereby a sy stem close to a transition point reacts more and more slowly to external perturbations than in other
419
situations when it is far from criticality . Both features are characteristic of self-organization and both have been observed experimentally in movement sy stems (for recent reviews see Kelso/Schöner/Scholz/Haken 1987; Kelso/ Schöner 1988; Schöner/Kelso 1988). What are the collective variables and control parameters in the speech production sy stem? There are many possible modifiers of articulation that might lead the sy stem through different coordinative patterns and hence reveal the underly ing coordination dy namics. These control parameters include, but are not limited to, stress, loudness, speaking rate and speaking sty le. If the nonspecific influence of a continuously vary ing control parameter results in a change of pattern, then one should be able to identify collective variables that correspond to the observed patterns and determine their dy namics through an analysis of stability. The identification of relevant collective variables for a given behavior is not trivial and will be addressed further in Section 3.3. Assume, for the moment, that a set of collective variables has been found that characterizes the articulatory pattern for a given phonetic string and that can be expressed by a low-dimensional vector x. Underly ing the dy namic view is the assumption that = (t), where t is time, obey s a dy namical law on a macroscopic scale: (1) ẋt= f(xt, parameters, noise) where f is, in general, a nonlinear function of the ty pically high-dimensional state vector xt. This function may also depend on a number of parameters representing, for example, the speaking sty le or rate, as well as random noise that reflects the many degrees of freedom acting on the sy stem but which are unaccounted for in the state vector xt. For a large class of functions f, special solutions of the equation (called ‚attractors’) exist. By definition, an attractor is (asy mptotically ) stable, that is, all neighboring solutions converge in time to the attractor solution. In the present formulation, phonological units may well correspond to stable collective states, or attractors, of the order parameter dy namics (cf. Schöner/Kelso 1988). In Section 2.1., we described a simple dynamical sy stem, a mass-spring sy stem, that has been used to model speech production. A mass-spring sy stem is a form of point attractor, the simplest attractor ty pe. Recent work has explored sy stems that support richer dy -
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namics, such as periodic attractors, as more appropriate for modelling speech production. Many more complicated attractor ty pes exist, giving rise to very complex behavior of the solutions of Eq.1. In general, low-dimensional nonlinear dy namical sy stems can exhibit extremely rich behavior, including multistability , switching, bifurcations, intermittency , and even deterministic chaos. Many of these features have been observed in human movement coordination (see for review Kelso/DeGuzman/Holroy d 1991) and to a more limited extent in speech production and perception. 3.3. Empirical Evidence A dy namical account of multiarticulator coordination that includes complicated attractor ty pes holds promise for understanding the flexibility or change of articulatory patterns, thus allowing phonetically rich sequences. In many theories of speech, and of motor control in general, there is a tendency to account for the appearance of new patterns as resulting from the selection of a new motor program, or motor engram. An alternative strategy recognizes that in multidegree of freedom sy stems in which component interactions occur, new patterns of organization and behavior appear that are not easily predictable from the preceding ones. This ‚sy mmetry breaking’ occurs in phy sical sy stems, as well as biological and psy chological ones and the new spatiotemporal patterns are sometimes referred to as ‚emergent properties’. There is already a hint in the literature that certain kinds of phonetic and sy llabic change correspond directl y to phase transitions among articulatory gestures (see Kelso/Saltzman/Tuller 1986) and hence may enable us to specify relevant collective variables. Consider an example provided by Stetson (1951; also Kelso/Munhall 1988), who observed that gradual increases in rate of producing a repetitive sy llable string (such as at, at, at ...) causes a change in the phasing of component gestures and hence of the sy llable affiliation of the consonant (ta, ta, ta ... is produced). Stetson thought that the need to simplify coordination caused the sy llable-final consonant to become sy llable-initial because the final consonant was “off-phase, out of step with the sy llable movement (p. 96).” One interpretation of Stetson’s data is that phasing among component gestures is the collective variable, or order parameter, underly ing both
stability and change in sy llabic structure and that consonant-initial sy llables are more stable than vowel-initial sy llables, particularly at fast rates. The relative stability of consonant-initial and vowel-initial sy llables has been explicitly investigated in recent work by Tuller/Kelso (1990). The work exploits the abrupt change in interarticulator phasing observed by Stetson (1951) as a special entry point for understanding both the stability and change of articulatory patterns. The phenomena Stetson observed allow the necessary and nontrivial step of identify ing the collective variables that characterize a given articulatory pattern (an enterprise closely affiliated with the ecological approach to perception and action, advocated by Gibson (1966; 1979) and his school, for example, Turvey /Shaw/Mace 1979). In addition, the dy namics of the collective variables can be determined through an analy sis of stability . This involves a step bey ond the phenomena, namely , a mapping onto a dy namical model which in turn generates predictions. In the Tuller/Kelso (1990) study , subjects said /ip/ or /pi/ repetitively , at increasing speaking rates, while their acoustic speech signal and glottal and lip movements were recorded. For repetitive sequences of /pi/ across the range of speaking rates, the subject’s peak glottal opening maintained a stable phase lag relative to minimum lip aperture. For repetitive sequences of /ip/, interarticulator relative phasing often changed markedly as speaking rate increased. At slow rates, peak glottal opening occurred temporally close to minimum lip aperture; at some critical value of rate an abrupt shift in relative phase value occurred to that observed for /pi/. In followup perceptual experiments, listeners perceived the consonant’s sy llable affiliation to change abruptly from sy llable-final to sy llable-initial on precisely the same sy llable as the observed shift in interarticulator relative phase (Tuller/ Kelso 1990; 1991). The greater relative stability observed for consonant-initial sy llables, as compared with vowel-initial sy llables, is consistent with the linguistic descriptions of distributional frequency of sy llable ty pes (e. g., Jakobson 1966). The finding also suggests that at slower speaking rates several attractors with different basins of attraction coexist (a feature called multistability ). As speaking rate increases, the change in available articulatory patterns arises solely as a result of the dy namics of the sy stem (the patterns are self-organ-
37. Dynamical Systems and Speech
ized). The finding also points to the importance of relative phase as a key collective variable for characterizing the articulatory pattern as a low-dimensional vector (see also Lisker/Abramson 1964; Löfqvist/Yoshioka 1981). 3.4. Modelling Approaches Empirical analy ses of speech production are complemented by modelling of the communicative process. For example, Lindblom/ MacNeilage/Studdert-Kenned y (1983) explored whether phonological structure could be understood as an emergent property that arises from the interaction of subsy stems. First, they defined a universal signal space with seven possible stop closures as beginnings, and nineteen possible vowel-like endpoints (133 resulting ‚sy llable’ patterns). Thus the trajectories assumed as primitives were consistent with a consonant-initial sy llable. Next, they postulated two talker-based constraints and two listener-based constraints on combinations of start- and endpoints that maximized perceptual effect and minimized articulatory cost. A computer program selected the twenty -four sy llable subset that best satisfied the four constraints. Remarkably , the program quickly converged on a common set of sy llables regardless of which item was used as the initial seed for the calculation. Moreover, the set contained many instances of ‚minimal pairs’, whose members differed only in initial closure position, or vowel end position, but not both. Note that neither the number of start and end combinations nor the constraints themselves in any way required the resulting segmental structuration. These striking results suggest that structuration of phonological universals such as segments and features may be an emergent property arising from the constrained interaction of system elements. Various other modelling studies of speech production have successfully used a dy namical sy stems approach. Of particular interest is Jordan’s (1986) connectionist model of speech patterning over time. At the lowest level of the model are output units that represent values of abstract phonetic features, such as voicing, nasality , and lip rounding. Unlike distinctive feature theory , the model allows values of the output units to vary continuously . At the highest level of the network are state units whose actions are defined by an equation of motion. In essence, the equation of motion defines an intrinsic tem-
421
poral evolution for sequential speech motions in much the same way that the equation of motion defines the displacement-velocity relationship in a mass-spring sy stem. The state units and output units are connected, using a nonlinear mapping, by a lay er of hidden units. A second set of inputs to the hidden units is provided by plan units, which increase sy stem flexibility by allowing the network to ‚learn’ a single set of weights for production of several different speech sequences. The ‚learning’ procedure uses the ‚back propagation’ method, or ‚generalized delta rule’ of Rumelhart/Hinton/Williams (1986) in which error signals generated at the output units are projected back into the network, allowing the hidden units to change their weights in a manner proportional to the sum of the errors received. An engineer might refer to this as a sophisticated technique for sy stem’s identification. Jordan trained the network to produce sequences of phonemes, where each phoneme is defined as a bundle of context-independent target values for the features. After training, the network produced continuous trajectories for the feature values (not articulatory movement patterns). The feature trajectories showed context-dependent anticipatory and carry over coarticulation effects whose temporal extent fit remarkably well with empirical studies of acoustic and kinematic effects of coarticulation. Jordan’s simulation sheds light on a longstanding debate in the speech production literature on whether timing control in speech is intrinsic (e. g., Fowler 1977; 1980) or extrinsic (e. g., Kozhevnikov/Chistovich 1965; Lindblom 1983). Note that the temporal ordering among the output units of the model is not explicitly represented any where in the network; there is no extrinsic timing device. Rather, the temporal structure is an implicit consequence of the input-output relationship of the sy stem elements, the pattern of connections among the elements, and the strengths of each connection. In this sense, the patterning over time of the output units (and thus the temporal extent of coarticulatory effects) is an emergent property of the intrinsic network dy namics (as proposed by Kelso/Tuller 1987). Jordan’s model relies on a list of abstract phonetic features as dimensions for the output units and thus is some distance removed from articulatory movement patterns. An approach to the modelling of speech patterns
III. Acquired Organic Pathologies of Language Behavior:Neurophonetic Disorders
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that is tied explicitly to articulatory gestures was proposed by Saltzman (1986) and Saltzman/Kelso (1987; see also Kelso/Saltzman/ Tuller 1986). In their ‚task-dy namic’ model of speech production, articulator y patterns emerge from a dy namical sy stem with functionally distinct but interacting levels. At one level, active gestural units organize the articulators temporarily and flexibly into functional groupings (coordinative structures) that accomplish particular gestural goals (such as the formation and release of constrictions). The influence of the gestural units on articulator trajectories waxes and wanes over time, thus introducing variability across segmental contexts and suprasegmental changes. The model’s strength lies in capturing the essential features of interarticulatory coordination patterns observed during unperturbed and experimentally perturbed speech. A persistent shortcoming of the model has been its reliance on an explicit proscription of the activation intervals for gestural units. Recently , Saltzman/Munhall (1989) have proposed incorporating Jordan’s serial network into the task-dy namic modelling. This provides the possibility for a dy namic model of speech production that is more closely tied to the articulatory gestures and allows sequential timing to evolve from the network structure and dy namics without an explicit temporal score.
4.
Conclusions
Dy namical sy stems theory offers a powerful and theoretically unified account of articulatory patterns generated during speech. Empirical observations and computer simulations have converged on dy namical accounts of the temporal unfolding of articulatory patterns and their relative stability despite changing segmental context, speaking rate, speaking sty le, or stress. Dy namical approaches to modelling speech have also reproduced the experimentally -observed stability of the articulatory sy stem in adjusting to unanticipated, externally -applied perturbations and its flexibility in switching from one configuration to another. The concepts and tools of dy namical sy stems theory is likely to be of value for understanding speech disorders. In a model of stuttering that dovetails nicely with the dy namical approach, Nudelman/Herbrich/ Hoy t/Rosenfield (1989) propose that when
the phase lag increases between speech motor control sy stems with different characteristic time scales, the total sy stem becomes unstable and speech dy sfluencies result (see also Zimmerman/Brown/Kelso et al. 1988 for a related idea). Two aspects of their model particularly suggest the utility of dy namical sy stems theory for an understanding of stuttering. First, the relative phasing of the hy pothesized speech motor control sy stems may vary continuously without producing dy sfluencies. Instabilities (and hence dy sfluencies) only occur when the control sy stems reach a critical value of relative phase. Second, the standard deviation of relative phase, not the mean value, is the best predictor of stuttering frequency . Stability is thus implicated as a more meaningful concept than invariance in understanding stuttering behavior (see Section 3). Our interpretation of these data is that the appearance of a dy sfluency is indicative of a phase transition from a more to a less ordered state. In contrast, the shift from vowel-initial to consonant-initial sy llables produced by fluent speakers as speaking rate increases is a transition between two ordered states. Demonstrations of nonlinear phase transitions are much more numerous in perception and production of nonspeech behaviors. Nevertheless, these initial foray s into speech production and phonological structure have proven insightful and offer new way s to attack old problems.
5.
References
Abbs, J. H., Gracco,V. L., & Cole, K. J. (1984). Control of multimovement coordination: Sensorimotor mechanisms in speech motor programming. Journal of Motor Behavior, 16, 195—232. Bernstein, N. S. (1967). The Coordination and Regulation of Movements. Oxford: Pergammon. Boy lls, C. C. (1975). A theory of cerebellar function with applications to locomotion. II. The relation of anterior lobe climbing fiber function to locomotor behavior in the cat. COINS Technical Report, 76—1. Department of Computer and Information Science, University of Massachusetts. Butcher, A. & Weiher, E. (1976). An electropalatographic investigation of coarticulation in VCV sequences. Journal of Phonetics, 4, 59—74. Daniloff, R. & Hammarberg, R. (1973). On defining coarticulation. Jo u rnal of Phonetics, 1, 239—248. Easton, T. A. (1972). On the normal use of reflexes. American Scientist, 60, 591—599.
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Fowler, C. A. (1977). Timing Control in Speech Produ ction. Bloomington, IN: Indiana University Linguistics Club. Fowler, C. A. (1980). Coarticulation and theories of extrinsic timing control. Jou rnal of Phonetics, 8, 113—133. Fowler, C. A., Rubin, P., Remez, R. E., & Turvey , M. T. (1980). Implications for speech production of a general theory of action. In B. Butterworth (Ed.), Langu age Produ ction. 373—420. New York: Academic. Gay , T., Ushijima, T., Hirose, H., & Cooper, T. S. (1974). Effect of speaking rate on labial consonantvowel articulation. Journal of Phonetics, 2, 46—63. Gel’fand, I. M., Gurfinkel, V. S., Fomin, S. V., & Tsetlin, M. L. (1971). Models of the stru ctu ral-fu nctional organization of certain biological systems. Cambridge, MA: MIT Press. Gentil, M., Harris, K. S., Horiguchi, S., & Honda, K. (1984). Temporal organization of muscle activity in simple disy llables. Jou rnal of the Acou stical Society of America, 75, S23. Gibson, J. J. (1966). The Senses Considered as Perceptual Systems. Boston: Houghton-Mifflin. Gibson, J. J. (1979). The Ecological Approach to Visual Perception. Boston: Houghton-Mifflin. Haken, H. (1975). Cooperative phenomena in sy stems far from thermal equilibrium and in nonphy sical sy stems. Review of Modern Physics, 47, 67—121. Haken, H. (1983). Synergetics, An Introdu ction: Non-equ ilibriu m Phase Transitionsand Self-organization in Physics, Chemistry, and Biology. Berlin: Springer. Jakobson, R. (1966). Implications of language universals for linguistics. In J. H. Greenberg (Ed.), Universals of Langu age 263—278. Cambridge, MA: MIT Press. Jordan, M. I. (1986). Serial order in behavior: A parallel distributed processing approach. Technical Report 8604, University of California, Institute for Cognitive Science, Dan Diego. Kelso, J. A. S., DeGuzman, G. C., & Holroy d, T. (in press). Sy nergetic dy namics of biological coordination with special reference to phase attraction and intermittency . In H. Haken & H. P. Koepchen (Eds.), Synergetics of Rhythms. Berlin: Springer. Kelso, J. A. S., DelColle, J. D., & Schöner, G. S. (1990). Action-perception as a pattern formation process. In M. Jeannerod (Ed.), Attention and Performance XIII. 139—169. Hillsdale, NJ: Erlbaum. Kelso, J. A. S. & Munhall, K. G. (1988). R. H. Stetson’s Motor Phonetics: A Retrospective Edition. San Diego: College Hill. Kelso, J. A. S., Saltzman, E. L., & Tuller, B. (1986). The dy namical perspective on speech production:
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Lindblom, B., Lubker, J., & Gay , T. (1979). Formant frequencies of some fixed-mandible vowels and a model of speech motor programming by predictive simulation. Jou rnal of Phonetics, 7, 147—161. Lindblom, B., MacNeilage, P., & Studdert-Kennedy , M. (1983). Self-organizing processes and the explanation of phonological universals. In B. Butterworth, B. Comrie, & O. Dahl (Eds.), Explanations of Lingu istic Universals. 181—203. The Hague: Mouton. Lindblom, B. & Sundberg, J. (1971). Acoustical consequences of lip, tongue, jaw and lary nx movement. Jou rnal of the Acou stical Society of America, 50, 1166—1179. Linville, R. (1982). Temporal aspects of articu lation: Some implications for speech motor control of stereotyped produ ctions. Unpublished Doctoral Dissertation. University of Iowa, Iowa City, Iowa. Lisker, L. & Abramson, A. (1964). A cross-language study of voicing in initial stops: Acoustical measurements. Word, 20, 384—422. Löfqvist, A. (1986). Stability and change. Journal of Phonetics, 14, 139—144. Löfqvist, A. & Yoshioka, H. (1981). Interarticulator programming in obstruent production. Phonetica, 38, 31—34. Lubker, J. (1983). Comment on ‚Temporal invariance in the production of speech’ by Harris, Tuller and Kelso. Paper presented at Conference on invariance and variability in speech processes. M.I.T. Cambridge, MA, U.S.A., October 1983 MacNeilage, P. F. & DeClerk, J. (1969). On the motor control of coarticulation in CVC monosy llables. Jou rnal of the Acou stical Society of America, 45, 1217—1233. Munhall, K. G. (1985). An examination of intraarticulator relative timing. Jou rnal of the Acou stical Society of America, 78, 1548—1553. Nittrouer, S., Munhall, K., Kelso, J. A. S., Tuller, B., & Harris, K. S. (1988). Patterns of interarticulator phasing and their relation to linguistic structure. Jou rnal of the Acou stical Society of America, 84, 1653—1661. Nudelman, H. B., Herbrich, K. E., Hoy t, B. D., & Rosenfield, D. B. (1989). A neuroscience model of stuttering. Jo u rnal of Fl u ency Disorders, 14, 399—427. Ostry , D. J. & Munhall, K. (1985). Control of rate and duration in speech. Jou rnal of the Acou stical Society of America, 77, 640—648. Riordan, C. J. (1977). Control of vocal tract length in speech. Jou rnal of the Acou stical Society of America, 62, 998—1002. Rumelhart, D. E., Hinton, G. E., & Williams, R. J. (1986). Learning internal representations by error propagation. In D. E. Rumelhart & J. L. Mc-
Clelland (Eds.), Parallel Distribu ted Processing: Explorations in the microstru ctu re of cognition, Vol. 1. Fou ndations 318—362. Cambridge, MA: MIT Press. Saltzman, E. L. (1986). Task dy namic coordination of the speech articulators: A preliminary model. Experimental Brain Research, Ser. 15, 129—144. Saltzman, E. L. & Kelso, J. A. S. (1987). Skilled actions: A task-dy namic approach. Psychological Review, 94, 84—106. Saltzman, E. L. & Munhall, K. G. (1989). A dy namical approach to gestural patterning in speech production. Ecological Psychology, 1, 333—382. Schmidt, R. C. (1982) Motor Control and Learning. Illinois: Human Kinetics. Schöner, G. S. & Kelso, J. A. S. (1988). Dy namic pattern generation in behavior and neural sy stems. Science, 239, 1513—1520. Shaiman, S. (1989). Kinematic and electromy ographic responses to perturbation of the jaw. Journal of the Acoustical Society of America, 86, 78—88. Sternberg, S., Knoll, R. L., & Turock, D. L. (1990). Hierarchical control in the execution of action sequences: Tests of two invariance properties. In M. Jeannerod (Ed.), Attention and Performance XIII. 1—56. Hillsdale, NJ: Erlbaum. Stetson, R. H. (1951). Motor Phonetics: A Stu dy of Speech Movements in Action. Amsterdam: NorthHolland. Tuller, B. & Kelso, J. A. S. (1984). The timing of articulatory gestures: Evidence for relational invariants. Jou rnal of the Acou stical Society of America, 76, 1030—1036. Tuller, B. & Kelso, J. A. S. (1990). Phase transitions in speech production and their perceptual consequences. In M. Jeannerod (Ed.), Attention and Performance XIII. 429—452. Hillsdale, NJ: Erlbaum. Tuller, B. & Kelso, J. A. S. (1991). The production and perception of sy llable structure. Jou rnal of Speech and Hearing Research, 34, 501—508. Tuller, B., Kelso, J. A. S., & Harris, K. S. (1982). Interarticulator phasing as an index of temporal regularity in speech. Jou rnal of Experimental Psychology: Hu man Perception and Performance, 8, 460—472. Tuller, B., Kelso, J. A. S., & Harris, K. S. (1983). Converging evidence for the role of relative timing in speech. Jou rnal of Experimental Psychology: Hu man Perception and Performance, 9, 829—833. Turvey , M. T. (1977). Preliminaries to a theory of action with reference to vision. In R. Shaw & J. Bransford (Eds.), Perceiving, Acting, and Knowing: Toward an Ecological Psychology. 211—266. Hillsdale, NJ: Erlbaum. Turvey , M. T., Shaw, R. E., & Mace, W. (1979). Issues in a theory of action: Degrees of freedom, coordinative structures and coalitions. In J. Requin
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(Ed.). Attention and Performance VII. Hillsdale, NJ: Erlbaum. Vatikiotis-Bateson, E. (1988). Lingu istic stru ctu re and articu latory dynamics: A cross-langu age stu dy. Unpublished Doctoral Dissertation, Indiana University, Indiana. von Bertalanffy , L. (1973) General System Theory. London: Penguin. Zimmerman, G., Brown, C., Kelso, J. A. S., Hurtig,
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R., & Forrest, K. (1988). The association between acoustic and articulatory events in a delay ed auditory feedback paradigm. Jou rnal of Phonetics, 16, 437—451. [Work supported yb NIDCD grant R29 DC00411, NIMH grant R01-MH-42900, and BRS grant S07-RR07258.]
Betty Tuller/J. A. Scott Kelso, Boca Raton, Florida (USA)
38. Pathophysiology of Disordered Articulation 1. 2. 3. 4. 5.
1.
Viewpoint Basic Speech Motor Actions Classification of Motor Speech Disorders Considerations for Classification of Motor Speech Disorders References
Viewpoint
The present chapter provides an overview of neurologic speech disorders and some perspectives on how these problems can be evaluated, studied, and understood. In the last two decades, these disorders increasingly have been viewed as fundamental neurobiological impairments. Efforts in this direction, starting just about the time of the publication of the seminal work yb Darle y /Aronson/Brown (1969 a; b), reflect the perspective that while speech and language have behavioral, social, linguistic and ecological consequences, they are fundamentally biological actions. This emphasis was most strongly articulated by individuals with clinical or medical interests in disorders of speech. It has been suggested that if one is to diagnose, understand, and treat disorders of speech and take advantage of modern medical advances, it is necessary to consider explicitly the underly ing nervous sy stem functions and dy sfunctions. — A medical approach to neurologically based speech disorders draws upon the principle that effective diagnosis and treatment are related to (1) the knowledge of underly ing pathophy siology and (2) the extent to which reliable assessment procedures are devised to exploit that knowledge. In this respect, speech motor difficulties present special clinical problems because of the complexity of speech generation. If used in isolation, the classical means of assessment,
largely consisting of listening to and classify ing a patient’s speech errors, are particularly limiting when it comes to identify ing pathophy siology . — Basically , many observable speech events are not simple reflections of underly ing neurobiological processes; surface analy sis procedures (i. e., intelligibility measures, severity ratings, etc.) offer few perspectives regarding etiology or directions for possible treatment. For example, an observed speech error (say ‚distortion’) in a disordered speaker could be due to a multitude of factors including (1) anatomical properties of the vocal conduit (orofacial anomalies, tongue grooving or muscle tissue loss in motor neuron disease), (2) unsteady or weak muscle contraction (due to loss of motoneurons, neocortical py ramidal cells, cerebellar inputs), (3) disruption of reflex or long latency corrective adjustments (at medullar, pontine motor nuclei or neocortical somatic sensory -to-py ramidal cells), (4) aberrant prediction of upcoming movements by nervous sy stem motor programming centers (cerebellum, basal ganglia, premotor or supplementary motor cortices), (5) inappropriate transmission of learned speech motor objectives (from cerebellar or parietal cortical centers), (6) unsuccessful corrections for speech element selection errors (posterior parietal or lateral precentral cortex — Brodmann’s Area 44), (7) improper selection of proper linguistic features (posterior parietal), (8) faulty neural communication among these or several other levels of the speech motor control process, or (9) dozens of other, but y et different, motor control and coordination functions. — Extending this argument, consider the common problem in dy sarthric subjects of unsteady or weak muscle contractions. Patients with amy otrophic
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lateral sclerosis, multiple sclerosis, cerebellar disease, upper motoneuron damage, and even Parkinson’s disease display these problems; obviously while their underly ing nervous sy stem damage is quite different, the slowed and somewhat odd-sounding speech, due possibly to weakness and unsteadiness, is almost a universal and ubiquitous feature. — Obviously the mere presence or absence of a given speech sign, or its influence upon speech understanding, does not y ield much clinical information. It is this realization that has provided motivation for a stronger focus upon the biological bases of motor speech disorders, and in turn upon the manner in which normal speech movements are generated.
2.
Basic Speech Motor Actions
Speech motor functions are perhaps less well understood or appreciated than similar motor behaviors of like complexity , due in part to the fact that the multiple movements are not entirely visible, as in locomotion, for example. Fortunately , speech movements do not appear to be controlled differently than most other movements; there appears to be a fair amount of similarity in the basic neural control of speech motor actions and other related behaviors (i. e., locomotion, handwriting, ty ping, dance). As a first step in appreciating these neural control processes, it is illuminating to outline what it is that the nervous sy stem is controlling. At the same time, considering these motor output requirements sets the proper stage for appreciating many disorders of speech described in other chapters in this volume. — Often, in introductory texts on speech three ‚components of the speech production apparatus’ are identified, the socalled respiratory , phonatory , and articulatory (upper airway ) sy stems. While this is a step in the correct direction, the implied separation cannot be justified functionally . Interactions among respiratory , lary ngeal, and upper airway neural control processes are well-described and of major importance. Related to this concern, it is useful to consider a more basic description. For generation of even a single vowel or consonant, approximately 70 muscles are involved. These muscles actively control (1) the respiratory movements of the rib cage, diaphragm, and abdomen, (2) lary ngeal movements of the thy roid, cricoid, and ary tenoid cartilages, and (3) the upper airway actions of the phary nx, tongue, soft palate, lips, and jaw. Many of
these muscles contribute to both respiratory and lary ngeal actions (extrinsic lary ngeal muscles, adductors and abductors of the glottal opening) and likewise to lary ngeal and upper airway gestures (my lohy oid, phary ngeal constrictors, anterior belly of diagastric). The interdependent neural control of these different muscle groups also is reflected in their ubiquitous brain stem interconnections. — These muscles contribute in generating movements with several functional consequences, including air volume/pressure manipulation, sound generation, and vocal tract resonances. Specifically , movements of the tongue not only act to change the shape of the upper air way for vowel-related resonances, but also reduce or enlarge the air volume for stop consonants and occlude air flow as part of sound generation for fricatives and for stop consonant release. — A major component of speech motor control involves the orchestration of all these muscles and movements as well as parceling their different contributions to the final acoustic output. Furthermore, because actions for a given element must follow and precede actions for adjacent elements, there is a major sequencing component as well. All of these considerations raise issues as to what might be the most fragile elements of this process, or conversely what aspects of control are most likely to be lost or impaired with damage to the nervous sy stem. In a word, because multiple motor actions are involved both in parallel and sequentially , it is apparent that the most critical problem faced by the nervous sy stem in the generation of speech is c o o r d i n a t i o n. The brain must keep track of all of the parts, their status, intended changes to meet upcoming objectives, the degree to which those objectives are met, or are going to need correction, etc. All of these factors are i n t e r d e p e n d e n t. These considerations lead to the next component of this chapter, namely what kind of neuromotor control processes are involved in this rather remarkable effort. — In understanding speech motor disabilities associated with brain damage, it becomes important to have an understanding of how the parallel and sequential actions described above are generated. In this respect, a long standing issue in the brain’s control of the complex movements for speech involves the degree to which the events described above are (1) each specified in advance and then play ed out subsequently , or rather (2) generated on-line and afresh each time production of a given speech
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event is repeated. If the muscle contraction patterns for each speech event are stored and then simply regurgitated each time that event is called for, outputs would be stereoty pic and there would be no need for sensory input. However, as described in chapter 45, Feedback Impairments in Dy sarthria, in recent y ears, studies from several different laboratories have shown that both the coordination among the multiple movements for speech and their sequencing are dependent, to a considerable degree, on sensory influences. For example, the coordination among the upper lip, lower lip, and jaw in control of oral opening and closing is flexibly manipulated via sensory monitoring of the positions of each of these articulators and moment-to-moment motor adjustments. — Critical to this issue is the importance of multi-movement coordination in speech. Most important features of speech (oral occlusions, vocal tract resonances, respiratory or upper airway volumes) are not generated by a single movement. Rather, combinations of jaw, lip, and tongue movements produce oral occlusions/constrictions, while rib cage, abdominal, and diaphragm movements combine to control respiratory volumes and hence air pressures. Regarding speech motor functions and dy sfunctions, these observations indicate that the primary controlled outputs for speech production are not individual upper airway , lary ngeal, or respiratory movements, but rather overall vocal tract or respiratory configurations. — While several studies support sensory -based coordination, it is apparent from simple consideration of speech. The orofacial sy stem obviously serves multiple functions of chewing, swallowing, and breathing, superimposed upon and in parallel with speech. Less natural intrusions include a cigarette between the lips, a pipe between the teeth, etc. Because most or all of these activities can be performed simultaneously , without major interference or conscious adaptation, a nervous ys stem capability for on-line adjustment among the multiple movements and muscle contracitons is most appealing. — The recent acknowledgement that individual muscle contractions and movements are adjusted via sensory input also is consistent with research on the primate nervous sy stem indicating that all major brain centers classically associated with motor functions are likewise centers of sensorimotor integration. This is discussed further in chapter 45, Feedback Impairments in Dy sarthria. In this respect, it is likely that
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many dy sarthric sy mptoms and signs may well be as critically dependent upon problems of sensorimotor integration as they are upon problems of pure motor function.
3.
Classification of the Motor Speech Disorders
Historically , the term dy sarthria (or anarthria in its complete form) has referred solely to disturbed articulation, subsequent to neurologic impairment. Grewel (1957) is credited, however with the concept that dy sarthria — or more precisely , the dy sarthrias — are more complex than articulatory dy sfunction and may , in fact, have localizing value. Canter (1967) first attempted to differentiate and classify the dy sarthrias based on site of lesion using the terms peripheral dy sarthria for those secondary to primary muscle, my oneural junction cell body and/or axon involvement and central dy sarthria representing bilateral upper motor neuron, extrapy ramidal and cerebellar sy stem disease. He recognized also that dy sarthria represented “a disturbance in the execution of motor patterns for speech due to paraly sis, weakness or discoordination of the speech musculature” (Canter 1967, 660), and thus potentially involves not only articulation but the other subsy stems of speech as well. These include phonation, respiration, resonation and speech prosody (e. g., rhy thm, intonation, inflection, stress, etc.). Although Canter’s work is noteworthy , his report was basically tutorial and descriptive in nature and thus suffered from an absence of data driven, quantified support. This matter was rectified, in part, by Darley /Aronson/ Brown (1969 a; b) in their now classic studies concerning the perceptual characteristics of dy sarthria, although the conceptual framework has been challenged. In their definition, dy sarthria represents a group of speech disorders which was characterized by disturbances in speech muscular control due to paraly sis, paresis, weakness, slowness, incoordination and/or altered tone that may encompass one or more of the basic motor speech subs y stems mentioned previousl y . Subsequent research has stressed not only the perceptual/acoustic characteristics of the dy sarthrias, but co-occurring neurophy siologic bases for the disorders as well. — Like Canter, Darley /Aronson/Brown recognized six dy sarthria subty pes, four of which were associated with central lesions, one which implied lower
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motor neuron involvement and one which represented both central and peripheral impairment. Recently , Hartmann/Abbs (1989) quantified and described a seventh ty pe of dy sarthria felt to have localizing value. — Although each of the dy sarthrias appear to have distinct perceptual/acoustic and neurophy siologic characteristics, the neuropathologic substrate underly ing each of the dy sarthrias is not as clear. The clinician, therefore, relies on c a r d i n a l motor speech sy mptoms and signs frequently in conjunction with other neurologic findings to achieve diagnoses. — Apraxia of speech has been described as a motor speech planning disorder. Whether it is a speech or language disorder or a combination thereof has been a point of controversy . This topic is dealt with elsewhere. — Table 38.1 presents site of lesion, ty pical conditions, primary neurologic manifestations, and dy sarthric sequelae. The table is not intended to be all inclusive. Also, many of the conditions listed may present with more than one ty pe of dy sarthria. For example, while multiple sclerosis classically presents with sy mptoms and signs associated with cerebellar impairment, as the disease progresses cortical white matter involvement y ields a mixed ataxic/spastic dy sarthria. A brief commentary on each motor speech disorder is provided, as means of orientation. 3.1. Unilateral Upper motor neuron Dysarthria Focal lesion of one corticobulbar tract produces different motor speech signs than noted for bilateral involvement. The one prospective study to date reported that diminished loudness, lack of pitch flexibility (monopitch), consonant imprecision, short phrases and decreased speaking rate e n t o t a l were unique for this particular dy sarthria. Consonant imprecision may be an outstanding feature due, primarily , to involvement of contralateral facial and lingual musculature. However, unlike the spastic dy sarthria, related pathologic reflexes are uncommon suggesting that bilateral py ramidal tract damage is necessary for disinhibition to occur on a central level. 3.2. Spastic Dysarthria Bilateral damage to the corticobulbar tracts innervating the cranial motor nuclei V, VII, IX—XII at the cortical, subcortical or brain stem level produces a disinhibitory phenomenon along with weakness, hy pertonicity and paresis of those muscles involved. Both laugh-
ing and cry ing as well as pathologic sucking, jaw-jerk, biting, palmomental and phary ngeal reflexes are evident. Speech is labored and slow, while voice quality is characterized by vocal straining and a quality not dissimilar from that heard in volitional cry ing. The respiratory support for speech is comparably diminished. Similarly , involvement of the velophary ngeal musculature may result in either continuous or intermittent abnormal resonance consisting of hy pernasality with nasal air escape. The strain-strangle or wail-like quality , particularly in severe forms of the disorder is pathognomonic. 3.3. Apraxia of Speech Apraxia of speech has been described as a motor planning (programming) disorder characterized yb relativel y unpredictable sound omission, substitution, and/or addition errors. These errors are influenced by articulatory complexity and include sound repetitions and prolongations, articulatory groping as the speaker seeks the accurate (intended) target and prosodic alterations including variable or slowed rate and stuttering (dy sfluency ). Co-occurring oral apraxia is not uncommon. The signs are not adequately explained on the basis of weakness, altered tone, or language impairment. Discoordinated movements are said to bear a resemblance to ataxic dysarthria as seen in cerebellar disease. 3.4. Ataxic Dysarthria The dy srhy thmic characteristics of cerebellar involvement are manifested in a dy sarthria by variable articulatory imprecision with frequent omission and/or distortion of sounds, particularly at word, phrase or sentence endings; irregular prosodic pattern characterized by variations in stress without respect to context; and frequently a harsh voice quality . The intoxicated character of ataxic dy sarthric speech is notable and conceivably represents generalized discoordination of motor speech control. 3.5. Hypokinetic Dysarthria Selectice unilateral or bilateral lesions of the substantia nigra or its projections result in a diminution of movement frequently accompanied by a resting tremor. Dy sarthric manifestations include limitations in pitch variability , decreased loudness, imprecise articulation, inappropriate silences or pausing within an utterance and short rushes of what
38. Pathophysiology of Disordered Articulation
Site of Lesion Unilateral Upper Motoneuron (UUMN) Bilateral Upper Motoneuron Broca’s Area Cerebellum Basal Ganglia
Lower Motoneuron
Typical Conditions Cerebrovascular Disease Cerebrovascular Disease Cerebrovascular Disease Friedreich’s Ataxia, Olivopontocerebellar Syndrome, Multiple Sclerosis Parkinsonism, Dystonia, Dyskinesias, Athetosis, Huntington’s Disease, Tourette’s Syndrome Amyotrophic Lateral Sclerosis, Myotonic & Muscular Dystrophy, Myasthenia Gravis, Möbius Syndrome
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Cardinal Neural Signs Contralateral Weakness, Spasticity Spasticity, Brisk Reflexes Weakness, Disinhibition None, if a focal lesion* Discoordination, Intention Tremor, Hypotonia, Dysmetria Rigidity, Bradykinesia, Tremor, Abnormal Posturing, Tics, Adventitious Movement, Writhing Muscle Atrophy, Weakness, Absent/Reduced Reflexes, Abnormal EMG
Speech Disorder UUMN Dysarthria Spastic Dysarthria Apraxia of Speech Ataxic Dysarthria Hypo- or Hyperkinetic Dysarthria Flaccid Dysarthria
* Typically presents with concurrent contralateral facial-limb weakness implying pyramidal tract involvement as well of spastic (spasmodic) dy sphonia may Table 38.1: Disorders or articulation
might be perceived as rapid speech. The term hy pokinetic dy sarthria is broadly sy nony mous with parkinsonism of which paucity of movement is pathognomonic. Parkinsonian features including yh pokinetic yd sarthria, however, are frequently co-occurring manifestations of multisy stem disease including multiple sy stems atrophy with dy sautonomia (Shy -Drager sy ndrome) and progressive supranuclear pals y (Steele-Richardson-Olszewski syndrome) (see Hartman/Abbs 1988). 3.6. Hyperkinetic Dysarthria Whereas hy pokinetic dy sarthria is characterized by limitation of movement, hy perkinetic dy sarthria, which can be described in terms of slow, quick or tremor forms, is characterized by a preponderance or an exacerbation of movement that may or may not be involuntary (see Hartman/Abbs 1988). Although essentially true for all dy sarthrias, the impact that hy perkinetic dy sarthria has on speech production and intelligibility seems to be dependent more so on those speech subsy stems directly involved in the movement disorder. Lesions of the striatum (putamen, caudate nucleus) and/or pallidum (globus pallidus) and/or their tracts appear responsible for these aberrations of movement. 3.6.1. S l ow Fo r m s include dy stonia, (tardive) dy skinesia and athetosis. Certain forms
be fo r m f r u st e of a more generalized widespread movement disorder or remain a focal sign of lary ngeal involvement in some patients. The presence of adductory or abductory voice arrest or combinations thereof are cardinal signs of spastic dy sphonia. Although they generally represent neurologic disease, in some patients they are manifestations of psy chopathology thus warranting careful investigation and differential diagnosis. — Neuroleptic toxicity may produce adventitious mouthing, chewing, and tongue protruding. Conversely , parkinsonism with co-occurring oral motor manifestations may also result from protracted use of neuroleptics in some patients. Speech manifestations have been described as “stuttering” and altered prosody including audible inspiration and voice tremor. — Athetoid movements are frequently a component of congenital cerebral palsy or may be seen in conjunction with chorea. Motor speech signs include short sentences, articulatory imprecision due, in part, to inappropriate positioning of the tongue, prolonged transition time for articulatory movements and discoordinated velophary ngeal closure (Kent/Netsell 1978). Neilson/ O’Dwy er (1981; 1984) have pointed out that the dy sarthria of athetosis may be, in part, due to compensatory postures and thereby represent abnormal voluntary attempts at modification rather than variable involuntary muscle activity.
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3.6.2. Q u i ck Fo r m s of hy perkinetic dy sarthria include the speech changes that accompany Huntington’s disease with imprecise consonant production, prolonged pause times, variable speaking rate, limited pitch variability , harsh voice quality and variable alterations in loudness or excess loudness. There is some question as to whether the dy sarthric features demonstrated with Huntington’s disease are a manifestation of degenerative changes within the basal ganglia or a consequence of the chorea itself (Caligiuri/Murray 1984; Ramig 1986). The motor and vocal tics associated with (Gilles de la) Tourette’s sy ndrome include involuntary vocalization, coprolalia, palilalia and echolalia. Abnormal dopamine metabolism or dopamine hy peractivity is felt to be responsible for the aberrations of movement seen in Tourette’s syndrome.
dy sarthric ty pes mentioned previously , flaccid dy sarthria can result from isolated subsy stem involvement. For example, a lesion of the recurrent lary ngeal nerve produces vocal fold paraly sis with resultant phonatory signs, e. g., hoarseness and breathiness, but with spared articulation and resonance. Conversely , multiple lower motoneuron involvement as in the case of my oneural junction disease, e. g., my asthenia gravis may present with compromised velophary ngeal function with resultant hy pernasality ; articulatory dy sfunction with associated sound distortion and variably impaired intelligibility ; lary ngeal involvement with hoarseness and breathiness; respiratory involvement with resultant decreased support for speech and prosodic involvement with compromised rate and intonation patterns. 3.8. Mixed Dysarthria
3.6.3. Tr e m o r Fo r m s. Regular and relatively rhy thmic contractions of the soft palate, posterior phary ngeal wall, base of tongue and lary nx at rest are pathognomonic of palatal-phary ngeal-lary ngeal my oclonus (palatal my oclonus, palatal ny stagmus). The cardinal features of this dy sarthria are audible changes in volume between 2 and 4 hertz notable on prolongation of the neutral vowel ah that cooccur with musculature contractions of involved structures. Movements are present at rest. The signs of palatal myoclonu s have been ascribed to lesions of the brain stem or cerebellum, particularly the dentato-rubro-olivary tracts. There is only one report concerning the dy sarthria associated with action my oclonus (Aronson/O’Neill/Kelly 1984). — Voice tremor, as a manifestation of the essential tremor sy ndrome (including benign heredofamilial tremor) is characterized by relatively regular and rhy thmic changes in phonation volume between 4 and 12 hertz. Unlike palatal my oclonus, however, movements are not present at rest. Certain forms of spastic dy sphonia are a manifestation of essential tremor. Changes within the extrapy ramidal sy stem were proposed as the cause of essential tremor.
Multisy stem neurologic involvement is potentially capable of producing py ramidal, extrapy ramidal, cerebellar and lower motor neuron signs concurrently . The manifestations of such signs depend on (1) the specific sites of involvement, and (2) when in the course of the disease the patient is examined. For example, amy otrophic lateral sclerosis commonly presents with primary bulbar involvement (e. g., progressive bulbar palsy ) with resultant flaccid (lower motoneuron) dy sarthria. As the disease progresses, upper motoneuron signs (corticobulbar tract) appear, resulting in a spastic component, thus flaccidspastic dy sarthria. Other conditions include Shy -Drager sy ndrome (multisy stem atrophy with dy sautonomia), with resultant hy pokinetic-flaccid mixed dy sarthria (which can include vocal fold paresis), Wilson’s disease (hepatolenticular degeneration), with resultant ataxic-h y pokinetic-spastic yd sarthria, and Steele-Richardson-Olszewski sy ndrome (progressive supranuclear palsy ) with hy pokinetic-spastic-ataxic yd sarthria. Olivopontocerebellar atrophy may be characterized by spastic-ataxic, flaccid-spastic (with stuttering) dysarthria.
3.7. Flaccid Dysarthria
4.
Involvement of one or more of the cranial or spinal nerves subserving motor speech control at the level of the nucleus, axon, my oneural junction or muscle results in lower motor neuron signs or flaccid dy sarthria. Unlike the
The classical studies by the May o Clinic group provided the most sy stematic and comprehensive framework for identify ing and classify ing dy sarthria and apraxia of speech. However, a comment on the nature of such classification and description is warranted. A
Considerations for Classification of Motor Speech Disorders
38. Pathophysiology of Disordered Articulation
very basic issue in this respect is the division of these disorders with respect to implied segregation of brain functions. Starting with dy sarthria, this is a speech production sy stem manifestation of a generalized problem of movement. Specifically , with damage or disease to various brain centers, motor functions of walking, manual manipulation, writing, balance, etc. are impaired along with those of speech. Damage of the cerebellum, basal ganglia, primary motor cortex, motoneurons, etc. all are agreed-upon etiologies for dy sarthria. By contrast, it is commonly claimed that apraxia of speech is not a dy sarthria, but due to “problem in programming or coordination of the movements of speech.” Indeed, several recent studies of motor control in this latter population support those descriptions. Unfortunately , it is not clear that problems in “coordination and programming” are not also experienced by patients with dy sarthria. For example, based upon extensive studies in nonhuman primates and in humans, impairments of the basal ganglia and the cerebellum are characteristic in manifesting ‚motor programming’ disorders. Likewise, the cerebellum, damage to which y ields ataxic dy sarthria, is commonly believed to be an primary center of movement coordination, with studies going back to the classic work of Gordon Holmes. — Similarly , if one argues that apraxia of speech results from brain damage to areas that are distinct from those y ielding dy sarthria, the distinction is further clouded. That is, if one accepts the argument that apraxia of speech is due to damage to Brodmann’s Areas 44/45 (lateral precentral cortex), recent data indicate that the primary outputs of the deep cerebellar dentate nucleus associated with orofacial function project not to the motor cortex, but rather to regions of the cortex overlapping Area 44. Yet other studies indicate that Area 44 has some direct projections to motor nuclei of the tongue, lips, and jaw, presumably acting in parallel to projections from primary motor cortex. Given these considerations, it is not surprising that it is only the rare patient who presents with a ‚pure’ apraxia, without either motor signs (i. e., unilateral facial weakness, tongue deviation) and/or serious problems with language expression or comprehension. — Difficulties of understanding are likely if one attempts to impose inappropriate distinctions among motor control, linguistic, and cognitive deficits. Specifically , motor control is now recognized to involve phenomena such as anticipation, adaptation, set, attention, instruc-
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tion, task goals, etc. Moreover, these factors appear to be operating via brain centers that were not classically considered to have cognitive functions, such as the basal ganglia, cerebellum, pre- and supplementary motor neo-cortices. For speech motor control, especially given its higher cortical nature, such cognitive factors must be intricately involved. Taking this argument to an obvious end, the demarcation between language and speech functions also is suspect. A number of linguistic factors influence the aspects of speech motor control, and conversely . Because language is manifest in the selection and sequencing of respiratory , lary ngeal, and upper airway movements to generate acoustic signals carry ing messages, one cannot separate that sequencing and selection from the neuromotor control of those movements. — Despite the aforementioned cautions, it is a matter of practical significance to categorize and evaluate the major features of the different forms of neurologic speech disorders. The continued challenge will be to develop increasingly biologically based criteria for such classification and have the flexibility to accept the elimination of some categories and merging of others.
5.
References
Aronson, A. E., O’Neill, B. P. & Kelly , J. (1984). The dy sarthria of action my oclonus. Presented at the Clinical Dy sarthria Conference, Tucson, AZ, 1984. Caligiuri, M. D. & Murray , T. (1984). Identification of a performance deficit in dy sarthria associated with Huntington’s disease. Presented at the Clinical Dysarthria Conference, Tucson, Arizona, 1984. Canter, J. (1967). Neuromotor pathologies of speech. American Jou rnal of Physical Medicine, 46, 659—666. Darley , F. L., Aronson, A. E. & Brown, J. R. (1969 a). Differential diagnostic patterns of dy sarthria. Jou rnal of Speech and Hearing Research, 12, 246—269. Darley , F. L., Aronson, A. E. & Brown, J. R. (1969 b). Clusters of deviant speech dimensions in the dy sarthrias. Jou rnal of Speech and Hearing Research, 12, 462—469. Grewel, F. (1957). Classification of dy sarthrias. Acta Psychiatrica Scandinavica, 32, 325—327. Hartmann, D. E. & Abbs, J. H. (1988). Dy sarthrias of movement disorders. In J. Jankovic & E. Tolosa (Eds.), Advances in Neu rology, Vol. 49: Facial Dyskinesias. 289—306. New York: Raven Press.
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Hartmann, D. E. & Abbs, J. H. (1989). Perceptual and phy siologic characteristics of unilateral upper motor neuron (UUMN) dy sarthria. Presented at the American Speech-Language-Hearing Association Meeting, St. Louis, Missouri, 1989. Kent, R. & Netsell, R. (1978). Articulatory abnormalities in athetoid cerebral palsy . Jou rnal of Speech and Hearing Disorders, 43, 353—373. Neilson, P. & O’Dwy er, N. (1981). The pathophy siology of dy sarthria in cerebral palsy . Jou rnal of Ne u rology Ne u ros u rgery and Psychiatry, 44,
1013—1019. Neilson, P. & O’Dwy er, N. (1984). Reproducibility and variability of speech muscle activity in athetoid dy sarthria of cerebral palsy . Jou rnal of Speech and Hearing Research, 27, 502—517. Ramig, L. (1986). Acoustic analy ses of phonation in patients with Huntington’s disease. Annals of Otology Rhinology and Laryngology, 95, 288—293.
James H. Abbs/David E. Hartman, Madison, Wisconsin (USA)
39. Assessment Methods in Neurophonetics: Speech Production 1. 2. 3. 4. 5.
1.
Introduction Assessment Techniques Assessment Paradigms Neurophonetic Assessment: Means and Ends References
Introduction
Phonetics is the science of speech, — of the motor processes associated with its production, of its characteristics as an acoustic signal, and of the auditory -perceptual processes associated with the comprehension of speech. ‘Neurophonetics’ thus encompasses the study of disturbed speech production and perception in neurologic patients. According to this definition, neurophonetics spans a wide field, ranging from the pathophy siologic nature of disturbed speech processes to the phonetic aspects of the resulting communication problems. A correspondingly wide range of diagnostic methods is employ ed to study these questions, including techniques adopted from e. g. phy siology , experimental psy chology , or signal processing. — This article reviews methodological approaches in the study of neurologically disordered s p e e ch p r o d u ct i o n, i. e. predominantly in motor speech disorders like dy sarthria and apraxia of speech. The field may be delimited from non-linguistic approaches, e. g. in cranial nerve neurology and reflexology , although the findings of these disciplines clearly have a strong impact on the understanding of disturbed speech functions. A further delimitation must be drawn towards ‘higher level’ processes in the production of spoken language, but the precise location of this border, which is often
characterized as separating motor speech functions from processes of language encoding, is controversial.
2.
Assessment Techniques
In the assessment of speech disturbances of neurogenic origin, speech events may be captured at rather different levels of their manifestation. Neurophonetic assessment ma y start out at the neuromuscular level, drawing on the electric muscle potentials associated with muscular activity in the speech organs, the muscular forces, or the kinematic aspects of speech movements. Or, it may deal with the aerody namic or acoustic effects of speech movements, and it may capture the perceptual features of disturbed speech. In this order of presentation, the different approaches roughly follow a hierarchy of decreasing pathophy siologic and increasing functional significance. 2.1. Movement Parameters The most natural approach towards an understanding of the pathophy siology underly ing the various neuromotor speech disorders would be to analy se the movement parameters generally used in studies of motor disorders, i. e. electrophy siologic, dy namic, and kinematic measures of movement. The recording of these parameters in the speech sy stem, however, is impeded by the fact that most speech organs are concealed deep in the oral and phary ngeal cavity and difficult to access by instrumentation. Moreover, since speech is a highly adaptive motor activity
39. Assessment Methods in Neurophonetics:Speech Production
even minimally obtrusive techniques might lead to alterations in the organization of the processes to be observed. For these reasons, the study of movement parameters in motor speech disorders is considerably less advanced than phy siologic research in the motor functions of the extremities. 2.1.1. Muscle Action Potentials In the execution of speech movements, the motor commands edited by the brain are transmitted to the motor units of the speech muscles involved, where electrical activation, i. e. m u s c l e a c t i o n p o t e n t i a l s (MAPs), can be measured. Electromy ographic measurements of MAPs are performed using either surface electrodes, needle electrodes, or hooked wire electrodes, the latter having the main advantage of being light, causing virtually no movement artifacts and stay ing in place even during rapid movements. — Electromy ographic techniques have been applied in virtually all muscles relevant for speaking and have, for example, been used in investigations of the specific roles of different speech muscles or in the study of interarticulatory relations. EMG applications to speech pathology have been focussed on easily accessible sy stems, i. e. predominantly on labial and mandibular muscles, but e l e c t r o myo g r a p hy of lingual or lary ngeal muscles in neurologic patients is not uncommon (Shipp/ Izdebski/Reed/Morrisey 1985). Clinical diagnostic applications are mainly concerned with the question of whether a particular muscle is, as a consequence of peripheral nerve involvement, insufficiently innervated (Hirano/ Nozoe/Shin 1987). In research, EMG methods have been used, for instance, to assess resting and background activity and reciprocal suppression in the context of spasticity or rigidity , to compare tremorous activities in different structures, or to measure temporal relationships in the activation patterns of sy nergistic or antagonistic muscle groups (e. g., Neilson/O’Dwy er 1981; Hunker/Abbs 1990). — The methodological value of electromy ography is characterized by its high pathophy siological significance. However, there are severe limitations to this method. A critical source of error is electrode placement (Gans/ Gorniak 1980). Normally , ‘calibration gestures’ are used to verify correct placement of electrodes, but this technique may cause problems in patients with motor speech disorders. Further, the probability of inserting a pair of electrodes into a functionally homogeneous
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population of muscle fibers is rather low, meaning that EMG based assertions on e. g. co-contraction among antagonistic muscles are of limited validity (Blair/Smith 1986). This problem is even more severe when surface electrodes are used. Thorough investigations into the psy chometric quality of electrode placement are therefore urgently needed (Tassinary/Caccioppo/Geen 1989). 2.1.2. Muscular Forces The immediate effect of electrical muscle activity is the build-up of contractile muscular force. However, the pattern of muscular forces in the speech sy stem reflects central processes much less directly than EMG patterns do, since muscle output force depends to a large extent on the mechanical properties of a muscle, i. e. its elasticity , velocity , and length. — The parameter of force is basic to important clinical conceptions of neuromotor disorders such as muscular weakness (e. g. in peripheral nerve involvement) or increased muscle tone (e. g. in spasticity ). Nevertheless, instrumental force measurements are sparse and have been restricted to the lips, the tongue, and the jaw. Force measurements in these structures are traditionally made using strain gage force transducers sensitive to accelerations along a given spatial vector (Barlow/Abbs 1983). Relevant questions include maximum voluntary closing forces and fine force control, the latter being operationally defined as the skill of holding a given force as constant as possible. Applications in neurological patients have also focussed on these variables, with the question of differential subsy stem impairment as an index of the role of muscle spindles in spasticity and Parkinsonian rigidity or of differential cranial nerve involvement in ALS (e. g. DePaul/Abbs/Caligiuri et al. 1988). — Closely related to the measures of active force control just described are measures of muscle stiffness, i. e. resistance of a muscle against passive displacement. The degree of muscle stiffness in the lower lip, operationally defined as the ratio of the force necessary to achieve lower lip displacement by a certain amount and the displacement amplitude, has been used as an index of labial rigidity in Parkinson’s disease (Caligiuri 1987). — Like EMG, force measures are considered rather specific to the pathophy siology underly ing a speech disorder. One should, however, bear in mind that force measurement techniques give no account of the contractile forces of single mus-
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cles, but rather of the effective forces resulting from contractions of various sy nergistic and antagonistic muscles in e. g. labial closure or tongue elevation. A second point to be made is that force measurements are exclusively related to nonspeech-tasks. This may , on the one hand, raise doubts as to their ecological validity and explain the lack of a correlation with measures of severity of dy sarthric impairment (DePaul/Abbs/Caligiuri et al. 1988). On the other hand, nonspeech tasks may help to determine whether a deficit is one of elementary motor functions of the speech organs or if language play s a crucial role (McNeil/ Weismer/Adams/Mulligan 1990). 2.1.3. Movement Kinematics Descending from the levels of electrical muscle activity and muscular forces to the kinematic aspects of speech movements, i. e. measures of displacement and velocity , an increasing number of peripheral influences becomes effective. Speech movements are not only the result of a complex interplay of actively controlled sy nergistic and antagonistic muscle contractions, but are also influenced by passive recoil forces, inertia and aerody namic processes. Nevertheless, kinematic measures of speech movements are considered a powerful inventory in the analy sis and description of motor speech disorders. The techniques applied in studies of speech movement kinematics differ depending on which subsy stem is to be observed. L i p s a n d j aw: The lips and the jaw are more easily accessible than the tongue, the velum, or the lary nx, and have therefore been studied more often than the latter. The technique which has been most successful in labial and mandibular kinematics so far is based on strain gage movement transducers measuring inferior-superior movements of upper lip, lower lip, and jaw (Barlow/Cole/Abbs 1983). Lip and jaw movement data can also be obtained by radiographic or electromagnetic techniques, which are specifically devised for the recording of tongue movements. — Much of the work on labial and mandibular movement kinematics in normals has been devoted to questions of movement timing and coordination and to the search for motor invariants in the perioral sy stem. In speech pathology , labial and mandibular kinematics have play ed a crucial role in studies of Parkinsonian dy sarthria (e. g. Forrest/Weismer/Turner 1989), with the main objective of demonstrating hy pokinesia and brady kinesia in the
speech movements of Parkinsonian patients. The core parameters used in these studies are movement amplitude, peak velocity , and movement time. — A particular problem lies in the high variability in normals over different studies. This impedes the interpretation of some of the reported results and explains why the applied kinematic measures are usually uncorrelated with dysarthria severity. To n g u e: The recording of tongue movements is one of the major challenges in articulatory phonetics, since the tongue may be considered the most versatile subsy stem in speech and, at the same time, an organ which is extremely difficult to observe. The many attempts to assess lingual kinematics can be classified in several way s, e. g. according to the underly ing phy sical technique (radiography , electromagnetic induction, ultrasound imaging, contact detection), or according to the analy sis plane (saggital vs. coronal). A further distinction can be made between point-tracking sy stems and imaging techniques. Each of the different measurement sy stems has its own advantages and limitations. — Two sy stems, which are similar in that they are based on point-tracking techniques and y ield saggital views of the articulators, are the X- r ay m i c r o b e a m (XRMB) and the e l e c t r o m a g n e t i c a r t i c u l o g r a p h (EMA). The two sy stems provide X-ray beam or electromagnetic trackings of a set of pellets or coils attached to the articulators of the experimental subject (Abbs/Nadler/Fujimura 1988; Schönle/Gräbe/Wenig et al. 1987). Unlike earlier radiographic techniques the XRMB y ields very low radiation exposures and offers negligible risk for both the experimental subject and the experimenter. The EMA sy stem contrasts with the XRMB in that it is biologically entirely safe, lower-dimensioned, and considerably less expensive. Both sy stems are particularly suited for recordings of the anterior, medial, and dorsal part of the tongue. The midsaggital analy sis plane allows investigation of horizontal and vertical tongue movements, whereas crosssectional articulations of the medial and lateral surface cannot be assessed. The temporal and spatial resolution is sufficient for the study of lingual movements during speaking. Users of the sy stems mostly claim that tongue pellets would not interfere with articulation, but Stone (1990) holds that the tongue tip should be excluded from recording since XRMB pellets feel cumbersome. — A particular methodological problem with point-
39. Assessment Methods in Neurophonetics:Speech Production
tracking measurements of lingual articulation lies in the separation of mandibular movement components from the observed pellet trajectories which contain information on both jaw- and tongue-related movements. According to Edwards/Harris (1990) the mandibular component of lingual movements should be modelled by a combined rotation and translation transform, which requires observation of two additional mandibular measurement points. — Applications of XRMB and EMA to normal aspects of lingual articulation are still sparse and much of our current knowledge e. g. on vowel articulation is still based on older cineradiographic techniques. One principal aim of this research is to build models which capture the many dimensions of tongue shape and the many degrees of freedom of lingual movements and thus may serve as a basis for future parametric investigations. — Studies of neuromotor impairments of lingual articulation have been restricted to a few individual cases so far. Qualitative descriptions of XRMB m ovem e n t t r aj e c t o r i e s and some quantitative data on tongue dorsum velocities in rapid sy llable repetitions of dy sarthric individuals have been reviewed by Hirose (1986). — The scarcity of useful data concerning neuromotor disturbances of the tongue indicates that point tracking techniques of lingual assessment have not y et reached the point where they can be successfully handled in neurologic patients. Besides multiple technical problems, a major difficulty is in the complexity of tongue shape deformations during articulation which can be grasped but insufficiently by a small set of measurement points. — A method which does not rely on single point tracking is u l t r a s o u n d i m a g i n g (Stone/ Sonies/Shawker et al. 1983). Sonography has the disadvantage that important reference structures such as the hy oid bone and the hard palate are not visualized. Further, the tongue tip cannot be measured by ultrasound techniques since there is usually some airfilled space beneath it which causes ultrasound wave reflection. In contrast, an important advantage is that sonography may provide information on the tongue shape in either the cross-sectional or the saggital plane, which renders it useful in tongue modelling (Stone 1990). Keller/Ostry (1983) used a simpler sonographic technique which measures tongue height at a single dorsal point and is confined to a one-dimensional assessment of tongue backing movements. Similar to other
435
tongue recording techniques, applications of sonography to motor speech disturbances are still restricted to very few single cases. — Information on cross-sectional tongue shape during articulation is also provided by e l e ct r o p a l a t o g r a p hy. In this method the subject wears an acry lic palate with a grid of sensors distributed over its surface. The contact pattern of the anterior part of the tongue with the hard palate during articulation is recorded and transmitted to a screen by wires led out through the corner of the mouth (Hardcastle/Jones/Knight et al. 1989). Due to the complexity of the signal which contains dy namic information on usually more than 60 electrodes it is important to apply suitable data reduction techniques (Hoole/Ziegler/ Hartmann/Hardcastle 1989). Palatometry is limited by its restriction to anterior lingual consonants and has the disadvantage that each subject must be provided with his/her own tailored palate. Moreover, subjects have to become accustomed to the device during a training period, which may impose particular difficulties to patients with motor learning impairments. Nevertheless, a number of problems can be adequately addressed by palatometric techniques, as for instance the characterization of articulatory configurations in lingual consonants and the assessment of coarticulation patterns. Applications to neuromotor disorders of speech have focussed on spatial and temporal abnormalities of anterior lingual articulations in dy sarthria and apraxia of speech (Hardcastle/Jones/Knight et al. 1989). Ve l u m: Unlike the tongue with its many degrees of freedom and its configurational versatility the velum is mostly described as a relatively simple ‘valve-like’ organ, with the essential function of controlling the airflow through the nasal cavity and thereby marking the distinction between oral and nasal sounds. The sy mptom of velophary ngeal incompetence found in several ty pes of dy sarthria is of high functional importance, since it usually results in severely distorted speech. — Direct observation of velar movements may be achieved by the XRMB or by v i d e o- e n d os c o py. Endoscopic views of the velum are inherently nonlinear, meaning that inferences regarding absolute displacement cannot be drawn, and between-subject comparisons of movement amplitude should be avoided. A less direct method of velar observation utilizes the transillumination technique to measure the amount of light passing through the velo-
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phary ngeal port when a fiberoptic light source is brought behind the velum and a photodetector is placed within one of the nostrils. While the photodetector signal is highly correlated with velar height it is also sensitive to lateral phary ngeal wall movements associated with velar closure and fails to discern velophary ngeal adaptations that may occur after closure (Zimmermann/Dalston/Brown et al. 1987). Similarly indirect measures of velar control are provided by aerody namic techniques (cf. 2.2.). — Questions ty pically addressed by the described methods are mainly concerned with the speed and timing of velar movements. The issue of velar timing was raised by Itoh/Sasanuma (1984) in their analy ses of aphasic and apraxic patients — a study which has had some impact on the discussion of the nature of aphasic speech errors (cf. 4.). — A problem which is particularly relevant in the case of velar movements concerns the functional significance of movement variables. It is known that normal speakers may differ in their patterns of lateral phary ngeal adaptation and velar elevation during velophary ngeal closure. Further, the velophary ngeal port need not be completely closed but may vary considerably in its size during the production of oral vowels and consonants. Examination of the velum alone therefore y ields a rather poor prediction of the actual quality of speech and even estimates of velophary ngeal port size should be carefully interpreted if implications concerning for instance the degree of perceived nasality are to be drawn in dysarthric patients. Vo c a l fo l d s: The notion of vocal fold movement may be understood in two different way s: in the sense of a c t i ve glottal ador abduction during running speech, predominantly used for distinguishing between voiced and voiceless sounds (‘lary ngeal articulation’), or in the sense of p a s s i ve, quasiperiodic oscillation of the adducted vocal folds during the production of voiced sounds. While the former are produced voluntarily and, in this respect, may be compared to the articulatory movements discussed so far, the latter are the result of an aerody namic and my oelastic process depending essentially on subglottal pressure, glottal width, and vocal fold stiffness and may therefore provide indirect information on the complex interplay between respiration, lary ngeal function, and articulation. A methodologically relevant difference lies in the temporal characteristics of both movement ty pes, with vocal fold oscil-
lations ty pically ranging between approximately 100 and 250 cy cles per second in adults, whereas voluntary repetitive lary ngeal ad- and abduction is ty pically performed at a rate of ca. 5 per second. — Lary ngeal behavior can be observed directly by telescopic or fiberoptic endoscopy . Endoscopic inspection of the lary nx and the hy pophary nx is clinically indispensible for the assessment of abnormal shapes or postures of lary ngeal or hy pophary ngeal structures, of abnormalities in the degree of adduction, or of involuntary lary ngeal movements. If lary ngeal articulations during speaking are to be assessed, transnasal endoscopy is required. Quantitative evaluation of lary ngeal movements is impeded by the shortcomings associated with the non-linearity of endoscopic views. If vocal fold oscillations are to be assessed in some detail, ultra high-speed photography is required. As may be expected, evaluation of high-speed films requires a high expenditure in frame-by -frame analy sis, if not automatic image processing techniques. — Part of the information contained in high-speed films may also be captured by e l e c t r o g l o t t og r a p hy ( E G G) or p h o t o g l o t t o g r a p hy ( P G G) (Baer/Löfqvist/McGarr 1983). EGG uses a pair of electrodes placed bilaterally on the neck at the level of the thy roid prominence to measure the electrical impedance of the lary nx, which is considered to vary reciprocally with the degree of vocal-fold contact. PGG ist based on the transillumination principle and may for instance utilize the light source of a nasal endoscope to measure the amount of light arriving at a phototransistor placed on the surface of the neck, below the cricoid cartilage. The method is susceptible to artifacts of various kinds, e. g. changes in light source or photodetector position or interposition of the epiglottis, and should therefore be controlled by parallel fiberoptic endoscopy . — EGG and PGG are considered to provide complementary information on the oscillatory cy cle of the vocal folds, with EGG convey ing information on the patterns of vocal fold contact and the PGG signal providing an index of peak glottal opening and glottal closure (Baer/Löfqvist/McGarr 1983). While EGG is predominantly used in phonation analy ses, PGG has proven particularly useful in the analy sis of lary ngeal gestures during articulation. — In motor speech disorders, EGG and PGG methods have, for instance, been applied to study lary ngeal dy namics in patients with spasmodic dy sphonia (Ludlow/
39. Assessment Methods in Neurophonetics:Speech Production
Connor 1987). Application of EGG and PGG methods to study the vibratory cy cle of vocal fold oscillations in dy sarthria is strongly suggested by Ward/Hanson/Gerratt et al. (1989). However, Childers/Hicks/Moore et al. (1990) are doubtful as to the diagnostic potentials of electroglottography , since for one thing, relevant ty pes of insufficient vocal fold contact remain undetected. Re s p i r a t o r y o rga n s: The term ‘ Re s p ir a t o r y k i n e m a t i c s’ usually refers to the anteroposterior movements of the thoracal and abdominal walls, which are the result of a rather complex interplay of active contractions of the diaphragm and the intercostals, of aerody namic processes, and of passive recoil forces of the chest wall (Weismer 1985). Kinematic parameters of speech breathing are assessed using either st r a i n ga ge b e l t p n e u m o g r a p h s o r m a g n e t o m e t e r s to measure changes in the circumference or AP-diameter of the rib cage and the abdomen (Murdoch/Chener y /Bowler/Ingram 1989; Hoit/Hixon/Watson/Morgan 1990). Volume calibration techniques are applied to estimate the relative contributions of thoracal and abdominal displacement to lung volume change (Reich/McHenry 1990). A large body of data has been collected to describe volume displacements of rib cage and abdomen in normal subjects, including populations vary ing in sex, age, or body ty pe (cf. Hoit/Hixon/ Watson/Morgan 1990). Up to now, examinations of neurologically impaired subjects have focussed on the detection of aty pical or paradoxical patterns in charts describing abdominal versus thoracal displacement over time (Weismer 1985; Murdoch/Chenery /Bowler/Ingram 1989). 2.2. Aerodynamic Parameters Whereas most of the parameters discussed above have their parallels in other motor sy stems, aerody namic parameters like a i r p r e ss u r e and vo l u m e ve l o c i t y are peculiar to speech. They reflect respiratory , lary ngeal, and articulatory maneuvers and as such may be used as an index of speech motor control. Yet, aerody namic parameters are rather indirect correlates of the motor processes associated with speaking since they combine a blend of different influences which are difficult to discern. — Relevant parameters are lung volume changes, subglottal, oral, and nasal pressures, and oral and nasal airflow rates. Lung volume measures of speech breathing are considered to reflect thoracal
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and abdominal activities and can be estimated from kinematic parameters of chest wall movements (cf. 2.1.3.). Oral and nasal pressure and airflow are a function of pulmonary pressure and their mutual relation is dependent on the velophary ngeal port area (Laine/ Warren/Dalston/Morr 1988). They can be measured using a differential pressure transducer with a catheter being inserted into the subject’s oral cavity or nostril. Subglottal pressure depends on lung volume and expiratory control and may be regarded as a major determinant of vocal intensity and, together with glottal width and vocal fold stiffness, one of the factors influencing vocal fold vibration (Holmberg/Hillman/Perkell 1988). Its direct measurement would require sensors to be placed below the glottis level or within the esophagus, which is highly invasive. A clinically applicable method to derive subglottal pressure from intraoral pressures is based on pressure measurements during complete oral closure and simultaneous glottal opening, as in /p/ (Kitajima/Fujita 1990). When this procedure is applied in dy sarthric patients, care must be taken that the lips are completely sealed and that air is prevented from passing through the nose. — Measures of a i r f l ow r a t e s are usually obtained by a pneumotachometer attached to an air-tight face mask (Holmberg/Hillman/Perkell 1988). If nasal and oral flow rates are to be differentiated, a two channel mask must be used. — Aerody namic parameters of speech disturbances of neurogenic origin have predominantly been applied to measure velophary ngeal function in dy sarthria (Hoodin/Gilbert 1989). Aerody namic measures of respiratory function have been assessed in Parkinsonian dy sarthria and in ALS, y et with a strong focus on basic nonspeech pulmonary function (Murdoch/Chenery/Bowler/Ingram 1989). 2.3. Acoustic Parameters The motor processes and associated aerody namic events described so far ultimately result in a sound pressure wave which is radiated from the lips and the nose and is the phy sical carrier of the speech code. Since the acoustic signal is the end-product of respiratory , lary ngeal, and articulatory movements, parameters extracted from it may be used to characterize the consequences of speech dy sfunctions at different levels. Compared to phy siologic and aerody namic techniques the recording of the speech wave is uncomplicated since it is usually performed outside the vocal
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tract and does not interfere with speaking. To be sure, the ease of assessment is gained at the expense of phy siologic significance, because the sound pressure wave integrates all motor activities associated with its production, and there is no straightforward way to single out the contribution of any of the different subsy stems. However, this shortcoming can be partly compensated for at least by using appropriate speech tasks (cf. 3.1.). On the other hand, speech wave parameters may capture the functionally relevant aspects of a patient’s speech impairment since they draw upon the signal by which the patient attempts to communicate. — The recording of the audio signal requires a high quality microphone and tape recorder and is usually performed in a sound-treated test booth. The extraction of acoustic parameters has long been based on analog devices like the sound spectrograph. In the meantime, these techniques have largely been substituted by digital signal processing methods, with microcomputer applications becoming increasingly important. — In principle, the speech signal can be analy zed in the temporal or the spectral domain, or by mathematical modelling techniques like l i n ea r p r e d i c t i ve c o d i n g ( L P C). Parameters of the temporal domain include, for instance, sound pressure level contours or durations of identifiable signal portions, whereas spectral analy sis draws upon the distribution of signal energy over the frequency band up to about 10 kHz. LPC analy sis over short signal portions y ields considerable data reduction and allows, for instance, the fast computation of smoothed spectra. — Applications to normal speech have been based on a multitude of measures characterizing, for instance, consonants produced at different places or with different manners of articulation, or sound contrasts based on voicing or nasality . Further relevant issues are the analy sis of phonatory parameters like fundamental frequency and the characterization of prosodic features. These investigations ty pically try to establish a correspondence between the acoustic parameter in question and some articulatory or perceptual correlate. — Acoustic descriptions of dy sarthric or apraxic articulation have largely been based on the signal parameters known from acoustic phonetics, e. g. formant frequencies in vowel articulation (Ziegler/ Hartmann/Hoole/Cramon 1990) or stop gap durations and voice onset times in plosive articulation (Caruso/Burton 1987). Measures of the variability of segment-, sy llable- or
word durations have been considered valuable in descriptions of ataxic dy sarthria or of aphasic speech disturbances (cf. Baum/Blumstein/Naeser/Palumbo 1990). Many of the measures studied so far have the disadvantage of rely ing on the presence of certain ‘landmarks’ in the speech signal, e. g. a clearly discernible plosive burst as is characteristic of the release of stop consonants in normals. In severe dy sarthria these landmarks may no longer be present so that alternative approaches towards temporal measures of dy sarthric speech are needed (Ziegler/Hartmann/ Hoole/Cramon 1990). — Acoustic analy ses of dy sphonia following lesions to the central nervous sy stem are surprisingly rare when compared to voice disorders of peripheral origin. A differentiation between several perceptually determined voice ty pes in patients with dy sarthria of traumatic and cerebro-vascular origin has been performed by Hartmann/Cramon (1984). A number of studies was focussed on acoustic features of spasmodic dy sphonia, such as voice tremor or the occurrence of phonatory aperiodicities and voice breaks (Ludlow/Connor 1987). — Finally , acoustic measures have been applied in the description of prosodic impairments, for instance in Parkinson’s disease, in aphasia, or in right hemisphere lesions (cf. Behrens 1989). The parameters used in these studies ty pically include measures of prosodic variation of fundamental frequency, intensity, and duration. 2.4. Auditory Parameters The goal of any kind of speech motor activity is the production of perceptually acceptable, intelligible speech. From the patient’s perspective the perceived quality of his/her speech output is the most relevant aspect of his/her speech disorder. Likewise, perceptual features provide the most relevant criterion for the severity of a speech disorder. It thus seems natural that any kind of clinical diagnostics is primarily based on auditory evaluation. Yet, the perceived quality of disturbed speech reflects the underly ing pathology even less directly than the acoustic signal does, since auditory parameters are mediated by the complex processes of auditory perception. — Attempts have been made to implement a standard inventory of terms to be used in the auditory assessment of dy sarthric speech (Darley /Aronson/Brown 1975), but the diagnostic methods based on such inventories are probably not sufficiently reliable (Zy ski/
39. Assessment Methods in Neurophonetics:Speech Production
Weisiger 1987). Moreover, such inventories are not founded on empiric perceptual investigations and many of the applied dimensions seem considerably unspecific or poorly defined (Sheard/Adams/Davis 1991). — The method traditionally used by phoneticians to describe the perceptual quality of speech is (narrow) p h o n e t i c t r a n s c r i p t i o n. This technique uses a standardized set of sy mbols, the ‘International Phonetic Alphabet (IPA)’, which serves to represent a wide range of sounds that can be produced by the human vocal apparatus. The IPA has been extended by diacritics which are specifically suitable for the transcription of disturbed speech (Duckworth/Allen/Hardcastle/Ball 1990). The method of phonetic transcription is widely accepted and a sufficiently high agreement can be obtained between trained transcribers. Transcription based analy ses become increasingly important in the evaluation of aphasia and apraxia of speech (Odell/McNeil/Rosenbek/Hunter 1990). Yet, applications in dy sarthria are rare (Vogel/Cramon 1983), probably since phonetic transcription is predominantly segment-oriented and requires high expenditure for assessing, segment-by -segment, the relatively constant features of dy sarthric speech. — More recent approaches have tried to establish psy chophy sical scaling techniques for the judgment of e. g. voice quality or speech naturalness (cf. Toner/Emanuel/ Parker 1990). The development of such scales is often based on sy nthetic or semi-sy nthetic stimuli or on voice samples from patients with peripheral lesions. Their reliabilty is known to improve with training (Bassich/Ludlow 1986). Apart from a few studies on speech quality in stuttering (Metz/Schiavetti/Sacco 1990), these methods have y et to be applied sy stematically to patients with neuromotor speech disorders. — A variable of considerable importance for evaluating the severity of a patient’s speech impairment is i n t e l l i g ib i l i t y. Psy chophy sical scales may be used to rate intellegibilit y (Fucci/Ellis/Petrosino 1990). However, such ratings fail to y ield an intelligibility ‘profile’ that would indicate which sound classes have the highest contribution to a patient’s disturbance. This information, which is crucial from the point-ofview of clinical management, is provided by intelligibility tests based on multiple choice word identification tasks with phonetically balanced materials (Ziegler/Hartmann/Cramon 1988).
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3.
Assessment Paradigms
3.1. Variation of Tasks Important in the investigation of motor dy sfunctions are the appropriate choice and the sy stematic variation of motor tasks. In motor speech disorders, this variation is achieved by choosing among different modalities of speaking (e. g. repetition vs. spontaneous production), among speech materials of different length (e. g. single sy llables vs. sentences) or different phonetic structure (e. g. labial sounds vs. lingual sounds), or by requiring maximum performance with respect to e. g. speed or effort. — The choice of the stimulus modality is guided by a number of considerations: Precise control over the target utterance to be produced is best achieved in repetition and reading tasks, but these tasks are poor models of ‘natural’ speech and are of only limited value in e. g. the assessment of prosodic deficits (Behrens 1989). — By choosing appropriate designs even indirect methods such as acoustic evaluation may y ield rather specific results. So, for instance, the influence of labial articulation can be inferred approximately from the speech signal by vary ing sy stematically between vowels contrasting in the amount of lip rounding required for their production (Ziegler/Hartmann/Hoole/Cramon 1990). A high selectivity can be achieved by using m i n i m a l p a i r s, i. e. pairs of utterances differing in exactly one segment (Ziegler 1987). — M a x i m u m p e r fo r m a n c e t a s k s are usually applied with the aim of increasing the diagnostic sensitivity by driving the motor sy stem to its limits. Examples are r a p i d s y ll a b l e r e p e t i t i o n, which imposes particular demands on articulatory motility and is generally considered as the speech equivalent of wrist diadochokinesis, or m a x i m u m vowe l o r f r i c a t i ve p r o l o n ga t i o n, which requires a high vital capacity , good expiratory control and skillful lary ngeal or articulatory valving (Kent/Kent/Rosenbek 1987). A special case of maximum performance testing is the measurement of r e a c t i o n t i m e in the initiation of speech. Suitable variation of stimulus-response conditions in reaction-time testing may give insight into specific speech onset and motor programming problems. — A problem inherent to all kinds of maximum performance tasks in neurological patients is that the degree to which these patients can be motivated to optimum performance is influenced by various neuropsy chological factors,
III. Acquired Organic Pathologies of Language Behavior:Neurophonetic Disorders
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and the results often cannot be explained solely in motor terms. Further, most of these tasks need a high number of repetitions, when stable measures are to be obtained (Kent/ Kent/Rosenbek 1987). 3.2. Variation of Constraints A further approach in the study of speech motor performance uses experimental manipulation of the motor constraints in speaking. This approach is motivated by questions concerning the integrity of motor programs or the processing of sensory information that would be necessary to control the implementation of a motor program under altered conditions. The paradigm which has been studied most thoroughly in normals encompasses the unpredicted perturbation of lip movements during closure (cf. Gracco/Abbs 1989). This research aims at an analy sis of sensory -motor interaction in movement programming, with a particular focus on the issue of m o t o r e q u i va l e n c e, i. e. the capability of the speech motor sy stem to achieve a desired motor goal in several different way s. So, for instance, immediate adaptations of the upper lip and the jaw compensate for unpredicted lower lip perturbations to achieve the goal of bilabial closure for /b/ or /p/ (Gracco/Abbs 1989). — This kind of articulatory flexibility has stimulated hy potheses and investigations in neurophonetics. DePaul/Abbs/Caligiuri et al. (1988) reported on particular problems of their ALS patients to compensate for the altered conditions imposed by a bite-block. A sy stematic investigation of the effects of jawfixing on vowel articulation in Broca’s aphasia was carried out by Sussman/Marquardt/ Hutchinson/NacNeilage (1986). A similar issue was raised by Marshall/Gandour/Windsor (1988) in their report on a Broca’s aphasic whose articulation deficit was profoundly influenced by application of an electronic artificial lary nx, i. e. by a reduction of the degrees of freedom within the complex lary ngeal-articulatory sy stem. Variation of the conditions under which the speech apparatus works is further applied in studies of speech breathing, with examinations often being performed on subjects in both an upright and a supine body position.
4.
Neurophonetic Assessment: Means and Ends
Each of the assessment techniques described in this chapter has its own strengths and
weaknesses, and therefore any question to be answered in neurophonetics requires careful selection of the most appropriate assessment method. — The most straightforward way to study the pathophy siologic nature of neurogenic speech dy sfunctions is certainly by phy siologic examinations, i. e. EMG, force, or kinematic measurements. However, if other motor sy stems like the extremities are taken as a model in such research, a number of differences should be considered. Unlike the extremities, many of the speech organs are difficult to access and often only indirect measures of their movements can be obtained. Moreover, the single-joint movement model, which play s a major role in the extremities, is generally not applicable in the speech sy stem. A most striking example is the tongue, which is not only difficult to observe but even more difficult to be grasped in a parametric model. Further, the calibration of measurement sy stems often requires active and skillful cooperation of the subject which cannot be taken for granted in neurologic patients. Still more fundamental than these difficulties, however, seems the problem of how to choose the movement parameters that are relevant in the description of speech motor control and its disturbances. Most of the kinematic parameters discussed in the literature demonstrate considerable within- and between-subject variability and the problem of movement invariants in speech is still open. Taking bilabial closure, for example, it is not only the case that the upper lip, the lower lip, and the jaw may be adjusted independently to realize closure with a high functional flexibility , but also that complete closure is not even absolutely necessary to achieve a perceptually acceptable bilabial stop consonant. The same is true for other subsy stems, e. g. the velophary nx (cf. 2.1.3.). The spatial aspects of movements therefore seem to play fundamentally different roles in speech, with its acoustically defined goals, and in e. g. grasping, where motor goals are defined in terms of an external spatial metric. This may be one reason why kinematic measures of dy sarthric speech have failed to be ecologically valid thus far (cf. 2.1.). At the same time, acoustic and perceptual methods obtain an important status in assessing whether a speech target has been realized adequately . — A special case of the issue of how speech motor goals are realized is encountered in questions concerning the nature of aphasic speech errors. In a traditional view the occurrence of phonemic paraphasias represents a failure at the level of
39. Assessment Methods in Neurophonetics:Speech Production
‘phoneme selection’, i. e. the selection of discrete and abstract motor goals. This view is supported by studies based on phonemic (‘broad’) transcription, which tends to neglect subtle deviations in the realization of a speech sound. More generall y , perception-based analy sis methods seem to foster a discrete model of sound substitution, due to the tendency of the auditory sy stem to perceive categorically . However, investigations based on kinematic or acoustic measures have shown that both perceptually adequate and paraphasic speech sounds may demonstrate gradual aberrations from normal, which is generally interpreted as a failure in the implementation of motor goals (Ziegler/Hoole 1989). An important though controversial contribution to this issue comes from c o a rt i c u l a t i o n studies investigating the transition between sounds and the anticipation of speech targets (Ziegler/Cramon 1986; Katz/ Machetanz/Orth/Schönle 1990). The coarticulation paradigm seems particularly useful in differentiating between phoneme selection and implementation models. — Besides questions embarking on the nature of motor speech dy sfunctions, a wide field of neurophonetic applications is concerned with the implications these dy sfunctions may have for a patient’s communicative abilities. From the point of view of neurologic rehabilitation, this issue is of primary relevance. As pointed out above, the movement parameters examined so far do not y ield valid indices of a patient’s overall speech impairment and may not be used as predictors of e. g. the ‘naturalness’ or the intelligibility of a patient’s speech. In this domain, therefore, perception-based methods remain relevant and great efforts should be taken to improve their psy chometric quality . In the future, considerable support can also be expected from speech acoustics, which may for instance be used in the modelling of intelligibilit y (Weismer/Kent/Hodge/Martin 1988). — A further important domain of neurophonetics are those assessment methods directly oriented at therapeutic applications. An example is the recording of speech parameters that may be used in fe e d b a ck t h e r a py . In principle, any acoustic, aerody namic, or movement parameter may be applied, provided that it can be determined in realtime and is specific to the motor function to be trained. However, the fundamentals of feedback-based motor learning in neuromotor speech disorders and the details of therapeutic applications are still to be elaborated.
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5.
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Sheard, C., Adams, R. D. & Davis, P. J. (1991). Reliability and agreement of ratings of ataxic dy sarthric speech samples with vary ing intelligibility . Jou rnal of Speech and Hearing Research, 34, 285—293. Shipp, T., Izdebski, K., Reed, C. & Morrissey , P. (1985). Intrinsic lary ngeal muscle activity in a spastic dy sphonia patient. Jou rnal of Speech and Hearing Disorders, 50, 54—59. Stone, M. (1990). A three-dimensional model of tongue movement based on ultrasound and x-ray microbeam data. Jou rnal of the Acou stical Society of America, 87, 2207—2217. Stone, M., Sonies, B. C., Shawker, T. H., Weiss, G. & Nadel, L. (1983). Analy sis of real-time ultrasound images of tongue configuration using a griddigitizing ys stem. Jo u rnal of Phonetics, 11, 207—218. Sussman, H., Marquardt, T., Hutchinson, J. & NacNeilage, P. (1986). Compensatory articulation in Broca’s aphasia. Brain and Language, 27, 56—74. Tassinary , L. G., Cacioppo, J. T. & Geen, T. R. (1989). A psy chometric study of surface electrode placements for facial electromy ographic recording. I. The brow and cheek muscle regions. Psychophysiology, 26, 1—16. Toner, M. A., Emanuel, F. W. & Parker, D. (1990). Relationship of spectral noise levels to psy chophy sical scaling of vowel roughness. Jou rnal of Speech and Hearing Research, 33, 238—244. Vogel, M. & Cramon, D. von (1983). Articulatory recovery after traumatic midbrain damage: A follow-up study. Folia Phoniatrica, 35, 294—309. Ward, P. H., Hanson, D. G., Gerratt, B. R., Berke, G. S. (1989). Current and future horizons in lary ngeal and voice research. Annals of Otology Rhinology Laryngology, 98, 145—152.
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Weismer, G. (1985). Speech breathing: Contemporary views and findings. In R. Daniloff (Ed.), Speech Science: Recent Advances. 47—72. San Diego: College-Hill Press. Weismer, G., Kent, R. D., Hodge, M. & Martin, R. (1988). The acoustic signature for intelligibility test words. Jou rnal of the Acou stical Society of America, 84, 1281—1291. Ziegler, W. (1987). Phonetic realization of phonological contrast in aphasic patients. In J. H. Ry alls (Ed.), Phonetic Approaches to Speech Produ ction in Aphasia and Related Disorders. 163—179. Boston: Little, Brown and Company. Ziegler, W. & Cramon, D. von (1986). Disturbed coarticulation in apraxia of speech: Acoustic evidence. Brain and Language, 29, 34—47. Ziegler, W., Hartmann, E. & Cramon, D. von (1988). Word identification testing in the diagnostic evaluation of dy sarthric speech. Clinical Lingu istics and Phonetics, 2, 291—308. Ziegler, W., Hartmann, E., Hoole, P. & Cramon, D. von (1990). Aku stische Dimensionen dysarthrischer Störungsmerkmale. München: GSF. Ziegler, W. & Hoole, P. (1989). A combined acoustic and perceptual analy sis of the tense-lax opposition in aphasic vowel production. Aphasiology, 2, 449—463. Zimmermann, G., Dalston, R. M., Brown, C., Folkins, J. W., Linville, R. N. & Seaver, E. J. (1987). Comparison of cineradiographic and photodetection techniques for assessing velophary ngeal function during speech. Jou rnal of Speech and Hearing Research, 30, 564—569. Zy ski, B. J. & Weisiger, B. E. (1987). Identification of dy sarthria ty pes based on perceptual analy sis. Journal of Communication Disorders, 20, 367—378.
Wolfram Ziegler, Munich (Germany)
40. Speech Apraxia 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
Definition Related Conditions History Signs of Speech Apraxia A Contemporary Portrait of Speech Apraxia Subtypes of Speech Apraxia Localization Explanations Diagnosis Conclusions
11.
References
After decades of debate, speech apraxia has earned a place in the nosology of neurogenic speech-language disorders. This development may well owe less to strong arguments from true believers than to natural processes that guarantee all conflicts — regardless of right — eventually end. Opponents get tired and interests change. If the conflicts are among older practitioners, positions soften and mature. More and better data accumulate; best
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of all, doubts creep in. This chapter will be about selected arguments, data, and accords. It will also be about doubts.
1.
Definition
Liepmann (1913) was among the first to identify a speech apraxia and differentiate it from aphasia. He said, “In 1900 I called the aphasia of my patient apraxia of the speech muscles” (97). It was from these and other historical materials that Darley (1969) built what has become, for many , the standard definition of speech apraxia, “An articulatory disorder resulting from impairment, as a result of brain damage, of the capacity to program the positioning of speech musculature and the sequencing of muscle movements for the volitional production of phonemes. No significant weakness, slowness, or incoordination in reflex and automatic acts. Prosodic alterations may be associated with the articulatory problem, perhaps in compensation for it” (Darley 1969, 2). This definition of speech apraxia was complete enough to earn the disorder a place in the taxonomy of neurogenic speech-language disorders. However, the boundaries of that place, its actual location in relation to other conditions such as conduction aphasia and dy sarthria, and even the label itself with its implications for underly ing mechanisms have fostered decades of debate and much remains to be resolved. What goes undebated is recognition that brain-damaged speakers exist whose speech is more marred by articulatory substitutions, distortions, distorted substitutions, and dy sprosody than their sensation, cognition, language, and strength and tone suggest it should be. Careful testing usually confirms the diagnosis of what will be called speech apraxia in this chapter.
2.
Related Conditions
Speech apraxia has been called a sy nony m for a variety of other terms including aphemia, cortical dy sarthria, anarthria, and phonetic disintegration (Johns/Darley 1970). Probably each of these terms, as used by at least one group of scholars, refers to a pattern of speech impairment identical to what is being called speech apraxia in this chapter. It is impossible to know for sure, however, until the sound of persons with each of these diagnoses is heard. Unfortunately , clinical sci-
entists seem never to have committed to an exchange of tapes. That leaves published descriptions. Prior to Alajouanine/Ombredane/ Durand (1939), published reports contained so little carefully collected speech-language data that modern readers are left to guess about the similarity of the writer’s and their own use of terms. Compounding the difficulty is that even some modern reports contain insufficient speech-language and neurologic data for confident comparison of subject groups called by different names. However, one condition, Broca’s aphasia, has been described frequently and completely enough to support the position that it is not a sy nony m for speech apraxia. To make the terms sy nony ms is damaging to the conceptual underpinnings of the nosology in neurogenic speech-language disorders. Broca’s aphasia is a language disorder characterized by agrammatism; speech apraxia is not. One related condition, oral apraxia, deserves special attention. Hughlings Jackson’s description (1878) of a patient’s inability to protrude his tongue upon request but ability to do so when eating and drinking is cited as one of the earliest written reports about the condition. Oral apraxia is usually differentiated from speech apraxia, although until recently , co-occurrence was assumed to be common and the two conditions were often described as representing nothing more than different severities of a common deficit in praxis. Data by DeRenzi/Pieczuro/Vignolo (1966) demonstrating that oral apraxia could occur in the absence of speech deficit and could accompany even fluent aphasia helped to change that assumption. The contemporary conclusion seems to be that oral, nonspeech movements and speech movements may be under different patterns of neuromotor control and may be differentially involved.
3.
History
Speech pathologists, neurologists, psy chologists, and linguists (Head 1926; Critchley 1970; Lecours/Nespoulous/Pioger 1987; Lebrun 1976; Benton 1981) appear to have agreed that modern understanding of speech apraxia began with Broca’s description of an expressive abnormality he called aphemia. Broca’s contributions, it is traditionally argued, did not spring from barren soil unnourished by any thing but his own clinical case studies, however. Buckingham (1981) de-
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scribes the influence of the phrenologists and of practitioners such as Bouillaud. Darley ’s papers on apraxia of speech (1968; 1969) are another benchmark in speech apraxia’s history . Not only did Darley write an enduring definition, he provided a durable description of the apraxic speaker’s performance. This description included inconsistent ‚phonemic’ errors of substitution, distortion, omission, and addition accompanied by effortful, trial and error groping. For nearly two decades this description dominated clinical research and education. The y ears between Broca and Darley were not an intellectual wasteland. Alajouanine/ Ombredane/Durand’s description (1939) of what they called the sy ndrome of phonetic disintegration is noteworthy because the experimenters controlled the testing materials and completed both auditory perceptual and acoustic analy ses of speech. Bay (1962) used auditory perceptual evaluation and the glossogram, which measured changes in pressure of the tongue against the palate during a variety of nonspeech tasks, to study a motor speech deficit he called cortical dy sarthria. Shankweiler/Harris (1966) published a carefully designed auditory perceptual analy sis of speech by five patients with the sy ndrome of phonetic disintegration. After Darley ’s papers, an unprecedented flood of studies and position papers, all of which have been reviewed extensively (Wertz/ LaPointe/Rosenbek 1984), appeared. These y ears were also marked by mordant debates, usually fueled by at least a soupcon of data, between those who felt that speech apraxia was a motor disorder and those who felt it was a language disorder. No publication marks the end of what can be called speech apraxia’s history . No wall fell. No treaty of scientific cooperation was signed. No voice was raised that shifted the paradigm for conceptualizing, study ing, and interpreting the data in speech apraxia. Instead what seems to have happened gradually is that the experimental soil began to be worked by fewer researchers and ones less interested in defending what was assumed to be true and more interested in discovering what might be true or at least replicable.
4.
Signs of Speech Apraxia
The goal of this next section is to develop and evaluate a modern profile of speech
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apraxia. Signs of speech apraxia have been identified at three levels of analy sis, the auditory perceptual, the acoustic, and the phy siologic. 4.1. Auditory Perceptual Analysis Auditory perceptual analy sis takes the form of either broad or narrow phonetic transcription. Most of the data contained in the earliest modern descriptions of speech apraxia resulted from broad transcription and suggested that speech sound substitutions were the most frequent apraxic error ty pe. Narrow phonetic transcriptions, while limited in number, are now increasingly common. One of the earliest (Square/Darley /Sommers 1982), revealed that distortions of both consonants and vowels were more frequent than substitutions. Odell/McNeil/Rosenbek/Hunter (1990) followed with a narrow phonetic transcription of consonant productions in words by four pure apraxic subjects. Distortions were the most frequent error ty pe (25%), followed by omissions, substitutions, distorted substitutions, and additions. Odell/ McNeil/Rosenbek/Hunter (1991) also reported the narrow phonetic transcription of vowels for the same four subjects. The mean error rate for vowels was 49% with considerable intra-subject variability . Distortions were the most frequent error ty pe (65%) for three of the four subjects. In another report, Odell/McNeil/Rosenbek/Hunter (1991) had two judges rate three categories of prosodic deviation: abnormalities in sy llabic stress, deviations in intraword temporal parameters, and what were called repeated production difficulties. Sy llabic stress errors were frequent, as were difficulties in making transitions from one sound to the next and in initiating speech. Unfortunately , the data do not say any thing about the degree to which prosodic disturbances are a primary part of apraxic sy mptomatology . A study adequate to the challenge of answering that question appears not to have been done. The most significant finding to emerge from the auditory perceptual data is that speech sound distortions are a prominent part of apraxic sy mptomatology . Another finding for which there was some historical precedent (Lebrun/Buy ssens/Henneaux 1973) is that vowels are as likely to be involved in some apraxic speakers as are consonants. Finally , the data add specificity to the description of prosodic disturbances.
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4.2. Acoustic Analysis Acoustic analy sis has certain advantages in the study of speech apraxia. A major one is that many acoustic features have known relationships to both perceptual phenomena and phy siologic events (Weismer 1984). Acoustic data, therefore, are important in speech apraxia research where increasingly the emphasis is on both description and explanation. The most frequent acoustic analy sis has been of voice onset time (VOT) (Blumstein/ Cooper/Zurif/Caramazza 1977; Blumstein/ Cooper/Goodglass et al. 1980; Shewan/Leeper/Booth 1984; Hoit/Murry /Knopp 1983; Itoh/Sasanuma/Tatsumi et al. 1982) despite controversy over how the data are to be interpreted (Tuller 1984; Ziegler 1984; Blumstein 1981). VOT errors identified in speakers labelled or assumed to be apraxic are usually interpreted as providing evidence of speech sound distortion resulting primarily from dy scoordination of lary ngeal and oral-lingual movements (Freeman/Sands/Harris 1978). A variety of other acoustic abnormalities have also been identified. These include: 1) abnormally long, but highly variable, speech sound durations (Duffy /Gawle 1984; Ry alls 1981); 2) abnormalities in intensity and fundamental frequency variation, especially the latter (Kent/Rosenbek 1983); 3) lingual-lary ngeal, lingual-velar, and lingual-labial phrasing abnormalities (Ziegler/von Cramon 1986); 4) abnormall y long intersegmental durations (Strand/McNeil 1987); 5) longer than normal transitions from sound to sound (Kent/Rosenbek 1983); 6) longer than normal verbal response times even with time to prepare (Strand 1987); and 7) difficulty adjusting speaking rate (Kent/McNeil 1987; McNeil/ Liss/Tseng/Kent 1990) especially in increasing it. 4.3. Physiologic Analysis Phy siologic analy ses, or analy ses using instrumentation to measure movements, are beginning to appear in the speech apraxia literature. A substantial review of the phy siologic data was prepared by McNeil/Kent (1990). They divide the studies into those of force and position control (McNeil/Weismer/Adams/Mulligan 1990); intraarticulator kinematics, including movement duration, velocity , and displacement (Itoh/Sasanuma 1987; Itoh/Sasanuma/Hirose et al. 1980; Robin/ Bean/Folkins 1989; McNeil/Adams 1991;
McNeil/Caligiuri/Rosenbek 1989; McNeil/ Liss/Tseng/Kent 1990); interarticulator kinematics or timing and coordination (Itoh/Sasanuma/Ushijima 1979; Itoh/Sasanuma/Hirose et al. 1980; Hardcastle 1987); and elecy trom ograph y (Shankweiler/Harris/Ta y lor 1968; Forrest/Adams/McNeil 1991; Hough/ Klich 1987; Towne/Crary 1988; McNeil/Prescott/Lemme 1976). The procedures and data in most of these studies are complex and best read in the original. Some tentative conclusions about the data are possible, however. The phy siologic data support the conclusions from other methods of analy sis that distortion and variability are cardinal features of apraxic performance. They also begin lay ing the foundation for a more sophisticated understanding of why apraxic speech sounds the way it does. Dy scoordinated movements of the speech structures seem to be a critical influence. In addition, selected of the data suggest that the perceptual impression of apraxic slowness may have more to do with range than velocity of movement. An even stronger message from the data about the socalled slowness of apraxic speech is that its movement correlates are complex and still to be explored (Adams/McNeil/Weismer 1989). Indeed the relationship of all phy siologic signs to auditory -perceptual signs in speech apraxia is yet to be established. 4.4. Caveats It is easy to exaggerate the power of instruments. For several reasons speech apraxia research’s march toward methods requiring the latest technology is not necessarily a march toward truth. Methods are being used with impaired speakers before sufficient normative data, especially from geriatric control subjects, have been collected. Intuition and informal extrapolation from limited normative data are frequently the shaky bases for conclusions about abnormal speech, including apraxic speech, and the pathophy siology underly ing it. Forrest/Weismer/Adams (1990) discuss the dangers of such an approach. In the absence of sufficient normative data, researchers risk being trapped by the assumption that performance on some measure by one or more apraxic talkers is apraxic performance and that such performance somehow explains the accompany ing speech signs. Probably some of the extant data from apraxic speakers will turn out to be signs of normal aging, some will turn out to reflect
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generalized effects of brain damage or of illness, and some will turn out to be unrelated to speech movement abnormalities. It may result that some of the phy siologic data are less useful and more misleading than are the perceptual despite the greater ‚subjectivity ’ of perceptual analysis. Phy siologic data, and indeed most of the data gathered from apraxic speakers, are threatened from another source as well. Munhall (1989) observes that very few studies have been designed to measure or control variability in speech apraxia. Munhall’s notion is that all speech is variable, and he urges studies of apraxia designed specifically to reveal the variability that is apraxic. Among the few studies designed to separate normal from apraxic variability are those by LaPointe/ Horner (1976) and Deal (1974). Until more studies designed with Munhall’s caveat in mind appear, conclusions about speech apraxia’s nature, and even about its signs, must be tentative indeed.
5.
A Contemporary Portrait of Speech Apraxia
Apraxic speech is lawfully variable, is especially sensitive to phonetic influences such as response length and complexity , and is characterized by a mixture of speech sound distortions and substitutions with distortions and distorted substitutions predominating. Variations in fundamental frequency and intensity are abnormally reduced in some utterances. Apraxic speech is slow because of prolonged transitions, steady states, and intersy llabic pauses. Apraxic speakers have difficulty controlling rate and initiating speech even when they know the utterance to be produced. Movements underly ing the perceptual and acoustic signs are variable but dy scoordination is prominent. A speaker with this pattern of speech and movement performance, if language and cognition including attention and memory , are near normal, can be hy pothesized with a high degree of confidence to have a speech apraxia.
6.
Subtypes of Speech Apraxia
It is traditional to divide apraxic limb and body movements into limb kinetic, ideomotor, and ideational ty pes. Liepmann (1913), a major contributor to this division, say s “There is a moment of fiction in the theoret-
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ical statement” differentiating yt pes of apraxia, but the “division is a very helpful guide in an otherwise very dark sphere” (100). Speech scientists have used Liepmann’s light to aid the search for ty pes of speech apraxia (Luria 1970; Deutsch 1984). Square/Darley / Sommers (1982) studied four apraxic speakers, three with cortical lesions and one with a subcortical lesion. A unique error pattern may have emerged from the analy sis of the subcortical speaker who was described as sounding “pseudo-foreign.” Kertesz (1984) compared 10 cases with what he calls verbal apraxia resulting from lesions of the striatum with twelve patients having cortical lesions. He reported that individual subcortical cases may be different from the cortical group because of ‚lower’ rate, volume, and fluency and that some of the subcortical patients had severe dy sgraphia, a combination also reported by Rosenbek/McNeil/Teetson et al. (1981). It is critical to be cautious with assumptions about speech apraxia subty pes (Robin/ Schienberg 1990). However, with increasingly sophisticated imaging techniques and experimental designs, the time is ripe to go looking for them. The clinical and research dividends may be considerable.
7.
Localization
Mohr and his colleagues (Mohr/Pessin/Finkelstein et al. 1978) published what for many has become the classic reference on speech apraxia’s localization. They identify two sy ndromes characterized by disproportionate difficulty with speech which they call little (probably a sy nony m for speech apraxia) and big Broca aphasia. In little Broca aphasia the lesion is limited to Area 44, or Broca’s area, in the frontal operculum. Mutism which quickly evolves into ‚effortful articulation’ and rapidly resolving language deficit are the signs of little Broca aphasia. Big Broca aphasia, characterized by significant deficits across all language modalities and agrammatic speech, results from a larger lesion involving much of the frontal operculum, insula, and underly ing white matter. This large lesion suggests involvement of the upper division of the left middle cerebral artery , while the lesion in little Broca aphasia suggests involvement of one branch of that division. It has also been posited that speech apraxia may result from parietal (Luria 1970) and subcortical, including basal ganglia (Square/Darley /Sommers 1982) and striatum (Kertesz 1984) lesions. All
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these reports antedate modern brain imaging methods such as positron emission computed tomography (PET) and magnetic resonance imaging (MRI). Modern methods of imaging the brain, autopsy data, and phonetically and linguistically sophisticated motor speech and language testing will refine our understanding of the parietal lobe and basal ganglia’s contributions to motor speech control. Even the extant data, however, support a series of testable hy potheses about the cortical-subcortical network responsible for speech performance. It can be hy pothesized that a region shaped roughly like a py ramid and involving frontal and parietal opercula and the basal ganglia constitute a motor control mechanism. Damage to any part of this mechanism may cause speech apraxia.
8.
Explanations
By calling a speech abnormality apraxia, the clinical scientist is specify ing at least something about the disturbed mechanism underly ing the signs and sy mptoms. Praxis refers to skilled movement and is the responsibility of what might be called a psy chomotor level of motor control (Darle y /Aronson/Brown 1975). In a hierarchical organization of the neural substrates supporting verbal expression, the psy chomotor level resides between the executive and language processing levels. It corresponds in neurolinguistic terms to the third articulation (Lecours/Lhermitte 1969) or interface (Lesser 1978) where phonemic units interact with movement parameters. Buckingham (1979) and Mlcoch/Noll (1980) have published perspicacious reviews of explanatory concepts in apraxia of speech. Buckingham evaluated the early centers and connections approaches to explanation in apraxia. A variety of other explanations, most of which can be called either primarily linguistic or primarily motoric, and debates about which was superior were also reported even in the earliest literature (Buckingham 1979), but were more common after Darley . One modern form of the controversery involving linguistic and motoric explanations, especially popular in the 1970’s and 80’s, was whether the errors in speech apraxia were phonemic/phonologic or phonetic. The phonemic/phonologic-phonetic distinction is increasingly unpopular (Abbs/Rosenbek 1985; Kent/Rosenbek 1983), however. One reason for the unpopularity is that the distinction is
simplistic. Another is that making it requires the highly subjective interpretation of data. Both speech sound substitutions and distortions, for example, may be manifestations of either linguistic (phonemic/phonologic) or motor (phonetic) performance deficits. Another reason is that data supporting it are limited (Folkins/Bleile 1990). The search for better explanations continues. Folkins/Bleile (1990) suggest new terminology , including the term phonomotor, and new research strategies as aids to explaining apraxic signs. They propose tasks which hold phonologic requirements stable while articulatory or motor requirements are being sy stematically altered. Having subjects perform the same utterance several times at different rates or with and without a bite block (Netsell 1985) to stabilize the jaw are examples. It can be hy pothesized that a motor performance deficit would function differently under different conditions while an intact motor performance sy stem would be relatively uninfluenced or no more influenced than the normal speaker’s system. Other neural scientists are also advocating different models and experimental paradigms to guide the next generation of research into the mechanisms underly ing conditions such as speech apraxia. Despite some reservations (Reed 1982), the movement appears to be toward adapting models of motor control, many of which are constructed hierarchically and thereby capable of accommodating the now popularly recognized interactions of cognitive, linguistic, and motor sy stems. Rosenbek/Kent/LaPointe (1984) review a variety of these explanatory concepts. One of the most elaborate attempts to apply models to normal and apraxic movements belongs to Kent/ McNeil (1987). They try to account for the influence of a host of cognitive, affective, linguistic, and motor variables on normal and apraxic speech performance. Their model, like the others previously alluded to, deserves to be studied in the original. They are introduced here primarily as support for the observation that the challenges to explain speech apraxia continue.
9.
Diagnosis
Speech diagnosis requires creating and testing hy potheses about what a speaker has until the number of possibilities is as small as can be and confidence in one of those possibilities is as high as can be. Speech apraxia’s signs
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frequently co-exist with the signs of other similar conditions. In addition, speech apraxia shares many signs, such as speech sound distortions, with other conditions, such as dy sarthria. Therefore, diagnosis requires a battery of speech and oral motor tests and measures of language, cognition, and any other ability such as hearing, which, if impaired, could contribute to a speaker’s sounding apraxic. It also requires considerable clinical acumen. Wertz/LaPointe/Rosenbek (1984) describe an elaborate battery . They recommend formal language tests such as the Boston Diagnostic Aphasia Examination (Goodglass/Kaplan 1972) and the Aachen Aphasia Test (Huber/ Poeck/Willmes 1984). Such tests of reading, writing, auditory and reading comprehension, and special skills are necessary especially to establish the presence and severity of aphasia. Wertz/LaPointe/Rosenbek (1984) also suggest a speech evaluation involving tasks to elicit spontaneous and imitiative speech, diadochokinesis, and measures of variability . These tasks provide controlled responses which the clinician can evaluate for signs of speech apraxia. Comparing spontaneous and imitative speech informs about the possibility of a conduction aphasia, because conduction aphasia and speech apraxia can sound similar in connected speech and different during imitation. Diadochokinetic testing can help rule out a dy sarthria. Because all slowness or irregularity on such testing is not necessarily dy sarthric, however, there is an additional need for a measure of variability such as having the speaker say the same utterance several times. Most dy sarthric speakers will be reasonably consistent and most apraxic speakers will be reasonably variable on such a task. Even this much testing may leave the diagnosis in doubt, however. Repeating the test battery , or portions of it, or using more sensitive tests of one or more ability may help. Kent/Kent (1988) created a flow chart that orders the special procedures that may increase a diagnostician’s confidence about the diagnosis. They recommend four ty pes of assessment. The first is the evaluation of prosody . The second is a collection of ‚performance load tests’ in which response length, rate, phonetic complexity , and other variables known to influence speech apraxia are sy stematically manipulated. The third is the traditional measurement of bulbar function during nonspeech tasks, including procedures contained in oral, nonverbal apraxia testing
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(DeRenzi/Pieczuro/Vignolo 1966). The fourth is maximum performance testing, including vowel prolongation and diadochokinesis with and without a bite block. All these procedures have their pitfalls (Kent/Kent/Rosenbek 1987), but all may help the insightful clinician make decisions. In the acute stage the best diagnostic test may be treatment. Apraxic speakers respond to different treatments than do speakers with the forms of aphasia and dy sarthria. Apraxic speakers hear and try to self-correct with no prompting from the clinician. Apraxic speakers anticipate and try to prevent errors. They are predictably variable and often move closer to targets if the clinician is alert to proper stimulus selection and cueing. Apraxic speakers retain and generalize the lessons of each session. Aphasic and dy sarthric speakers may do some or all of these things, but often not to the same degree; hence the value of experience and acumen in sorting through all these responses and arriving at a confident diagnosis.
10. Conclusions Speech apraxia has been called many things. Some labels seem never to pass across national boundaries, and even if a particular term does travel, the national enthusiasm for its appropriateness is often stopped at the border. Fortunately , neuroscience does not require one vocabulary , and a single enthusiasm would be its death knell. It does require thoughtful hy potheses, careful subject selection and description, exquisite experimental designs and procedures, and clear reporting. Speech apraxia is beginning to benefit from all four. Broca would probably be as pleased as Darley is.
11. References Abbs, J. H. & Rosenbek, J. C. (1985). Some motor control perspectives on apraxia of speech and dy sarthria. In J. Costello (Ed.), Speech disorders in adults. 21—58. San Diego: College-Hill Press, Inc. Adams, J. G., McNeil, M. R. & Weismer, G. (1989, unpublished). Speech movement velocity profiles in neurogenic speech disorders. Paper presented to the American Speech and Hearing Association. St. Louis, Missouri. Alajouanine, T., Ombredane, A. & Durand, M. (1939). Le syndrome de disintegration phonetiqu e dans l’aphasic. Paris: Masson.
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Bay , E. (1962). Aphasia and nonverbal disorders of language. Brain, 85, 411—426. Benton, A. (1981). Aphasia: Historical perspectives. In M. T. Sarno (Ed.), Acqu ired aphasia. 1—25. New York: Academic Press, Inc. Blumstein, S. (1981). Phonological aspects of aphasia. In M. T. Sarno (Ed.), Acqu ired aphasia. 192—255. New York: Academic Press, Inc. Blumstein, S. E., Cooper, W. E., Goodglass, H., Statlender, S. & Gottlieb, J. (1980). Production deficits in aphasia: A voice-onset time analy sis. Brain and Language, 9, 153—170. Blumstein, S. E., Cooper, W. E., Zurif, E. B. & Caramazza, A. (1977). The perception and production of voice-onset time in aphasia. Neuropsychologia, 15, 371—383. Buckingham, H. W. (1979). Explanation in apraxia with consequences for the concept of apraxia of speech. Brain and Language, 8, 202—226. Buckingham, H. W. (1981). A pre-history of the problem of Broca’s aphasia. In R. H. Brookshire (Ed.), Clinical aphasiology: Conference proceedings, 1981. 3—16. Minneapolis: BRK Publishers. Critchley , M. (1970). Aphasiology. London: Edward Arnold. Darley , F. L. (1968, unpublished). Apraxia of speech: 107 y ears of terminological confusion. Paper presented to the American speech and Hearing Association. Denver, Colorado. Darley , F. L. (1969, unpublished). Input and output disturbances in speech and language processing. Paper presented to the American Speech and Hearing Association. Chicago, Illinois. Darley , F. L., Aronson, A. E. & Brown, J. R. (1975). Motor speech disorders. Philadelphia: W. B. Saunders Company. Deal, J. L. (1974). Consistency and adaptation in apraxia of speech. Jou rnal of Commu nication disorders, 7, 135—140. DeRenzi, E., Pieczuro, A. & Vignolo, L. A. (1966). Oral apraxia and aphasia. Cortex, 2, 50—73. Deutsch, S. E. (1984). Prediction of site of lesion from speech apraxic error patterns. In J. C. Rosenbek, M. R. McNeil & A. E. Aronson (Eds.), Apraxia of speech: Physiology-acou stics-lingu istics-management. 113—134. San Diego: College-Hill Press, Inc. Duffy , J. R. & Gawle, C. A. (1984). Apraxic speakers’ vowel duration in consonant-vowel-consonant sy llables. In J. C. Rosenbek, M. R. McNeil & A. E. Aronson (Eds.), Apraxia of Speech: Physiology-aco u stics-ling u istics-management. 167—196. San Diego: College-Hill Press, Inc. Folkins, J. W. & Bleile, K. M. (1990). Taxonomies in biology , phonetics, phonology , and speech motor control. Jou rnal of Speech and Hearing Disorders, 55, 596—611. Forrest, K., Adams, S. & McNeil, M. R. (1991).
Perioral EMG activity in aphasic, apraxic, and dy sarthric speakers. In C. Moore, D. Beukelman & K. Yorkston (Eds.), Motor speech disorders: Management approaches. 147—171. Austin: pro-ed. Forrest, K., Weismer, G. & Adams, S. (1990). Statistical comparison of movement amplitudes from groupings of normal geriatric speakers. Jou rnal of Speech and Hearing Research, 33, 286—389. Freeman, F. J., Sands, E. S. & Harris, K. S. (1978). Temporal coordination of phonation and articulation in a case of verbal apraxia: A voice onset time study. Brain and Language, 6, 106—111. Goodglass, H. & Kaplan, E. (1972). The assessment of aphasia and related disorders. Philadelphia: Lea and Febiger. Hardcastle, W. J. (1987). Electropalatographic study of articulation disorders in verbal dy spraxia. In J. H. Ry alls (Ed.), Phonetic approaches to speech prod u ction in aphasia and related disorders. 113—136. Boston: A College-Hill Publication, Little, Brown and Company. Head, H. (1926). Aphasia and kindred disorders of speech. Volu me 1. London: Cambridge University Press. Hoit, J., Murry , T. & Kopp, H. G. (1983). Voice onset time production and perception in apraxic subjects. Brain and Language, 20, 329—339. Hough, M. S. & Klich, R. J. (1987). Effects of word length on lip EMG activity in apraxia of speech. In R. H. Brookshire (Ed.), Clinical aphasiology, Volu me 17. 271—276. Minneapolis: BRK Publishers. Huber, W., Poeck, K. & Willmes, K. (1984). The Aachen aphasia test. In F. C. Rose (Ed.), Advances in neu rology, volu me 42, progress in aphasiology. 291—303. New York: Raven Press. Itoh, M. & Sasanuma, S. (1987). Articulatory velocities of aphasic patients. In J. H. Ry alls (Ed.), Phonetic approaches to speech produ ction in aphasia and related disorders. 137—161. Boston: A CollegeHill Production, Little, Brown and Company. Itoh, M., Sasanuma, S., Hirose, H., Yoshioka, H. & Ushijima, T. (1980). Abnormal articulatory dy namics in a patient with apraxia of speech: X-ray microbeam observation. Brain and Langu age, 11, 66—75. Itoh, M., Sasanuma, S., Tatsumi, I., Murakami, S., Fukusako, Y. & Suzuki, T. (1982). Voice onset time characteristics in apraxia of speech. Brain and Language, 17, 193—210. Itoh, M., Sasanuma, S. & Ushijima, T. (1979). Valar movements during speech in a patient with apraxia of speech. Brain and Language, 7, 227—239. Jackson, H. (1878). Remarks on non-protrusion of the tongue in some cases of aphasia. Lancet, 1, 716. Johns, D. F. & Darley , F. L. (1970). Phonemic variability in apraxia of speech. Jou rnal of Speech and Hearing Research, 13, 556—583.
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Kent, R. D. & Kent, J. F. (1988). Motor speech disorders. In D. E. Yoder & R. D. Kent (Eds.), Decision-making in speech-lang u age pathology. 154—155. Toronto: B. C. Decker, Inc. Kent, R. D., Kent, J. F. & Rosenbek, J. C. (1987). Maximum performance tests of speech production. Jou rnal of Speech and Hearing Disorders, 52, 367—387. Kent, R. D. & McNeil, M. R. (1987). Relative timing of sentence repetition in apraxia of speech and conduction aphasia. In J. H. Ry alls (Ed.), Phonetic approaches to speech produ ction in aphasia and related disorders. 181—220. Boston: A College-Hill Production, Little, Brown and Company. Kent, R. D. & Rosenbek, J. C. (1983). Acoustic patterns of apraxia of speech. Jou rnal of Speech and Hearing Research, 26, 231—249. Kertesz, A. (1984). Subcortical lesions and verbal apraxia. In J. C. Rosenbek, M. R. McNeil & A. E. Aronson (Eds.), Apraxia of speech: Physiology-aco u stics-ling u istics-management. 73—90. San Diego: College-Hill Press, Inc. LaPointe, L. L. & Homer, J. (1976). Repeated trials of words by patients with neurogenic phonological selection-sequencing impairment (apraxia of speech). In R. H. Brookshire (Ed.), Clinical aphasiology: Conference proceedings. 261—277. Minneapolis: BRK Publishers. Lebrun, Y. (1976). Neurolinguistic models of language and speech. In H. Whitaker & H. A. Whitaker (Eds.), Stu dies in neu rolingu istics, Volume 1, 1—30. New York: Academic Press. Lebrun, Y., Buy ssens, E. & Henneaux, J. (1973). Phonetic aspects of anarthria. Cortex, 9, 126—135. Lecours, A. R. & Lhermitte, F. (1969). Phonemic paraphasias: Linguistic structures and tentative hy potheses. Cortex, 5, 193—228. Lecours, A. R., Nespoulous, J. L. & Pioger, D. (1987). Jacques Lordat or the birth of cognitive neuropsy chology . In E. Keller & M. Gopnik (Eds.), Motor and sensory processes of langu age, 1—16. New Jersey : Lawrence Erlbaum Associates, Publishers. Lesser, R. (1978). Lingu istic investigations of aphasia. London: Edward Arnold. Liepmann, H. (1913). Motor aphasia, anarthria, and apraxia. Translations of the 17th international congress of medicine (London). Section X 1, Part 2, 97—106. Luria, A. R. (1970). Trau matic aphasia: Its syndromes, psychology and treatment. The Hague: Mouton. McNeil, M. R. & Adams, S. (1991). A comparison of speech kinematics among apraxic, conduction aphasic, ataxic dy sarthric and normal geriatric speakers. In T. E. Prescott (Ed.), Clinical aphasiology, Volume 19. 279—294. Austin: pro-ed. McNeil, M. R., Caligiuri, M. & Rosenbek, J. C.
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(1989). A comparison of labio-mandibular kinematic durations, displacements, velocities and dy smetrias on apraxic and normal adults. In T. E. Prescott (Ed.), Clinical aphasiology, Volu me 18. 173—193. Boston: A College-Hill Production, Little, Brown and Company. McNeil, M. R. & Kent, R. (1990). Motoric characteristics of adult aphasic and apraxic speakers. In G. R. Hammond (Ed.), Advances in psychology: cerebral control of speech and limb movements. 349—386. New York: Elsevier/North Holland. McNeil, M. R., Liss, J., Tseng, C.-H. & Kent, R. D. (1990). Effects of speech rate on the absolute and relative timing of apraxic, and conduction aphasic sentence production. Brain and Langu age, 38, 135—158. McNeil, M. R., Prescott, T. E. & Lemme, M. L. (1976). An application of electromy ographic biofeedback to aphasia/apraxia treatment. In R. H. Brookshire (Ed.), Clinical aphasiology: Conference proceedings, 1976. 151—171. Minneapolis: BRK Publishers. McNeil, M. R., Weismer, G., Adams, S. & Mulligan, M. (1990). Oral structure nonspeech motor control in normal, dy sarthric, aphasic and apraxic speakers: Isometric force and static position control. Jou rnal of Speech and Hearing Research, 33, 255—268. Mlcoch, A. G. & Noll, J. D. (1980). Speech production models as related to the concept of apraxia of speech. Speech and Language, 4, 201—238. Mohr, J. P., Pessin, M. S., Finkelstein, S., Funkenstein, H. H., Duncan, G. W. & Davis, K. R. (1978). Broca aphasia: Pathologic and clinical. Neurology, 28, 311—324. Munhall, K. G. (1989). Articulatory variability . In P. Square-Storer (Ed.), Acqu ired apraxia of speech in aphasic adu lts. 64—83. London: Tay lor and Francis. Netsell, R. (1985). Construction and use of a biteblock in evaluating and treating speech disorders. Jou rnal of Speech and Hearing Disorders, 50, 103—106. Odell, K., McNeil, M. R., Rosenbek, J. C. & Hunter, L. (1990). Perceptual characteristics of consonant productions by apraxic speakers. Journal of Speech and Hearing Disorders, 55, 345—359. Odell, K., McNeil, M. R., Rosenbek, J. C. & Hunter, L. (1991). A perceptual comparison of prosodic features in apraxia of speech and conduction aphasia. In T. E. Prescott (Ed.), Clinical aphasiology, Volume 19. 295—306. Austin: pro-ed. Odell, K., McNeil, M. R., Rosenbek, J. C. & Hunter, L. (1991). Perceptual characteristics of vowel and prosody production in apraxic, aphasic, and dy sarthric speakers. Jou rnal of Speech and Hearing Research, 34, 67—80. Reed, E. S. (1982). An outline of a theory of action systems. Journal of Motor Behavior, 14, 98—134.
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41. 1. 2. 3. 4. 5.
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Minneapolis: BRK Publishers. Strand, E. A. (1987, unpublished). Acoustic and response time measures in utterance production: A comparison of apraxic and normal speakers. Doctoral dissertation, University of Wisconsin-Madison: Madison, Wisconsin. Strand, E. A. & McNeil, M. R. (1987). Evidence for a motor performance deficit versus a misapplied rule sy stem in the temporal organization of utterances in apraxia of speech. In R. H. Brookshire (Ed.), Clinical aphasiology, Volu me 17. 260—270. Minneapolis: BRK Publishers. Towne, R. L. & Crary , M. A. (1988). Verbal reaction time patterns in aphasic adults: Consideration for apraxia of speech. Brain and Langu age, 35, 138—153. Tuller, B. (1984). On categorizing aphasic speech errors. Neuropsychologia, 22, 547—557. Weismer, G. (1984). Acoustic descriptions of dy sarthric speech: Perceptual correlates and phy siological inferences. In J. C. Rosenbek (Ed.), Current views of dysarthria. 293—314. Seminars in speech and language. Volume 5, Number 4. New York: Thieme Inc. Wertz, R. T., LaPonte, L. L. & Rosenbek, J. C. (1984). Apraxia of speech in adu lts: The disorder and its management. Orlando, Florida: Grune and Stratton. Ziegler, W. (1984). What can the spectral characteristics of stop consonants tell us about the realization of place of articulation in Broca’s Aphasia? A reply to Shinn and Blumstein. Brain and Language, 23, 167—170. Ziegler, W. & von Cramon, D. (1986). Timing deficits in apraxia of speech. Eu ropean Archives of Psychiatry and Neurological Sciences, 236, 44—49.
John C. Rosenbek, Madison, Wisconsin (USA)
Spastic Dysarthria Introduction Attributes of Spastic Dysarthria The Pathophysiology of Spasticity Management of the Individual with Spastic Dysarthria References
Introduction
Spastic dy sarthria designates a speech disorder resulting from an inferred or demonstrated neurologic condition of spasticity , or
upper motor neuron lesion. The description of the speech disorder therefore is twofold: analy sis of the speech abnormalities, and consideration of the underly ing pathophy siology in relation to the speech disturbances. 1.1. Terminology Spasticity is a neurologic term that denotes a sy ndrome of hy pertonus with exaggeration of stretch reflexes, resulting from lesions to the corticobulbar or corticospinal tracts. A frequently cited definition of spasticity is from
41. Spastic Dysarthria
Lance (1980): spasticity is a motor disorder characterized by a velocity -dependent increase in tonic stretch reflexes (“muscle tone”) with exaggerated tendon jerks, resulting from hy perexcitability of the stretch reflex, as one important component of the upper motor neuron sy ndrome. Clinically , spasticity is usually accompanied by paresis so that characterization of the motor impairment is twofold (Delwaide/Young 1985). 1.2. Relationship between Speech and Neurologic Impairment First, it should be stressed that spasticity is a heterogeneous disorder, with the severity , distribution, and nature of clinical signs vary ing with the localization and combination of lesions as well as with the time between examination and insult (Delwaide/Young 1985). Not all individuals with spasticity have a speech disturbance. Unilateral damage often is associated with spastic hemiplegia, in which speech disturbances tend to be transient or mild, but bilateral damage, or pseudobulbar palsy , is more serious and can produce severe dy sarthria (Edwards 1984; Love/Webb 1986). The unilateral form is less impairing to speech because the speech muscles generally receive bilateral innervation from the cranial nerves. The dy sarthria associated with spasticity is variously termed spastic dy sarthria, upper motor neuron dy sarthria, or pseudobulbar dy sarthria. The speech disturbances often result from impairments in the respiratory , lary ngeal and upper airway (supraglottal) sy stems. Spastic dy sarthria is distinguished from spastic (spasmodic) dy sphonia which has different characteristics and perhaps a different etiology, or etiologies (Schaefer 1983).
2.
Attributes of Spastic Dysarthria
The speech characteristics associated with spastic dy sarthria have been reported for both acquired dy sarthria (pseudobulbar palsy ) and congenital dy sarthria (the latter appearing in children with spastic cerebral palsy ). Reports in the literature usually discuss these two forms of the disorder separately and this account will do likewise. 2.1. Pseudobulbar Dysarthria In the classic description and classification of dy sarthria, Darley /Aronson/Brown (1969 a, b; 1975) rated 38 auditory -perceptual dimensions of dy sarthric speech and identified the
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most prominent clusters of dimensions for several ty pes of dy sarthria. Their data for acquired spastic yd sarthria (pseudobulbar palsy ) indicated the following ranked dimensions characteristic of the speech disorder: 1 — imprecise consonants; 2 — monopitch; 3 — reduced stress; 4 — harsh voice; 5 — monoloudness; 6 — pitch level; 7 — rate; 8 — hy pernasal; 9 — strained-strangled voice; and 10 — short phrases. Several of these dimensions (imprecise consonants, monopitch, harsh voice, monoloudness, rate, hy pernasal and short phrases) were commonly associated with other dy sarthric ty pes identified by Darley et al. The dimensions of pitch level, reduced stress and strained-strangled voice were more narrowly associated with spastic dy sarthria. It is noteworthy that the deviant dimensions embrace a number of voice and resonance qualities. Enderby ’s work (1983; 1986) paralleled that of Darley /Aronson/Brown in her attempts to identify distinguishing characteristics of dy sarthric groups. With respect to spastic dy sarthria, she reported the main characteristics to be: poor movement of the tongue in speech, slow rate of speech, poor phonation and intonation, poor intelligibility in conversation, reduced alternating movements of the tongue, poor lip movements in speech, reduced maintenance of palatal elevation, poor intelligibility of description, hy pernasality and lack of control in volume. As in the case of the Darley /Aronson/Brown studies, Enderby ’s analy ses point to several dimensions of speech and voice impairment. Whereas perceptual rating is the predominant method used in clinical assessment, acoustic and phy siologic methods are an increasing source of information in clinical practice and research. Acoustic measurements of diadochokinetic sy llable repetition reported by Portnoy /Aronson (1982) showed that spastic patients were both slower and more variable than normal-speaking controls. X-ray observations of spastic dy sarthria indicate that the speech movements are slow and of restricted range (Kent/Netsell/Bauer 1975; Hirose/Kiritani/Sawashima 1980). Ziegler/von Cramon (1986) concluded from an acoustic study that gross lingual movements were more impaired for the dorsum than for the blade. The acoustic measures also showed that spastic subjects, relative to normals, had increased word and sy llable duration, centralized vowels and ineffectively articulated plosives. The spastic subjects tended to have
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a retracted tongue position, which was judged to contribute to their speech difficulties. Ziegler/von Cramon (1986) reported that spastic subjects often had considerable difficulty with the task of rapid diphthong repetition. Some subjects experienced an articulatory breakdown shortly after beginning the task, whereas others accomplished the task with slow, prolonged articulatory movements. The interpretation for this difficulty was that the spastic subjects were impaired in their ability to alter rapidly the sy nergistic-antagonist patterns of muscle activation. These x-ray and acoustic data help to explain the high ratings for the dimension of imprecise consonants in the Darley /Aronson/ Brown (1969 a) results for spastic dy sarthria. They also help to identify sensitive tasks for speech assessment. For example, the Ziegler/ von Cramon (1986) study suggests that rapid repetition of diphthongs is a sensitive speech task.
ger/Kent study of congenital spastic vs athetoid cerebral palsy and the results obtained by Darley /Aronson/Brown for the similar neurologic pairing of spastic (pseudobulbar) vs slow hy perkinesia (dy stonia) dy sarthria in adults. The uniquely characterizing features for the two groups studied by Darley /Aronson/Brown were: Spastic — low pitch; hy pernasality , pitch breaks, breathy voice, and excess and equal stress; slow hy perkinesic — irregular articulatory breakdowns, inappropriate silences, prolonged intervals and phonemes, excessive loudness variation and voice stoppage. Common features between the congenital and acquired forms of spastic dy sarthria are hy pernasality , breathy voice, and change in voice quality or pitch. Common features between congenital athetoid and acquired dy stonic dy sarthria are voice stoppages and slow rate (the latter being equivalent to prolonged intervals and phonemes).
2.2. Dysarthria in Spastic Cerebral Palsy
3.
Early reports on the dy sarthria in spastic cerebral palsy in children were inconsistent in their description of speech characteristics. Many of these studies attempted with little success to define the differences in speech and voice between athetoid and spastic cerebral palsy (By rne 1959; Hedges 1955; Irwin 1955; Leith 1954; Rutherford 1939; Shapiro 1960). More recently , Workinger/Kent (1991) reported that although the differences between the two ty pes of dy sarthria are subtle, the most characteristic dimensions of each were as follows: spastic — consistent hy pernasality , breathy voice, and voice quality change; athetoid — reduced stress, inappropriate voice stoppage or release; and slow rate. The most characteristic dimensions for the children with spastic cerebral palsy pertained to resonance and voice quality , whereas the most characteristic dimensions for the athetoid group indicated difficulties with timing and coordination of movements. Workinger/Kent also reported that experienced listeners could distinguish spastic and athetoid speakers. Earlier research with inexperienced listeners failed to demonstrate a differentiation of the two types (Hedges 1955, Shapiro 1960).
The usual neurologic characterization of spasticity is in terms of increased limb tone (claspknife ty pe of resistance to passive movement), exaggerated tendon jerks and clonus, Babinski responses in the lower extremities, and impairment of voluntary control of skeletal muscles. The pathophy siology has been described in terms of a twofold imbalance between excess excitation (such as increased phasic stretch reflexes) and deficient inhibition (such as suppression of the tonic vibration reflex, reflex irradiation and abnormal silent intervals in an electromyogram). y M klebust/Gottlieb/Penn/Agarwal (1982) drew attention to another neurological feature in patients with spasticity resulting from perinatal suprasegmental insults. They determined from electromy ographic recordings that these patients had a “reciprocal excitation,” a phenomenon in which segmental stretch reflexes are simultaneously expressed in the agonist, stretched muscle and the antagonistic, shortening muscle. This pattern contrasts with the normal pattern of reciprocal inhibition. M y klebust/Gottlieb/Penn/ Agarwal concluded that their results require an expansion of the classic definition of cerebral palsy as a disorder involving solely the brain. Their suggested redefinition includes damage to the “immature suprasegmental structure that imposes a secondary , developmental disorder on the spinal cord” (My klebust/Gottlieb/Penn/Agarwal 1982, 373).
2.3. Similarities between the Acquired and Congenital Dysarthrias Some similarities can be seen between the results summarized above from the Workin-
The Pathophysiology of Spasticity
41. Spastic Dysarthria
The nonspeech (feeding) movements of biting, sucking, swallowing and chewing were compared with speech articulation in a group of 60 cerebral-palsied subjects by Love/Hagerman/Taimi (1980). Although the nonspeech and speech performances were related, individual subjects did not necessarily exhibit the group pattern. For example, of 19 subjects who were rated as having no speech, two of them had adequate feeding skills. Love/Hagerman/Taimi also reported that there was no sy stematic relationship between speech ability and the presence of abnormal oral reflexes. Barlow/Abbs (1984) investigated the ability of subjects with congenital spasticity to regulate fine forces in the lips, tongue and jaw. These three muscle sy stems differ in the density of muscle spindles and presence of monosy naptic reflexes. The lips apparently lack spindles, the tongue contains a modest number of spindles in some fibers, and the jaw is comparatively well endowed with spindles. If hy peractivity of muscle-spindle monosy naptic reflexes were a primary determinant of the motor impairment in spasticity , then it would be predicated that the three muscle sy stems would be impaired to different degrees. The results indicted that, generally , force control was poorest for the tongue and nearly equivalent for the lips and jaw. This result argues against the explanation of impaired orofacial movements in terms of hy peractivity of muscle-spindle monosy naptic reflexes. Although Barlow/Abbs reported that their spastic subjects had difficulties in fine force control, Ziegler/von Cramon (1986) observed relatively little impairment in the ability of their spastic subjects to sustain a fricative articulation (which was considered to be a task involving fine force control). Neilson/O’Dw y er (1981) similarl y concluded that hy pertonus is a not a causal factor in the impaired speech movements of spastic subjects. In asking what does cause the dy sarthria in cerebral palsy , they pointed to a possible motor learning deficit as proposed by Kent/Netsell (1978) for athetoid cerebral palsy . They explained that if “motor commands are generated on the basis of previously learned correlations between motor events and their sensory consequences ..., then impairment of sensory -motor integration processes involved in establishing such correlations should disrupt the ability to formulate appropriate motor commands” (Kent/ Netsell 1978, 1018). In this connection, the results of M y kelbust/Gottlieb/Penn/Agarwal
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should be recalled: a developmental disorder may contribute to the motor impairment in spastic cerebral palsy . Evarts (1985) proposed that the negative sy mptoms following py ramidal tract lesions could be explained in terms of emergent features in the motor cortex. Specifically , he pointed to impairment of emergent properties of py ramidal tract neurons associated with short-latency , goal-oriented and set-dependent movements. A direction for future research, then, is to identify the aspects of spasticity that are most closely associated with impaired movements. Recent research does not indicate that hy pertonus is the only , or even the primary , cause of the movement disorder. Particularly with respect to speech movements, it may be necessary to consider the participation of the motor cortex in the regulation of the affected musculature.
4.
Management of the Individual with Spastic Dysarthria
Medical management ty pically relies on chemotherapy for the spasticity (accompany ing paraly sis is not treatable by such means). The primary agents are benzodiazepines (especially diazepam), baclofen and dantrolene (Helme 1986). Phy sical therapy often is useful, especially to prevent contracture. Less frequently used managements include peripheral nerve blockade, electrical stimulation of the cerebellum, and intrathecal phenol injection. Suggestions for speech management have been discussed by Aten (1983), who relied heavil y on the Darle y /Aronson/Brown (1969 a) rating sy stem to identify the speech abnormalities and plan respective treatments. Aten recommended that treatment begin with the most deviant perceptual dimension. He suggested specific interventions aimed at the following objectives: facilitating air flow, improving intelligibility , reducing hy peradduction of the vocal folds, reducing length of utterance, and achieving muscular and emotional balance. Linebaugh/Wolfe (1984) noted that intelligibility and naturalness decreased as sy llable duration increased in spastic speakers. This result may mean that reduction of word and sy llable durations is a reasonable goal for speech management. However, there is no clear evidence to show that shortening of durations will of itself lead to improved intelligibility . Vogel/von Cramon (1983) de-
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scribed articulatory recovery in five patients with traumatic mutism, three of whom presented with spasticity . Recovery of articulatory ability was summarized in terms of four stages, which, with the exception of one patient, spanned an interval of three months or less.
5.
References
Aten, J. L. (1983). Treatment of spastic dy sarthria. In W. H. Perkins (Ed.), Cu rrent Therapy of Commu nication Disorders. Dysarthria and Apraxia. 69—77. New York: Thieme-Stratton. Barlow, S. M. & Abbs, J. H. (1984). Orofacial fine motor control impairments in congenital spasticity : Evidence against yh pertonus-related performance deficits. Neurology, 34, 145—150. By rne, M. (1959). Speech and language development of athetoid and spastic children. Jou rnal of Speech and Hearing Research, 24, 231—240. Darley , F. L., Aronson, A. E., & Brown, J. R. (1969 a). Differential diagnostic patterns of dy sarthria. Jou rnal of Speech and Hearing Research, 12, 246—269. Darley , F. L., Aronson, A. E., & Brown, J. R. (1969 b). Clusters of deviant speech dimensions in the dy sarthrias. Jou rnal of Speech and Hearing Research, 12, 462—496. Darley , F., Aronson, A., & Brown, J. (1975). Motor Speech Disorders. Philadelphia: W. B. Saunders. Delwaide, P. J. & Young, R. R. (1985). Clinical Neu rophysiology in Spasticity. Amsterdam: Elsevier. Edwards, M. (1984). Disorders of Articu lation. Wien: Springer-Verlag. Enderby , P. (1983). Frenchay Dysarthria Assessment. San Diego: College-Hill. Enderby , P. (1986). Relationships between dy sarthric groups. British Jou rnal of Disorders of Communication, 21, 189—197. Evarts, E. V. (1985). Emergent features in motor cortex as key s to negative sy mptoms following py ramidal tract lesions. In P. J. & Delwaide R. R. Young (Eds.), Clinical Neu rophysiology in Spasticity. 13—25. Amsterdam: Elsevier. Hedges, T. A. (1955). The relationship between speech understandability and the diadochokinetic rates of certain speech musculatures among individuals with cerebral palsy . Unpublished doctoral dissertation, Ohio State Universit y , Columbus, Ohio, U.S.A. Helme, R. D. (1986). Movement disorders. In M. A. Samuels (Ed.), Manu al of Neu rologic Therapeu tics, 3rd Ed. 316—334. Boston: Little, Brown. Hirose, H., Kiritani, S., & Sawashima, M. (1980). Patterns of dy sarthric movements in patients with am y otrophic lateral sclerosis and pseudobulbar
palsy . Annu al Bu lletin of the Research Institu te of Logopedics and Phoniatrics (Tokyo) 14, 263—272. Irwin, O. C. (1955). Phonetic equipment of spastic and athetoid children. Jou rnal of Speech and Hearing Disorders, 20, 54—57. Kent, R. D. & Netsell, R. (1978). Articulatory abnormalities in athetoid cerebral palsy . Jou rnal of Speech and Hearing Disorders, 43, 353—373. Kent, R. D., Netsell, R., & Bauer, L. L. (1975). Cineradiographic assessment of articulatory mobility in the dy sarthrias. Jou rnal of Speech and Hearing Disorders, 40, 467—480. Lance, J. W. (1980). Sy mposium sy nopsis. In R. G. Feldman, R. R. Young, & W. P. Keollo (Eds.), Spasticity: Disordered Motor Control. 485—494. Chicago: Year Book Publishers. Leith, W. R. (1954). A comparison of judged speech characteristics of athetoids and spastics. Unpublished master’s thesis, Purdue University , West Lafayette, Indiana, U.S.A. Linebaugh, C. W. & Wolfe, V. E. (1984). Relationships between articulation rate, intelligibility , and naturalness in spastic and ataxic speakers. In M. R. McNeil, J. C. Rosenbek, & A. E. Aronson (Eds.), The Dysarthrias: Physiology, Acou stics, Perception, Management. 197—205. San Diego: College-Hill Press. Love, R. J., Hagerman, E. L., & Taimi, E. G. (1980). Speech performance, dy sphagia and oral reflexes in cerebral palsy . Jou rnal of Speech and Hearing Disorders, 45, 59—75. Love, R. J. & Webb, W. G. (1986). Neu rology for the Speech-Langu age Pathologist. New York: Butterworths. My klebust, B. M., Gottlieb, G. L., Penn, R. D., & Agarwal, G. C. (1982). Reciprocal excitation of antagonistic muscles as a differentiating feature in spasticity. Annals of Neurology, 12, 367—374. Neilson, P. D. & O’Dwy er, N. J. (1981). Pathophy siology of dy sarthria in cerebral palsy . Journal of Neu rology, Neu rosu rgery and Psychiatry, 44, 1013—1019. Portnoy , R. A. & Aronson, A. E. (1982). Diadochokinetic sy llable rate and regularity in normal and in spastic and ataxic dy sarthric speakers. Journal of Speech and Hearing Disorders, 47, 324—328. Rutherford, B. (1939). Frequency of articulation substitutions in children handicapped by cerebral palsy . Jou rnal of Speech and Hearing Disorders, 4, 285—287. Schaefer, S. (1983). Neuropathology of spasmodic dysphonia. Laryngoscope, 93, 1183—1204. Shapiro, J. (1960). An investigation of the ability of auditors to assess athetoid and spastic cerebral palsy by listening to speech samples. Unpublished master’s thesis, Sy racuse University , Sy racuse, New York, U.S.A. Workinger, M. S. & Kent, R. D. (1991). Perceptual analy sis of the dy sarthrias in children with athetoid
42. Flaccid Dysarthria
and spastic cerebral palsy . In C. Moore, K. Yorkston & D. Beukelman (Eds.), Dysarthria and Apraxia of Speech: Perspectives on Management. Baltimore, Maryland: Brookes Publishing Co. Vogel, M. & Cramon, D. von (1983). Articulatory recovery after traumatic mutism. Folia Phoniatrica, 35, 294—309.
457
Ziegler, W. & Cramon, D. von (1986). Spastic dy sarthria after acquired brain injury : An acoustic study . The British Jou rnal of Disorders of Commu nication, 21, 173—187.
Raymond D. Kent, Madison, Wisconsin (USA)
42. Flaccid Dysarthria 1. 2.
3. 4. 5.
1.
Introduction Peripheral Neuromuscular Structures and Speech Characteristics Associated with Flaccid Dysarthria Neurological Causes of Flaccid Dysarthria Management References
Introduction
Flaccid dy sarthria (also referred to as ‚peripheral dy sarthria’, or ‚lower motor neuron dy sarthria’) results from damage to the peripheral nervous sy stem (PNS). The PNS can be affected by a wide variety of disease processes, and the damage to speech functions can be quite selective. This chapter, therefore, will present an overview of the peripheral neuromuscular structures involved in speech, and will look at those disorders of the PNS which lead to dy sarthric speech sy mptoms. The structures involved include the brainstem nuclei of the cranial nerves mentioned below which carry motor and/or sensory information, the anterior horn cells and the peripheral nerves involved in breathing, the neuromuscular junction, and the muscles. The clinical results of lower motor neuron disease are most obvious when there is complete damage to the peripheral nerve as caused by trauma. The immediate effect is complete paraly sis of dependent muscles, regional loss of sensation, and progressive atrophy of the muscles as a result of disuse; the degree of atrophy is proportional to the number of damaged nerve fibers. Reflexes are absent. The muscles also become lax (flaccid). Electromy ographic investigation shows characteristic changes. In most neurogenic diseases the effects of denervation appear more slowly than in the case mentioned above. The resistance of muscles to passive movements is decreased, a condition known as hy potonia. Further clinical
signs of neurogenic disorders are fasciculations (visible twitches of muscle), and fibrillations which are only detectable by electromy ography . Fasciculations are yt pical for slowly progressing diseases and are uncommon in peripheral neuropathies.
2.
Peripheral Neuromuscular Structures and Speech Characteristics Associated with Flaccid Dysarthria
More than any other ty pe of dy sarthria, flaccid dy sarthria is far from being a uniform sy ndrome. The speech sy mptoms vary depending upon which particular nerve(s) and/ or muscles are primarily affected. The neurology of flaccid dy sarthria therefore necessitates a sy stematic evaluation of several components of the vocal tract, including respiratory , lary ngeal, velophary ngeal and orofacial structures. A differentiated knowledge of neuromuscular structures and functions is essential for the clinician so that he/she can identify the overall pattern of motor speech dy sfunction and can recognize subtle changes which occur in progressive diseases. 2.1. Respiration The primary muscles of the respiratory sy stem (inspiratory : diaphragma, external intercostals, and interchondral portion of the internal intercostals; expiratory : rectus abdominis, external and internal oblique abdominis, and transversus abdominis) are innervated by a sy stem involving the multiple innervation patterns provided by the brachial and cervical plexus and direct spinal nerves. The sites of the cell bodies comprise the 3rd—5th cervical and 1st—12th thoracic and 1st lumbar segments of the spinal cord. Clinically significant
458
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sy mptoms of flaccid paraly sis of respiratory function (vary ing depending on the site of motor neuron lesion) may be marked weakness of inspiratory and/or expiratory breathing, short or inadequate linguistic phrasing, decreased vital capacity , reduced loudness, and asy mmetrical or abnormal breathing patterns (e. g. “reversed breathing” as defined by Davis 1987). (For details relating to methods of investigation of respiratory function as well as respiratory dy sfunction in flaccid dy sarthria see Hixon/Putnam/Sharp (1983).) 2.2. Phonation Two branches of the vagus nerve (X) — the external branch of the superior lary ngeal nerve and the recurrent lary ngeal nerve are essential to phonatory functions. The intrinsic muscles of the lary nx — except the cry cothroid — are all supplied by the recurrent lary ngeal nerve, a main branch of the cranial nerve X. The external branch of the superior lary ngeal nerve carries motor axons to the cricothy roid muscle. — Sensory information from the mucous membrane of the lary nx above the level of the vocal folds is carried by branches of the internal lary ngeal nerve. The mucous membrane below the level of the vocal folds is supplied by the recurrent lary ngeal nerve. Both, the internal and the recurrent lary ngeal nerve carry afferent fibers from stretch receptors of the intrinsic lary ngeal muscles. Flaccid dy sphonia may result from damage to the vagus nerve at any point along its pathway from the nucleus ambiguus in the brainstem to the lary ngeal musculature. A lesion above the bifurcation of the phary ngeal branches paraly zes the cricothy roid muscle and all other intrinsic lary ngeal muscles on the side of the lesion. The unilateral paraly sis or weakness produces breathy or hoarse voice quality , reduced range of pitch and loudness. The affected vocal fold is fixed in an abducted position. In the case of bilateral lesions only whispery voice (aphonia) is possible. If there is a lesion of the recurrent lary ngeal nerve only , the vocal fold is fixed in a paramedian position, and voice quality is breathy or hoarse. Bilateral lesion would make breathing difficult. Superior and recurrent lary ngeal nerves may be damaged simultaneously or selectively . Consequently , the functions of the intrinsic lary ngeal musculature will be either spared or disturbed. Details on the effects of lesions on the vagus nerve as well as information regarding examination techniques and differential diagnosis are described in Aron-
son (1985, 79—98). 2.3. Articulation The motor innervation of the articulators of speech is mainly provided by the cranial nerves V, VII, XI, and XII. The supralary ngeal mechanism serves not only as an acoustic resonator but also as a sound generator, with the velophary ngeal valve play ing a major role. The principal motor innervation of velar muscles is derived from the cranial accessory nerve, which arises from the nucleus ambiguous in the medulla oblongata. It travels with the vagus nerve, and clinically , disorders of the cranial accessory are regarded as disorders of the vagus nerve. A unilateral lesion will normally cause slight hy pernasality . Incomplete velophary ngeal closure caused by bilateral paraly sis reduces intraoral pressure and consequently the sharpness of oral consonant production, reducing sound production to only nasal vowels and consonants in its most severe form. Insufficient velophary ngeal valving may also have a major impact on respiration (premature exhaustion of air support) and phonation (loss of voicing contrasts, compensatory hy pertension of the vocal folds) as result of nasal air escape. All intrinsic and extrinsic tongue muscles except the palatoglossus muscle receive their motor innervation from the hy poglossal nerve. It exits the brainstem between the py ramid and the inferior olive, leaving the cranium via the hy poglossal foramen and running caudally and anteriorly to the level of the hy oid bone. Along its route through the tongue it branches off to the extrinsic and intrinsic tongue muscles. In unilateral flaccid paraly sis the tongue deviates to the paraly zed side, thus the place of articulation will be slightly shifted. This normally leads to only mild distortion of the lingual consonants. The client frequently judges the impairment to be more severe. Bilateral hy poglossal nerve lesions results in severe loss of the ability to elevate and protrude the tongue as well as to change the shape of the tongue. Depending upon the degree of paresis this condition will primarily affect the manner of articulation, and in cases of severe impairment, articulatory movements are only approximate blurring the differences between vowel and consonant articulation. Motor innervation for the craniomandibular complex is provided by the mandibular division of the trigeminal nerve. The anterior division of the mandibular branch contains most of the motor nerves supply ing the
42. Flaccid Dysarthria
groups opening and closing the jaw. Unilateral trigeminal lesion does not disturb articulatory sound production. Bilateral lesions will, however, severely affect labial consonant and vowel production as well as tongue adduction movements. Labial movements are mainly controlled by the buccal and mandibular branches of the facial (VII) nerve. The facial nerve emerges from the lateral aspect of the brainstem at the lower border of the pons. According to Bernstein/Nelson (1984) the branches of the facial nerve show some variability in their pathway . The buccal branch innervates the orbicularis oris superior, levator labii, buccinator, and zy gomaticus muscles, and the muscles of the side of the nose. The mandibular branch innervates the orbicularis oris inferior, depressor anguli oris, depressor labii, and mentalis muscles. Unilateral weakness of the lips following lesions of the facial nerves disturbes production of labial vowels and consonants, particularly clusters of several labial sounds. In bilateral flaccid paraly sis, labial sounds are often unintelligible. Finally , it should be mentioned, that changes in the amount of saliva produced in the oral cavity due to damage of the superior salivatory nucleus or to the parasy mpathetic preganglionic of the facial nerve, will make articulation very labored. The afferent innervation of the articulators concerned with proprioception is complex. The supply of the articulatory apparatus with muscle spindles varies considerably , and cannot be discussed here in detail. Further research into the role of noncontractile element innervation of the speech apparatus would be of considerable value in understanding flaccid dy sarthria more fully . For a comprehensive review of the neuroanatomy and neurophy siology of the speech mechanism, see Kuehn/Lemme/ Baumgartner (1989). The clinical characteristics of flaccid dy sarthria established yb Darle y /Aronson/ Brown (1969), Carrow/Rivera/Mauldin/ Shamblin (1974), and Enderby (1986) refer mainly to those sy ndromes with multiple damage to lower motor neurons. The rank order of deviant speech dimensions in these studies differ considerably . As indicated earlier, occurrence and prominence of particular speech characteristics depend on which nerves and muscles are affected. Aside from this aspect, they have some prominent features in common, like imprecise consonants, breathiness, hy pernasality , harsh voice, and short phrases.
459
3.
Neurological Causes of Flaccid Dysarthria
The following is a brief overview of the major groups of neurologic diseases which may affect the lower motor neurons controlling the muscles used for speech, and the diseases of the muscles themselves. For details see Swash/ Schwartz (1988), and Adams/Victor (1985). 3.1. Neurogenic Disorders Neurogenic disorders are generally classified according to the site of the major pathological process involved. 3.1.1. Motor Neuron Disease This is a progressive disorder often of unknown origin which may involve both lower and upper motor neurones. A subdivision of motor neuron disease is progressive bulbar palsy with progressive degeneration of the motor nuclei of the lower brainstem. The clinical signs are progressive wasting and weakness of the speech muscles; in later stages the weakness also affects the respiratory muscles. When weakness spreads to the hands, arms, and legs, this condition is then usually referred to as amy otrophic lateral sclerosis. — Prognosis depends on the severity of bulbar involvement; the duration of the disease is generally 2—5 y ears. Less frequent diseases with progressive bulbar weakness and atrophy are the spinal muscular atrophies where dy sarthria and dy sphagia may develop after several y ears. — Other rare anterior horn cell diseases with bulbar involvement are sy ringobulbia, herpes zoster, poly omy elitis or Creutzfeldt-Jakob disease. 3.1.2. Brainstem Lesions Brainstem sy ndromes which involve caudal cranial nerves may be caused by vascular disturbances, e. g. occlusion of the vertebral or posterior inferior cerebellar artery leading to ipsilateral cranial nerve V, IX, X, and XI palsy (e. g. Wallenberg or other vascular sy ndromes). Other causes are tumors, encephalitic processes, or multiple sclerosis. 3.1.3. Damage to Cranial Nerves Isolated or multiple injuries to the cranial nerves are of vary ing origins. The nerves may be damaged by intra- or extracranial tumors (e. g., acoustic neurinoma causing compression of the 7th cranial nerve) or meningeal carcinomatosis, aneury sm (e. g., compression of the left lary ngeal nerve by an aortic arch
III. Acquired Organic Pathologies of Language Behavior:Neurophonetic Disorders
460
aneury sm), trauma (e. g., extensive fractures of the skull), or iatrogenic damage (e. g., to the recurrent lary ngeal nerve during thy roid surgery , or damage to the phrenical nerve during puncture of the jugular vein). 3.1.4. Polyneuropathies Poly neuropathies may be caused by inflammation (viral, bacterial, allergic reactions), intoxication (medication, enviromental toxins), vascular diseases, deficiency diseases, or they may be of genetic origin. Speech may be affected as well as by paresis of particular respiratory muscles (e. g., paresis of the intercostal muscles as in post-diphteric poly neuropathy ) and/or by muscles innervated by cranial nerves. The most frequently affected cranial nerves are the facial nerves followed by the glossophary ngeal and vagus nerves. One common acute form is idiopathic poly radiculoneuropathy or Guillain-Barré ys ndrome. Weakness develops more or less sy mmetrically in distal muscles over a period of a few day s or weeks. Trunk, speech, and respiratory muscles are usually affected later, the facial nerves being more frequently affected than the caudal cranial nerves. 3.2. Disorders of the Neuromuscular Junction The most common form of this ty pe of disorder is my asthenia gravis. An autoimmune mechanism is thought to operate at the neuromuscular junctions. Repeated or persistent activity of a muscle group exhausts contractile power leading to a progressive paresis; rest may restore strength. Impairment of the muscles involved in speech is an early sy mptom in 30% of cases. 3.3. Myopathies In general, the term my opathy refers to all primary muscle disorders. In poly my ositis weakness of facial, phary ngeal, and lary ngeal muscles as well as of the respiratory muscles may occur. Muscular dy strophy is highly variable in its clinical sy mptoms. In some cases selective involvement of speech muscles is described, e. g. as lary ngeal and phary ngeal weakness in oculophary ngeal dy strophy or in my otonic dy strophy . Metabolic or endocrine myopathies are rarely relevant.
4.
Management
In some cases it may be necessary to focus
initial intervention procedures on facilitating vital functions such as chewing or swallowing rather than on optimizing motor speech deficits. The evaluation and management of the patient with disordered oral feeding is discussed in Logeman (1983). — Patients, who are unable to communicate using speech may require a combination of approaches. In addition to dy sphagia therapy the patient is provided with an alternative communication sy stem (e. g. a simple alphabet board, or an electronic device). Excellent reviews are available that address this area (Beukelman/Yorkston/Dowden 1984). At a later stage the focus of therapy shifts to the specific treatment of the impaired motor speech. In the acute stage of bulbar palsy , respiratory functions may also be severely affected due to paraly sis of respiratory muscles or the vocal cords. Respiratory assistance or tracheostomy may be necessary. — As it is the case with management of all ty pes of dy sarthria, treatment must be based on an accurate evaluation of the speech motor apparatus. This applies particularly to flaccid dy sarthria because, as mentioned previously , the different speech muscles may be selectively affected. Linebaugh (1983) recommends process-specific procedures. The choice of treatment focus depends on the relative involvement and the mutual speech process interdependencies. Efficient use of expiratory air flow can best be achieved by elimination of velophary ngeal incompetence by fitting a palatal lift prosthesis and then strengthening respiratory muscles. In Linebaugh’s approach, strengthening exercises are assisted by biofeedback methods. — Patients may compensate for their poor respiratory support by using auxiliary respiratory muscles, as reported by Hixon/ Putnam/Sharp (1983). Phonatory exercises focus on tension-producing maneuvers. Unilateral recurrent nerve paraly sis may be compensated by means of adduction of the intact vocal fold across the midline. Surgical intervention like nerve transfer or Teflon injection may be successful (Crumley /Izdebski/McMiken 1988). In severe articulatory deficits as well as in selectively affected muscle control non-speech drills and tactile stimulation (pressure, stretching, tapping) might be most appropriate. Electrostimulation to restore innervation is not recommended because isometric muscle contraction is not possible. Patients with progressive disease are candidates for learning compensatory strategies, counseling can help to prevent maladaptive strategies or to optimize the ‚communication environment’.
43. Hypo- and Hyperkinetic Dysarthria
5.
References
Adams, A. D. & Victor, M. (1985). Principles of Neu rology. New York: Mac Graw-Hill Book Company. Aronson, A. E. (1985). Clinical voice disorders. 2nd ed. New York/Stuttgart: Thieme. Bernstein, L. & Nelson, R. (1984). Surgical anatomy of the extraparotid distribution of the facial nerve. Archives of Otolaryngology, 110, 177. Beukelman, D. R., Yorkston, K. M., & Dowden, P. A. (1984). Commu nication au gmention: a casebook of clinical management. San Diego: CollegeHill Press. Carrow, E., Rivera, V., Mauldin, M. & Shamblin, L. (1974). Deviant speech characteristics in motor neuron disease, Archives of Otolaryngology, 100, 212—218. Crumley , R. L., Izdebski, K., & McMiken, B. (1988). Nerve transfer versus Teflon injection for vocal fold paralysis. Laryngoscope, 98, 1200—1204. Darley , F. L., Aronson, A. E., & Brown, J. R. (1969). Differential diagnostic patterns of dy sarthria. Jou rnal of Speech and Hearing Research, 12, 246—269.
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Davis, L. F. (1987). Respiration and Phonation in cerebral palsy : a developmental model. Seminars in Speech and Language, 8, 101—106. Enderby , P. (1986). Relationships between dy sarthric groups. British Jou rnal of disorders of Communication, 21, 151—165. Hixon, T. J., Putnam, A. H. B., & Sharp, J. P. (1983). Speech production with flaccid paraly sis of the rib cage, diaphragm, and abdomen. Jou rnal of Speech and Hearing Disorders, 48, 315—327. Kuehn, D. P., Lemme, M. L., & Baumgartner, J. M. (1989). Neu ral bases of speech, hearing, and lang u age. Boston/Toronto/London: College-Hill Press. Linebaugh, C. W. (1983). Treatment of flaccid dysarthria. in Cu rrent therapy of commu nication disorders: dysarthria and apraxia. New York: ThiemeStratton. Logeman, J. A. (1983). Evalu ation and treatment of swallowing disorders. San Diego: College-Hill Press. Swash, M. & Schwartz, M. (1988). Neuromuscular diseases. Berlin/Heidelberg/New York: Springer.
Mathias Vogel, Munich (Germany)
43. Hypo- and Hyperkinetic Dysarthria 1. 2. 3. 4. 5.
6.
1.
Types of Hypokinetic and Hyperkinetic Dysarthria Disorder Characteristics Symptom Modulation Pathophysiology Characteristics of the Speech Execution System Based on the Hypo- and Hyperkinetic Dysarthrias References
Types of Hypokinetic and Hyperkinetic Dysarthria
Hy pokinetic dy sarthria is characterized by reduced movement and occurs in patients with either Parkinson’s disease, Multiple Sy stems atrophy (or Shy Drager Sy ndrome) or progressive supranuclear palsy (Steele Richardson Sy ndrome). Hy pokinetic dy sarthria is one subty pe of akinesia, the inability to move, or speak, at will. The phy siological abnormality which interferes with patients’ abilities to move at will, has received considerable attention in both the speech and the movement disorders fields. Parkinson’s disease is the
form of hy pokinetic dy sarthria most often studied. The hy perkinetic dy sarthrias have received much less attention. Patients with these motor control disorders are unable to r e g u l a t e their willed movements. In some ty pes of hy perkinetic dy sarthria, such as tardive dy skinesia and Huntington’s chorea, an involuntary movement may interfere with the execution of the desired movement pattern. In other ty pes, such as oral-mandibular dy stonia and the spasmodic dy sphonias, some component of the willed movement is excessive and interferes with the execution of the remainder of the movement pattern. The hy perkinetic dy sarthrias are less well understood but have several intriguing characteristics which shed light on the organization of speech motor control in the central nervous sy stem. Both the hy po- and hy perkinetic dy sarthrias are thought to be the result of disease processes affecting the basal ganglia (Marsden 1982). Although the hy pokinetic and hy perkinetic dy sarthrias differ in their speech production impairments, both represent a lack of control
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during speech execution. In this chapter, first, the characteristics of these disorder are reviewed regarding independent processing stages during speech execution such as: Speech planning, programming during movement execution, speech initiation, movement velocity range, and accuracy , and speech rate. Second, factors which modulate speech sy mptom occurrence/severity will be discussed and underly ing pathophy siology . Finally , a review of these disorders suggests characteristics of the speech execution system.
2.
Disorder Characteristics
2.1. Movement Abnormalities Movement slowing can be manifested in two way s; by delay ed movement onsets (akinesia) and by increased movement durations once movement has been initiated (bradykinesia). 2.1.1. Delayed Initiation Times On limb movement tasks, Parkinson’s disease (PD) patients are slower than controls on simple reaction time tasks but not on choice reaction time tasks (Sheridan/Flowers/Hurrell 1987). On simple reaction time tasks, the response ty pe is known and advance planning can be performed before the ‘go’ signal while in choice reaction time paradigms, planning must be performed after the ‘go’ signal. Normal subjects are slower on choice than on simple reaction time tasks involving limb movements (Sheridan/Flowers/Hurrell 1987), possibly because movement planning must be performed after the ‘go’ signal. Because Parkinson patients have the same latency on both simple and choice reaction time tasks and are slower than normal primarily on simple reaction time tasks, their slow performance has been taken to indicate a movement planning disorder (Marsden 1982). On s p e e ch simple reaction time tasks, however, PD patients are not impaired in comparison with normal (Ludlow/Connor/Bassich 1987), suggesting that speech planning, and initiation, is not impaired in PD patients. In hy perkinetic disorders such as spasmodic dy sphonia (SD), speech initiation reaction times are slower than normal (Ludlow/ Connor 1987), although in other ty pes of hy perkinetic disorders, such as patients with Huntington’s chorea, speech reaction times are normal (Ludlow/Connor/Bassich 1987). The increased speech reaction times in SD, however, are not due to a planning disorder
because lary ngeal movement onset after the ‘go’ signal was at the same time or earlier than normal, even though the speech onset was delay ed (Ludlow/Connor 1987). These patient’s delay s, then, were due to an execution problem rather than motor planning deficits. 2.1.2. Reduced Movement Speed In limb movements studies, PD patients have prolonged movement times and reduced movement velocities (Hallett/Khosbin 1980). In speech, however, jaw and lip movement durations are normal (Connor/Abbs/Cole/ Gracco 1989) and word, phrase and sentence durations are not prolonged in PD patients (Ludlow/Bassich 1983; 1984; Ludlow/Connor/Bassich 1987). The differences in PD patients performance of limb and speech movement tasks was addressed by Connor/Abbs (1991). The same jaw movement was measured in patients and controls during visual tracking, production of a speech sy llable and production of the sy llable in a sentence. The PD patients differed from the controls only on the visual tracking task and not on the two speech tasks. The non-speech and speech production tasks differed in their degree of familiarity , complexity and reliance upon visual guidance. The results suggest that complexity is not important in determining the deficits of PD patients. Connor/Ludlow/ Schulz (1989) found that acoustic mesaures of sy llable production in isolated and repeated productions were similar, and not more impaired with increased task complexity or length. In fact, in the Connor/Abbs/Cole/ Gracco (1989) study , the greatest movement amplitudes and velocities were found on the sequential speech task in comparison with the isolated sy llable production task. Therefore, the differences in movement slowing between limb and speech tasks does not seem to be due to task complexity . The reason for these differences is as y et unclear. Most limb movement tasks are visually guided, while speech is not. Alternatively , learning is usually required for skilled performance of many limb movement tasks while speech is a previously learned and higly practiced motor skill in adults. In yh perkinetic disorders, Huntington’s disease (HD) patients have increased speech production times for sentences, slower sy llable repetition rates, and increased pause lengths between phrases (Ludlow/Connor/ Bassich 1987). Brady kinesia has also been
43. Hypo- and Hyperkinetic Dysarthria
reported in finger movement studies (Hefter/ Hömberg/Lange/Freund 1987). In SD patients, sentence durations are increased from normal and are improved with treatment (Ludlow/Naunton/Sedory et al. 1989). In hy perkinetic speech disorders, however, it is not known whether the brady kinesia is due to slow voluntary movements or the intrusion of involuntary movements. 2.2. Loss of Control 2.2.1. Speaking Rate in PD Clinically , PD patients give the impression that they are speaking at an uncontrollably fast rate, often referred to as ‘speech rushes’ (Darley /Aronson/Brown 1969 a; 1969 b). Some PD patients exhibit palilalia (LaPointe/ Homer 1981; Kent/LaPointe 1982) which is uncontrolled repetition of sy llable and words. The sy mptom is similar to acquired stuttering following brain injury (Ludlow/Rosenberg/ Salazar et al. 1987). Impaired speech performance with continued speech can be improved in both PD and palilalia by regulating speech rate either by external pacing either using a pacing board, or auditory cues such as a metronome or delay ed auditory feedback (Hanson/Metter 1983; Downie/Low/Lindsay 1977). Quantitative studies of speech rate have failed to substantiate these impressions (Ludlow/Bassich 1983; Caligiuri 1989). An acoustic study of reiterative palilalia demonstrated that the perceptual impression of an increasingly rapid rate of repetition was not substantiated; the final utterance of a repetition train was either longer in duration or equivalent to preceding productions (Kent/LaPointe 1982). Further, when the change in rate during sy llable repetition was computed in PD, patient’s rates demonstrated the opposite, greater slowing than normal over 5.5 seconds (Ludlow/Connor/Bassich 1987). The perceptual impression of increasing speech rate may be due to reductions in movement amplitude and accuracy with continued speech production (Caligiuri 1989). The reduced range is often referred to as rigidity in PD and may be unrelated to akinesia and brady kinesia. Although movement duration is not impaired during speech in PD patients, movement range for the upper lip and jaw is reduced and motor coordination may be affected (Connor/Abbs/Cole/Gracco 1989). In another study , formant transition rates were reduced in PD patients both in isolated and
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repeated sy llables suggesting that movement accuracy is reduced (Connor/Ludlow/Schulz 1989). Caliguiri (1989) studied lip movement displacements in PD patients and controls at different speech rates. He found PD patient’s reductions in movement amplitude from normal became more pronounced as the PD patients speech rate increased to a normal rate (Caliguiri 1989). The decreased movement accuracy during speech production may underlie the perceptual impression of uncontrolled rate in PD patients speech. Therefore, of the three movement abnormalities in PD, akinesia, brady kinesia and rigidity (reduced movement amplitude), rigidity seems to affect speech production to the greatest degree. 2.2.2. Involuntary Movements in Hyperkinetic Dysarthria Involuntary movements occur in patients with tardive dy skinesia (TD), oral-mandibular dy stonia (OMD), HD and SD. There are large differences however, in the characteristics of these intrusive movements. In tardive yd skinesia, continual grimacing, tongue writhing, lip smacking and teeth grinding usually occur at rest and are usually suppressed by speech or other voluntary movements. Therefore, although the involuntary movements are severe in these patients, often speech production is relatively spared. In oral-mandibular dy stonia (OMD), patients have involuntary abnormal sustained postures such as constant jaw opening, jaw closing, sustained tongue protrusion and grimacing. These postures are sustained while the patient is awake and interfere with voluntary movement such as speech. Quantitative studies are needed to address whether OMD is a constant hy pertonia of some muscles interfering with the activation of muscle antagonists, or if the total pattern of muscle activation is disturbed. That is, if the nonhy pertonic muscles, normally active for voluntary movement, are suppressed. If this is the case, the disorder may be more one of movement programming rather than execution. This might explain why injection of hy pertonic muscles with botulinum toxin is not as beneficial in OMD as in other dy stonias (Jankovic/Schwartz/Donovan 1990). In SD, both spasmodic bursts and hy pertonia of several of the lary ngeal muscles interfere with movement. In adductor SD, uncontrolled spasmodic bursts occur in both the thy roary tenoid and cricothy roid muscles and both muscles evidence hy peractivation (Lud-
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low/Hallett/Sedory et al. 1990). In addition, the thy roary tenoid is increased over resting levels to a much greater percentage than the cricoth y roid (Ludlow/Baker/Naunton/Hallett 1987; Ludlow/Naunton/Sedory et al. 1990). Therefore, the pattern of lary ngeal muscle activation both at rest and during speech and swallow is abnormal, suggesting a movement programming disorder.
3.
Symptom Modulation
3.1. Task Specificity For many y ears, SD was thought to be a psy chogenic disorder. The basis for this belief was the observation that adductor SD patients can usually cough, sing, and whisper and only have difficulty when they attempted to speak. Similarly , patients with abductor SD can normally perform throat clearing, coughing, laughter and cry ing but are breathy or have intermittent voice loss when speaking. More recently , this has become better understood as a characteristic of the focal dy stonias (Rosenbaum/Jankovic 1988). The patients will develop abnormal posturing during one task but be clinically unaffected during another task using similar movements. This is also evident in OMD; often patients will be more impaired during speech than during chewing or vice versa (Paulson/Barnes 1988). This intriguing feature of the focal dy stonias suggests that the neural substrates for different tasks can be independent in the central nervous sy stem and that the pathway s for one task can be affected while others controlling the same muscles are unaltered. Task specificity in SD is not dependent upon whether or not a task is a vegetative non-learned movement or a movement dependent upon a previously learned skill. These patients are often dramatically more impaired in speaking than in singing and whispering, which are all skilled tasks. Task specificity may also be a feature of the hy pokinetic dy sarthrias. Differences in impairment for the same jaw movement whether it is used for a non-speech visually guided movement or used for isolated or embedded speech sy llables were demonstrated in PD patients (Connor/Abbs 1991). However, as suggested earlier, these tasks differ in other respects; the use of visual guidance and the degree of previous skill. Certainly , task differences are not as clinically dramatic in PD
as they are in the focal dy stonias. Additional studies are needed to determine whether task specificity is a feature of PD. 3.2. Variations in Performance Situational and temporal factors can alter speech performance in both the hy pokinetic and hy perkinetic dy sarthrias. Most hy perkinetic dy sarthric patients are better early in the day . This is most likely due to the exacerbation of muscle hy pertonia by muscle activation. Hy pokinetic PD patients fluctuate widely during the day and variations in performance can be particularly dramatic in patients on medications (Nutt 1990). Usually patients are less rigid between one and two hours after dopamine medication and then rigidity will return within 3 to 4 hours after medication. Some patients develop dy skinesias and can have hy perkinetic dy sarthria sy mptoms in one to two hours after their medication. Rapid swings between hy pokinesia and hy perkinesia in PD patients being treated with dopamine is known as the ‘onoff’ phenomenon and develops after a patient has been treated for several y ears. Although not formally investigated, patients usually report their speech improved during dy skinesia over hypokinesia. 3.2.1. Exacerbated by Stress Patients have daily fluctuations in their sy mptom severity and can usually report whether it is a good day or bad day for their disorder. Stress seems to exacerbate sy mptoms and can also be related to periods of waxing and waning in sy mptoms over several day s or weeks. Often patients first notice their sy mptoms after a stressful event. High expectations of successful treatment often can depress sy mptoms, while depression and anxiety can exacerbate them. This can alter responses to treatment making the need for controlled studies of treatment effects necessary . Random assignment to a treatment and control group with some intervention in both groups or double blind placebo versus treatment are the designs which can provide accurate assessment of treatment effects in both the hy perkinetic and hypokinetic dysarthrias. 3.2.2. Improvements with Task Constraints One of the most frustrating experiences in study ing patients with motor control disorders, are the differences between their per-
43. Hypo- and Hyperkinetic Dysarthria
formance in every day situations and their performance in a controlled testing environment. When the parameters of a task are significantly controlled, the patients’ performance usually improves markedly . Therefore, a structured speech test with repetition of limited speech items or the elicitation of well defined speech items will not provide samples representative of a patient’s dy sarthria. Relatives observing such testing often remark how much better the patient performs during speech testing in the clinical setting than at home. This is the effect of constraining the performance parameters and directing the patient’s attention to controlling particular behavioral factors. 3.3. Focal Disturbance The most focal disturbances occur in the dy stonias, such as spasmodic dy sphonia and oral mandibular dy stonia, where sy mptoms are confined to one component of the vocal tract such as the lary ngeal musculature or the jaw and facial muscles. Although sy mptoms appear in one area, however, subclinical abnormalities may be present in other regions, such as abnormal blink reflexes in SD (Cohen/ Ludlow/Warden et al. 1989). In assessing the dy sarthrias, Netsell (1986) proposed that functional components be examined independently for involvement. Evaluations of PD patients have consistently demonstrated that voicing control is often more disturbed that other aspects of speech on tests of speech articulation (Logemann/Fisher/ Boshes/Blonsk y 1977; Logemann/Fisher 1981). Darley /Aronson/Brown (1969) found that ratings reflecting voice quality such as breathiness, monopitch and monoloudness were included in the most affected characteristics of PD. Objective acoustic measures similarly found that measures of phonation were also most affected (Canter 1963; Ludlow/Bassich 1983; Weismer 1984). However, no phy siological comparisons of muscle activation or movement reductions have been conducted across functional components. It could be that lary ngeal control appears most affected because the speed demands on control of vocal fold position for speaking is more constrained for normalcy than other aspects of speech control. Voicing onset and offset must be accurate within a few milliseconds for distinctions between voiced and voiceless consonants. Therefore, hy pokinesia may be more evident in lary ngeal control because of the
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very precise timing required for voicing contrasts in speech. Tongue movement is usually much slower and labial control must only be rapid for the production of /p/. The early and severe involvement of vocal fold movement in Shy Drager Sy ndrome (multiple sy stems atrophy ) is an important feature of the disorder (Bassich/Ludlow/Polinsky 1984; Hanson/Ludlow/Bassich 1983). Few other dy sarthrias have been investigated from a functional component approach examining for selective impairment of one component. However, studies of the basal ganglia and the basal forebrain pathway s suggest a topographic organization (DeLong/Alexander/Mitchell/Richardson 1988; Koliatsos/ Martin/Walker et al. 1988). Such an organization would certainly support selective focal involvement of one body part with relative sparing of another in basal ganglia disease.
4.
Pathophysiology
Few formal studies have been conducted of the pathophy siology of the dy sarthrias. Such studies have been conducted on patients with other movement control disorders to examine whether they have exaggerated responses to sensory stimuli. In studies of H reflex responses to stimulation of spindle afferents, patients with limb dy stonia had reduced inhibition of responses in comparison with normal (Panizza/Lelli/Nilsson/Hallett 1990). This suggests that muscle activation feedback produces greater motoneuron activation than normal in dy stonia. One study has been conducted in SD patients of blink reflex responses to stimulation of the supraorbital nerve. Reduced inhibition of the blink reflex in response to electrical stimulation was found in SD patients in comparison with normal. This suggests that inhibition is reduced in response to afferent stimuli to other cranial motoneurons in SD (Cohen/Ludlow/Warden et al. 1989). The blink reflex is also heightened in PD patients (Estaban/Gimenez-Roldan 1975) as well as peroral responses to mechanical stimuli (Caligiuri/Abbs 1987). Therefore, in general, a loss of normal inhibition seems to be present in many of these disorders. De Long (1990) has suggested that in hy pokinesia excessive tonic and phasic inhibitory output from the basal ganglia to the thalamus results in reduced responsiveness of cortical mechanisms because of a reduction in thalamocortical activation. The findings of
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a more slowly rising bereitschaftspotential in PD would support this model (Dick/Rothwell/Day et al. 1989). Hy perkinetic disorders, on the other hand, may be the result of disinhibition of the thalamus due to a reduction in output from the motor globus pallidus. This makes the thalamocortical neurons increasingly responsive and more likely to discharge spontaneously . These models of the hy po- and hy perkinetic dy sarthrias are in agreement with the fluctuating characteristics or these disorders. That is, the movement planning and programming for speech production is intact but movement regulation and control is not.
5.
Characteristics of the Speech Execution System Based on the Hypoand Hyperkinetic Dysarthrias
In addition to the need to better understand speech disorders for improved treatment, the study of speech production disorders can also improve our understanding of the speech motor control sy stem. Some of the characteristics of the hy po- and hy perkinetic dy sarthrias suggest the following characteristics. (a) Speech production deficits may differ from limb movement deficits in basal ganglia disease. (b) Reduced movement range may interfere with speech intelligibility to a greater degree than brady kinesia (movement slowing) or akinesia (movement initiation difficulties). (c) Highly skilled over-learned motor control tasks may be less affected than new or visually guided tasks by basal ganglia disease. (d) Alterations in movement accuracy can alter impressions of speaking rate on listeners. (e) The motor control of vocal tract gestures for chewing and other activities is independent from that for speech. (f) Speech performance can be improved by reducing the number of parameters which the speaker must control at one time. (g) Individual vocal tract components can be independent in their neural control. (h) The role of the basal ganglia in speech production is one of modulation of speech execution. Its function may alter the range and accuracy of speech movements but not the planning or programming of previously learned speech gestures.
6.
References
Bassich, C. J., Ludlow, C. L., & Polinsky , R. J. (1984). Speech sy mptoms associated with early signs of Shy Drager sy ndrome. Jou rnal of Neu rology, Neurosurgery, and Psychiatry, 47, 995—1001. Caligiuri, M. P. (1989). The influence of speaking rate on articulatory hy pokinesia in parkinsonian dysarthria. Brain and Language, 36, 493—502. Caligiuri, M. M. & Abbs, J. H. (1987). Response properties of the perioral reflex in Parkinson’s disease. Experimental Neurology, 98, 563—577. Canter, G. J. (1963). Speech characteristics of patients with Parkinson’s disease: I. Intensity , pitch, and duration. J. Speech Hear. Dis., 28: 221—229. Cohen, L. G., Ludlow, C. L., Warden, B. S., Estegui, M. D., Agostino, R., Sedory , S. E., Holloway , E., Dambrosia, J., & Hallett, M., (1989). Blink reflex excitability recovery curves in patients with spasmodic yd sphonia. Ne u rology, 39, 572—577. Connor, N. P. & Abbs, J. H. (1991). Task-dependent variations in Parkinsonian motor impairments. Brain, 114, 321—332. Connor, N. P., Abbs, J. H., Cole, K. J., & Gracco, V. L. (1989). Parkinsonian deficits in serial multiarticulate movements for speech. Brain, 112, 997—1009. Connor, N. P., Ludlow, C. L., & Schulz, G. S. (1989). Stop consonant production in isolated and repeated sy llables in Parkinson’s disease. Neuropsychologia, 27, 829—838. Darley , F., Aronson, A. E., & Brown, J. (1969 a). Differential diagnosis patterns of dy sarthria. Journal of Speech and Hearing Research, 12, 246—269. Darley , F. L., Aronson, A. E., Brown, J. R. (1969). Clusters of deviant speech dimensions in the dy sarthrias. J. Speech Hear. Res.; 12, 469—496. DeLong, M. R. (1990). Primate models of movement disorders of basal ganglia origin. Trends in Neuroscience, 13, 281—285. DeLong, M. R., Alexander, G. E., Mitchell, S. J., & Richardson, R. T. (1986). The contributions of basal ganglia to limb control. In H. J. Freund, U. Buttner, B. Cohen, & J. Noth (Eds.), Progress in Brain Research. 161—174. Amsterdam: Elsevier Science Publishers. Dick, J. P. R., Rothwell, J. C., Day , B. L., Cantello, R., Buruma, O., Gioux, M., Benecke, R., Berardelli, A., Thompson, P. D., & Marsden, C. D. (1989). The bereitschaftspotential is abnormal in Parkinson’s disease. Brain, 112, 233—244. Downie, A. W., Low, J. M., & Lindsay , D. D. (1981). Speech disorders in Parkinsonism: Usefulness of delay ed auditory feedback in selected cases. Jou rnal of Neu rology, Neu rosu rgery, and Psychiatry, 44, 852—853. Estaban, A. & Gimenez-Roldan, S. (1975). Blink reflex in Huntington’s chorea and in Parkinson’s
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disease. Acta Ne u rologica Scandinavia, 52, 145—157. Hallett, M. & Khoshbin, S. (1980). A phy siological mechanism of bradykinesia. Brain, 103, 301—314. Hanson, D. G. Ludlow, C. L., & Bassich, C. J. (1983). Vocal fold paresis in Shy -Drager sy ndrome. Annals of Otology, Rhinology, and Laryngology, 92, 85—90. Hanson; W. R. & Metter, E. J. (1983). Speech rate modification in Parkinson’s disease: A report of two cases. In W. R. Berry (Ed.), Clinical Dysarthria. 231—251. San Diego, CA: College-Hill Press. Hefter, H., Hömberg, V., Lange, H. W., & Freund, H. J. (1987). Impairment of rapid movement in Huntington’s disease. Brain, 110, 585—612. Jankovic, J., Schwartz, K., Donovan, P. T. (1990). Botulinum toxia treatment of cranio-cervical dy stonia, spasmodic dy sphonia, other focal dy stonias and hemifacial spasm. Jou rnal of Neu rology Neu rosurgery and Psychiatry, 53, 633—639. Kent, R. D. & LaPointe, L. L. (1982). Acoustic properties of pathologic reiterative utterances: a case study of palilalia. Jou rnal of Speech and Hearing Research, 25, 95—99. Koliatsos, V. E., Martin, L. J., Walker, L. C., Richardson, R. T., DeLong, M. R., & Price, D. L. (1988). Topographic, non-collateralized basal forebrain projections to amy gdala, Hippocampus, and anterior cingulate cortex in the rhesus monkey . Brain Research, 463, 133—139. LaPointe, L. L. & Horner, J. (1981). Palilalia: A descriptive study of pathological reiterative utterances. Jou rnal of Speech and Hearing Disorders, 46, 34—38. Logemann, J. A. & Fisher, H. B. (1981). Vocal tract control in Parkinson’s disease: Phonetic feature analy sis of misarticulations. Jou rnal of Speech and Hearing Disorders, 46, 348—352. Logemann, J. A., Fisher, H. B., Boshes, B., & Blonsky , R. (1977). Frequency and cooccurrences of vocal tract dy sfunctions in the speech of a large sample of Parkinson patients. Jou rnal of Speech and Hearing Disorders, 42, 47—57. Ludlow, C. L., Baker, M., Naunton, R. F., & Hallett, M. (1987). Intrinsic lary ngeal muscle activation in spasmodic dy sphonia. In R. Benecke, B. Conrad, & C. D. Marsden (Eds.), Motor Distu rbances. 119—130. Orlando: Academic Press. Ludlow, C. L. & Bassich, C. J. (1983). The results of acoustic and perceptual assessment of two ty pes of dy sarthria. In W. Berry (Ed.), Clinical dysarthria. 121—153. San Diego: College-Hill. Ludlow, C. L. & Bassich, C. J. (1984). Relationships between perceptual ratings and acoustic measures of hy pokinetic speech. In M. R. McNeil,
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J. C. Rosenbek, & A. E. Aronson (Eds.), The dysarthrias. 163—195. San Diego: College-Hill. Ludlow, C. L. & Connor, N. P. (1987). Dy namic aspects of phonatory control in spasmodic dy sphonia. Jou rnal of Speech and Hearing Research, 30, 197—206. Ludlow, C. L., Connor, N. P., & Bassich, C. J. (1987). Speech timing in Parkinson’s and Huntington’s disease. Brain and Language, 32, 195—214. Ludlow, C. L., Hallett, M., Sedory , S. E., Fujita, M., & Naunton, R. F. (1990). The pathophy siology of spasmodic dy sphonia and its modification by botulinum toxin. In A. Beradelli, R. Benecke, M. Manfredi, & C. D. Marsden (Eds.), Motor Disturbances. 274—288. Orlando: Academic Press. Ludlow, C. L., Naunton, R. F., Sedory , S. E., Schulz, G. S., & Hallett, M. (1989). Effects of botulinum toxin injection on speech in spasmodic dy sphonia. Neurology, 30, 123—456. Ludlow, C. L., Rosenberg, J., Salazar, A., Grafman, J., & Smutok, M. (1987). Site of penetrating brain lesions causing chronic acquired stuttering. Annals of Neurology, 22, 60—66. Marsden, C. D. (1982). The my sterious motor function of the basal ganglia: The Robert Wartenberg lecture. Neurology, 32, 514—530. Netsell, R. (1986). A neu robiologic view of speech produ ction and the dysarthrias, San Diego, CA: College-Hill Press, 3—4. Nutt, J. G. (1990). Levodopa-induced dy skinesia: Review, observations, and speculations. Neurology, 40, 340—345. Panizza, M., Lelli, S., Nilsson, J., & Hallett, M. (1990). H-reflex recovery curve and reciprocal inhibition of H-reflex in different kinds of dy stonia. Neurology, 40, 824—828. Paulson, G. W. & Barnes, J. (1988). Oral facial dy stonia triggered by speech. Psychosomatics, 29, 236—238. Rosenbaum, F. & Jankovic, J. (1988). Task specific focal tremor and dy stonia: Categorization of occupational movement disorders. Ne u rology, 38, 522—527. Sheridan, M. R., Flowers, K. A., & Hurrell, J. (1987). Programming and execution of movement in parkinson’s disease. Brain, 110, 1247—1271. Weismer, G. (1984). Articulatory characteristics of Parkinsonian dy sarthria: Segmental and phraselevel timing, spirantization, and glottal coordination. In M. R. McNeil, J. R. Rosenbek, & A. E. Aronson (Eds.), The Dysarthrias: Physiology, Acou stics, Perception, Management. 101—130. San Diego: College-Hill.
Christy L. Ludlow, Bethesda, Maryland (USA)
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44. Cerebellar Dysarthria 1. 2. 3. 4. 5. 6. 7. 8.
1.
Introduction Clinical Perceptual Attributes of Cerebellar Dysarthria Phonetic Attributes Acoustic Attributes Kinematic Attributes Pathophysiological Mechanisms in Cerebellar Dysarthria Management of Patients with Cerebellar Dysarthria References
Introduction
Cerebellar dy sarthria results from damage to the cerebellum and/or its afferent or efferent connections due to structural or functional (e. g. alcohol intoxication) alterations. It comprises a somewhat inhomogeneous sy mptomatology which is a consequence of the functional complexity the cerebellum play s in motor control. Yet, the inhomogeneity has not been worked out to a sy ndromatic level comparable to the aphasic sy ndroms. Often, ataxic dy sarthria is used as a sy nony mous term to label cerebellar speech deficits (Darley /Aronson/Brown 1975; Kent/Netsell/Abbs 1979). The review will take into account the anatomical and functional aspects of the cerebellum, give a description of cerebellar breakdown of speech production at the perceptual, phonetic, acoustic, and kinematic levels. 1.1. Neuroanatomical, Neurophysiological and Clinical Aspects The cerebellum contains complete sensory and motor representations of the body ; y et lesions lead neither to muscle weakness nor to disorders of perception. However, the cerebellum controls the timing and the pattern of muscles activated during movement. Furthermore, the cerebellum modulates spinal cord and brain stem mechanism involved in postural control. Therefore, lesions of the cerebellum produce disturbances in the coordination of limb, ey e, and orofacial movements as well as disorders of muscle tone and posture. The neocerebellum (pontocerebellum), the evolutionary latest portion to develop after the archicerebellum (vestibulocerebellum) and the paleocerebellum (spinocerebellum), play s a major role in planning and initiation
of movements (especially with its lateral parts of the cerebellar hemispheres) and is of primary interest to speech. Sy mptoms of damage to the lateral cerebellar hemispheres comprise 1) abnormalities in timing and build-up of force (intentional movements (grasping/ pointing) are slower, delay ed in initiation and termination resulting in overshoot, slowness of alternating movements (dy sdiadochokinesis), 2) loss of fine tuning and irregular decomposition of voluntary movements with errors in direction, deviations of proper course, discontinuity , dy smetria (mostly overshoot), and tremor (increasing with proximity to target). The temporal composition of the exact time sequence of a complex program is deranged which involves multiple functional subunits of agonist-antagonist interactions composing a coordinate action (sy nergism, asy nergia). This ataxic sy mptomatology — commonly seen in the limbs — has also been shown to occur in the orofacial motor sy stem (Schönle 1988). 1.2. Hemisphericity and Localization of Speech in the Cerebellum The predominantly contralaterality of the cerebrocerebellar connections suggests a right hemisphere dominance of the cerebellum for speech motor control. Premotor and motor cortical areas (Brodmann area 4 and 6) project through the cortico-pontocerebellar tract to the contralateral neocerebellar hemispheres and their output is convey ed back to these cerebrocortical areas via red nucleus and the thalamus. However, clinical observations are equivocal with respect to hemispheric lateralization and localization of speech functions. While Holmes (1917; 1922) localized speech functions to the vermis (cerebellar midline structure) Amici/Avancini/Pacini (1976) found cerebellar dy sarthria most often with damage to the paravermal and lateral parts of the hemispheres. Disordered speech was uncommon with vermal destruction. In a review of 162 case histories collected over 30 y ears Lechtenberg/Gilman (1978) observed a significant association of dy sarthria with left cerebellar hemisphere lesions in the superior paravermal segment. Consequently , left-sided dominance for cerebellar speech motor control was assumed by the authors. However, close look at the diagnostic categories reveals 141 tumor cases versus 6 infarctions only (3 right hemisphere patients (2 with dy sarthrias)
44. Cerebellar Dysarthria
and 3 left hemisphere patients (3 with dy sarthrias). Given the poor localizing value of tumors and given that CCT-information was available only in 65 cases the question of cerebellar speech dominance remained unsettled. In the most thorough clinico-neuro-radiological MRI (magnetic resonance imaging) study of 12 patients with cerebellar infarction Ackermann/Vogel/Petersen/Poremba (1991) found the paravermal region of the superior portions of the cerebellum to be of critical importance for speech motor control. The 8 patients with infarctions in the territory of the posterior inferior cerebellar artery (PICA) (five on the left side) sparing the superior parts showed no speech deficits. Of the four patients with superior cerebellar artery infarcts three had right-sided lesions and one a bilateral infarct. These data — despite the small case number — question a left hemisphere dominance for speech in the cerebellum and leave the problem open for further MRI-investigations. 1.3. Diseases of the Cerebellum Affecting Speech Although the cerebellar sy mptomatology is alike in most cerebellar diseases speech alterations appear to be more prominent in some affections of the cerebellum e. g. in infarctions of the paravermal region of the superior portions of the cerebellum or some degenerative diseases. In hereditary cerebellar ataxia (NonnePierre-Marie, manifestation age: app. 35 y rs.), a multi-sy stem degenerative disease, a ty pe of cerebellar dy sarthria occurs which was clinically termed ‘vox leontina’ (lion’s voice). Phonation becomes deeper, harsh and louder; articulation is slurred, slow, and explosive with overshooting innervation (speaking with excessive loss of air). Some hereditary cerebellar ataxias only involve degeneration of the cerebellum and allow for better clinicoanatomical correlations than most other cerebellar diseases (e. g. Ackermann/Ziegler 1991). In the group of spino-ponto-cerebellar atrophies which also involve several neuronal ys stems, Friedreich’s ataxia (manifestation age: app. 13 y rs.) dy sarthria develops in the context of yd sdiadochokinesia, intention tremor and ny stagmus. Very often cerebellar dy sarthria occurs in multiple sclerosis presenting with the triad of Charcot (ny stagmus, intention tremor, and scanning speech). Al-
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coholic cerebellar degeneration, the most common acquired cerebellar degeneration, results in slurred speech only in an advanced stage. In contrast, acute alcohol intoxication leads to speech disturbances even at low blood levels (Schönle/Poser/Conrad 1988). In idiopathic paroxy smal ataxia, cerebellar dy sarthria occurs suddenly for seconds, reappearing over a variable time period together with other cerebellar sy mptoms (loss of balance, blurring of vision, ny stagmus). Netsell/ Kent (1976) reviewed 13 cases of paroxy smal ataxic dy sarthria and found multiple sclerosis to be the most likely etiology . Olivo-pontocerebellar degeneration (OPCA) is characterized by progressive ataxia, beginning with a disorder of gait and dy sarthria (mixed ataxicspastic), later evolving into a severe disturbance of coordinated movements of all limbs. — Lesions of the dentate — red nucleus — central tegemental tract — ipsilateral olive circuit result in palatal my oclonus in which patients show a continuous tremor of facial and phary ngeal muscle with distortion of speech production. The multisy stem nature of many of the cerebellar diseases make careful selection, investigation, and description of patient population a perequisite when study ing purely cerebellar dysarthria.
2.
Clinical Perceptual Attributes of Cerebellar Dysarthria
Since the early characterization of cerebellar speech disturbances (Bonhoeffer 1908; Charcot 1877) auditory perceptual descriptors of cerebellar dy sarthria have become commonly accepted in clinical use including features like scanning, slow, slurring, staccato, explosive, intermittent, jerky , irregular, hesitant and garbled speech and altered accent (Brown/Darley /Aronson 1970). The sum of the difficulties with the regulation of speech in cerebellar diseases was called dy sprosody by Holmes (1917). The most easily recognized feature, scanning speech, was first described by Charcot (1877) as a ‘peculiar difficulty of enunciation’ with speech production slowed and words ‘measured or scanned’. — Darley and coworkers (Darley /Aronson/Brown 1969 a; b; 1975; Brown/Darley /Aronson 1970) designed a classification sy stem for basic abnormalities of speech (‘deviant dimensions’) and investigated 30 patients with cerebellar lesions. They found 10 speech dimensions to be severely deviant (above 1.5 of their severity scale): imprecise consonants, excess and equalized
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stress, irregular articulatory breakdown, distorted vowels, harsh voice, prolonged phonemes, prolonged intervals, monotone pitch, monotony of loudness, and slow rate. Other deviant speech characteristics with lower ranking in severity occured in 14 out of the 30 patients: low pitch, excess loudness variations, hy pernasality , strain-strangled sound, pitch breaks, and voice tremor. Unfortunately , diagnoses were not specified nor was the presence of other neurological sy mptoms commented upon and no information about lesion localization was provided. — However, Gilman/Kluin (1984), based on their clinical experience, questioned the findings of Darley / Aronson/Brown (1969 a; b; 1975) that cerebellar dy sarthria includes continuously low pitch, monotony of pitch, monotony of loudness, and strain-strangled sounds. In a careful study they compared the speech output of patients with olivo-pontocerebellar atrophy (OPCA) and Friedreich’s ataxia. While the OPCA-patients exhibit signs of upper neuron disease such as hy peractive gag reflex, enhanced jaw stretch reflex, limited range of facial movement (as seen in pseudobulbar palsy ), the Friedreich’s patients did not and, therefore, presented a more ‘pure’ cerebellar disorder without cortibulbar involvement. — Perceptual analy sis of the speech production of the Friedreich’s ataxia patients revealed ‘pure’ ataxic dy sarthria with imprecise consonants, excess and equalized stress, irregular articulatory breakdowns, distorted vowels, harsh voice, prolonged phonemes, prolonged intervals and slow rate but without continuously low pitch, monotony of pitch, monotony of loudness, or strain-strangled sound. These signs were observed, however, in the OPCA patient group. While Darley /Aronson/ Brown (1969 a; b; 1975) rated articulation as the most deviant dimension in cerebellar patients, Gilman/Kluin (1984) found the phonatory and prosodic dimensions to be the most aberrant in patients with ataxic dy sarthria from Friedreich’s disease. Strain-strangled sounds resulting from effortful squeezing of air through the glottis, or obstruction of the exhaled airstraim appears to be a sign of corticobulbar tract involvement seen in OPCA (in form of a mixed ataxic spastic dy sarthria) or in pseudobulbar palsy and upper motor neuron involvement in amy otrophic lateral sclerosis. The results of Gilman/Kluin were in accord with studies by DeJong (1979) and Joanette/ Dudley (1980). DeJong described sudden
pitch changes and ataxic, staccato and explosive elements as prominent speech disturbances in Friedreich’s disease. In a study of 22 patients with Friedreich’s disease Joanette/ Dudley (1980) found two groups of speech characteristics, defining two distinct subgroups of patients: a) a general dy sarthric factor and b) a pattern of phonatory stenosis. The former included imprecise consonants and prolonged phonemes as most prominent variables. These together with most of the variables in Darley ’s et al. clusters constitute ataxic dy sarthria with explosive -hesitant and scanning speech. The second factor, phonatory stenosis, involved harshness and pitch breaks, but not monotony of pitch, monotony of loudness or strained-strangled sound. Transient harshness was also found in the Gilman/Kluin study (1984) but was linked to fluctuating pitch levels as harsh voice is generally associated with low pitch (Boon 1979). Taken these studies together, ‘pure’ ataxic dy sarthria (i. e. in patients without upper motor neuron involvement) is mainly characterized by prosodic/phonatory changes fluctuating pitch levels, ‘explosive’ transients, breathiness, alternating loudness, excess and equalized stress patterns and audible inspirations; other features such as slow and dy sry thmic rate, prolonged phonemes and prolonged intervals, occasional imprecise consonants, irregular breakdown of articulation, mild hy pernasality and harsh voice represent the spastic component of mixed spastic ataxic dysarthria.
3.
Phonetic Attributes
In their study of speech deficits in patients with circumscribed cerebellar ischemic lesions Ackermann/Vogel/Petersen/Poremba (1991) assessed speech functions with a comprehensive phonetic test battery . Articulatory deficits were evaluated by phonetic analy sis of speech samples drawn from spontaneous speech, repetition tasks (including all consonants and cardinal vowels), reading a short story and diadochokinetic tasks. For assessment of prosodic features patients had to realize stress contrasts and different intonation patterns; lary ngeal functions, voice quality and stability , pitch, and loudness, were evaluated perceptually. As the most prominent feature of ataxic dy sarthria fluctuation and irregularity in speech production was identified by Ackermann/Vogel/Petersen/Poremba including ir-
44. Cerebellar Dysarthria
regular articulatory breakdown, fluctuations of pitch and loudness, and voice tremor. Articulatory precision was reduced with slurred pronunciation of single consonants and consonant clusters; occasionally , stop consonants were exaggerated due to lengthening. The articulator y deficits occurred inconsistentl y throughout all speech samples (irregular articulatory breakdown). Fluctuations of pitch and loudness were observed in the more impaired patients. Two patients revealed sy llabic speech with segregation of words into sy llables. Slowing of speech tempo was noted in all patients. Breathy voice, variable speech rate, audible inspirations, excess and equalized stress, and impaired intelligibility was not observed in contrast to the Gilman/Kluin (1984) and Darle y /Aronson/Brown (1975) studies; this may be due to Ackermann/Vogel/ Petersen/Poremba’s small number of patients and their lower degree of severity . — As the principal outcome of Ackermann’s study irregularity and fluctuation in speech production represent the core deficit in cerebellar dy sarthria which can be considered to be the only deficit in circumscribed paravermal cortical lesions.
4.
Acoustic Attributes
Kent/Netsell/Abbs (1979) performed an acoustic analy sis of ataxic dy sarthric speech from five patients with degenerative diseases of the cerebellum. As the most consistent and marked abnormalities they observed changes of the normal timing pattern with lengthening of a variety of segments, equalization of sy llable duration and separation of sy llables. Disproportional segment lengthening, particularly of unstressed vowels, resulted in a disruption of the normal stress and timing pattern of speech. In words with a consonantvowel-consonant sequence the measures of vowel formant frequency were normal except for longer durations of sy llables and formant transitions, and occasionally , voice onset times. With increasing severity the number of lengthened segments increased as well as the length of individual segments itself. Durational adjustments of the sy llables in a word was inconsistent; when suffixes were added ataxic subjects made smaller reductions than normal speakers. Abnormal contours of fundamental frequency , particularly monotone and sy llable-falling patterns, frequently accompanied disturbances of sy llable timing. Equal duration and regular separation of sy l-
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lables were found to constitute scanning speech. — The articulation rate of spastic and ataxic speakers was compared by Linebaugh/ Wolfe (1984) using acoustic measurements. No significant differences were found for the two groups in contrast to the perceptual findings of Darley /Aronson/Brown (1969 a) whose spastic dy sarthric patients were significantly slower than the ataxic group. Portnoy / Aronson (1982) also found no significant differences in mean sy llable durations between their spastic and ataxic dy sarthric subjects. This discrepancy has to remain unresolved as no information is provided about severity of dy sarthria, patient selection criteria, neurological symptomatology or diagnoses.
5.
Kinematic Attributes
With the development of new techniques (cineradiograph y (Kent 1972; Kent/Netsell/ Bauer 1975; the X-ray microbeam sy stem (Kiritani/Itoh/Fujimura 1975) and electromagnetic articulograph y (Schönle/Wenig/ Schrader et al. 1983; Schönle/Gräbe/Wenig et al. 1987) attempts have been made to directly investigate movements in patients with speech motor disorders including cerebellar dy sarthria. In a cineradiographic study of an ataxic dy sarthric patient with cerebellar degeneration Kent/Netsell 1975 observed abnormalities in speaking rate, stress patterns, articulatory placements for vowels and consonants. Velocities of movements were abnormally reduced and durations of vowel steady states and consonant constrictions abnormall y lengthened. Some consonant constrictions were missed entirely , others were inappropriately formed. Range of movements was restricted not only for complex but even for ‘simple’ movements, e. g. during production of isolated vowels. — In a cineradiographic study of a patient with paroxy smal ataxic dy sarthria Netsell/Kent (1976) found the same disturbances as in the above subject, in particular with regard to rate, range and direction of movements. — Using the X-ray microbeam sy stem Hirose/Kiritani/Ushijima/ Sawashima (1978) performed a kinematic analy sis in a patient with ataxic dy sarthria from spinocerebellar degeneration. The y found inconsistencies in range and velocity of jaw and lip movements during repetition of the monosy llable /pa/. Alternation of movement direction was sluggish in comparison to normals. Velocities of lip displacement were
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extremely inconsistent in the ataxic, however, maximum velocities reached normal values. — Hunker/Bless/Weismer (1981) observed in a plethy smographic study of the respiratory sy stem that circumferential size changes of the rib cage and abdomen were abnormal in the same ataxic speaker described by Kent/ Netsell (1975). While in normal speakers rib cage and abdominal wall move in a coordinated way , they were moving in opposition (paradoxically ) in the ataxic patient. As a consequence, this discoordination between the rib cage and the abdomen could have resulted in some interference with lung volume control and subglottal air pressure with the effect of uncontrolled phonatory changes. — In a kinematic analy sis of ataxic dy sarthria with electromagnetic articulography (Schönle 1988) interarticulatory temporal coordination and the kinematics of orofacial movements were investigated in 12 patients (eight patients with multiple sclerosis, three with cerebellar infarcts, one with Friedreich’s heredoataxia) who showed marked cerebellar pathology on clinical testing, in particular cerebellar ataxia and dy sarthria. Interarticulatory timing was evaluated for the coordination of jaw opening movements and lary ngeal activities during repetitive production of 25 /pa/ sy llables. While normal control subjects showed a highly cor-
related temporal relationship between jaw cy cles and phonatory activities, opening movements for the /p/ and initiation of vocal cord vibration ran loose in the ataxic patients with a complete loss of the temporal coordination. The good correlation in the normal subjects was taken as evidence that the interarticulatory timing is precisely controlled during normal speaking while precise control of interarticulatory temporal coordination is impaired in cerebellar patients. Loss of coordinative structures (Turvey 1977) and functional sy nergies (Rondot/Bathien/Toma 1979) were concluded to be part of the pathophy siological mechanisms underly ing cerebellar dysarthria. With respect to orofacial kinematics the influence of aberrant articulatory movements on speech production due to cerebellar impairment was demonstrated for the first time (Schönle 1988, 86). Some representative data from this study are presented in figures 44.1—3. Fig. 44.1. demonstrates ataxic alterations of movement trajectories during jaw opening in four successive trials of repetitive production of /pa/. In contrast to the smooth, sinusoidal opening and closing movement of the jaw in a normal speaker the movements are segmented and jerky with untimely speed changes resulting in decomposed and dy s-
Fig. 44.1: Jaw opening trajectories in four successive trials of repetitive production of /pa/ (j: jaw, v: acousticspeech signal).
44. Cerebellar Dysarthria
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Fig. 44.2: Production of /pa/ at a spontaneous rate (left side); two oscillations of an intention tremor occurat the end of the jaw opening movement interfering with interarticulatory timing. Fast production of /pa/(right side): note an instability of movement amplitudes from one utterance to the next.
Fig. 44.3: Trajectories of tongue blade and jaw during repetitive utterance of /ka/ at a spontaneous rate(tongue pellet position 45 mm from the tongue tip); utterances of a normal speaker (left side) and of apatient with cerebellar impairment (right side).
metric trajectories. As a consequence, these intra-articulatory changes lead to an alteration of the geometry of the vocal tract from which a distortion of the acoustic of the speech output results. Speech production may also be altered by intention tremor (fig. 44.2, left side), amplitude instability (fig. 44.2, right side), and loss of end-positional control (fig. 44.3). The occurrence of oscillatory movements in the final phase of the jaw opening (fig. 44.2) results in a disturbance of the temporal coordination of mandibular and phonatory movements, voicing onset is delay ed until the end of the
oscillatory activity of the jaw. As a consequence on the behavioral level the /pa/-production falls apart and is perceived as segmented. Inspection of the lingual movement (upper trace in fig. 44.2) reveals that the tongue does not perform oscillatory motions as would be the case if the tongue would passively follow the jaw movements. Obviously , the tongue is controlled well in advance to counteract and compensate for the mandibular oscillations in order to reach a stable target positioning for the /a/-production. Fig. 44.3 shows tongue blade movement trajectories during repetitive utterance of /ka/
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at a spontaneous rate. In the normal speaker (fig. 44.3. left side) the tongue movements form a highly consistent pattern with exact closure of the tongue at the palate for the /k/ and exact target positioning for the /a/. In contrast, when the patient in fig. 44.3. (right side) produces sequences of /ka/ both amplitudes and directions of the movements change from one production to the next. This impairment of end-positional control leads to changes in the configuration of the vocal tract which results in aberrant speech acoustics ranging from almost correct to highly abnormal speech sounds. — A loss of endpositional control and alterations in the control of temporal coordination between jaw movements and phonatory activity during repetitive production of /pa/ sy llables was also observed in functional impairments of the cerebellum after alcohol ingestion even at low levels of blood alcohol (Schönle/Poser/Conrad 1988).
6.
Pathophysiological Mechanisms in Cerebellar Dysarthria
The kinematic studies revealed detailed and rich information about the pathophy siological mechanisms underly ing ataxic dy sarthria. While speech gestures are appropriate in their overall gestalt they lack precision in their temporo-spatial metrics due to impaired motor control. Control variables such as force, velocity , amplitude, direction and timing appear to be affected in cerebellar dy sarthria in much the same way as in cerebellar disturbances of limb and eye movements. Loss of the ability to modulate force generation due to cerebellar hy potonia may be responsible for slowness of movements, prolongation of speech segments, and the tendency to equalize segment length as observed in scanning speech. Loss of exact timing between articulators with ‘random coordination’ underlies what is perceived at the behavioral level as irregular breakdown of the speech output and inconsistency in speech movements, be it in the articulatory , phonatory or respiratory subsystems.
7.
Management of Patients with Cerebellar Dysarthria
No commonly used and generally accepted pharmacological therapeutic regimens exist currently for cerebellar ataxia. While Rosenbeck/La Pointe (1978) stated
that no specific treatment programs exist for the different ty pes of dy sarthria, Yorkston/ Beukelman (1981) developed a treatment program which they specifically designed for four patients with ataxic dy sarthria. The treatment sequences were based on intelligibility and prosodic considerations. Control of speaking rate was used to increase intelligibility . Normal prosodic patterning was not achieved due to the inability to learn precise coordination of fundamental frequency , loudness and timing adjustments for expression of stress. However, durational adjustments could be made and target words were stressed appropriately. In a single case study Simmons (1983) applied acoustic analy sis to monitor the treatment program in one ataxic speaker which was based on Yorkston/Beukelman (1981) approach. In a hierarchy of tasks four treatment phases were applied over a period of one y ear: 1) loudness and pitch variation to reduce monotone speech quality ; 2) modification of word and sentence stress patterns: 3) shortening of overall sy llable durations; 4) increase of naturalness to decrease exaggerated pitch and loudness variations and smoothing word transitions. The program led to compensated speech rather than to normal speech as was expected. Acoustic analy sis could be shown to improve the efficiency of the therapeutic interventions. — Berry /Goshorn (1983) applied immediate visual feedback using a storage oscilloscope in the treatment of an ataxic patient who spoke too rapidly and loudly . The treatment goal was to slow the speaking rate and thus to improve intelligibility . Over a period of five weeks the patient learned to control loudness and to slow the rate of speech by prolonging pauses. Intelligibility improved not only in the experimental but also in natural settings. Taken together, further research is necessary to develop new intervention strategies which focus on specific patho-phy siological processing deficits and apply results from kinematic and acoustic analy ses for remediation of dy sarthric speech. Communicative effects should be controlled at the perceptual level by perceptual rating scales (e. g. Sheard/Adams/Davis 1991).
8.
References
Ackermann, H., Vogel, M., Petersen, D., & Poremba, M. (1991). Speech deficits in ischemic cerebellar lesions. Unpublished manuscript.
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Ackermann, H. & Ziegler, W. (1991). Cerebellar voice tremor: an acoustic analy sis. Jou rnal of Neu rology, Neurosurgery, & Psychiatry, 54, 74—76. Amici, R., Avancini, G., & Pacini, L. (1976). Cerebellar Tu mors. Monographs in Neu ral Sciences, Vol. IV. Karger Basel 4. Berry , W. R. & Goshorn, E. L. (1983). Immediate Visual Feedback in the Treatment of Ataxic Dy sathria: A Case Study . In W. R. Berry (Ed.), Clinical Dysarthria. 253—265. College Hill Press, San Diego. Bonhoeffer, K. (1908). Über den Einfluß des Zerebellums auf die Sprache. Monatsschrift f. Psychiat. u. Neurol., 24, 88—92. Boon, D. R. (1979). The Voice & Voice Therapie. Englewood Cliffs: Prentice-Hall. Brown, J. R., Darley , F. L., & Aronson, A. E. (1968). Deviant Dimensions of Motor Speech in Cerebellar Ataxia. Trans. Am. Neu rol. Assoc., 93, 193—196. Brown, J. R., Darley , F. L., & Aronson, A. E. (1970). Ataxic Dy sarthria. Internat J. Neu rol. 7, 302—316. Charcot, J. M. (1877). Lectu res on the Diseases of the Nervou s System. Vol. 1. London: The New Sy denham Society. Darley , F. L., Aronson, A. E., & Brown, J. R. (1969 a). Differential diagnostic patterns of dy sarthria. Jou rnal of Speech and Hearing Research, 12, 246—249. Darley , F. L., Aronson, A. E., & Brown, J. R. (1969 b). Clusters of deviant speech dimensions in the dy sarthrias. Jou rnal of Speech and Hearing Research, 12, 462—296. Darley , F., Aronson, A., & Brown, J. (1975). Motor Speech Disorders. W. B: Saunders Company . Philadelphia. DeJong, R. N. (1979). The Neu rologic Examination. 4th ed., Hagerstown: Harper & Row. Delawaide, P. J. & Young, R. R. (1985). Clinical Neu rophysiology in Spasticity. 13—25. Amsterdam: Elsevier. Gilman, S. & Kluin, K. (1984). Perceptual Analy sis of Speech Disorders in Friedreich Disease and Olivopontocerebellar Atroph y . in J. R. Bloedel, J. Dichgans, & W. Precht (Eds.), Cerebellar Fu nctions. 148—163. Berlin: Springer. Hirose, H., Kiritani, S., & Sawashima, M. (1980). Patterns of dy sarthric movements in patients with amy otrophic lateral sclerosis & pseudobulbar palsy . Annu al Bu lletin of the Research Institu te of Logopedics and Phoniatrics (Tokyo) 14, 263—272. Hirose, H., Kiritani, S., Ushijima, T., & Sawashima, M. (1978). Analy sis of Abnormal Articulatory Dy namics in two Dy sarthric Patients. Jou rnal of Speech and Hearing Disorders, 43, 96—105. Holmes, G. (1917). The sy mptoms of acute cere-
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bellar injuries due to gunshot injuries. Brain 40, 461—535. Holmes, G. (1922). The Croonian Lectures on the Clinical Sy mptoms of Cerebellar disease and their interpretation. Lancet 1, 1177—1182, 1231—1237; 2, 59—65, 111—115. Hunker, C., Bless, D., & Weismer, G. (1981). Respiratory Inductive Pleth y smograph y : A Clinical Technique for Assuring Respiratory Function for Speech. Paper Presented at the Meeting of the American Speech-Language-Hearing Association Convention in Los Angeles. Cited from Abbs, J. H., Hunker, Ch. J., & Barlow, St. M. (1983). Differential Speech Motor Subsy stem Impairments with suprabulbar lesions: Neuroph y siological Framework and Supporting Data. In W. R. Berry (Ed.), Clinical Dysarthria. 21—56. San Diego: College Hill Press. Joanette, Y. & Dudley , J. G. (1980). Dy sarthric Sy mptomatology of Friedreich’s Ataxia. Brain and Language 10, 39—50. Kent, R. D. (1972). Some considerations in the cinefluorographic analy sis of tongue movements during speech. Phonetica, 26, 16—32. Kent, R. & Netsell, R. (1975). A case of an ataxic yd sarthric: Cineradiographic and spectographic observations. Jou rnal of Speech and Hearing Disorders, 40, 115—134. Kent, R. D., Netsell, R., & Abbs, J. H. (1979). Acoustic characteristics of dy sarthria associated with cerebellar disease. Jou rnal of Speech and Hearing Research, 22, 627—648. Kent, R. D., Netsell, R., & Bauer, L. L. (1975). Cineradiographic assessment of articulatory mobility in the dy sarthrias. Jou rnal of Speech and Hearing Disorders, 40, 467—480. Kiritani, S., Itoh, K., & Fujimura, O. (1975). Tongue-Pellet Tracking by a Computer-Controlled X-Ray Micorbeam Sy stem. Jou rnal of the Acou stical Society of America, 57, 1516—1520. Lechtenberg, R. & Gilman, S. (1978). Speech Disorders in Cerebellar Disease. Annals of Neu rology, Vol. 3, 285—290. Linebaugh, C. W. & Wolfe, V. E. (1984). Relationships between articulation rate, intelligibility , and naturalness in spastic and ataxic speakers. In M. R. McNeil, J. C. Rosenbek & A. E. Aronson (Eds.), The Dysarthrias: Physiology, Acou stics, Perception, Management. 197—205. San Diego: College Hill Press. Netsell, R. & Kent, R. D., (1976). Paroxy smal ataxic dy sarthria, Jou rnal of Speech and Hearing Disorders, 41, 93—109. Portnoy , R. A. & Aronson, A. E. (1982). Diadochkinetic sy llable rate and regularity in normal and in spastic and ataxic dy sarthric speakers. Journal of Speech and Hearing Disorders, 47, 285—287.
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Rondot, P., Bathien, N., & Toma, S. (1979). Phy siopathology of cerebellar movement. In J. Massion, K. Sasaki (Eds.), Cerebro-cerebellar interactions. 203—230. Amsterdam: Elsevier. Rosenbek, J. C. & LaPointe, L. L. (1978). The Dy sarthrias: Description, Diagnosis, and Treatment. In Johns, D. F. (Ed.), Clinical Management of Neu rogenic Commu nication Disorders. Boston: Little, Brown and Company. Schönle, P. W. (1988). Elektromagnetische Artiku lographie. Ein neu es Verfahren zu r klinischen Untersu chu ng der Sprechmotorik. Springer: Berlin, Heidelberg, New York. Schönle, P. W., Gräbe, K., Wenig, P., Höhne, J., Schrader, J., & Conrad, B. (1987). Electromagnetic articulatory : use of alternating magnetic fields for tracking movements of multiple points inside and outside the vocal tract. Brain and Langu age, 31, 26—35. Schönle, P. W., Poser, W. E., & Conrad, B. (1988). Änderungen der Sprechmotorik unter niedrigen Blutalkoholspiegeln. In W. Arnold, W. E. Poser, M. R. Möller (Eds.), Su chtkrankheiten, Diagnose, Therapie u nd analytischer Nachweis. 228—232. Berlin: Springer. Schönle, P. W., Wenig, P., Schrader, J., Gräbe, K.,
Bröckmann, E., & Conrad, B. (1983). Ein elektromagnetisches Verfahren zur simultanen Registierung von Bewegungen im Bereich des Lippen-, Unterkiefer- und Zungensy stems. Biomed. Tech. 28, 263—267. Sheard, Ch., Adams, R. D., & Davis, P. J. (1991). Reliability and Agreement of Ratings of Ataxic Dy sarthric Speech Samples With Vary ing Intelligibility . Jou rnal of Speech and Hearing Research, 34, 285—293. Simmons, N. N. (1983). Acoustic Analy sis of Ataxic Dy sarthria: An Approach to Monitoring Treatment. In W. R. Berry (Ed.), Clinical Dysarthria. College Hill Press, San Diego, 283—294. Turvey , M. T. (1977). Preliminaries to a theory of action with reference to vision. In R. Shaw, J. Bransford (Eds.), Perceiving, acting, and knowing: Toward an ecological psychology. Hillsdale: Erlbaum. Yorkston, K. & Beukelman, D. (1981). Ataxic Dy sarthria: Treatment sequences based on intelligibility and prosodic considerations. Jou rnal of Speech and Hearing Disorders, 46, 398—404.
Paul W. Schönle/Berthold Gröne, Allensbach (Germany)
45. Feedback Impairments in Dysarthria 1. 2. 3. 4. 5. 6.
1.
Background Possible Sensory Impairments in Dysarthria Clinical Assessment of Sensorimotor Integrity Implications for Treatment Conclusions References
Background
Theories regarding the role of sensory information in the control of speech production and deficits therein as potential etiologies for speech disorders have a very long history . Modern research on this issue began with the discovery in the post-WWII period that delay of the speech auditory signal caused severe disruption of speech. In the 1950s and 1960s, coincidental with popularization of cy bernetics, investigators used a number of sensory disruption techniques to verify the exact role of sensory feedback in speech. Unfortuntely , most experiments addressing this hy pothesis were directed toward a general either-or resolution, with little focus on specific mechanisms or the benefit of the concept that con-
tributions of sensorimotor processes might vary with different articulators, different ty pes of speech movements, or during different phases of a given movement. Due to this approach, until about 15 y ears ago, unequivocal experimental evidence to document the role of sensory information in the control of speech movements was basically lacking. Many of the early experiments involved overt disruption of sensory information, via auditory masking, delay of auditory feedback, or different regimen of topical or trigeminal nerve anesthesia. In most cases, there was substantial intersubject variability and measures very often were limited to the numbers and kinds of speech errors that could be detected by listeners. In retrospect, these studies appear to have suffered from a lack of full appreciation of the plasticity and adaption of the nervous sy stem; specifically , subjects were able, more or less successfully , to utilize alternate sensory inputs to accomplish the same speech motor goals. As noted, “claiming that sensation is not essential for speech motor control, from those early data, is analogous
45. Feedback Impairments in Dysarthria
to claiming that vision is not important to upright posture and equilibrium, simply because the blind can stand and balance themselves” (Abbs 1991, 133). In the last few y ears, a different experimental paradigm has been utilized that documents sensorimotor contributions to speech production. Specifically , the critical experiment involved disruption of the ongoing speech movements mechanicall y , without anticipation or prior knowledge by the subject, and observation of the extent to which those induced errors were corrected. Since 1975, a number of experiments have employ ed this technique and the results are quite decisive. Specifically , if one introduces an unanticipated mechanical disturbance on jaw elevation during the execution of lip closure for a bilabial stop sound [p], relatively short latency (< 100 msec.) articulatory adjustments are observed which effectively eliminate any speech manifestations of the induced error. Because these kinds of adjustments are observed in naive subjects the very first time a disruption is introduced, it has been surmised that the sensorimotor adjustments responsible are a natural part of the speech motor process (Abbs/Gracco 1984; Gracco/Abbs 1985; 1989; Shaiman 1989). Demonstration of an important role for sensory information in the control of speech is entirely consistent with results from parallel studies in the last decade on sensorimotor control of arm, hand, ey e, head, and locomotion movements. With this background, questions naturally are raised regarding the possible contributions of sensory or feedback aberrations in the movement control deficits associated with many speech disorders.
2.
Possible Sensory Impairments in Dysarthria
Perhaps the most convincing documentation of the sensory bases for so-called speech motor disorders is the wide-spread neuroanatomical coincidence between sensory and motor functions throughout the nervous sy stem. Fortunately , modern techniques in neurophy siology and neuroanatomy have dramatically improved the data that address this overlap. Specifically , brain studies in nonhuman primates were for many y ears confined to recording and stimulation under deep anesthesia, revealing only a select set of sensory and motor connections. Recent techniques, pioneered by the late Ed Evarts, permitted microelectrode recording and stimu-
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lation in the central nervous sy stem of awake animals, in many cases revealing sensory activity in association with motor task performance. These studies revealed a ubiquitous interconnection of sensory and motor processes, such that the latter is seldom manifest without the former, and conversely . The sections that follow provide a brief review of these interconnections and some indications as to how certain classes of motor speech disorders may involve both motor and sensory impairments. 2.1. Cerebral Cortex The importance of sensory information in the control of movements has changed dramatically with the observation in awake primates that stimulation of the lips or tongue elicits short latency responses in py ramidal cells of primary motor cortex (Brodmann’s area 4) and lateral regions of premotor cortex (Brodmann’s area 6 and 44). This observation can only mean that those cortical cells, some with single sy napse connections to lingual and labial motoneurons — the py ramidal cells, are directly responsive to powerful sensory input. Similar observations have been made regarding sensory inputs to other regions of cerebral cortex, with equally important implications. The classic view of the neocortex in the control of speech has been one of posterior cortical function in language components with transmission of information anteriorly for speech motor execution. While this perspective is not incorrect it is lacking the essential component of how sensory input influences these processes. Based upon research in waking primates and parallel observations in humans using improved imaging techniques, it appears that sensory information is involved at all levels of this process. For example, orofacial sensory inputs shown to project to the posterior parietal area have been argued to contribute to the monitoring of general overall vocal tract goals, as are associated with phonological elements (Abbs 1986; Abbs/Welt 1985). By contrast, sensory inputs to the primary motor cortex (Brodmann’s area 4) and regions more lateral and anterior (Brodmann’s areas 6 and 44) appear to have somewhat different functions. While the different influences of sensory input to different regions of the cerebral cortex associated with speech are outside the scope of this chapter, the implications for disorders of speech seem obvious. First, because of the ever-present
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overlap between sensory and motor functions on the cerebral cortex, damage to any of these areas is likely to y ield both motor and sensory deficits. In fact it may not be possible, despite classic sensory -motor stratification of clinical nosology , to separate sensory from motor manifestations. This observation is borne out in certain studies of speech disordered populations with cerebral damage. For example, patients with so-called apraxia of speech long have manifested difficulty in processing orofacial sensory input (Rosenbek/Wertz/Darley 1973). Interestingly , it has been argued that apraxia of speech is a disorder of speech movement coordination — a motor function increasingly believed to require sensorimotor processes (Abbs/Connor 1989); to this point is the observation that sensory input to Broca’s cortical speech area (Brodmann’s area 44) converge from multiple orofacial sites, as would be necessary for motor control of such coordinative functions. 2.2. Cerebellar Functions The cerebellum has been described as the head ganglion of the somatic sensory sy stem. This statement reflects the dense projections to the cerebellum from tendon, joint, and skin receptors and muscle afferents that project to the cerebellum. The role of sensory projections to the cerebellum has been somewhat elusive; however, increasingly it has been hy pothesized that the role of sensory inputs to the cerebellum is in integrating multiple movements that are a necessary aspect of most natural movements, including speech. In a general respect, the cerebellum has also been implicated in the on-line sensorimotor correction of potential movement errors, particularly longer latency corrections for errors that might be anticipated. Specifically , cerebellar output has been shown to be modified with experience such that the need for ongoing corrections might be anticipated and hence correction would be enhanced or expedited. Of particular importance to the motor control of speech is the fact that projections from the orofacial sy stem, particularly skin and mucosal receptors, are particularly numerous. Conversely , lingual muscle spindle afferents, unlike muscle spindles from jaw and respiratory muscles, do not project to cerebellar sites. To the extent that muscle spindles are thought to play an important role in speech motor control, these data would argue for a different role for the cerebellum in control of tongue than in control of the jaw or
respiratory sy stem. To this point, while lip muscles lack muscle spindles, and hence also do not have spindle afferents that project to the cerebellum, there are dense cerebellar projections from mechanoreceptors in the facial skin and in the mucosal tissue of the lips and tongue. Damage to the cerebellum leads to ataxic dy sarthria, a condition characterized by unsmooth, jerky movements (cf. Winstein/ Muller/Abbs 1990) and some evidence of reduced muscle tone. While sensory impairments as contributing factors in this disorder are equivocal, investigators have reported specific problems in coordination among movements of the rib cage, abdomen and diaphragm — said to be due to inadequate modulation of motoneuron activity by spindle afferents — a modulation shown to be influenced by the cerebellum. 2.3. Basal Ganglia Putative motor control functions assigned to the basal ganglia have often been a subject of controversy . It appears generally clear that this brain center is however important in speech motor control and motor control in general. In particular, based upon recording of single neurons in awake primates during the production of movement, the basal ganglia have been documented as a site for integration of sensory inputs with motor outputs. Indeed, recent studies have involved sensory mapping of orofacial and upper limb projections to the basal ganglia. In parallel with observations in the motor cortex, basal ganglia (pars reticulata and globus pallidus) neurons receiving sensory input from a given skin region also show discharge in association with spontaneous movement of that region. In parallel with the sensorimotor connections of the cerebral cortex and cerebellum, the basal ganglia have also been thought to contribute to sensorimotor error correction in movement control. The dy sarthria associated with Parkinson’s disease is the most common speech motor disturbance resulting from damage to the basal ganglia. Clearly these patients manifest an inability to self monitor their speech and manifest inappropriate control of loudness and rate, suggesting abnormal utilization of auditory information. Interestingly , Parkinson’s patients appear to manifest different kinds of impairments in speech movements of the lips versus those of the jaw (Connor/Abbs/Cole/Gracco 1989), a difference quite possibly related to the presence of spindles in jaw muscles and their
45. Feedback Impairments in Dysarthria
absence in the muscles of the lips. In this respect, Parkinson’s patients show hy peractive trigeminal reflexes; stretching of the facial skin in normal subjects elicits no muscle responses, while Parkinson’s patients manifest these abnormal reflexes quite readily (Caligiuri/Abbs 1987). These results have been interpreted to indicate that the basal ganglia have a role in gating of sensory information from the orofacial region; with damage, that gating is disturbed. While conclusive proof is lacking, the multiple speech problems in Parkinson’s patients are as likely due to impaired sensory function as motor deficits, especially given the substantial interdependence of these two processes in normal speech motor control.
3.
Clinical Assessment of Sensorimotor Integrity
Because many speech disorders appear to have underly ing sensory as well as motor deficits, several researchers have attempted to devise techniques for testing orofacial somatic sensory integrity . Obviously the normal sensory inputs associated with orofacial motor function are due to muscle contraction forces and length changes, displacements and skin deformation produced by contraction, and air pressure variations in the vocal tract. One problem in testing whether these inputs are received and processed normally is devising mechanical stimuli that are natural. A second issue is in developing a means for determining the degree that such stimuli are processed normally ; it is clear that most sensory input for control of motor actions is processed subliminally . Asking patients to give verbal reports regarding psy chophy sical properties of such stimuli is obviously an artificial process. Finally , classical psy chophy sical testing using even natural stimuli is very far removed from normal sensorimotor function and is dependent on the faulty premise that the brain is a passive sensory processor. The very aspect of function being ignored with discrete presentation of test stimuli to a passive subject — active processing of inputs related to ongoing motor tasks — may be the critical component that is impaired in patients with speech disorders. Based on these concerns, such testing, while properly motivated in a general respect, obviously must be conducted and interpreted very carefully.
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4.
Implications for Treatment
The recognition that some of the manifestations of so-called motor speech disorders may , in fact, be due to sensorimotor difficulties does offer some insights for potentially new treatment techniques as well as explanations as to the success and failure of some existing treatments. For example, if speech movements are guided, corrected, and refined by moment-to-moment sensory input, loss or impairment of that input would require a greater rote learning of such movements. The effectiveness of treatments that stress articulation drill might be due to the need to generate these movements without such on-line correction and refinement — sort of like building up a set of fixed motor programs. Similarly , the value of delay ed auditory feedback or masking noise with some dy sarthric groups (such as Parkinson’s patients) may require that they more consciously monitor articulatory output, hence improving their control. However, the most promising treatment for speech disorders with an etiology of impaired sensorimotor function would appear to be biofeedback. Specifically , with biofeedback treatment patients are provided with instrumentally -enhanced sensory information (usually visual) of an important motor output parameter; it is expected that they will utilize that information to regain control in noninstrumental settings. Some successes have been reported with this technique, largely in the form of case reports. However there are a number of variables that are said to contribute to success or failure. Speech is a complex motor behavior and consciously monitoring more than one or may be two of the critical motor output parameters is not an easy task, especially for an individual with brain damage. As such, biofeedback successes in speech motor disorders have most generally occurred in training regimes focused on single dimensioned, static variables such as background muscle tone, overall strength (in nonspeech tasks), or control of limited movements in articulators like the velum (cf. Rubow, 1984, for a review). Other complicating factors or issues that need to be resolved include the issue of whether training for a slow, non-speech control will have a positive transfer to control of more complex speech movements. In the 15 y ears since the advent of biofeedback as a treatment for speech disorders, many answers remain unresolved. Obviously , scientists and clinicians must work to
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practically address these complications before such treatment will be successfull for more than a few cases.
5.
Conclusions
While sensory functions associated with the control of speech are inseparable from motor functions, using that knowledge in the assessment and treatment of speech disorders remains a difficult prospect. Nevertheless, full appreciation of such ubiquitous sensorimotor integration is a key element to research and practice on many speech disorders.
6.
References
Abbs, J. H. (1986). Invariance and variability in speech production: A distinction between linguistic intent and its neuromotor implementation. In J. Perkell & D. H. Klatt (Eds.), Invariance and Variability in Speech Processes. 202—219. Hillsdale, NJ: Lawrence Erlbaum Associates. Abbs, J. H. (1991). Evaluation of somatic sensory processes contributing to the production of speech: From the laboratory to the clinic. In Assessment of Speech and Voice Produ ction: Research and Clinical Applications. NIDCD Monographs. 132—138, in press. Abbs, J. H. & Connor, N. P. (1989) Motor coordination for functional human behaviors: Perspectives from a speech motor data base. In S. A. Wallace (Ed.), Perspectives on the Coordination of Movement. 157—183. New York: Elsevier Science Publishers. Abbs, J. H. & Gracco, V. L. (1984). Control of complex motor gestures: Orofacial muscle responses to load perturbations of the lip during speech. Journal of Neurophysiology, 51, 705—723. Abbs, J. H. & Welt, C. (1985). Structure and function of the lateral precentral cortex: Significance
for speech motor control. In R. Daniloff (Ed.), Recent Advances in Speech Science. 155—191. San Diego: College Hill Press. Caligiuri, M. P. & Abbs, J. H. (1987). Response properties of the perioral reflex in Parkinson’s disease. Experimental Neurology, 98, 563—572. Connor, N. P., Abbs, J. H., Cole, K. J., & Gracco, V. L. (1989). Parkinsonian deficits in serial multiarticulate movements for speech. Brain, 112, 997—1009. Gracco, V. L. & Abbs, J. H. (1985). Dy namic control of the perioral sy stem during speech: Kinematic analy ses of autogenic and nonautogenic sensorimotor processes. Jou rnal of Neu rophysiology. 54, 418—432. Gracco, V. L. & Abbs., J. H. (1989). Sensorimotor characteristics of speech motor sequences. Experimental Brain Research. 75, 586—598. Rosenbek, J. C., Wertz, R. T., & Darley , F. L. (1973). Oral sensation and perception in apraxia of speech and aphasia. Jou rnal of Speech and Hearing Research, 16, 22—36. Rubow, R. (1984). Role of feedback, reinforcement, and compliance on training and transfer in biofeedback-based rehabilitation of motor speech disorders. In M. R. McNeil, J. C. Rosenbek, & A. Aronson (Eds.), The Dysarthrias: PhysiologyAco u stics-Perception-Management. 207—230. San Diego: College Hill Press. Shaiman, S. (1989). Kinematic and electromy ographic responses to perturbation of the jaw. Journal of Acoustical Society of America, 86, 78—88. Winstein, C. J. Muller, F., Abbs., J. H., Connor, N. P., Dichgans, J., & Diener, H. C. (1990). Discoordination of multiarticulate movements in patients with diffuse cerebellar atrophy : evidence from speech. Movement Disorders, 5 (Supplement 1). 5.
James H. Abbs/Roxanne DePaul, Madison, Wisconsin (USA)
46. Therapy of Dysarthrias and Speech Apraxia 1. 2. 3. 4.
1.
Definitions Therapy of the Dysarthrias Treatment of Speech Apraxia References
Definitions
The term ‘dy sarthria’ is generally used in a rather broad sense to denote the effect of a movement disorder on respiratory , phonatory
as well as articulatory functions involved in speech sound production. More accurately might be the designation ‘dy sarthrophonia’, or even ‘d y sarthrophonopneumia’, which have been proposed as terminological improvements (Netsell 1984). Speech apraxia is less well defined: “... there is little consensus of opinion regarding underly ing disrupted mechanisms and sy mptomatology , and no definitive guidelines for
46. Therapy of Dysarthrias and Speech Apraxia
the selection of the most efficacious treatment procedures for individual verbally apractic patients ...” (Square-Storer 1989 a, XV). There is an ongoing debate as to whether the deficit in speech apraxia is phonological, i. e. aphasic, or articulatory , i. e. motor, in nature (for a discussion, see Square-Storer/ Roy , 1989). In the context of this chapter, speech apraxia will be regarded as a disturbance of the programming of the spatial and temporal coordinates of speech movements. This contribution first presents some general guidelines for dy sarthria therapy . It then goes on to discuss more specific treatment measures designed to alleviate the respiratory , phonatory and articulatory dy sfunctions hindering speech production. The final section of the paper handles treatment methods for speech apraxia.
2.
Therapy of the Dysarthrias
The dy sarthrias have been broadly classified into the spastic (or central paretic), paretic, hy pokinetic, hy perkinetic and ataxic varieties and dy sarthria with feedback impairment. Although the underly ing movement disorders of the spastic, paretic, and hy pokinetic ty pe are clearly distinct (central and peripheral paresis, extrapy ramidal disease), the articulatory performance in these disorders, as evident in acoustic parameters, is usually quite similar (Darle y /Aronson/Brown 1975). Imprecise consonants, monopitch and monoloudness are noted in all three varieties. Hy pernasality and shortening of phrases occur in both central and peripheral paretic types. According to Netsell/Rosenbek (1986) and Vogel/Ziegler/Morasch (1988), treatment is based upon a phy siologically oriented speech analy sis aiming at those pathophy siological mechanisms and interactions which cause anomalous movements and coordination. Netsell (1983) has stressed that evaluation must focus on how the perceived speech abnormalities relate to the integrity of each functional component of the speech sy stem. These include the following anatomical structures: the diaphragm, the abdomen and the rib cage for respiration, the lary nx for phonation, and the velophary nx, the tongue blade and tip, the lips and the jaw for articulation. In treatment planning, a target sy mptom is usually selected which is critical for the patient’s comprehensibilit y . A yh pothesis concerning the pathophy siological and func-
481
tional basis of this target sy mptom is then formed. Finally , this hy pothesis is used to set a sequence of therapeutic goals. Such phy siologically oriented diagnostic evaluation may reveal, e. g., that an imprecise consonant production is the result of inadequate intraoral air pressure and not a sy mptom of articulatory impairment (Kearns/Simmons 1988). This example demonstrates that a malfunction in one component may seriously influence perceptual characteristics associated with others. Darle y /Aronson/Brown (1975, 270—271) advanced the following underly ing principles of dysarthria therapy: — Compensation by functional utilization of those neuronal and muscular capacities that are retained following damage. The patient learns to “work around” the impairment that has altered his/her speech habits. — Purposeful activity: The patient must now learn to do what he had been doing automatically before by means of conscious voluntary control and must become sensitive to the obstacles that interfere with the listener’s understanding. The goal of being heard and understood replaces the former goals of being quick and expressive in a personal way. — Monitoring: As he/she speaks, the patient must be self-critical and recognize and, if necessary, correct errors. He/she must learn from mistakes how to do better next time. — An early start of treatment. With progressive diseases, therapy started early helps retard speech impairment, and with static lesions, maladaptive and inefficient speech habits may be prevented. — Motivation is maintained by structuring the clinician-patient relationship so as to provide emotional support, concern and understanding and minimize feelings of panic, discouragement, and despair. Briefly , treatment consists of improving what patients have and improving what patients do with what they have (Rosenbek/ LaPointe 1985). The overall goal of treatment is rarely normal speech, but rather to establish maximal intelligibilit y (Rosenbek/LaPointe 1985), which may be obtained by: — learning to improve the residual speech motor abilities — learning to improve coping with the speech motor deficit
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— reducing maladaptations — acquiring functional compensatory behaviour — adapting the structure of the articulatory system. With respect to speech breathing, a direct improvement of residual abilities can frequently be achieved by training the transition from the resting respiratory pattern to the speech pattern, correction of posture and recruitment of both thoracic and abdominal respiration. Coping with the speech motor deficit may be improved, e. g., by adapting phrase length to a reduced expiratory phase, by reducing speech rate or by developing a strategy of producing a phrase syllable by syllable. Reduction of maladaptations may include the use of biofeedback to reduce movements or tonus of ys nergistic muscles. A functional compensation for the production of phonemes that require isolated elevation of the tongue tip (e. g. /l/, /t/, /s/, /n/) may be achieved by elevating the tongue blade instead. Moreover, a palatal lift prothesis may be used as a substitute in such cases in which comprehensibility is severely compromised by paresis or malfunction of the soft palate (Netsell/Rosenbek 1986). Most authors (e. g. Darle y /Aronson/ Brown 1975, Kearns/Simmons 1988, Vogel/ Ziegler/Morasch 1988) agree that the therapy of the dy sarthrias tends to be more sy mptom than sy ndrome specific. That is to say , the treatment of, e. g., spastic dy sarthria is not necessarily different from that of hy pokinetic dy sarthria. The presentation of treatment methods will therefore be organized according to the anatomical components involved in speech production and not by sy ndromes or diseases. No consideration will be given to pharmacological therapy , although especially in the case of hy pokinetic dy sarthria in Parkinson’s Disease, the optimal medication is the basis of speech therapy . In this condition, changes in medication may have a dramatic effect upon articulatory proficiency. 2.1. Treatment of Respiratory Dysfunction Dy sarthria treatment only rarely focusses on non-speech breathing (for methods, compare Vogel/Ziegler/Morasch 1988). On the other hand, many if not most dy sarthric patients suffer from either a markedly decreased expiration phase during articulation (Ziegler/ Hartmann/Hoole/von Cramon 1990), an in-
ability to provide sufficient subglottal pressure (Netsell/Daniel 1979) or an inability to switch in a controlled way from the nonspeech breathing pattern to a coordinated pattern of speech breathing. The non-speech breathing pattern is characterized by a similar duration of inspiration and expiration with blood gas levels as the regulated variable. In contrast, the pattern of breathing during speech consists of short inspiration and prolonged expiration with subglottal pressure as target parameter (Kim 1968, Hixon/Goldman/Mead 1973). Both volume and force of expiration can be increased by changes in posture. Usually , various positions must be tried out and their corresponding effect upon speech analy zed (Kearns/Simmons 1988). Phy siotherapy including sensory stimulation (Farber 1974; Tegart/Mitto 1987) can improve strength and tonus of the respiratory musculature, and the patient may learn to increase abdominal breathing and also make use of auxiliary breathing muscles. Aerody namic biofeedback measuring subglottal pressure has been used successfully in dy sarthria treatment (Netsell/ Daniel 1979). There are various methods to increase expiration length and control that include phonatory and articulatory as well as isolated breathing tasks and strategies to adapt speech planning to reduced respiratory capacities. These approaches either focus on drill or on enhanced monitoring and control (for descriptions, see Kearns/Simmons 1988, Vogel/Ziegler/Morasch 1988). 2.2. Treatment of Phonatory Dysfunction In cases of mutism, anarthria and aphonia two approaches, frequently in combination, are used to trigger phonation (Vogel/Ziegler/ Morasch 1988): — passive manipulation of the larynx, such as pressure upon or upward movement of the thyroid cartilage, — sensory stimulation by vibration or massage. Adequate control of respiration is a prerequisite for success. The same manipulations may be employ ed in training coordination between phonation and articulation. Darle y /Aronson/Brown (1975) stressed that most dy sarthric patients produce excessively low pitch and therefore have access to only a limited pitch range. Feedback may be used to help these patients to perform at their optimum pitch level thus providing a greater
46. Therapy of Dysarthrias and Speech Apraxia
range of variation. Frequently , pitch control is difficult to establish. Vogel/Ziegler/Morasch (1988) point out that prosodic contour may be more easily obtained by variations in volume. With the exception of Parkinson patients, dy sarthric speakers tend to speak excessively loudly and, except for those with ataxic and hy pokinetic dy sarthria, do not vary loudness to a great degree. Feedback should train patients to reduce loudness to a level appropriate for conversation (Berry / Goshorn 1983). Collaterally , left on their own, these patients attempt to increase intelligibility by slowing the rate of speech, frequently producing one sy llable at a time with equal stress and loudness. A therapy plan geared towards approximating normal speech would help the patient to train pitch and loudness variation, to vary vowel length and to increase the length of unpaused productions. Parkinson patients, on the other hand, may avoid a drop in loudness and intelligibility by learning to produce shorter phrases. Parkinson patients have proved able to reduce their speech rate by use of delay ed auditory feedback (Hanson/Metter 1983). The harsh voice quality of many dy sarthric speakers may be amerliorated by postural adjustments. Further, relaxation techniques can help minimize phonatory effort. In more severe cases, phonation can begin with voiced sighing and gradually progress towards a sustained breathy phonation (Darley /Aronson/ Brown 1975). 2.3. Treatment of Articulatory Dysfunction Following Rosenbek/LaPointe (1985), we distinguish between the velophary ngeal and orofacial regions of articulation. Hy pernasality is the most common dy sarthric sy mptom associated with velophary ngeal dy sfunction. It is caused by central or peripheral paresis or hy pokinesia of the soft palate. Among other things, treatment approaches can pinpoint nasal air emission as the target sy mptom. Feedback can be provided by holding a mirror under the nares or by electronically measuring nasal air flow (Kearns/Simmons 1988). Further treatment methods include sensory stimulation of the soft palate by massage, vibration, or ice application together with voluntary movement. Another strategy for diminishing nasal emission is increasing oral egress. In severe cases, application of a palatal lift prosthesis or palatal surgery may be required.
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Isotonic and isometric exercises can be applied in the treatment of paresis and hy pokinesia of the orofacial articulators (Rosenbek/LaPointe 1985). With severe, especially posttraumatic dy sarthria, Vogel/Ziegler/Morasch (1988) propose focussing first upon restoring oral sensibility and modulating pathological reflexes by apply ing sensory stimuli which serve to either inhibit or facilitate these reflexes. They advocate using passive support of articulatory movements in order not to trigger off associated movements. With nonverbal movements, the patient should learn to move articulators individually and differentially using adequate strength and speed to ultimately reach the correct target. Shaping of articulation then starts with vowels and those consonants that are produced in a steady state, i. e., those that require a constant position of articulators. Occasionally , biofeedback is used to reduce excess movement or muscle tone (Netsell/Cleeland 1979). In patients with oral sensory deficits, the phonetic placement technique (van Riper/ Irwin 1958) may be used to improve movement control, or oral sensory awareness may specifically be trained. Phonemes are embedded in sy llables as early as possible. Many patients will have to learn to overarticulate in order to overcome slurred speech. Special attention should be paid to medial and final consonants. Again, intelligibility and not normality of production is generally the central goal of treatment. If a patient proves unable to make contact between the tip of the tongue and the alveolar ridge or hard palate, he/she may be able to compensate by elevating the tongue blade. Bilabials may be approximated by contact between the upper teeth and the lower lip and consequent mandibular movement (Darle y /Brown/Aronson 1975). In cases of ataxic and hy perkinetic dy sarthria, a bite block may be useful to stabilize the jaw during speech (Netsell 1985). In milder cases or after some therapeutic success, the transfer of treatment gain into every day communication may become a major problem. Many patients learn to articulate quite acceptably when they focus attention upon speech production. However, in real life communication, attention is usually distracted by the social surroundings, perception of information and to the content of the intended message. At this stage, communicative acts in patient groups or other settings become the primary target of therapy.
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3.
III. Acquired Organic Pathologies of Language Behavior:Neurophonetic Disorders
Treatment of Speech Apraxia
Most speech apraxic patients also suffer from aphasia. Only when the apraxic impairment becomes critical for speech production, will its treatment be the central goal of therapy. Most approaches focus upon a key apraxic sy mptom (for a more detailed review and requirements for use of the different therapies, compare Square-Storer 1989 b): 1) In apraxic mutism and in severe speech apraxia, phonetic derivation of phonemes from non-speech sounds is attempted (van Riper/Irwin 1958). 2) When distorted production of phonemes is the central problem, the content network approach (Shewan 1980) is called for. Its goal is to develop voluntary access to articulation by using multimodal stimulation (auditory , visual, tactile and combinations) and to establish multiple means of feedback and control. 3) When the sequencing of speech sounds is the prominent deficit, the so-called speech sound sequencing intervention strategy (Dabul/Bollier 1976) may be applied. Its central feature is drilling the production of phoneme sequences of alternating place of articulation. Vogel/Ziegler/Morasch (1988) recommend guidance of the individual treatment by phonetic criteria, e. g. under consideration and sy stemic variation of place and mode of articulation. 4) In those cases, in which word initialization is the greatest obstacle, the key -word technique is often helpful (Irwin/Griffith 1973). This approach utilizes the patient’s ability to produce some words constantly and with little effort. The patient is trained to produce these key words under volitional control and derive from them other words with the same initial. As an alternative, Willbold/Johannsen-Horbach/Wallesch (1984) have described a technique in which the intact praxis of the upper limb is employ ed as a trigger or as a motor model for articulation of the initial phoneme. 5) As the impairment tends to increase with effort, relaxation techniques with EMG-feedback have been administered with some success (Rosenbek/Kent/LaPointe 1984). 6) Vogel/Ziegler/Morasch (1988) also emphasize that fluency and comprehensibility , but not accuracy are the primary goals of treatment of speech apraxia. Therefore, the patient’s attempts at self correction should only be encouraged, if his/her comprehensibility is
impaired. In most patients, fluency is the communicatively more important aim. 7) The Melodic Intonation Therapy Program, which attempts to carry speech production by an accentuated prosodic contour (Sparks/Helm/Albert 1974) has also been reported to improve production in speech apraxics (Tonkovich/Marquardt 1977). A more phy siologically oriented strategy , Prompts for Restructuring Oral Muscular Phonetic Targets (PROMPT), has recently been described yb Square-Storer/Ha y den (1989). In this strategy , the patient is provided with an “enhanced and, initially , cliniciancontrolled somatosensory description of the postural fixators or articulatory end-points, velocities, and trajectories of movements, and the ‘phasing’ or temporal assembly of motor subroutines. The clinician acts as an ‘external programmer’. After having mapped the program, he/she then ensures that the patient remains motorically but not sensorily passive. Immediately following, the patient is allowed motoric control while the clinician continues to provide somatosensory support for the constraints and patterns of movement. Eventually , the patient appears to internalize the program for each target and (...) begins to generate related programs ...” (Square-Storer/ Hay den, 192). According to the authors, the underly ing phy siological rationale is that the programming of motor events is directly influenced and potentially guided step by step by somatosensory information. This guidance is thought to compensate for the defect in program generation in speech apraxia. The intact linguistic plan of the intended utterance may be utilized to facilitate stepwise motor program processing. PROMPT differs from the other approaches outlined above (with the exception of Melodic Intonation) in that it is applied predominantly at the phrase level. Square-Storer/Hay den (1989) obtained impressive results with this therapy program. Comparative studies with other treatment programs are being presently conducted.
4.
References
Berry , W. R. & Goshorn, E. L. (1983). Immediate visual feedback in the treatment of ataxic dy sarthria: a case study . In W. R. Berry (Ed.), Clinical dysarthria. 253—265. San Diego: College Hill. Dabul, B. & Bollier, B. (1976). Therapeutic approaches to apraxia. Jou rnal of Speech and Hearing disorders, 41, 268—276.
46. Therapy of Dysarthrias and Speech Apraxia
Darley , F. L., Aronson, A. E., & Brown, J. R. (1975). Motor Speech Disorders. Philadelphia: Saunders. Farber, D. S. (1974). Sensorimotor evalu ation and treatment for allied health personnel. Indianapolis: University of Indiana Foundation. Hanson, W. R. & Metter, E. J. (1983). DAF speech rate modification in Parkinson’s disease: a report on two cases. In W. R. Berry (Ed.), Clinical dysarthria. 231—251. San Diego: College Hill. Hixon, T., Goldman, M., & Mead, J. (1973). Kinematics of the chest wall during speech production. Jou rnal of Speech and Hearing Research, 16, 78—115. Irwin, J. V. & Griffith, F. A. (1973). A theoretical and operational analy sis of the paired stimuli technique. In W. D. Wolfe & D. J. Goulding (Eds.), Articu lation and Learning: New dimensions in research, diagnostics, and therapy. 156—194. Springfield: Thomas. Kearns, K. P. & Simmons, N. N. (1988). Motor speech disorders: The dy sarthrias and apraxia of speech. In N. J. Lass, L. V. McRey nolds, J. L. Northern, & D. E. Yoder (Eds.), Handbook of Speech-Lang u age Pathology and u A diology. 592—621. Toronto: Decker. Kim, R. (1968). The chronic residual respiratory disorder in post-encephalitic Parkinsonism. Journal of Neu rology, Neu rosu rgery and Psychiatry, 31, 393—398. Netsell, R. (1983). Speech motor control: theoretical issues with clinical impact. In W. R. Berry (Ed.), Clinical dysarthria. 1—19. San Diego: College Hill. Netsell, R. (1984). A neurobiologic view of the dy sarthrias. In M. R. McNeil, J. C. Rosenbek, & A. E. Aronson (Eds.), The dysarthrias: physiology, acou stics, perception, management. 1—36. San Diego: College Hill Press. Netsell, R. (1985). Construction and use of a bite block for evaluating and treating speech disorders. Jou rnal of Speech and Hearing Disorders, 50, 103—106. Netsell, R. & Cleeland, C. (1979). Modification of lip hy pertonia in dy sarthria using EMG feedback. Jou rnal of Speech and Hearing Disorders, 38, 131—141. Netsell, R. & Daniel, B. (1979). Dy sarthria in adults: ph y siological approach to rehabilitation. Archives of Physical Medicine and Rehabilitation, 60, 502—508. Netsell, R. & Rosenbek, J. C. (1986). Treating the dy sarthrias. In R. Netsell (Ed.), A neu robiologic view of speech produ ction and the dysarthrias. 123—152. San Diego: College Hill Press. Rosenbek, J. C., Kent, R. D. & LaPointe, L. L. (1984). Apraxia of speech: an overview and some
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perspectives. In J. C. Rosenbek, M. R. McNeil, & A. E. Aronson (Eds.), Apraxia of speech: physiology, acou stics, lingu istics, management. 1—72. San Diego: College Hill Press. Rosenbek, J. C. & LaPointe, L. L. (1985). The dy sarthrias: description, diagnosis and treatment. In D. F. Johns (Ed.), Clinical management of neu rogenic commu nication disorders. 97—129. Boston: Little, Brown. Shewan, C. M. (1980). Verbal dy spraxia and its treatment. Human Communication, 5, 3—12. Sparks, R., Helm, N., & Albert, M. (1974). Aphasia rehabilitation resulting from melodic intonation therapy. Cortex, 10, 303—316. Square-Storer, P. (1989 a). Preface. In P. SquareStorer (Ed.), Acqu ired apraxia of speech in aphasic adults. XV—XVII. London: Taylor & Francis. Square-Storer, P. (1989 b). Traditional therapies for apraxia of speech — reviewed and rationalized. In P. Square-Storer (Ed.), Acqu ired apraxia of speech in aphasic adu lts. 145—161. London: Tay lor & Francis. Square-Storer, P. & Ha y den (Chumpelik), D. (1989). PROMPT Treatment. In P. Square-Storer (Ed.), Acqu ired apraxia of speech in aphasic adu lts. 190—219. London: Taylor & Francis. Square-Storer, P. & Roy , E. A. (1989). The apraxias — commonalities and distinctions. In P. SquareStorer (Ed.), Acqu ired apraxia of speech in aphasic adults. 20—63. London: Taylor & Francis. Tegart, L. & Mitto, H. (1987). Die Therapie der spastischen Dy sarthrie. In L. Springer & G. Kattenbeck (Eds.), Aktu elle Beiträge zu r Dysarthrophonie und Dysprosodie. 25—58. München: tuduv. Tonkovich, J. D. & Marquardt, T. P. (1977). The effects of stress and melodic intonation on apraxia of speech. In R. H. Brookshire (Ed.), Clinical aphasiology conference proceedings. 97—102. Minneapolis: BRK. Van Riper, C. & Irwin, J. (1958). Voice and articulation. Englewood Cliffs: Prentice Hall. Vogel, M., Ziegler, W. & Morasch, H. (1988). Sprechen. In D. von Cramon & J. Zihl (Eds.), Neu rophysiologische Rehabilitation. 319—359. Berlin: Springer. Willbold, B., Johannsen-Horbach, H., & Wallesch, C. W. (1984). Zur Therapie der artikulatorischen Apraxie. Sprache—Stimme—Gehör, 8, 24—26. Ziegler, W., Hartmann, E., Hoole, P., & von Cramon, D. (1990). Entwicklu ng von diagnostischen Standards u nd von Therapieleitlinien für zentrale Stimm- u nd Sprechstör u ngen (Dysarthrophonien). München: Gesellschaft für Strahlen- und Umweltforschung.
Helga Johannsen-Horbach/Claus- W. Wallesch, Freiburg (Germany)
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47. 1. 2. 3. 4. 5. 6.
1.
Effects of Anatomical Alterations on Fully Developed Articulation Introduction Maxillary Resections Ablation of the Soft Palate Mandibulectomy Glossectomy References
Introduction
The cognitively intact adult with normal speech who suffers sudden loss of parts of the speech mechanism through ablative surgery constitutes an interesting research opportunity for linguists. What adjustments or maladjustments does the individual make in phonetic output and other linguistic behavior? Such individuals provide a research population for investigating the plasticity of the speech production mechanism, that is, for study ing the minimum phy sical requirements for normal speech production or for exploring aberrant speech production which nevertheless recognizably realizes the phonological sy stem. In addition, adjustments in speech production are influenced by idiosy ncratic factors as well as by the particular ablative procedures and subsequent reconstructions, further challenging the linguist in teasing apart the role that each factor play s in speech. The purpose of this chapter is to orient the linguist to the area of orofacial ablative surgery with respect to opportunities for the analy sis of the phonetic realization of phonological structures. Information is organized according to ty pe of resection and, when appropriate, to effects of surgical or prosthetic treatment on speech production. Combination resections of multiple oral structures are common, but information on speech in such reports is often missing (e. g., Kavanagh/Hinkle 1987) and, if offered, is presented only in general terms.
2.
Maxillary Resections
Articulation is imperiled by removal of normal dental, alveolar and palatal contacts; resonance is altered if the ablation destroy s the normal separation between the oral and nasal cavities (Arndt/Shelton/Bradford 1965; Fletcher/Sooudi/Frost 1974; Majid/Weinberg/Chalian 1974). The consensus of clinical reports is that most patients regain intelligibility once fitted with appropriate prosthetic
devices (Kipfmueller/Lang 1972; Majid/Weinberg/Chalian 1974; Plank/Weinberg/Chalian 1981). See Peterson-Falzone 1988, for summary.
3.
Ablation of the Soft Palate
These resections are ty pically accompanied by partial or total maxillectomy , and result in loss of velophary ngeal closure, with the expected effects of nasal air loss on obstruent consonants and hy pernasal resonance on vowels and vocalic segments. Correction of the phy sical defect may be approached surgically or prosthetically ; few data are available delineating benefits of one approach over the other, probably due to individual factors affecting adjustments to prostheses (obturators for the velophary ngeal port) versus surgical approaches. Casey /Emrich (1988) reported development of ‘compensatory ’ motion of the phary ngeal musculature (commonly called Passavant’s ridge) in 83% of patients undergoing soft palatectomy , but had no data on presence or absence of such movement preoperatively . (Inward movement of phary ngeal musculature is known to be of significant benefit in prosthetic treatment of patients with clefts and other forms of velophary ngeal insufficiency [Karnell/Rosenstein/ Fine 1987]). Minsley /Warren/Hinton (1988) reported that four patients with oronasal defects due to resection of the maxilla and/or soft palate increased respiratory volumes four-fold following the resections, thus maintaining supralary ngeal vocal tract air pressures within the normal range despite the reduction in vocal tract resistance. This compensation is similar to that evidenced by speakers with cleft palate. Significant differences were found in the respiratory volumes accompany ing voiced and voiceless consonants; thus the linguistic contrast was retained even with the elevated volumes.
4.
Mandibulectomy
Reports on speech after mandibulectomy are usually descriptions of cases involving partial or total ablation of the tongue (following section). Most articles focus on surgical technique and discuss speech only in terms of “intelligibility ” after reconstruction (e. g., Jewer/Boy d/Manktelow et al. 1989; Weissler/ Goldsmith/Martinkosk y 1988). Hemimandi-
47. Effects of Anatomical Alterations on Fully Developed Articulation
bulectomy causes little disturbance in function if the bone resection does not pass the midline (Bloomer/Hawk 1973).
5.
Glossectomy
A very large body of clinical data on the effects of partial or total glossectomy on speech is available, much of it difficult to interpret. Several reports have described the ability of some patients to develop intelligible speech without prosthetic or surgical reconstruction (Bloomer/Hawk 1973; Dugua y 1964; Goldstein 1940; Herberman 1958). Goldstein (1940) even went so far as to conclude that the tongue was n o t an indispensable articulator. However, the descriptions given by these early authors are often lacking in details regarding individual phones, and even the definition of ‘intelligible’ is unspecified. The literature on glossectomy indicates that impairment in function is not alway s proportional to the amount of tissue removed. Skell y /Spector/Donaldson et al. (1971) reported remarkably similar (and low) intelligibility for partial and total glossectomees. However, Rentschler/Mann (1980) reported a correlation of — .726 between extent of surgery and intelligibility . More important than the difference between partial or subtotal glossectomy and total glossectomy is the fact that most of these occur as part of combined ablations of the floor of the mouth, mandible, phary nx and even lary nx. In an early report on a patient with a partial glossectomy (Lehman/Hulicka/Mehringer 1966), the “total lack of speech” was due to concomitant lary ngectomy rather than to resection of lingual tissue. Some reports on partial glossectomees describe articulatory adjustments developed either spontaneously or with training. Backus (1940) described a boy who substituted labial consonants for tongue-tip phonemes after anterolateral excision of one-third of the tongue. Bloomer/Hawk (1973) described a hemiglossectomee who substituted a lingual-alveolar constriction for midline lingual grooving on sibilants. Skelly /Spector/Donaldson et al. 1971) described a therapy program, later elaborated by Skelly (1973), for teaching compensatory articulations to partial and total glossectomees. Intelligibility for the partial glossectomees increased from a pre-therapy rating of 6—24% to post-therapy values of 24—46%.
487
For the total glossectomees, 0—8% intelligibility increased to 18—42%. The partial glossectomees were observed to make marked use of the residual stump rather than resorting to the more varied substitutions used by the total glossectomees, some examples of which were production of /z/ by bilabial tension obstruction of the airstream (also described by LaRiviere/Seilo/Dimmick 1975); production of /g/ by phary ngeal constriction, with slight bulging of the retroglossal phary ngeal wall; and production of /d/ by lower lip contact with the maxillary teeth, or in edentulous patients, with the maxillary alveolar ridge. Skell y /Donaldson/Schinsk y (1972) emphasized consistency of phoneme substitution as critical in intelligibility , and stated that usable gains in compensatory articulation required 6 to 8 months in total glossectomees. Duguay (1964) supplied a list of “acceptable acoustic approximations” drawn from his own observations and from a survey of the literature. These included production of tip-alveolars either by elevation of the floor of the mouth or by retraction and elevation of the lower lip to contact the upper incisors; substitution of labiodental for interdental consonants; production of sibilants by airflow through the teeth, lips protruded; substitution of glottal stops for the stop feature of affricates; production of linguavelar consonants by contact of buccinator muscles with the molars, or by ‘movements approximating the palatal arches,’ or replacement of /k/ and /g/ by glottal stops and /ng/ by nasalization of the preceding vowel; and replacement of /r/ by a ‘laryngeal’ or uvular articulation. LaRiviere/Seilo/Dimmick (1975) described speech in a patient left with a small remnant of lingual tissue posterior to the faucial pillars. Bilabial and labiodental consonants were highly intelligible, as would be expected, but so were /t, s, n, l/ and the voiced affricate. Intelligibility of vowels ranged from 90% for /ae/ to 9% for vocalic /r/, with a mean of 45.8%. Sentence intelligibility was 88.8%. Listeners confused /t, p/ and /d, b/, and acoustic analy sis revealed that the durations of these pairs had been reversed. However, /s/ and /f/ were also confused perceptually and their durational values were not similar. This suggests that durational differences cannot compensate for all ambiguous acoustic properties although they may add to the confusion if inappropriate. Linguadental stops and interdental fricatives were produced by movements normally associated with bilabial
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III. Acquired Organic Pathologies of Language Behavior:Neurophonetic Disorders
stops and labiodental fricatives. Sibilants were produced by blowing air through closed teeth. In general, the speaker preserved manner and voicing of consonants while necessarily sacrificing place of production. Some information on effects of lingual ablation on vowel intelligibility is available (Ballard/Kerner/Ty son 1986; Gillis/Leonard 1983; Landahl/Karnell 1990; LaRiviere/Seilo/Dimmick 1975; Skelly 1973; Skelly /Donaldson/ Fust/Townsend 1972). Skell y /Donaldson/ Fust/Townsend (1972) noted that the value of F1 extended over a wide range in less intelligible speakers, that is, exhibited a greater than normal bandwidth, and the intensity of F2 was diminished. In line with the findings of psy choacoustic investigations on perception of vowels produced by normal speakers, intelligibility increased as F1 decreased in bandwidth and F2 became more defined. In the patient described by LaRiviere/Seilo/ Dimmick (1975), vowels were neutralized both perceptually and acoustically , with F1 more stable than F2. Gillis/Leonard (1983) reported 48% vowel intelligibility in single words in their glossectomy speaker. Georgian/Logemann/Fisher (1982) provided extensive perceptual and acoustic data on a patient following resection a n d r e c o nst r u c t i o n of the tongue and floor of the mouth. The speech samples were CVC sy llables consisting of voiced and voiceless bilabial and tip-alveolar stops in various vowel contexts. The greatest perceptual misidentification was observed when both bilabials and tip-alveolars occurred in context with /i/. (Note that many glossectomy speakers described in the literature spontaneously substitute, or have been taught to substitute, labial consonants for tongue tip consonants.) Among the acoustic findings were absence of stop bursts, weakened F3, and frequent convergence of F2 towards F1. Negatively sloped transitions, as opposed to normally positively sloped, were observed for all bilabial productions except /bi/. Landahl/Karnell (1990) also compared perceptual to acoustic data on two glossectomee speakers, one whose speech was rated as 80% intelligible and the other at 50% intelligible. They reported that, for the latter, removal of poorly identified vowel information enhanced listeners’ identification of the consonants. For the less impaired speaker, full CV’s were well identified while removal of vowel information diminished correct consonant identification. The authors concluded that, when onset spectra are ambiguous, the
vowel transitions weight the onset spectrum to influence identification of the consonant place of articulation, in some instances away from the intended category. Several reports have described patients undergoing glossectomy combined with partial mandibulectomy (Ballard/Kerner/Ty son et al. 1986; Cantor/Curtis/Shipp et al. 1969; Curtis/ Cantor 1974; Knowles/Chalian/Shanks 1984; Wheeler/Logemann/Rosen 1980); two reports have described patients who have undergone glossectom y with total mandibulectom y . Shedd (1976) said his patient was 70 to 80% intelligible, but gave no details on articulatory compensations or treatment procedures. The patient described yb Me y erson/Johnson/ Weitzman (1980) lost the mandible together with the anterior one-half of the tongue with excision of the my lohy oid, hy oglossus, genioglossus and digastric muscles. After multiple surgical reconstructions, all consonants except /h/ were severely distorted. Bilabial consonants were affected due to lack of bony support for the lower lip. Intelligibility was zero at the initial evaluation, and 50% eighteen months later, before formal therapy was initiated. Speakers were taught to use phary ngeal constrictions to approximate velar stops. Linguoalveolar stops were approximated by contact between the lower lip and upper teeth. A slower rate of speech was encouraged to increase intelligibility , which was 80% by the conclusion of therapy . Acoustical analy sis at this time showed the vowel space to be diminished in comparison to normal speakers, with the most limitation in the range of F2. Prosthetic approaches to rehabilitation have y ielded interesting results recently , although many reports are poorly detailed. These consist of attempts (a) to provide a prosthetic tongue, and (b) to lower the palatal arch to facilitate articulatory contacts. Cantor/Curtis/Shipp et al. (1969) reported the latter devices to facilitate velar consonant production for patients with severe restrictions in lingual mobility but negative effects for those with modest restriction. Wheeler/Logemann/Rosen (1980) described a series of patients with 10 to 90% of the tongue excised whose speech intelligibility ranged from 72% to 81% (note that even the patient with 90% of the tongue extirpated had not lost more than 18% of his intelligibility ). Without their “maxillary reshaping prostheses,” no patient exceeded 90% intelligibility ; with these devices, 6 of 10 reach this criterion. In 3 of 4
47. Effects of Anatomical Alterations on Fully Developed Articulation
patients provided with “thickening of the maxillary denture” (Lauciello/Vergo/Schaaf/ Zimmerman 1980), both articulation and resonance were reported to improve. A similar approach was used by Knowles/Chalian/ Shanks (1984). Araman y /Downs/Beer y /Aslan (1982) suggested palatal augmentation prostheses for partial glossectomees, mandibular tongue prostheses for total glossectomees. Palatography (mapping of articulatory contacts sensed by electrodes imbedded in a palatal plate) was suggested by both Christensen/Hutton/Hasegawa/Fletcher (1983) and McKinstr y /Araman y /Beer y /Sansone (1985) for optimal fitting of prostheses, but patient material was limited. Mandibular tongue prostheses have been described in several reports (Ballard/Kerner/ Ty son et al. 1986; Belsky 1978; deSouza/Martins 1975; Moore 1972; Gillis/Leonard 1983) offering somewhat my stify ing descriptions of the devices and little specific information on speech. (There are multiple articles on surgical reconstruction attempting either to restore lingual function or to prepare the mandible and floor of the mouth to support a lingual prosthesis; unfortunately , these reports discuss recovery of function primarily in terms of deglutition rather than speech.) Moore (1972) fashioned a prosthesis with a “highly flexible tip” so that his patient could produce tongue-tip sounds, but there was not note of how the tip was controlled. Gillis/Leonhard (1983) designed several experimental prostheses for their patient, but did not describe in detail which design produced the best speech results, which were improvements in vowel intelligibility from 48% to 64% and consonant intelligibility from 82% to 90% in single words. Ballard/Kerner/Ty son et al. (1986) noted that their patient who had been fitted with a combination mandibular/tongue prosthesis shifted the anterior-to-posterior position of the mandible to achieve tip-alveolar and linguavelar consonants. It is worth noting that the most comprehensive speech habilitation program for glossectomy patients is still the “compensatory phy siologic phonetics” of Skelly and associates, despite the fact that the work is now nearly 20 y ears old (1971, 1972 a, 1972 b, 1973). In addition to the compensatory gestures taught in an effort to achieve approximations of normal consonants, Skelly and coworkers sought to improve intelligibility through manipulation of vowel duration, vocal intensity , pause length, habitual pitch, pitch range and variation in pitch patterns.
489
No follow-up reports have appeared, but no other speech pathologists have replaced or significantl y augmented Skell y ’s work. Clearly , improvements in therapeutic approaches will be dependent upon investigations which relate the phy siology with acoustic output and the perceptual responses of listeners.
6.
References
Aramany , M. A., Downs, J. A., Beery , Q. C., & Asian, Y. (1982). Prosthodontic rehabilitation for glossectomy patients. Jou rnal of Prosthetic Dentistry, 48, 78—81. Arndt, W. B., Shelton, R. L., & Bradford, L. J. (1965). Articulation, voice, and obturation in persons with acquired and congenital palatal defects. Cleft Palate Journal, 2, 377—383. Backus, O. (1940). Speech rehabilitation following excision of the tip of the tongue. American Jou rnal of the Disabled Child, 60, 368—370. Ballard, J. L., Kerner, E., Ty son, J., Ashford, J., & Rees, R. (1986). Adenocarcinoma of the tongue complicated by hemimandibulectomy : Soft tissue support for a tongue prosthesis in an edentulous glossectomy patient. Jou rnal of Prosthetic Dentistry, 56, 470—473. Belsky , M. W. (1978). Prosthetic reconstruction of mandibular tongue prostheses. Jou rnal of Prosthetic Dentistry, 39, 650—653. Bloomer, H. H. & Hawk, A. M. (1973). Speech considerations: Speech disorders associated with ablative surgery of the face, mouth and phary nx — ablative approaches to learning. ASHA Report No. 8: Orofacial Anomalies: Clinical and Research Implications. 42—61. Washington, D. C.: American Speech and Hearing Association. Cantor, R., Curtis, T. A., Shipp, T., Beumer, J., & Vogel, B. S. (1969). Maxillary speech prostheses for mandibular surgical defects. Jou rnal of Prosthetic Dentistry, 22, 253—260. Casey , D. M. & Emrich, L. J. (1988). Passavant’s ridge in patients with soft palatectomy . Cleft Palate Journal, 25, 72—77. Christensen, J. M., Hutton, J. E., Hasegawa, A., & Fletcher, S. G. (1983). Evaluation of the effects of palatal augmentation on partial glossectom y speech. Jo u rnal of Prosthetic Dentistry, 50, 539—543. Curtis, T. A. & Cantor, R. (1974). The forgotten patient in maxillofacial prosthetics. Jou rnal of Prosthetic Dentistry, 31, 662—679. DeSouza, L. J. & Martins, O. J. (1975). Swallowing and speech after radical total glossectomy with tongue prosthesis. Oral Surgery, 39, 356—360.
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Duguay , M. J. (1964). Speech after glossectomy . New York State Jo u rnal of Medicine, 64, 1836—1838. Fletcher, S. G., Sooudi, I., & Frost, S. D. (1974). Quantitative and graphic analy sis of prosthetic treatment for “nasalance” in speech. Jou rnal of Prosthetic Dentistry, 32, 284—291. Georgian, D. A., Logemann, J. A. & Fisher, H. B. (1982). Compensatory articulation patterns of a surgically treated oral cancer patient. Jou rnal of Speech and Hearing Disorders, 47, 154—159. Gillis, R. E. & Leonard, R. J. (1983). Prosthetic treatment for speech and swallowing in patients with total glossectomy . Jou rnal of Prosthetic Dentistry, 50, 808—814. Goldstein, M. A. (1940). Speech without a tongue. Journal of Speech Disorders, 5, 65—69. Herberman, M. A. (1958). Rehabilitation of patients following glossectomy . Archives of Otolaryngology, 67, 182—183. Karnell, M. P., Rosenstein, H., & Fine, L. (1987). Nasal videoendoscopy in prosthetic management of palatophary ngeal dy sfunction. Jou rnal of Prosthetic Dentistry, 58, 479—484. Kavanagh, K. T. & Hinkle, W. G. (1987). Reconstruction of the soft palate after jaw, tongue, neck dissection with subtotal palatectomy (velophary ngoplasty). Laryngoscope, 97, 1461—1463. Kipfmueller, L. J. & Lang, B. R. (1972). Presurgical maxillary prosthesis: An analy sis of speech intelligibilit y . Jo u rnal of Prosthetic Dentistry, 28, 620—625. Knowles, J. C., Chalian, V. A. & Shanks, J. C. (1984). A functional speech impression used to fabricate a maxillary speech prosthesis for a partial glossectomy . Jou rnal of Prosthetic Dentistry, 51, 232—237. Landahl, K. L. & Karnell, M. P. (1990). Acoustic invariants in glossectomee speech. Manuscript in preparation. LaRiviere, C., Seilo, M. T. & Dimmick, K. C. (1975). Report on the speech intelligibility of a glossectomee: Perceptual and acoustic observations. Folia Phoniatrica, 27, 201—214. Lauciello, F. R., Vergo, T., Schaaf, H. G. & Zimmerman, R. (1980). Prosthodontic and speech rehabilitation after partial and complete glossectomy . Journal of Prosthetic Dentistry, 43, 204—211. Lehman, W. L., Hulicka, I. M. & Mehringer, E. J. (1966). Prosthetic treatment following complete glossectomy . Jou rnal of Prosthetic Dentistry, 16, 344—350. Majid, A. A., Weinberg, B. & Chalian, V. A. (1974). Speech intelligibility following prosthetic obturation of surgical acquired maxillary defects. Journal of Prosthetic Dentistry, 323, 87—96. McKinstry , R. E., Aramany , M. A., Beery , Q. C. & Sansone, F. (1985). Speech considerations in pros-
thodontic rehabilitation of the glossectomy patient. Journal of Prosthetic Dentistry, 53, 384—387. Mey erson, M. D., Johnson, B. H. & Weitzman, R. S. (1980). Rehabilitation of a patient with complete mandibulectom y and partial glossectom y . American Journal of Otolaryngology, 1, 256—261. Minsley , G. E., Warren, D. W. & Hinton, V. (1988). Maintenance of intraoral pressure during speech after maxillary resection. Jou rnal of the Acou stical Society of America, 83, 820—824. Moore, D. J. (1972). Glossectomy rehabilitation by mandibular tongue prosthesis. Jou rnal of Prosthetic Dentistry, 28, 429—433. Peterson-Falzone, S. J. (1988). Speech disorders related to craniofacial structural defects, Part I. In N. J. Lass, L. V. McRey nolds, J. L. Northern & D. E. Yoder (Eds.), Handbook of speech-langu age pathology and au diology. 442—476. Toronto: B. C. Decker. Plank, D. M., Weinberg, B. & Chalian, V. A. (1981). Evaluation of speech following prosthetic obturation of surgically acquired maxillary defects. Journal of Prosthetic Dentistry, 45, 626—638. Rentschler, G. J. & Mann, M. B. (1980). The effects of glossectomy on intelligibility of speech and oral perceptual discrimination. Jou rnal of Oral Su rgery, 38, 348. Shedd, D. (1976). Rehabilitation problems of head and neck cancer patients. Jou rnal of Su rgical Oncology, 8, 11—21. Skelly , M., Donaldson, R. C. & Schinsky , L. (1972), Substitution consistency as a factor in glossectomee intelligibility . Jou rnal of the Missou ri Speech and Hearing Association, 5, 21—23. Skelly , M., Donaldson, R. C., Fust, R. S. & Townsend, D. L. (1972). Changes in phonatory aspects of glossectomee intelligibility through vocal parameter manipulation. Jou rnal of Speech and Hearing Disorders, 37, 379—389. Skelly , M. (1973). Glossectomee speech rehabilitation. Springfield, II.: C. C. Thomas. Skelly , M., Spector, D. J., Donaldson, R. C., Brodeur, A. & Paletta, F. X. (1971). Compensatory phy siologic phonetics for the glossectomee. Journal of Speech and Hearing Disorders, 36, 101—114. Weissler, M. C., Goldsmith, M. M. & Martinkosky , S. (1988). A method of closure after resection of anterior floor of mouth cancers. OtolaryngologyHead and Neck Surgery, 99, 315—320. Wheeler, R. L., Logemann, J. A. & Rosen, M. S. (1980). Maxillary reshaping prostheses: Effectiveness in improving speech and swallowing of postsurgical oral cancer patients. Jou rnal of Prosthetic Dentistry, 43, 313—319.
Sally J. Peterson-Falzone, San Francisco, California (USA)/Karen L. Landahl, Chicago, Illinois (USA)
48. Disorders of Phonation
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48. Disorders of Phonation 1. 2. 3. 4. 5.
1.
Introduction Organic Voice Disorders Functional Voice Disorders Central Voice Disorders Following Craniocerebral Injury Trauma (CIT) References
Introduction
This article starts with a discussion of the voice with respect to its role in communication. Then the anatomic, phy siological and pathological foundations of voice production will be introduced as a backdrop for the understanding of the relationships to be presented here. In view of the space available for the chapter on disorders of phonation in this handbook, only a very general overview of the various causes of phonation disorders can be given in favor of a more thorough treatment of the effects of craniocerebral injury and other brain diseases on the lary nx and its functions. After that, the direct effects of these brain diseases on the center controlling lary ngeal functions will be examined. Finally , we will look into those effects actually resulting from interventions, such as long-term intubation, that had been necessary in the acute phase of the illness. The realization of communication demands precise coordination of respiration, phonation and articulation. The disturbance of a part of the sy stem disrupts the whole and may even cause it to break down entirely . This contribution handles the voice and its disorders, well knowing that a voice disorder is often caused by an impediment in the coordination of the three different functions, and therefore signals a more encompassing disorder. In this case, the voice disorder may be the initial sy mptom of another illness which may progress and affect other functions. Or, the voice disorder may not occur until other disorders are apparent. A normal voice tells more about its carrier than his or her speech. A person’s voice often has quite individual and unmistakable sound properties, that vary within a certain range and depend on the speaker’s phy sical and psy chological state. The singularity of each voice is determined by the anatomic structures in the lary nx and in the vocal tract. Interestingly , one can hardly voluntarily influence this set up to change one’s special
sound of voice. In fact, a normal speaker will even have difficulty attempting to alter learned speech behaviors, which have been partly influenced by ‚vocal’ role models, such as volume, pitch level, intonation and other parameters. A person’s voice will only be perceived as being appropriate, when its pitch level and sound characteristics reflect the appearance and the personality of the speaker and when its volume meets the demands of the situation. Even minor deviations from the modalities mentioned lead to a noticeable clash between the speaker and his or her voice, usually arousing negative emotions or downright rejection on the part of the hearer. The human voice is produced in the lary nx, which is situated at the top of the trachea, at the point where the trachea and the esophagus branch. The lary nx consists of a cartilage box (Fig. 48.1), which is held together by ligaments, muscles and mucous membranes. The joint linking the cricoid cartilage to the 2 ary tenoid cartilages is flexible enough to allow the lary nx to carry out opposing functions. That is, the lary nx must open for respiration and close for phonation (Fig. 48.2). Almost all of the muscles involved in voice production have an effect on these joints, to open or to close the glottis or to tense the vocal folds. These muscles receive their nervous impulses from two branches of the vagus nerve (X), the superior and inferior lary ngal nerves (N. lary ngicus superior et N. lary ngicus inferior = N. recurrens), and regulate the position of the vocal folds and their tension. The vibrations of the vocal folds, which give rise to the primary sound production of the lary nx, are caused by a breath stream coming from the trachea and flowing against the closed glottis. The air flow induces quite even, regular movements in both vocal folds (my oelastic-aerody namic theory of voice production; van den Berg 1956; 1958). Immediately after passing through the vibrating vocal cords, this primary sound of the lary nx is but y et a still completely undifferentiated sound pattern with a lot of overtones. It must then be transformed into the diverse sounds of speech by means of free resonance in the vocal tract, that is in the entrance of the lary nx, the low and middle phary nx, the oral and nasal cavity and the nose. (For further details about the anatomy
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III. Acquired Organic Pathologies of Language Behavior:Neurophonetic Disorders
Fig. 48.1: Posterior (a) and lateral (b) views of the hyoid bone and the laryngeal and tracheal cartilages andtheir connecting membranes
Fig. 48.2: Normal larynx in indirect laryngoscopy during respiration (a) and phonation (b)
and phy siology of phonation, see Aronson’s (1990) textbook on clinical voice disorders.) Not only do the manifold functions of the normal voice just mentioned depend on intact centers, neurons and pathway s from the motor control center to the lary nx, not to mention the condition of the lary nx itself, but they also depend on the emotional affective state of the speaker. With this in mind, the diversity of disorders that can affect voice function is no surprise. Clinicians treating disorders of phonation are faced with certain hindrances. One diffi-
culty is the lack of knowledge about premorbid idiosy ncrasies or even possible disorders of phonation in the patients to be treated. A further difficulty is posed by the fact that several different factors can alter phonation in an individual patient. Thus primary and secondary effects on pitch are hard to differentiate. For example, many voice disorders, no matter whether they are organic, functional (in a narrow sense) or psy chogenic in origin can cause the patient to compensate in such a manner that the illness inducing factors are masked.
48. Disorders of Phonation
Furthermore, certain voice disorders do not clearly fit into the categories mentioned. At the top of this list is adductor (spastic) dy sphonia, which is probably a generic term for phonation disorders of different origins, these being neurological as well as psy chological and having the same or similar vocal sy mptoms (Aronson 1990). Among other things, this uncertainty may have led to the fact that international researchers have not been able to agree on a standard classification of voice disorders. On the other hand, this lack of standardization, may also be a sign that the use of constantly refined diagnostic instruments has put us in a better position to create more and more closed and distinct subcategories for both centrally as well as peripherally -induced voice disorders. (For more detailed information on voice disorders, see the excellent articles by Habermann (1980) and Schultz-Coulon (1980) as well as the textbook by Aronson (1990).) Well aware that a binding categorization cannot be undertaken here either, I will nevertheless dare to make a tentative one for the sake of providing an overview of all of the disorders of phonation. This will also allow me to classify the voice disorders arising after craniocerebral injury trauma (to be looked at more closely below), as well as those resulting from the therapy of such injuries. Finally , I will attempt to present these disorders in a comprehensive classification (Table 48.1; without claim to completeness). The table distinguishes between organic and functional voice disorders. An organic voice disorder can be brought about by an anatomic disease of the lary nx itself. Alternatively , it may result from a general illness also affecting the lary nx or an illness befalling the structures controlling the lary nx. In contrast, a functional voice disorder is considered to be a disturbance of pitch and/or vocal performance without primary organic damage. A further division of functional voice disorders is based on that of Perelló’s (1962). In his classification sy stem, phonoponoses are considered to be the result of improper, uneconomical voice production or a constant strain on the organs of speech. Thus they are generally of mechanical origin. In contrast, phononeuroses are mainly attributed to psy chological alterations. Indeed, this dualistic division into mechanical and psy chological causes is subject to criticism. Despite the fact that it represents numerous overlapping and hy brid illnesses, it oversim-
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plifies and distorts the ty pical multifactorial genesis of the functional dy sphonias (Pascher 1982). In addition, it appears to be problematic to group every psy chologically -induced voice disorder among the (phono)neuroses, a term which is not alway s appropriate. Clinical practice has repeatedly shown that individual cases can prove difficult to classify according to these two groups. This is usually the case, since there are no distinguishing criteria either in the sy mptoms or in the results of the voice and larynx examination.
2.
Organic Voice Disorders
Whatever their pathogens, infections lead to alterations of the audible sounds produced by phonation to vary ing degrees. Infectious cells infiltrate the mucous membrane of the lary nx and possibly even that of the vocal fold muscles. Here, they upset the periodic shift of the mucous membrane of the vocal folds on the tensed Mm. vocales to different degrees. If the infection persists, is repeated or progresses, permanent changes in the mucous membrane may occur, such as those in chronic lary ngitis. The sy mptoms are worsened by toxic substances like cigarette smoke, alcohol or industrial fumes. Tumors may also provoke changes in the voice production, in that they alter the mass of the oscillating vocal folds. Aside from severe fractures of the cartilage supporting the lary nx and endolary ngeal lesions following intubation, external mechanical influences can cause hemorrhaging, granulation, or ruptures in fibers. These reactions may end in permanent changes in the structure of the vocal folds and consequently in the clearness of the voice. Vocal fold paresis after long-term intubation will be discussed more thoroughly below. The organic voice disorders stemming from neurological illnesses can be differentiated according to whether they involve vocal fold paraly sation or more extensive neurological illnesses. Paraly sis of the vocal folds may have a wide variety of causes, because of the great length of the lary ngal nerves and their connection to the base of the skull as well as to different throat and thorax organs (Tucker 1980). Vocal fold paresis is usually the result of paraly sis of the recurrent lary ngeal nerve, a main branch of the cranial nerve which transmits nervous impulses to all intrinsic
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Table 48.1: Classification of voice disorders (*: see p. 495)
48. Disorders of Phonation
muscles of the lary nx except for the m. cricothy roideus. The cricothy roid muscle is innervated by the external branch of the superior lary ngeal nerve. Therefore, impairment of this nerve alone is not sufficient to cause any significant movement deficit in the vocal cords. However, impairment of the superior lary ngeal nerve combined with recurrent lary ngeal nerve paresis will indeed cause paralysis of the vocal folds. Vocal folds paresis accompanied by hoarseness due to its corresponding position outside the median line of the vocal tract, is a sy mptom, not an illness in its own right. Therefore, in the case of an illnes in which the cause and effect cannot be easily determined, such as in strumectomy , for instance, additional neurological, medical, and radiological examinations are called for. A voice disorder may occur as an initial sy mptom of an extensive neurological disorder. Usually , however, a voice disorder develops later, in conjunction with dy sarthria (also referred to as dy sarthrophonia) and disturbances in swallowing (dy sphagia). The vocal changes occurring in dy sarthrophonia after craniocerebral injury will be discussed in detail below. Another cause of organic voice disorders are hormonal illnesses, which lead to fine tissue changes of the vocal folds and subsequently to alterations of the sound. Particularly evident is the dependence of the voice as a secondary sex characteristic on the sex hormones, such that all illnesses involving hy per- or hy pogonadism in male and female patients often lead to quite ty pical voice disorders (Pascher/Johannsen 1975). However, not all mutational voice disorders are caused by hormones, but rather they may also stem from defective auditive control of phonation in non-musicality , or in a strong mother-son bond with inadequate separation.
3.
Functional Voice Disorders
Above I made a distinction between phonoponoses, functional voice disorders in a narrow sense caused by strain, and phononeuroses, psy chogenic voice disorders. The most common form of the phonoponoses is the hy perfunctional dy sphonia, which is characterized by a non-phy siological overfunctioning of the muscle sy stems involved in phonation, articulation and respiration, exceeding the boundaries of economic functioning.
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The major cause is a discrepancy between individual vocal performance and its demands on vocal function. In hy pofunctional dy sphonias, the tension and the function of the muscle sy stems are reduced, often coinciding with a consumptive illness. This disorder may also result after several y ears hy perfunction, when the muscle tonus can no longer be maintained. The ventricular dy sphonia (= dy sphonia plicae ventricularis) can be viewed as an extreme form of hy perfunctional dy sphonia. In this disorder, phonation does not take place on the level of the vocal folds, but on the false or ventricular vocal folds. This may even be desirable, when one or both true vocal folds can no longer oscillate, for example after an operation removing a carcinogenic vocal fold. Conversely , voice production on the ventricular vocal fold level is undesirable, when it would otherwise be possible on the vocal fold level. Psy chological voice disorders clearly show what a finely -tuned indicator of the psy chological state of the carrier, the human voice really is. All different kinds of acute and chronic disorders are expressed in the voice of the patient. The severity of the disorder, in hy per- as well as in hy pofunctional form, can range from mild hoarseness to voicelessness (Kramer 1963). An extreme form of the psy chogenic voice disorders are considered to be part of the adductor (spastic) dy sphonias, whose etiology was mentioned above. Phonoponoses and phononeuroses are not mutually exclusive. A voice disorder can alternate between the two, not only because of multifactoral causes, but also in the course of the disease. The challenge this poses for the clinician is not to be underestimated. In the following, central and possible peripheral voice disorders arising after craniocerebral injury will be presented in more detail. In the more extensive section on central voice disorders, I will discuss the dy sarthrophonias, disorders affecting the three functional areas of respiration, phonation and articulation. The section on peripheral voice disorders looks at cases requiring artificial respiration with endotracheal intubation over a long period of time, possibly made necessary by trauma or respiratory depression in the acute phase of illness, marked by a * in Table 48.1. Special demands face the diagnostician, when a central voice disorder is complicated by an additional peripheral voice disorder by intubation.
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4.
III. Acquired Organic Pathologies of Language Behavior:Neurophonetic Disorders
Central Voice Disorders Following Craniocerebral Injury (CI)
After severe CI, patients’ sy mptoms eventually stabilize allowing classification. But first, the sy mptoms of large portions of these patients develop in quite characteristic stages of recovery of speech and voice function (von Cramon 1981; Morasch/von Cramon 1984). The recovery stages proceed from an initial mute stage, to one of whispering and culminate in a stage of voiced phonation. This is especially the case following traumatic midbrain syndrome. In the mute stage which coincides with complete anarthria, the patients are not capable of voluntarily moving their lips. In effect, they are voiceless. Sound utterances can only be stimulated by means of the cough and gag reflex. At this point of the illness, lary ngoscopic examination of the lary nx shows nothing unusual. The vocal folds are normall y abduced. Respiration-dependent movements of the vocal folds are apparent. There is no change in reaction upon request to phonate. Von Cramon/Vogel (1981) believe the cause of this lary ngeal akinesis to lie in a functional disturbance of supranuclear neurons in the oral brain stem. In the ensuing whispering stage, which only lasts a few day s, the adduction movements of the vocal folds increase as the patient attempts to phonate. The patient, however, cannot voluntarily perform a glottal stop. In the subsequent stage of voiced phonations, the disturbance of the voluntary adduction movements of the vocal folds continues to improve. The voices of such patients still sound breathy , however, because the vocal folds are not y et closed (Ziegler/von Cramon 1987). An endoscopy of the lary nx at this time would reveal signs of a rapidly developing spasm (Aronson 1990), which may favor one side depending on the localization of the lesion. Not until the next stage do distinct groups of disorders appear. These include: the rigid, the spastic and the atactic dy sarthrophonias (Hermann 1965) as well as the mixed dy sarthrophonias (Ziegler/von Cramon 1987). This classification schema is based on that by Darle y /Aronson/Brown (1975). Man y researchers object to the application of the same disorder categories of the extremity motoric to the articulation and phonation movements. However, at present there is no better pathogenetic classification system to replace it.
4.1. Rigid Dysarthrophonia The lary ngoscopic finding in this form of dy sarthrophonia is characterized by incomplete adduction of the tense and stretched vocal folds. The voice of these patients sounds harsh and breathy ; pitch and volume remain constant. 4.2. Spastic Dysarthrophonia These patients have a markedly squeezed and strained voice of rather low volume. As in rigid dy sarthrophonia, pitch and volume vary minimally . Such voice quality characteristics correspond to the shortening and thickening of the vocal folds seen in hyperadduction. 4.3. Atactic Dysarthrophonia The ring of the voice of these patients ranges from harsh to squeezed and strained. More peculiar to the atactic dy sarthrophonias, however, are involuntary , sometimes erratic variations in pitch and volume, which consequently have a striking effect on prosody . These noticeable traits arise from constantly changing glottal size and vocal fold length as the lary nx repeatedly attempts and fails to meet the demands of the target. 4.4. Mixed Dysarthrophonia Approximately a third of the patients do not fall into any of the three categories mentioned above (Ziegler/von Cramon 1987). One reason for this is that sy mptoms belonging to different subgroups may be observed simultaneously . Or, the changes taking place in the various functional areas of phonation and articulation do not fit in the same subgroup. Furthermore, the patient’s constellation of sy mptoms can be complicated by damage to the peripheral cranial nerves coming into play. As far as the voice of such patients with CI is concerned, the presence of vocal function disturbances in addition to those of dy sarthrophonia must be recognized. The frequent co-occurrence of centrally induced voice disorders with those disorders caused by peripheral voice disturbances, especially in those patients requiring long-term artificial respiration by means of intubation, has been indicated above. Under these conditions, it is easy to see how mucous membrane lesions such as edema, hemorrhages in one or both vocal folds or intubational granuloma can impede voice production. Results of longterm intubation even more important and more challenging for the diagnostician are
48. Disorders of Phonation
those disorders related to a paresis of one or both vocal folds. Vocal folds paresis tends to be an exception, although it is still the most common diagnosis. The diversity of the attempts to explain these kinds of pareses resulting from longterm intubation make the accuracy of such diagnoses seem doubtful, since they are extremely unlikely . And in view of the anatomic relationship between the lary nx, the trachea and the N. recurrens (see Johannsen 1984), explanations such as “pressure arising from an overinflated cuff of the endotracheal tube” really are almost impossible (Lim/Chia/Ng 1987). In fact, in the past 10 y ears several authors have indicated that direct damage to the lary nx and thus the especially to one or both of the cricoary taenoid joints is more logical and more likely (Berendes 1982; Johannsen 1984; Johannsen/Pirsig 1987; Gallivan/Dawson/ Robbins 1989). There are 3 way s intubation can cause immobility of one or both vocal folds: Cricoary taenoidanky losis, interary taenoidfibrosis and luxation of the ary tenoid cartilage. The latter can also occur after only brief intubation. 4.5. Cricoarytaenoidankylosis After intubation lasting only 2 day s, the pressure of the tube can lead to lesions of the mucous membrane or the cartilage in the area processus vocales of the ary tenoid cartilages or the posterior plate of the cricoid cartilage (see Fig. 48.1). These lesions serve as an entrance way for germs causing infection. In this manner, the cricoary taenoid joint can become infected with an anky losis as a consequence (Johannsen 1984; Johannsen/Pirsig 1987). Since there is usually a delay between the extubation of a patient and the ensuing lary ngeal diagnosis, signs of acute infection are no longer apparent upon examination. Patients in the initial mute stage following traumatic mid-brain sy ndrome are clearly at risk for anky losis, since in addition to intentional vocal fold mobility , reflectory mobility , as in coughing for example, is impaired. Therefore, cricoary taenoidanky losis therapy must mobilize the joint by tearing scarred connective tissue or even shattering a cartilage buildup in the joint (Johannsen/Pirsig 1987). 4.6. Interarytaenoidfibrosis Much rarer than anky losis is the likelihood that an interary taenoidfibrosis with its scar tissue will bind both ary tenoid cartilages
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(Beck/Mann 1978; Schlöndorff/Elies 1985). The sheet of scar tissue on the ventral side of the posterior plate of the cricoid cartilage can hardly ever be seen in an indirect lary ngoscopic or lary nxendoscopic examination. This disorder can be clearly distinguished from the mute state of mid-brain sy ndrome: In fibrosis, the vocal folds remain near the medial line, so that some patients in the acute stage require a tracheotomy a few day s after the extubation. In contrast, in patients in the mute stage, the vocal folds are in the normal respiration position. Moreover, in interary taenoidfibrosis as well as in anky losis, reflexive movements are no longer possible. The excision of the sheet of scar tissue is recommended, which may have to be repeated in some cases. 4.7. Luxation of the Arytenoid Cartilage Compared to the large number of intubations, luxations of one or even both ary tenoid cartilages are very rare (Quick/Merwin 1978; Rudert 1974). This fact is caused by the extensive passive flexibility of the cricoary taenoid joints with its’ extremely limp joint capsule. The luxation of the ary tenoid cartilage occurs dorsally more often than ventrally . It is obviously the convex curvature of the distal third of the tube that is pressing against the ary tenoid cartilage. The ensuing asy mmetry of the lary nx makes the diagnosis straightforward, that is, as long as this possibility is taken into account. The ary tenoid cartilages can almost alway s be successfully repositioned. The sy ndromes of voice disorders are presented here as part of the mostly more extensive disorders of the communicative ability of the patients with CIT. Although they appear to be quite distinct, in actuality , these constellations are much more diffuse. This places high demands on the diagnostician, requiring him or her to precisely calculate intricate findings. It also means that he or she must have extensive experience examining and treating such patients.
5.
References
Aronson, A. E. (1990). Clinical voice disorders. 3rd ed. New York: Thieme. Beck, C. & Mann, W. (1978). Das immobilisierte Ary höckergelenk. Archiv für Ohren-, Nasen- u nd Kehlkopfheilkunde, 219, 494—495. Berendes, J. (1982). Organisch bedingte Funktionsstörungen des Kehlkopfes. In J. Berendes, R.
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Link & F. Zöllner (Eds.), Hals-Nasen-Ohrenheilku nde in Praxis u nd Klinik. Bd. 4/1. 5.1—5.30. Stuttgart: Thieme. Darley , F. L., Aronson, A. E. & Brown, J. R. (1975). Motor speech disorders. Philadelphia, London, Toronto: W. B. Saunders. Gallivan, G. J., Dawson, J. A. & Robbins, L. D. (1989). Videolary ngoscopy after endotracheal intubation: Implications for voice. Jou rnal of Voice, 3, 76—80. Habermann, G. (1980). Funktionelle Stimmstörungen und ihre Behandlung. Archiv für Ohren-, Nasenund Kehlkopfheilkunde, 227, 171—345. Hermann, K. (1965). Post-traumatic yd sarthria. Proceedings of the 8th International Congress of Neurology. Wien: 1, 135—137. Johannsen, H. S. (1984). Stimmlippenstillstand nach Intubation — neurogen oder durch Anky lose des Cricoary taenoidgelenkes? Laryngologie Rhinologie Otologie, 63, 255—256. Johannsen, H. S. & Pirsig, W. (1987). Therapie der Anky lose des Krikoary taenoidgelenkes nach Intubation. Laryngologie Rhinologie Otologie, 66, 82—83. Jürgens, U. (1986). The squirrel monkey as an experimental model in the study of cerebral organization of emotional vocal utterances. European Archives of Psychiatry and Neu rological Sciences, 236, 40—43. Kramer, E. (1963). Judgement of personal characteristics and emotions from nonverbal properties of speech. Psychological Bulletin, 60, 408—420. Lim, E. K., Chia, K. S. & Ng, B. K. (1987). Recurrent lary ngeal nerve palsy following endotracheal intubation. Anaesthesia and Intensive Care, 15, 342—345. Morasch, H. & von Cramon, D. (1984). Lary ngoskopische Befunde bei Dy sphonie nach traumatischem Mittelhirnsyndrom. HNO, 32, 13—16. Pascher, W. (1982). Funktionelle Krankheiten der
Stimme. In J. Berendes, R. Link & F. Zöllner (Eds.), Hals-Nasen-Ohrenheilku nde in Praxis u nd Klinik. Bd. 4/1. 7.1—7.45. Stuttgart: Thieme. Perelló, J. (1962) Dy sphonies foncitonelles. Folia phoniatrica (Basel) 14, 150—205. Pascher, W., Johannsen, H. S. (1975). Angewandte Phoniatrie. III. Juvenile Stimmstörungen, hormonelle Stimmstörungen. HNO, 23, 383—391. Quick, C. A. & Merwin, G. E. (1978). Ary tenoid dislocation. Archives of Otolaryngology, 104, 267—270. Rudert, H. (1984). Über seltene Intubationsbedingte innere Kehlkopftraumen. HNO, 32, 393—398. Schlöndorff, G. & Elies, W. (1985). Stimmbandstillstand mit Stridor infolge Interary taenoidfibrose — eine Komplikation in der Intensivpflege. Laryngologie Rhinologie Otologie, 64, 403—404. Schultz-Coulon, H.-J. (1980). Die Diagnostik der gestörten Stimmfunktion. Archiv für Ohren-, Nasen- und Kehlkopfheilkunde, 227, 1—169. Tucker, H. M. (1980). Vocal cord paraly sis 1979: etiology. The Laryngoscope, 90, 585—590. Van den Berg, J. W. (1956). Phy siology and phy sics of voice production. Acta Physiologica et Pharmacologica Neerlandia, 5, 40—55. Van den Berg, J. W. (1958). My oelastic-aerody namic theory of voice production. Jou rnal of Speech and Hearing Research, 1, 227—244. Von Cramon, D. (1981). Traumatic mutism and the subsequent reorganization of speech functions. Neuropsychologica, 19, 801—805. Von Cramon, D. & Vogel, M. (1981). Der traumatische Mutismus. Nervenarzt, 52, 664—668. Ziegler, W. & von Cramon, D. (1987). Zentrale Stimmstörungen. In L. Springer & G. Kattenbeck (Eds.), Aktu elle Beiträge zu r Dysarthrophonie u nd Dysprosodie. 59—79. München: tuduv Verlag.
Helge S. Johannsen, Ulm (Germany)
49. Pure Word Deafness (Verbal Auditory Agnosia) 1. 2. 3. 4.
1.
Cortical Deafness Auditory Agnosia Pure Word Deafness References
Cortical Deafness
Since the late nineteenth century , various auditory disorders caused by cerebral lesions have been reported. The details of the clinico-
pathological correlations, however, remain unclear to this day . Bilateral cerebral lesions only exceptionally lead to severe hearing disturbance. This condition is generally called ‘cortical deafness’ (Earnest/Monroe/Yarnell 1977; Graham/Greenwood/Leck y 1980; Bahls/Chatrian/Mesher et al. 1988) since the primary auditory cortex (Heschl’s gy rus) is involved bilaterally in most cases. Recent studies on humans and animals, however,
49. Pure Word Deafness (Verbal Auditory Agnosia)
have questioned whether bilateral lesions in the primary auditory cortex cause severe hearing loss at all. As Vignolo (1969) pointed out, cases have been reported in which only minimal hearing loss was detected by audiometry , despite complete destruction of the primary auditory cortex and/or its underly ing white matter bilaterally . Abundant experimental evidence also shows that bilateral ablation of the primary auditory cortex in animals does not cause permanent deafness, although a transient decrease in acuity may be observed (Neff/Diamond/Casseda y 1975). Furthermore, severe, persistent hearing loss has been reported to be caused by bilateral lesions in the white matter adjacent to the putamen (Clark/Russell 1938) or underly ing the insular cortex and Heschl’s gy rus (Hirano 1973; 1983), with sparing of Heschl’s gyrus.
2.
Auditory Agnosia
Besides cortical deafness, inability to interpret the meaning of sounds has been reported in the presence of otherwise adequate hearing as measured by standard audiometry . This condition is called ‘auditory agnosia’. This term, however, has been used ambiguously (Albert/ Sparks/von Stockert/Sax 1972; Bauer/Rubens 1985), generally describing two different clinical conditions. In a broad sense it has been used to refer to impaired capacity to recognize both verbal and nonverbal sounds, and in a narrow sense to refer to a selective deficit in the recognition of nonverbal sounds only . The latter, often called auditory sound agnosia, is far less common than the former, probably because patients with auditory sound agnosia are less likely to seek medical advice than those with a disorder of speech comprehension and also because nonspecific auditory complaints are often discounted when pure tone audiometric and speech discrimination thresholds are normal (Bauer/Rubens 1985). Auditory sound agnosia has been reported in relation to unilateral lesions of the right (Spreen/Benton/Fincham 1965; Fujii/Fukatsu/Watabe et al. 1990) or of the left hemisphere (Spinnler/Vignolo 1966; Faglioni/ Spinnler/Vignolo 1969; Albert/Goldblum/ Benson/Hécaen 1971), and bilateral temporoparietal lesions (Albert/Sparks/von Stockert/Sax 1972). Recently , Motomura/Yamadori/Mori/Tamaru (1986) reported a patient with ty pical auditory agnosia caused by bilateral subcortical lesions neighboring the me-
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dial geniculate body . Their case was unique in that the clinical picture began with generalized auditory agnosia and changed, over two months, to auditory sound agnosia. This case suggests that the auditory processing mechanisms for nonverbal and verbal sounds may be different, even at a subcortical level.
3.
Pure Word Deafness
Selective impairment of verbal sound recognition has also been reported. This condition also can be regarded as an auditory agnosia; however, the term ‘pure word deafness’ has been widely employ ed (Brown 1974; Hécaen/ Albert 1978; Benson 1979; Bauer/Rubens 1985), although some authors have preferred the term ‘verbal auditory agnosia’ or ‘auditory agnosia for speech (Goldstein 1974) or linguistic material (Ulrich 1978)’. The neuroanatomic substrate of this disorder is better elucidated than those of other ‘cortical’ auditory disorders. Thus, the remainder of this article focuses on this impairment. Patients with pure word deafness cannot comprehend spoken words, although they can read, write, and speak in an almost normal manner. Comprehension of nonverbal sounds is relatively retained. The sy ndrome is ‘pure’ only in the sense that internal language is intact (Nielsen 1946), although many of the reported cases show sy mptoms of Wernicke’s aphasia (Brown 1974; Benson 1979; Bauer/ Rubens 1985). The key characteristic of ‘pure’ word deafness is the extreme disproportionality of the impairment in auditory comprehension when compared to other language functions. The disorder was first described by Kussmaul (1877), who coined the term ‘reine Worttaubheit’ (pure word deafness) to describe a patient unable to comprehend spoken words with otherwise intact speech production and hearing. He attributed this to the destruction of the left first temporal gy rus. Lichtheim (1885) defined the disorder as “the inability to understand spoken words unaccompanied by disturbance of spontaneous speech and by severe disturbance in writing and understanding of the printed words”. He called this sy ndrome ‘isolierte Sprachtaubheit (isolated speech deafness)’, and considered it to be the result of a disruption in the pathway from the auditory reception center to the auditory word impression center. Similarly , Bastian (1897) thought of the sy ndrome as arising from isolation of the auditory word center rather than its destruction.
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3.1. Lesion Anatomy
3.2. Auditory Processing Deficits
There was once uncertainty about the concept that pure word deafness was a distinct disorder of cerebral function. Freud (1891) suspected that a peripheral hearing loss was necessary for the development of an isolated word deafness. On the basis of two cases with laby rinthine dy sfunction, Freund (1895) concluded that the sy ndrome was primarily due to hearing loss. However, in a very carefully studied patient in whom ordinary deafness was clearl y excluded, Liepmann (1898) showed that this sy ndrome could be produced by a left unilateral cerebral lesion. The pathology was described in fuller detail by Liepmann/Storch (1902). The lesion, located subcortically in the left temporal lobe, had destroy ed the left auditory radiation as well as the callosal fibers from the right auditory region. The subsequent well-documented autopsy cases established the cerebral origin of the sy ndrome (Goldstein 1974). Freund himself later reported that one of his two patients clinically thought to have had word deafness due to bilateral laby rinthine dy sfunction actually had a tumor in the left first temporal yg rus (Hemphill/Stengel 1940; Goldstein 1974). Geschwind (1965) in his review of the disconnection sy ndromes noted that most cases had bilateral, usually cortical-subcortical lesions in the anterior part of the superior temporal gy rus, leaving Heschl’s gy ri essentially intact; and that the less common unilateral cases involved subcortical lesions that interrupted auditory radiation fibers as well as callosal fibers from the contralateral auditory cortex. He concluded that the sy ndrome ultimately represented a disconnection of the auditory cortex from Wernicke’s area. Recently , pure word deafness caused by bilateral infarctions of the primary auditory cortex (Coslett/Brashear/Heilman 1984) or by bilateral damage to its underly ing deep white matter (Brick/Frost/Schochet et al. 1985) has been reported. A patient with lesions similar to those described by Coslett/Brashear/Heilman (1984) has been reported previously by Kanshepolsk yy /Kelle /Waggener (1973). These indicate that, as Coslett/Brashear/Heilman (1984) suggested, comprehension of verbal sounds may be mediated by the pathway into and from Heschl’s gy rus, and comprehension of nonverbal sounds may be mediated by other cerebral structures such as the auditory association cortex.
Some investigators have recently attempted to characterize the nature of the deficit of this sy ndrome from a functional point of view, and have emphasized the defects in auditory processing (Jerger/Weikers/Sharbrough/Jerger 1969; Kanshepolsk y /Keller/Waggener 1973; Albert/Bear 1974; Auerbach/Allard/ Naeser et al. 1982), temporal resolution (Albert/Bear 1974), phonemic discrimination (Chocholle/Chedru/Botte et al. 1975; Denes/ Semenza 1975; Saffran/Marin/Yeni-Komshian 1976; von Stockert 1982), and prephonemic discrimination (Auerbach/Allard/Naeser et al. 1982). For instance, Jerger/Weikers/ Sharbrough/Jerger (1969) presented extensive audiologic data obtained from a patient with presumed bilateral temporoparietal lesions. They demonstrated impairments in the ability to discriminate the loudness of stimuli, to localize sounds in space, to identify the order in which different auditory events occur in time, and to perceive brief sounds. Albert/ Bear (1974) experienced a patient with probable left temporoparietal lesion in whom understanding of spoken language improved dramatically when the examiner spoke at an abnormally slow rate. To confirm this ratedependent comprehension, they examined the ability of the patient to count the number of clicks presented for one second (click counting), and the threshold at which two clicks could be distinguished as separate (click fusion). Their patient performed poorly for rates greater than 2 per second, and was unable to discriminate two clicks separated by less than 15 msec, whereas normals counted 8 to 11 clicks per second, and distinguished two clicks at 1 to 3 msec intervals. From these observations, they emphasized that one of the important factors for the development of pure word deafness was a defect in temporal resolution of auditory stimuli rather than in specific phonetic impairment. Saffran/Marin/ Yeni-Komshian (1976), on the other hand, showed that the auditory comprehension of their patient was facilitated significantly when the spoken words were drawn from a particular category and also when context was provided by placing the word at the end of a meaningful sentence (e. g., boat in the sentence, The boy sailed a boat.). Auerbach/Allard/Naeser et al. (1982) also observed a severe deficit in temporal resolution in a case of bilateral temporoparietal lesions, as in the case of Albert/Bear (1974). Based on their
49. Pure Word Deafness (Verbal Auditory Agnosia)
exceptionally detailed case study and a review of the literature, they regarded all the abnormalities in click fusion, click counting, and duration discrimination as ‘temporal auditory acuity disorder’ since all these measurements represent a function of time of the auditory sy stem. They considered it ‘prephonemic’ if a phonemic discrimination disorder could be attributed to a disorder in acoustic processing such as temporal auditory acuity . From these considerations, they suggested that two distinct ty pes of pure word deafness could be described. The first is a disorder of prephonemic temporal auditory acuity and has been associated with bilateral temporal lobe lesions. This ty pe is characterized by (1) particular difficulty with rapid formant transitions, leaving vowel discrimination relatively preserved; (2) improved performance with an increase in the number of distinctive features distinguishing two target phonemes; (3) a particular vulnerability for the distinctive feature of place of articulation when compared to the feature of voicing. The second ty pe of pure word deafness is a disorder in phonemic discrimination that cannot be attributed to a difficulty in temporal auditory acuity and has been associated with left unilateral temporal lesions (Denes/Semenza 1975; Saffran/Marin/ Yeni-Komshian 1976). This ty pe shows an inconsistent pattern in linguistic studies, that is, either a particular vulnerability for the feature of voicing compared to that of place of articulation (Saffran/Marin/Yeni-Komshian 1976) or no particucular pattern (Denes/Semenza 1975). Auerbach/Allard/ Naeser et al. (1982) suggested that the first ty pe is an apperceptive disorder secondary to pathology involving the auditory cortices whereas the second represents a higher disorder in phonemic discrimination, and may be considered a fragment of Wernicke’s aphasia. This division follows the classification of Lissauer (1890), who attempted to distinguish between the ability to sy nthesize sensory information into an adequate perception (apperception) and the ability to analy ze perception in relation to meaning and other perceptions (association) in discussing visual agnosia. More recently , Yaqub/Gascon/Alnosha/ Whitaker (1988) also have reported a patient with bilateral temporal lesions who showed a pattern similar to the first ty pe of Auerbach/ Allard/Naeser et al. (1982), supporting the view of the latter. We performed several sophisticated auditory tests in a case of pure word deafness
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caused by bilateral temporoparietal lesions (Tanaka/Yamadori/Mori 1987). Our patient also demonstrated extremely long auditory fusion threshold for clicks (300 msec) and markedly decreased ability to count the number of clicks (inaccurate for rates greater than 2 per second). These findings support the view of Albert/Bear (1974) who emphasized that the defect in auditory temporal resolution was an important factor for the development of word deafness. Our patient, however, presented a problem inexplicable by this hy pothesis. We presented two tones with the same duration and intensity , and asked the patient to report whether one or two tones were heard as the interval between the two tones was varied. The duration of a tone ranged from 20 to 500 msec. For each duration, sensation level was set at 20 dB above the threshold which had been measured in the thresholdduration function test. Our patient demonstrated marked improvement in the ability to discriminate two tones as the duration of a tone was prolonged. However, the auditory comprehension did not improve at all, even if the patient was spoken to slowly enough. This indicates that there are other factors besides a defect in auditory temporal resolution for the poor recognition of spoken words in our case. Our patient had marked impairment in perception of brief sounds and in discrimination of loudness, pitch and tone duration. These elemental auditory disturbances, especially impairment in discriminating sound duration, may be responsible for the poor recognition of spoken words in our case. In linguistic investigation with natural speech stimuli, our patient was able to identify vowels at a better than chance level but failed in consonant-vowel (CV) discrimination, with no particular pattern of error, even if the number of distinguishing features increased. In natural speech, vowel durations usually average 100 to 150 msec but may last as long as 400 msec. In CV combinations, the consonant is characterized by rapid frequency changes within the first 40 msec of stimulus onset (Auerbach/Allard/Naeser et al. 1982). Our patient required a duration difference of 380 msec to discriminate a duration of two tones correctly , whereas normals required a duration difference of only 20 to 30 msec. Accordingly , complete inability to identify and discriminate CV combinations, but some retained capacity to discriminate vowels in our patient may be explained by severe impairment in discriminating sound duration. If
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this is true, our patient must have a temporal auditory acuity disorder, the first ty pe proposed yb Auerbach/Allard/Naeser et al. (1982). Thus, a detailed analy sis of each patient with word deafness by means of sophisticated auditory tests probably sheds light on understanding of how speech sounds are processed by the human brain. Our patient produced another intriguing result during rhy thm discrimination testing: severe impairment in the recognition and reproduction of the simple rhy thm patterns at a fast rate regardless of the modalities of perception, i. e., either audition, vision, or touch. This finding supports the view of Mavlov (1980) who demonstrated a supramodal defect only in the recognition and reproduction of rhy thm patterns in a case of a professional musician following a vascular stroke in the left posterior parietal or parietotemporal region. However, in our patient, this condition improved significantly in all modalities when the rate was decreased, indicating that rhy thm sense is essentially preserved. Since perception of rhy thm requires registration of time intervals, this rate-dependent supramodal defect is attributable to a supramodal defect in temporal resolution. Indeed, our patient had a disturbance of temporal resolution in all the three sensory modalities tested, and the temporal resolution markedly improved in at least both audition and vision as the duration of the tone and the light increased. This finding has led us to speculate that there is a ‘time-organizing sy stem’ which is both independent of and central to the sensory mechanism. Therefore, rhy thm sense probably reflects one aspect of a ‘time-organizing sy stem’ situated in the temporoparietal region, predominantly in the left hemisphere. Thus, a deficit of temporal resolution described by Albert/Bear (1974) appeared to be related to rhy thm sense but not to auditory comprehension in our patient.
4.
References
Albert, M. L., Goldblum, M.-C., Benson, D. F., & Hécaen, H. (1971). Mechanisms of auditory comprehension. II. Cerebral dominance. Transactions of the American Neu rological Association, 96, 132—135. Albert, M. L., Sparks, R., von Stockert, T., & Sax, D. (1972). A case study of auditory agnosia: linguistic and non-linguistic processing. Cortex, 8, 427—443. Albert, M. L. & Bear, D. (1974). Time to understand: a case study of word deafness with reference
to the role of time in auditory comprehension. Brain, 97, 373—384. Auerbach, S. H., Allard, T., Naeser, M., Alexander, M. P., & Albert, M. L. (1982). Pure word deafness: analy sis of a case with bilateral lesions and a defect at the prephonemic level. Brain, 105, 271—300. Bahls, F. H., Chatrian, G. E., Mesher, R. A., Sumi, S. M., & Ruff, R. L. (1988). A case of persistent cortical deafness: clinical, neurophy siologic, and neuropathologic observations. Ne u rology, Cleveland, 38, 1490—1493. Bastian, H. C. (1987). Some problems in connexion with aphasia and other speech defects. Lancet i, 933—942, 1005—1017, 1131—1137, 1187—1194. Bauer, R. M. & Rubens, A. B. (1985). Agnosia. In K. M. Heilmann & E. Valenstein (Eds.), Clinical Ne u ropsychology. 209—217. New York: Oxford University Press. Benson, D. F. (1979). Pure word deafness. In D. F. Benson (Ed.), Aphasia, Alexia, and Agraphia. 133—134. New York: Churchill Livingstone. Brick, J. F., Frost, J. L., Schochet, Jr. S. S., Gutmann, L., & Crosby , T. W. (1985). Pure word deafness: CT localization of the pathology . Neurology, Cleveland, 35, 441—442. Brown, J. (1974). Aphasia, Apraxia and Agnosia: clinical and theoretical aspects. 127—135. Springfield, Illinois: Charles C. Thomas. Chocholle, R., Chedru, F., Botte, M. C., Chain, F., & Lhermitte, F. (1975). Étude psy choacoustique d’un cas de ‘surdité corticale’. Neuropsychologia, 13, 163—172. Clark, W. E. Le G. & Russell, W. R. (1938). Cortical deafness without aphasia. Brain, 61, 375—383. Coslett, H. B., Brashear, H. R., & Heilman, K. M. (1984). Pure word deafness after bilateral primary auditory cortex infarcts. Neu rology, Cleveland, 34, 347—352. Denes, G. & Semenza, C. (1975). Auditory modality -specific anomia: evidence from a case of pure word deafness. Cortex, 11, 401—411. Earnest, M. P., Monroe, P. A., & Yarnell, P. R. (1977). Cortical deafness: demonstration of the pathologic anatomy by Ct scan. Neu rology, Minneapolis, 27, 1172—1175. Faglioni, P., Spinnler, H., & Vignolo, L. A. (1969). Contrasting behavior of right and left hemisphere: damaged patients on a discriminative and a semantic task of auditor y recognition. Cortex, 5, 366—389. Fujii, T., Fukatsu, R., Watabe, S., Ohnuma, A., Teramura, K., Kimura, I., Sato, S., & Kogure, K. (1990). Auditory sound agnosia without aphasia following a right temporal love lesion. Cortex, 26, 263—268. Freud, S. (1891). Zu r Au ffassu ng der Aphasien: eine kritische Studie. Vienna: Franz Deuticke.
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Freund, C. S. (1895). Labyrinthta u bheit u nd Sprachtaubheit. Wiesbaden: Bergmann. Geschwind, N. (1965). Disconnexion sy ndromes in animals and man. Brain, 88, 237—294. Goldstein, M. N. (1974). Auditory agnosia for speech (‘pure word deafness’): a historical review with current implications. Brain and Langu age, 1, 195—204. Graham, J., Greenwood, R. & Lecky , B. (1980). Cortical deafness: a case report and review of the literature. Jou rnal of the Neu rological Science, 48, 35—49. Hécaen, H. & Albert, M. L. (1978). Hu man Neu ropsychology. 265—276. New York: John Wiley & Sons. Hemphill, R. E. & Stengel, E. (1940). A study on pure word-deafness. Jou rnal of Neu rology and Psychiatry, 3, 251—262. Hirano, M. (1973). On the ‘So-called’ cortical deafness. Psychiatria et Neu rologia Japonica, Tokyo, 75, 94—138 (in Japanese). Hirano, M. (1983). What is ‘Cortical Deafness’?: review of literature. Clinical Psychiatry, Tokyo, 25, 337—343 (in Japanese). Jerger, J., Weikers, N. J., Sharbrough, F. W., & Jerger, S. (1969). Bilateral lesions of the temporal lobe: a case study . Acta Oto-Laryngologica, Su pplement, 258, 1—51. Kanshepolsky , J., Kelley , J. J., & Waggener, J. D. (1973). A cortical auditory disorder: clinical, audiologic and pathologic aspects. Neu rology, Minneapolis, 23, 699—705. Kussmaul, A. (1877). Disturbances of speech. In H. von Ziemssen (Ed.), Cyclopedia of the Practice of Medicine. Volu me 14. 581—875. New York: William Wood. Lichtheim, L. (1885). On aphasia. Brain, 7, 433—484. Liepmann, H. (1898). Ein Fall von reiner Sprachtaubheit. In C. Wernicke (Ed.), Psychiatrische Abhandlungen. Breslau: Schletter. Liepmann, H. & Storch, E. (1902). Der mikroskopische Gehirnbefund bei dem Fall Gorstelle. Monatsschrift für Psychiatrie u nd Neu rologie, 11, 115—120. Lissauer, H. (1890). Ein Fall von Seelenblindheit nebst einem Beitrag zur Theorie derselben. Archiv
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für Psychiatrie und Nervenkrankheit, 21, 222—270. Mavlov, L. (1980). Amusia due to rhy thm agnosia in a musician with left hemisphere damage: a nonauditory supramodal defect. Cortex, 16, 331—338. Motomura, N., Yamadori, A., Mori, E., & Tamaru, F., (1986). Auditory agnosia: analy sis of a case with bilateral subcortical lesions. Brain, 109, 379—391. Neff, W. D., Diamond, I. T., & Casseday , J. H. (1975). Behavioral studies of auditory discrimination: central nervous sy stem. In W. D. Keidel & W. D. Neff (Eds.), Handbook of Sensory Physiology, Volume 5, Part 2. 307—400. Berlin: Springer. Nielsen, J. M. (1946). Agnosia, Apraxia, Aphasia. Their valu e in cerebral localization. 2nd edition. New York: Hoeber Publishing. Saffran, E. M., Marin, O. S. M., & Yeni-Komshian, G. H. (1976). An analy sis of speech perception in word deafness. Brain and Langu age, 3, 209—228. Spinnler, H. & Vignolo, L. A. (1966). Impaired recognition of meaningful sounds in aphasia. Cortex, 337—348. Spreen, O., Benton, A. L., & Fincham, R. W. (1965). Auditory agnosia without aphasia. Archives of Neurology, Chicago, 13, 84—92. Tanaka, Y., Yamadori, A., & Mori, E. (1987). Pure word deafness following bilateral lesions: a psy chophysical analysis. Brain, 110, 381—403. Ulrich, G. (1978). Interhemispheric functional relationships in auditory agnosia: an analy sis of the preconditions and a conceptual model. Brain and Language, 5, 286—300. Vignolo, L. A. (1969). Auditory agnosia: a review and report of recent evidence. In A. L. Benton (Ed.), Contribu tions to Clinical Neu ropsychology. 172—231. Chicago: Aldine Publishing. von Stockert, T. R. (1982). On the structure of word deafness and mechanisms underly ing the fluctuation of disturbances of higher cortical functions. Brain and Language, 16, 133—146. Yaqub, B. A., Gascon, G. G., Alnosha, M., & Whitaker, H. (1988). Pure word deafness (acquired verbal auditory agnosia) in an arabic speaking patient. Brain, 111, 457—466.
Yasufumi Tanaka, Tochigi (Japan)
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50. Speech Tics in Tourette’s Syndrome 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
Characteristics of Tourette’s Syndrome Characteristics of Tics in Tourette’s Syndrome Effects of Speech Behavior on Tic Frequency Position of Tics in Speech Are Tics Voluntary or Involuntary? Pathophysiology of Tic Behavior Associated Behaviors Relationships with Other Deficits Conclusions References
1.
Characteristics of Tourette’s Syndrome
Tic behaviors in Gilles de la Tourette’s sy ndrome (TS) include the random and stereoty pic production of complex oral and lary ngeal movements and sounds, sometimes sy llables and phrases, which are referred to as vocal or speech tics. The diagnostic criteria for TS (Diagnostics and Statistical Manual of Mental Disorders 1987) include: (a) both multiple and one or more vocal tics have been present at some time during the illness, although not necessarily concurrently; (b) the tics occur many times a day (usually in bouts), nearly every day or intermittently throughout a period of more than one year; (c) the anatomic location, number, frequency , complexity , and severity of the tics changed over time; (d) onset was before age 21; and (e) occurrence was not exclusively during y ps choactive substance intoxication or known central nervous system disease. The definition of whether a tic is simple or complex, motor or vocal, is important for identify ing TS separate from simple tic disorder, or chronic multiple tic disorder. Complex motor tics are differentiated from simple motor tics. The former include motor patterns such as jumping, hitting and finger tapping. These must be differentiated from simple motor tics such as a shoulder shrug, ey eblink, head twitch, or facial grimace. Simple vocal tics include throat clearing, squeaks, sniffing and grunting while complex vocal tics include words, echolalia, palilalia (sy llable repetition) and coprolalia (swearing). TS is differentiated from chronic multiple tic disorder which includes only vocal tics, or only motor tics, but not both.
TS occurs worldwide, is more frequent in caucasians than blacks or hispanics and all cases are now thought to have a genetic etiology . Prevalence is greater in males than females (3 : 1) and between .1 and .5 per thousand. Onset is usually well before 13 y ears of age and sy mptoms diminish or disappear in 70% before adulthood (Singer/Walkup 1991).
2.
Characteristics of Tics in Tourette’s Syndrome
Tics in TS are not the same as jerks or tremor in that they are complex motor patterns, sudden movements, gestures or utterances which mimic some aspect of the repertoire of normal behavoir. TS tics differ from movements in tardive dy skinesia which include repetitive continuous movements such as; bruxism, jaw opening and closing, licking or lip smacking. TS tics also differ from oromandibular dy stonia where a continuously abnormal posture interferes with speaking, such as sustained and uncontrolled jaw opening or jaw clenching. Tics are sudden, rapid and sporadic and may occur often in bursts or bouts and then will be absent for a time. Such bouts of tics may include a rapid stream of a variety of tics. The exact order and combination of tics usually differs each time. Many persons with TS report they can suppress tics for a short interval (30 minutes) but then must release them. Most persons affected with this disorder report that they have premonitary feelings or urges to perform a tic. They are usually aware of their tics and are annoy ed and embarrassed by them. However, more recently in family studies individuals have been identified with TS or chronic tics who are unaware of their disorder and have never sought medical assistance for their disorder (Kurlan 1989). Tics will wax and wane throughout the disorder and change over time. One ty pe of tic, such as facial grimacing may predominate over 6 months to be replaced by shoulder shrugs and coprolalia for 8 months and then may be replaced by lip smacking and/or ey eblinks the next y ear. Coprolalia, repeated swearing, is the most troubling of the sy mptoms but does not occur in all cases. Many of the vocal tics are less obvious such as oh boy, yup, and OK.
50. Speech Tics in Tourette’s Syndrome
2.1. Vocal Tic Types In our studies of TS (Ludlow/Polinsky /Caine et al. 1982; Caine/Polinsky /Ludlow et al. 1982; Caine/Ludlow/Polinsk y /Ebert 1984; Polinsky /Ebert/Caine et al. 1980), we divided tics into 10 categories with the following tic definitions: (a) Lary ngeal: throat clearing, coughing, humming, shriek, grunting, high pitched sounds, barks, squeaks, hooting, whistling. (b) Lingual: slurping, hiss, clicks. (c) Nasal: sniffing, snorting. (d) Respiratory Exhalations: sighs, blowing, wheezing. (e) Respiratory Inhalations: air gulping, gasps. (f) Labial: smacking, spitting, raspberry noises, bronx cheers, kissing sounds. (g) Words: stereoty pic or hesitation phenomena, interjected words, echolalia. (h) Palilalia: single or multiple strings. (i) Jargon: single or multiple meaningless syllables. (j) Coprolalia: swearing. All of the tics we identified were normal behaviors, although usually inappropriate in the social context. None were produced with a struggle; all were produced without effort in a quick fluid fashion. Classification of tics into the above categories was somewhat arbitrary , but used to measure how behavior changed over time and with treatment. Four of these categories include behaviors that would be classified as speech or verbal, while the remainder were non-speech vocal tract gestures. 2.2. Frequency of Tic Types The frequency with which TS patients exhibit these different categories of tics follows a somewhat regular pattern. In a study of 54 patients (Ludlow/Polinsky /Caine et al. 1982), the percentage of tics in each category was as follows: lingual 35.6%; lary ngeal 23.5%; nasal 14.5%; respiratory inhalation 8.9%; respiratory exhalation 4.7%; labial 5.5%; jargon 4.1%; and coprolalia 2.8%. Therefore, the most frequent tic ty pes were nonverbal categories and the least frequent were speech tics. When TS patients and controls were compared on the numbers of tics in each group within each category (Ludlow/Polinsky /Caine et al. 1982), the TS groups produced lary ngeal, nasal, inhalation, exhalation, labial, and coprolalia more frequently than the controls
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(p ≤ .03). Surprisingly , the TS patient and controls did not differ in the frequency of lingual tics, suggesting that not only was this a normal behavior but that it was not more frequent than normal. The only tic category that did not occur in the controls was coprolalia, however, this was the least frequent category in TS. Therefore, TS tics could be viewed as normal behaviors, only increased in frequency and intensity. 2.3. Severity and Tic Types Because differences appear in the frequency of tics in TS, the relationship between tic ty pes was examined to determine if there is a progression across tic ty pes in TS; that is, does one tic ty pe appear in mild forms of the disorder, while other ty pes only appear in more severe forms. We examined this issue in 13 TS patients. The mildest patient had lingual, lary ngeal and exhalation tics; four more impaired patients had lingual, lary ngeal, exhalation, and nasal tics; a further impaired patient had lingual, lary ngeal, exhalation, and coprolalia; the next four more severe patients had lingual, lary ngeal, exhalation, nasal, and coprolalia; a further impaired patient had lingual, lary ngeal, exhalation, nasal, and labial tics, the next more severe patient had lingual, lary ngeal, exhalation, nasal, coprolalia, and jargon while the most severely impaired patient had all tic ty pes. This suggests that tic categories were added in a progressive order with increased severity of the disorder from lingual in the mildest forms, through lary ngeal, exhalation, nasal, coprolalia, and labial, to jargon in the most severe cases. In fact when psy chiatrists’ ratings of patient severity were related with a) the number of tic categories produced, and b) the total number of tics produced in 2 minutes, Spearman Rank Correlation Coefficients demonstrated a higher relationship with the number of tic categories (R = .71) than with tic frequency (R = .57). Therefore, the number of tic categories present might be a better measure of patient severity than the frequency of tics.
3.
Effects of Speech Behavior on Tic Frequency
To examine how vocal tic production is modified by patients’ ongoing behavior, the frequency and ty pes of tics produced by TS patients while silent, during oral reading, and
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during speech conversation, was examined in 13 TS patients. The mean number of tics per minute in speech was 20.9, while it was 18.1/ min during oral reading and 14.2/min when patients were resting or listening to the examiner. Therefore, vocal tics tended to be more frequent during speaking than at other times. To determine whether the 13 TS patients would have similar ratings of severity whether their tic frequency was measured at rest, while speaking or reading, they were rank ordered based on their mean rate of tic production across all three conditions and this rank was related to their rank in each of the conditions. The Spearman Rank Correlation Coefficients were 0.85 between speaking and the mean for all conditions, 0.76 for reading and 0.53 in silence. Therefore, measures made while speaking were most representative of patients severities of tic production. Tic production was studied when changes in speaking rate were effected using delay ed auditory feedback and white noise. Although significant reductions in speaking rate were produced from 125 words/min to 80 words/min, no changes occurred in the rate of vocal tic production. Thus although tics are likely to occur more often during speech than at rest, they are not affected by speaking rate.
4.
Position of Tics in Speech
Several studies have addressed whether tics are randomly produced during speech by TS patients. Martindale (Martindale 1976; 1977) analy zed the location of tics in speech in one subject and found that tics occurred at points of low information in speech such as during pauses and before conjunctions and pronouns. He also found that tics were more frequent in longer sentences than short sentences. He suggested that non-inhibited subcortical centers inject tics into the speech stream when cortically based speech centers are less active. Frank (1978) studied the position of tics in speech in 3 TS patients examining the position relative to speech clauses and reported that tics occurred most frequently just before the first word of a clause, somewhat less frequently immediately after the final word, and third in pauses between clauses. Tics occurred much less frequently however, between words within a clause. The same issue was examined in 13 TS patients in our clinic with similar results: 72% of tics
occurred on speech initiation and only 28% occurred within speech; only 5% occurred within syllables. In summary, then, (a) vocal tics in TS are more frequent occurrences and socially inappropriate occurrences of normal behaviors; (b) the types of tic categories a patient exhibits, rather than the frequency , will indicate the severity of his disease; (c) more severely affected patients will have verbal or speech tics; (d) vocal tics occur more frequently during speaking than during silence, but occur during interruptions in speech flow; and (e) vocal tics occur at points of low information in speech.
5.
Are Tics Voluntary or Involuntary?
Most TS patients report premonitary feelings or urges before they produce a tic. Obsessive compulsive thoughts are often associated with this disorder (Frankel/Cummings/Robertson et al. 1986) and some have characterized the production of tics as compulsions to perform motor acts. Lang (1991) examined patients’ perceptions of sy mptom production sy stematically in 170 patients with various hy perkinesias and 60 tic disorder patients. Fifty -six of the sixty TS patients (95%) reported their tics were voluntary while 92.7% of the nontic movement disorder patients reported their movements were involuntary . Although the TS patients reported that their tics were voluntary , they did feel that the i n t e n t i o n to tic was involuntary , leading Lang to coin the phrase, “intentional unvoluntar y ” (Lang 1991, 227). Several patients have described their tic productions as intentional actions used to satisfy or eliminate unfulfilled sensations or urges. These observations emphasize that sensory experiences are a primary or dominant feature of the illness whereas the tics are considered only as responses to these sensory experiences (Lang 1991; Kurlan 1989).
6.
Pathophysiology of Tic Behavior
The phy siological basis for the TS sy ndrome is unknown but is thought to be due to striatal dopamine receptor supersensitivity . This hy pothesis is based on significant tic reductions with dopamine receptor antagonists and tic increases with drugs that enhance dopami-
50. Speech Tics in Tourette’s Syndrome
nergic neurotransmission (Caine/Ludlow/Polinsky/Ebert 1984; Kurlan 1989). Little information is available concerning the pathophy siology of this disorder. A comparison of the presence of the readiness potential preceding simple tics and volitional imitation of the same tics, demonstrated an absence of the readiness potential preceding spontaneous simple tics (Obeso/Rothwell/ Marsden 1981; 1982). Similar comparisons need to be made prior to spontaneous speech tics and patients’ imitations of speech tics because speech tics are usually more complex. Such findings might suggest that tics are produced by different brain regions than normal speaking behavior. This possibility is suggested by the occurrence of tics during all stages of sleep (Glaze/Frost/Jankovic 1983) and also by the observation that 30% of TS patients may not be aware of their tic production (Kurlan 1989).
7.
Associated Behaviors
During our studies of TS, we noted that an unexpectedly large percentage of our TS population had other speech and language deficits. Based on individual interviews of our TS patients, 45% reported a stuttering problem at some point in their lifetime, 45% reported language delay and 56% reported a reading disorder. We investigated this in a more formal manner in 54 TS patients and 54 age and sex matched controls (Ludlow/Polinsk y / Caine et al. 1982) using the only language testing tool available at that time which would span the age range to be studied from 5 to 60 y ears of age; the Neurosensory Center Comprehensive Examination for Aphasia with Gaddes/Crockett (1975) norms for children from 5 to 13 years of age and the Spreen/ Benton (1969) norms for those above 14 y ears. A similar pattern of language deficits was found across all age groups: significantly poorer scores than normal on language expression, written expression, writing to dictation and copy ing. The particular subtests with impaired performance included word fluency , sentence construction (in speaking and writing) reading names, writing names, and digit repetition. No significant relationship was found, however, between the number or frequency of tics and the degree of language deficit on these subtests, suggesting that these two functions were independent in TS. The language deficits were interpreted as demonstrating impaired language execution
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both in speaking and writing with normal speech repetition. Singer/Walkup (1991) have interpreted the neurophy siological deficits of TS patients as, “deficits in the executive function domain — the capacity to plan and sequence complex behaviors and to organize and sustain goal-directed activities” (Singer/ Walkup 1991, 22).
8.
Relationships with Other Deficits
Many behavioral and learning disorders frequently accompany TS such as obsessive compulsive disorder, attention deficit hy peractivity disorder, learning deficits, sleep abnormalities, dy slexia, phobias, depression and stuttering (Comings/Comings 1987 a; 1987 b; 1987 c; Kurlan 1989; Singer/Walkup 1991). Considerable controversy exists in the field today on whether a) these associated disorders are different expressions of the same gene (Comings/Comings/Knell 1989) or that only obsessive compulsive disorder and chronic multiple tics are expressions of the TS gene (Pauls/Leckman 1986). Comings and his coworkers examined the pedigrees of over 1200 TS families with information on other disorders gathered through indirect interview and have suggested that TS is inherited in a semidominant semi-recessive fashion with variable expression ranging from minimal tics to many disorders including obsessive compulsive disorder, stuttering, depression, and dy slexia (Comings/Comings/Knell 1989). In contrast, Pauls and his coworkers conducted direct interviews and segregation analy ses and suggested an autosomal dominant pattern with sex-specific and incomplete patterns (Pauls/ Leckman 1986). Their examination of familial patterns of obsessive compulsive disorder, chronic tic disorders and TS demonstrated that obsessive compulsive disorder and chronic multiple tic disorder are alternate phenoty pes of the TS gene with higher penetrance for males (.99) than for females (.70) (Pauls/Towbin/Leckman et al. 1986; Pauls/ Pakstis/Kurlan et al. 1990). On the other hand, although attention deficit hy peractivity disorder has been found to have an increased frequency in families of TS patients, when a rigorous family study was conducted, the two traits segregated independently (Pauls/Hurst/ Kruger et al. 1986). Further careful study is needed to determine whether there is a genetic relationship between TS and the other disorders reported to occur frequently in association with TS, such as anxiety , conduct dis-
III. Acquired Organic Pathologies of Language Behavior:Neurophonetic Disorders
508
orders, depression, dy slexia, mania, panic attacks, phobias, and stuttering (Comings/ Comings/Knell 1989).
9.
Conclusions
Speech tics in TS are intriguing to those interested in speech pathology because of their similarities and dissimilarities with chronic developmental stuttering. Both disorders seem to have a genetic component and in fact may be related in some way (Comings/Comings/Knell 1989). More males are affected by both disorders, both wax and wave in severity , have a great deal of heterogeneity , remit spontaneously in late childhood and later adolescence in a significant proportion of cases, both are frequently associated with language learning difficulties, and both respond well to haloperidol, a dopaminergic antagonist. There are some other marked differences in their manifestation in speech however, stuttering is reduced at slower than normal speaking rates and occurs within speech while tics in TS precede speech and are unaffected by changes in rate. The new methods of study ing the human genome and analy zing the locations and genetic materials responsible for these disorders may uncover biological mechanisms contributing to both disorders.
10. References Caine, E. D., Ludlow, C. L., Polinsky , R. J., & Ebert, M. H. (1984). Provocative drug testing in tourette’s sy ndrome: d- and l-Amphetamine and haloperidol. Jou rnal of the American Academy of Child Psychiatry, 23 : 2, 147—152. Caine, E. D., Polinsky , R. J., Ludlow, C. L., Ebert, M. H., & Nee, L. E. (1982). Heterogeneity and variability in Tourette Sy ndrome. In A. J. Friedhoff & T. N. Chase (Eds.), Gilles de la Tou rette Syndrome. 437—442. New York: Raven Press. Comings, D. E. & Comings, B. G. (1987 a). A controlled study of Tourette sy ndrome: IV. Obsessions, compulsions, and schizoid behaviors. American Journal of Human Genetics, 41, 782—803. Comings, D. E. & Comings, B. G. (1987 b). A controlled study of Tourette sy ndrome: VI. Early development, sleep problems, allergies, and handedness. American Jou rnal of Hu man Genetics, 41, 822—838. Comings, D. E. & Comings, B. G. (1987 c). A controlled study of Tourette sy ndrome: I. Attention deficit disorder, learning disorders and school problems. American Jou rnal of Hu man Genetics, 41, 701—741. Comings, D. E., Comings, B. G., & Knell, E.
(1989). Hy pothesis: Homozy gosity in Tourette Sy ndrome. American Jou rnal of Medical Genetics, 34, 413—421. Diagnostic and Statistical Manu al of Mental Disorders, Revised (1987). 3rd Ed.. Washington, D. C.: American Psychiatric Association. Frank, S. M. (1978). Psy cholinguistic findings in Gilles de la Tourette sy ndrome. Jou rnal of Communication Disorders, 11, 349—363. Frankel, M., Cummings, J. L., Robertson, M. M., Trimble, M. R., Hill, M. A., & Benson, D. F. (1986). Obsessions and compulsions in Gilles de la Tourette’s syndrome. Neurology, 36, 378—382. Gaddes, W. H. & Crockett, D. J. (1975). SpreenBenton aphasia tests, normative data as a measure of normal language development. Brain and Language, 2, 257—280. Glaze, D., Frost, J. D. Jr., & Jankovic, J. (1983). Sleep in Gilles de la Tourette’s sy ndrome: disorder of arousal. Neurology, 33, 586—592. Kurlan, R. (1989). Tourette’s sy ndrome: Current concepts. Neurology, 39, 1625—1630. Lang, A. (1991). Patient perception of tics and other movement disorders. u Ne rology, 41, 223—228. Ludlow, C. L., Polinsky , R. J., Caine, E. D., Bassich, C. J., & Ebert, M. H. (1982). Language and speech abnormalities in Tourette Sy ndrome. In A. J. Friedhoff & T. N. Chase (Eds.), Gilles de la Tou rette Syndrome. 351—361. New York: Raven Press. Martindale, C. (1976). The grammar of the tic in Gilles de la Tourette’s sy ndrome. Langu age and Speech, 19, 1—20. Martindale, C. (1977). Sy ntactic and semantic correlates of verbal tics in Gilles de la Tourette’s sy ndrome: A quantitative case study . Brain and Language, 4, 231—247. Obeso, J. A., Rothwell, J. C., & Marsden, C. D. (1981). Simple tics in Gilles de la Tourette sy ndrome are not prefaced by a normal premovement potential. Jou rnal of Neu rology, Neu rosu rgery and Psychiatry, 44, 735—738. Obeso, J. A., Rothwell, J. C., & Marsden, C. D. (1982). The neurophy siology of tourette sy ndrome. In A. J. Friedhoff & T. N. Chase (Eds.), Gilles de la Tou rette Syndrome. 105—114. New York: Raven Press. Pauls, D. L., Hurst, C. R., Kruger, S. D., Leckman, J. F., Kidd, K. K., & Cohen, D. J. (1986). Gilles de la Tourette’s sy ndrome and attention deficit disorder with hy peractivity : Evidence against a genetic relationship. Archives of General Psychiatry, 43, 1177—1179. Pauls, D. L. & Leckman, J. F. (1986). The inheritance of Gilles de la Tourette’s sy ndrome and associated behaviors: Evidence for autosomal domi-
50. Speech Tics in Tourette’s Syndrome
nant transmission. New England Jou rnal of Medicine, 315, 993—997. Pauls, D. L., Pakstis, A. J., Kurlan, R., Kidd, K. K., Leckman, J. F., Cohen, D. J., Kidd, J. R., Como, P., & Sparkes, R. (1990). Segregation and linkage analy sis of Tourette’s sy ndrome and related disorders. Jou rnal of American Academy of Child and Adolescent Psychiatry, 29, 195—203. Pauls, D. L., Towbin, K. E., Leckman, J. F., Zahner, G. E. P., & Cohen, D. J. (1986). Gilles de la Tourette’s sy ndrome and obsessive-compulsive disorder: Evidence supporting a genetic relationship. Archives of General Psychiatry, 43, 1180—1182.
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Polinsky , R. J., Ebert, M. H., Caine, E. D., Ludlow, C., & Bassich, C. J. (1980). Cholinergic treatment in the tourette sy ndrome. The New England Journal of Medicine, 302 : 23, 1310—1311. Singer, H. S. & Walkup, J. T. (1991). Tourette sy ndrome and other tic disorders: diagnosis pathophysiology, and treatment. Medicine, 70, 15—32. Spreen, O., & Benton, A. L. (1969). Neurosensory Center Comprehensive Examination for Aphasia, Victoria, B. C.: University of Victoria.
Christy L. Ludlow, Bethesda, Maryland (USA)
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IV. Pathologies of Language Use in Psychiatric Disorders
51.
Language Behavior in Alexithymia
1. 2. 3. 4. 5. 6.
Neurosis and Psychosomatic Disease Affect Verbalization and Alexithymia Communication of Emotional Meaning Content Analysis and Emotional Meaning Concluding Remarks References
1.
Neurosis and Psychosomatic Disease
As clues to individual psychological organization, stylistic properties of speech have been employed in medicine since the introduction of ‘talking cures’, particularly psychoanalysis. Verbal communication complemented traditional ‘medical gaze’ and emphasized dyadic and group interaction in diagnosis and treatment. — In psychoanalysis, the term ‘neurosis’ refers to a psychological organization developed in response to intense and partly repressed affects, especially anxiety and hostility. Language, one of the systems for dealing with such affects, may show relevant ‘defense mechanisms’. The psychoanalytic methods have also been applied to somatic disorders, first explained by principles similar to those proposed for neurotic symptoms, mostly conversion. It became evident that a h o m o gen e o u s model might be complemented with an h e t e r o ge n e o u s one, implying different organization for neurosis and somatic illnes. Ruesch (1948) distinguished between ‘arrested’ development, leading to psychosomatic disorder, and ‘pathological’ development, resulting in neurosis. Others indicated that verbal communication differs in bearers of neurosis and psychosomatic disorders (Lolas/von Rad 1989). — The term ‘neurosis’ is not employed in the ‘Diagnostic and Statistical Manual of the American Psychiatric Association’ (DSM-III-R) and is included only as adjective in the 10th revision of the ‘International Classification of Diseases’ (ICD-10). ‘Psychosomatic disease’ is no longer used as a nosological entity, being replaced by “psychological factors affecting physical condi-
tions” (DSM-III-R) and “behavioural syndromes and mental disorders associated with physiological dysfunction and hormonal disturbances” (ICD-10), categories replacing it within a multiaxial biopsychosocial framework. The group ‘somatoform disorders’, without organic basis or known pathophysiology, lies between ‘purely psychological’ and ‘purely organic’ disorders. — These comments highlight the problem of ascribing speech patterns to pathological entities without due regard to their true definition. What appeared in the past as ‘fixed’ or structural characteristics has often been reformulated as communication patterns or systemic attributes of dyads and groups.
2.
Affect Verbalization and Alexithymia
Irrespective of the way they choose to describe them, psychotherapists have long been aware of patients not inclined to verbalize feelings. Ferenczi and Zilboorg described people unable to establish affective rapport with therapists, in whom somatic affect is discordant with verbal expression. These “difficult patients” (Shands 1975) appear dull, boring and impoverished by comparison to psychologically-minded neurotics, more prone to verbal expression. Among the features Ruesch (1948) included in his concept of “infantile personality” were inability to discharge tension through verbal or creative symbolism and tendency to employ somatic expression. These impair people to cope with frustration and affects and could lead to somatic illnesses. The pattern overlaps with Shands ‘difficult patients’ who, aside from difficulties to describe feelings, are unable to use the pronoun I in emotionally meaningful contexts. Among subjects likely to exhibit this cognitive, affective and relationship pattern are those afflicted by ‘psychosomatic’ conditions, alcoholism, drug dependence and post-trau-
51. Language Behavior in Alexithymia
matic stress (Krystal 1988). From a psychodynamic point of view, French psychoanalysts (Marty/de M’Uzan/David 1963) described a cognitive style adhering to concrete facts, reduced dreaming and fantasy and a particular type of relatedness to others, whereby these are seen as stereotyped images of oneself. Constriction of emotional functioning, impoverishment of fantasy life and tendency to use action instead of language to deal with conflict were included in the concept of a l ex i t hy m i a, proposed by Sifneos (1973) as a cluster of features prevalent in ‘psychosomatic’ patients (psychosomatic meaning the “holy seven” diseases of Alexander (1950), with tissue changes and psychological mediating links in etiology and/or pathogenesis). The contrast between alexithymic and neurotic styles has greatly influenced research. Although the core disturbance is inability to verbally express feelings (‘a-lexithymia’), the concept was construed as a pervasive inhibition or block of self-caring and self-regulating functions and failure to identify and use emotionally meaningful nonverbal expressions as signals to the self. Somatization and regression to somatic forms of expression would result from an inability to cope verbally (‘mentally’) with stress and conflict. The behavior pattern was explained as dysconnection between cognition and affect, as inhibition of affect verbalization due to defenses or as sociocultural constraint. The relationship of alexithymia to bodily dysfunction, and its prevalence in otherwise normal populations, have been sources of debate and confusion.
3.
Communication of Emotional Meaning
Alexithymia and its related theories uncovered the importance of communication and interaction in diagnosis, prognosis and therapy. ‘Communication of emotional meaning’ has become a dimension descriptive of persons, dyads, groups, or situations (Lolas/von Rad 1982 a; b). Under this systemic viewpoint empirical studies can be reevaluated. — Operationalization of alexithymia has taken different forms. Psychometric questionnaires, studies of elicited and spontaneous speech, and physiological measurements have been used. Data from non-propositional speech probes (questionnaires) have differentiated alexithymia from other psychopathological labels and explored its prevalence in different
511
populations. For evaluating communication of emotional meaning studies of spontaneous natural speech seem appropriate, since the clinical dialogic situation was the primary observational setting of alexithymia.
4.
Content Analysis and Emotional Meaning
Content analysis is a technique for making replicable inferences from a t ex t to its c o nt ex t (cf. Koch/Schöfer (Eds.) 1986). The latter can refer to psychological, behavioral or situational features. Early studies emphasized structural aspects (i. e. number of words produced in an interview, number of times the pronoun I is used, number of verbs and adjectives per 1000 words, ‘affectladen words’), showing that alexithymic individuals produce less textual markers related to affect than psychoneurotics during monologues and dialogues (von Rad/Lolas 1978; Taylor/Doody 1985). Psychoneurotic patients express more anxiety at the first psychoanalytical interview, particularly in relation to guilt and shame, and more hostility directed towards the self, employing grammatical clauses as coding units (Gottschalk/Lolas/Viney 1986). When similar samples of patients were compared during monologues, differences appeared only for mutilation anxiety, with higher scores for psychosomatic patients. This illustrates the influence of situational context on the differences and cast doubt on any static characterization of subjects by means of speech measures alone (Lolas/von Rad/Scheibler 1981). Other authors find similar results in monadic situations (Taylor/Doody 1985). Using interview data, affect p a t t e r n i n g was investigated. While psychosomatic (alexithymic) subjects tend to associate hostility directed outwards with shame and anxiety, psychoneurotics show an association between hostility outwards and guilt anxiety. When both dyadic and monadic conditions are combined within the same session, differences between cardiac neurosis and ulcerative colitis patients do not appear during monologues (von Rad/Lolas 1982 a; b). Employing a form of content analysis based on single words and automatic processing, psychoneurotics were shown to agree more with interviewers, suggesting that alexithymia might be a dyadic feature depending upon thematic synchrony between patients and therapists (Lolas/von Rad 1982 a; b). Assuming a continuum along
IV. Pathologies of Language Use in Psychiatric Disorders
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the dimension communication of emotional meaning, content analysis scores differentiated between generalized anxiety disorder, irritable bowel and peptic ulcer patients. The latter were the less expressive, with irritable bowel subjects in an intermediate position between them and anxious patients (Lolas/ Heerlein 1986). Carefully planned studies conclude that the degree of association between alexithymia and other psychopathological features is not redundant (Taylor/Doody 1982 ). It has been suggested that expressive deficits are restricted to cognitive/functional and not to unconscious aspects (Ahrens 1985) and that it may affect more the expression of negative affects.
5.
Concluding Remarks
Research on the distinction between psychoneurosis and psychosomatic disease, kindled by psychoanalytical theory, has drawn attention to verbal communication of affect and emotion as diagnostic dimension. Restricted expression of feelings through words (alexithymia) has been described as part of a syndrome characterized by limited fantasy life and tendency to bodily expression. Although dependent on situational context and limited by prevailing nosologies, this research suggests that language has an homeostatic function in psychosomatic organization. Its control and self-regulation functions in biopsychosocial health are expressed in the dimension ‘communication of emotional meaning’, which may serve as a useful descriptive and diagnostic tool. Several techniques of content and meaning analysis can be employed for this purpose. Clause-based methods have been successfully used for differentiating different clinical pictures (Schöfer/Müller/von Kerekjarto 1979; Oxman/Rosenberg/Schnurr/ Tucker 1988). It should be kept in mind that a specific match between speech characteristics and clinical diagnoses depends to a great extent on prevailing nosologies and that the distinction between psychosomatic diseases and neuroses is in a state of revision. Caution should also be exercised when considering pauses, verbal productivity and other formal features of speech, as well as nonverbal behavior, as differentiating elements. As with language behavior, diagnostic usefulness of such sources of communication data depends on a critical balance between appropriate operationalization of relevant descriptive constructs and sound taxonomy of illnesses.
6.
References
Alexander, F. (1950). Psychosomatic medicine. New York: Norton. Ahrens, S. (1985). Alexithymia and affective verbal behaviour in three groups of patients. Social Science and Medicine, 20, 691—694. Gottschalk, L., Lolas, F., & Viney, L. (1986). Content analysis of verbal behaviour. Berlin — Heidelberg: Springer. Krystal, H. (1988). Integration and selfhealing: A ffects, trauma, and alexithymia. Hillsdale, N. J.: Analytic Press. Koch, U. & Schöfer, G. (Eds.) (1986). Sprachinhaltsanalyse in der psychiatrischen und psychosomatischen Forschung. Weinheim/München: PVU. Lolas, F. & Heerlein, A. (1986). Content category analysis of affective expression in irritable bowel, duodenal ulcer and anxiety disorder patients. Psychopathology, 19, 309—316. Lolas, F. & von Rad, M. (1982 a). Communication of emotional meaning: a biopsychosocial dimension in psychosomatics. In S. B. Day (Ed.), Life stress. 138—144. New York: Van Nostrand-Reinhold. Lolas, F. & von Rad, M. (1982 b). Psychosomatic disease and neurosis: a study of dyadic verbal behaviour. Comprehensive Psychiatry, 23, 19—24. Lolas, F. & von Rad, M. (1989). Alexithymia. In S. Cheren (Ed.), Psychosomatic medicine. 189—237. Madison, CT: International Universities Press. Lolas, F., von Rad, M., & Scheibler, D. (1981). Situational influences on verbal affective expression of psychosomatic and psychoneurotic patients. Journal of Nervous and Mental Disease, 169, 619—623. Marty, P., de M’Uzan, M., & David, C. (1963). L’investigation psychosomatique. Paris: Presses Universitaires de France. Oxman, T. E., Rosenberg, S. D., Schnurr, P. P., & Tucker, G. J. (1988). Diagnostic classification through content analysis of patient’s speech. American Journal of Psychiatry, 145, 464—468. Ruesch, H. (1948). The infantile personality. Psychosomatic Medicine, 10, 134—144. Schöfer, G., Müller, L., & von Kerekjarto, M. (1979). Die Differenzierung psychosomatischer Krankheitsgruppen mit der Gottschalk-GleserSprachinhaltsanalyse. Medizinische Psychologie, 5, 24—38. Shands, H. (1975). How are “psychosomatic” patients different from “psychoneurotic” patients? Psychotherapy and Psychosomatics, 26, 270—285. Sifneos, P. (1973). The prevalence of “alexithymic” characteristics in psychosomatic patients. Psychotherapy and Psychosomatics, 22, 255—262. Taylor, G., & Doody, K. (1982 ). Psychopathology and verbal expression in psychosomatic and psy-
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choneurotic patients. Psychotherapy and Psychosomatics, 38, 121—127. Taylor, G., & Doody, K. (1985). Verbal measures of alexithymia: What do they measure. Psychotherapy and Psychosomatics, 43, 32—37. von Rad, M. & Lolas, F. (1978). Psychosomatische und psychoneurotische Patienten im Vergleich. Un-
terschiede des Sprechverhaltens. Psyche, 32, 956— 973. von Rad, M. & Lolas, F. (1982 ). Empirical evidence of alexithymia. Psychotherapy and Psychosomatics, 38, 91—102.
Fernando Lolas, Santiago (Chile)
52. Pathology of Language Behavior in Affective Psychoses 1. 2. 3. 4. 5. 6. 7.
1.
Introduction Speech Production Syntax and Text Lexicon and Semantics Fluency and Speech Disruptions Conclusions References
Introduction
A multitude of psychological symptoms can be assessed by analysis of language behavior; as one might expect, because of the complexity of the biological language system, cerebral pathology can alter speech and language behavior in any of a number of ways. In contrast to language disorders like aphasia, the pathology of language and language behavior in depression and mania have been called language symptoms (Vetter 1969). The underlying abnormality may be, for example, a sign of disturbed emotionality or of tension. In such cases it is also possible to find signs of these disturbances in other domains like in gestures or the vegetative system. In other words the symptoms are not restricted to linguistic variables. It is very common to have the question, if a variable is affected by a thinking disorder, a pure language disorder or, for example, by a psychomotor disturbance. Besides this distinction, which depends on the predominance of the disturbance in one or several subsystems, there is a further distinction between more or less pure linguistic and para-linguistic variables. Taxonomies for the para-linguistic variables have been attempted to establish e. g. by Newman/Mather (1938) and Mahl/Schulze (1964). Indeed, in some cases it is difficult to distinguish clearly between linguistic and para-linguistic disturbances. Therefore it is important to identify those
of pathogenetic factors in affective psychoses, which interfere with the function of subsystems of the language system. This task has been undertaken by some investigators in order to find objective parameters of relevant psychopathological variables. The affective psychoses are subdivided into the unipolar major depressive disorder and the bipolar affective psychosis (see e. g. DSM III-R 1987), is a course of the illness characterized by depressive and manic phases. Many of the investigators did not report on the unipolar-bipolar distinction of their depressed patients and sometimes failed to report, whether the cases of depression were of a reactive (neurotic) or endogenous type (belonging to the affective psychoses). For this reason there is considerable inhomogeneity in most of the clinical samples of depression. In this chapter the symptoms regarding language and language behavior will be predominantly discussed for depression, since this disorder has been the object of the majority of investigations.
2.
Speech Production
2.1. Articulation and Phonematic Variables There is no clear evidence for defective articulation in either depression or mania. But ratings of the articulatory variables by trained phonetician do, in fact, demonstrate some abnormalities. For instance, Newman/ Mather (1938) described articulation as lax and Darby (1981) noted imprecise consonants after antidepressive drug treatment, reflecting a possible medication induced effect. The articulation time for, e. g., counting has been found to be within the normal range in depression, and is not changing with the clinical improvement of the illness (Szabady/Brad-
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shaw/Besson 1976; Greden/Carroll 1980; Nilsonne 1987; 1988). Contrary to these results Klos/Ellgring (1984) found a slightly prolonged articulation time. Formal aphasia testing of depressed patients has not revealed phonematic difficulties in depression (Faber/Reichstein 1981; Emery/ Breslau 1989; Newman/Sweet 1986). There are no reports of an increased frequency of slips of the tongue phonematic paraphasias or neologisms. Furthermore there is no disturbance in phoneme discrimination in depression (Kugler/Caudrey 1983). It seems justified to conclude from the existing data, that in affective psychoses there are no specific problems with the phonematic aspects of language. Many of the alterations in articulation, which may occur, can be related to psychopharmacological effects. 2.2. Voice Quality and Prosody 2.2.1. Voice Quality and Loudness Early studies characterized the quality of voice in depression (Newman/Mather 1938) as having a pharyngeal, sometimes nasal resonance with glottal rasping. In addition, a study involving speech deviation rating found signs of a hypokinetic extrapyramidal disturbance (Darby/Simmons/Berger 1984). In most cases the fundamental frequency of the speech of depressed patients was found to be lower than that of controls, but there is considerable variation within the group of depressed patients (Hargreaves/Starkweather/Blacker 1965; Starkweather 1967). No significant group effect between depressed patients and normal controls was reported by Zuberbier (1957) and Nilsonne (1987; 1988). In contrast, Scherer (1979 b) found about a 10% increase in fundamental frequency after clinical improvement of depression. Several investigators noted medication effects (Smith 198 2 ; Nevlund/Fann/Falk 1983; Helfrich/ Standke/Scherer 1985; Weiß 1987), whereas Andreasen/Alpert/Marty (1981) did not found medication effects on acoustic parameters. A hoarse voice as a side effect of tricyclic antidepressaent medication was reported by Rhoades/Lowel/Hedgepeth (1979). Depressed patients have been observed by clinicians to speak in a low or soft voice. The variable of loudnes has been measured by Whitman/Flicker (1966), Darby (1981) and Stassen/Kuny/Woggon/Angst (1989) and among others Hargreaves/Starkweather/ Blacker (1965) noted considerable variablity.
IV. Pathologies of Language Use in Psychiatric Disorders
It must be stressed that there are severe problems in clinically measuring the sound pressure level in depressed patients (Andreasen/ Alpert/Marty 1981). In summary, acoustic parameters of the voice of depressed patients are obviously altered, but there is a considerable variation within the group of depressed patients. 2.2.2. Prosodic Variables The dynamics of loudness have been found to be reduced in depressed patients by Zuberbier (1957). An early case study of depression, which analyzed both loudness and pitch, was performed by Zwirner (1930). Newman/Mather (1938) reported absent or rare emphatic accents, which include changes in loudness as well as changes in fundamental frequency. Clinical judgement of prosody as being monotonous is presumably caused by several factors, like changes in loudness and pitch — in syntax as well as in content (see below). Ratings by experienced phoneticians reflected several changes in the prosody of depressed patients (Newman/Mather 1938), i. e., narrow pitch range, and infrequent stepwise changes of perceived pitch. Moses (1954) stressed the observation of uniformity in the depressed voice with repetitions of a gliding down, (s. a. Darby/Hollien 1977). After technically masking the semantic content (content filtering), raters percieved the speech of depressed patients as sad, regardless of the content of the story the patients were telling. At the same time, however, according to a reliable rating of the verbal transcript the stories were considered as sad, happy or angry. The expression of the affects sadness and anger was rated as inappropriate (Levin/Hall/Knight/Alpert 1985). If these findings can be replicated, they might direct the attention to the question, whether there is a more widespread disturbance of affective expression in depression, than has been previously presumed, which might go undetected because of the constant sadness in the behavior of the patients. Depressed patients’ variation of pitch (standard deviation of the pitch) was reported to be reduced by Zuberbier (1957), Leff/Abberton (1981) and Nilsonne (1987; 1988). But whereas Zuberbier (1957) found less downward deflection of the melodic line at the end of the utterance, no significant difference in the variable for this prosodic feature was observed in the study by Nilsonne (1988). Interestingly Hargreaves/Starkweather/Blacker
52. Pathology of Language Behavior in Affective Psychoses
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(1965) noted a high interindividual variability of the predominant melodic line of depressed patients. Nilsonne (1988) also reported lower values for two further variables in depression, namely the standard deviation of the rate of change and the average speed of the change. It seems especially important to investigate, whether the monotonous voice of depressive patients is related to a general psychopathological symptom i. e., psychomotor retardation (Nilsonne 1988), or whether it is a normal expression of the emotional state of the patients. Andreasen/Alpert/Marty’s (1981) finding, that acoustic parameters are more related to the designation of patients as being emotionally flat versus non-flat, independent of the clinical diagnosis of depression, mania or schizophrenia, might be interpreted as an argument against nosological significance of these variables. A further interpretation (Nilsonne 1988) is the involvement of the presumably lateralized systems which regulate the prosody in depression.
whereas the depressed patients used more qualifying adverbs and first person pronouns, manic patients used more adjectives. Contradicting these findings, Lorenz/Cobb (1952 ) and Lorenz (1953) reported, that in mania — in addition to an increased amount of language production — there is an increase in the use of verbs and pronouns and less use of adjectives and prepositions. Text cohesion and text coherence was reported to be unimpaired in depression (Frommer/Tress 1989). Investigation of a 2 00-word sample with the cloze paradigm, which assesses the predictability of speech, reflected normal scores (0.55 in depression versus 0.55 in controls, Maher/Manschreck/Weisstein 1988) or even above normal scores (0.52 versus 0.47, Ragin/Oltmanns 1983). In contrast Maher/Manschreck/Weisstein (1988) found somewhat lower scores in their bipolar depressive patients. It can be summarized that the quantitative analysis of language production of depressed patients demonstrates no abnormalities in syntactical variables or text parameters and thus fail to indicate a disturbance of the syntax system. The low elaboration of syntactical structures of utterances reported in the evaluation of spontaneous speech of depressed patients are paralleled by difficulties in reading comprehension at higher levels of complexity and as well as tasks of increased syntactical complexity (Emery/Breslau 1989), which may be discussed as complexity effects and not as symptoms of a disturbance of the language system. In mania, on the contrary, a rich syntactic elaboration was reported, with diversified syntactic structures (Newman/Mather 1938). Quantitative linguistic investigations of manic patients have been done mostly in comparison with schizophrenic patients, which demonstrate more syntactical deviations (Andreasen/Grove 1979; Frommer/Tress 1989; Hoffman/Stopeck/Andreasen 1986; Wykes/ Leff 1982).
3.
Syntax and Text
Investigations of the language production of depressed patients (Newman/Mather 1938) report little effort to elaborate phrases. The construction of sentences were described as loose and fragmentary and the syntactical devices as being mostly of the additive type (coordination and parallelism). The verbal responses in psychodiagnostic tests (Schafer 1948) were described as showing little spontaneous elaboration or qualification, and in association tests the language production seemed generally dull, stereotyped and blocked. Surprisingly, Andreasen/Pfohl (1976) found no significant differences in syntactic complexity of depressed and manic patients. There have only been few quantitative investigations of specific syntactic parameters of depressed patients, which served mostly as psychiatric controls for schizophrenic patients. In one of these studies Pylyshyn (1970) found more negations and less qualifying subordinators in the language production of depressed patients. Moreover, he observed no significant differences for the type token ration of depressive patients, nor did Pinard/ Roy/Tetreault (1972 ). In a different approach Weintraub/Aronson (1962 ; 1967) and Hinchcliffe/Lancashire/Roberts (1971) also reported more use of negation in depression. Andreasen/Pfohl (1976) established that,
4.
Lexicon and Semantics
There are some studies which report reduced vocabulary scores, especially for older depressed patients, whereas vocabulary in normals actually increases with age (Savage/Britton/Bolton/Hall 1973; Kendrick/Gibson/Moses 1979; Reischies 1988). In formal aphasia testing no naming disturbances were seen in depression, Faber/
IV. Pathologies of Language Use in Psychiatric Disorders
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Reichstein (1981), Emery/Breslau (1989). Bucci/Freedman (1981), however, found a deficit in ‚referential activity function’, which relies essentially on naming, in older depressed patients. They interpret their finding as a failure of integration of symbolic processing. Word production with a speed component, like the word fluency tasks, e. g. finding words with a certain initial letter, are impaired in depression (Robertson/Taylor 1985; Reischies 1988; Reischies/von Spieß/Hedde 1990). But it has to be kept in mind that these tasks require a considerable effort, and it is likely that depressed patients fail in tasks which are effortful (Weingartner/Cohen/Murphy et al. 1982 ). In an untimed version of such a task Emery/Breslau (1989) also found word production deficits in depressed older patients, yet attributed them nevertheless to the task’s high effort demand. It is possible that certain word retrieval problems contribute to the reduced quantity of language production of depressed patients and to the vagueness in the verbal expression, which was reported by Andreasen/Pfohl (1976). Speech blockage has been reported as possible side effect of antidepressant medication (tricyclics, maprotiline and MAO-antagonists). It is characterized more often as “word blockage” in the sense of word finding problems (Schatzberg/Cole/Blumer 1978; Goldstein/Goldberg 1986), although articulation problems have also been abserved (Sandyk 1986). No disturbance in denotative versus connotative meaning has been found between depressed and manic patients in contrast to schizophrenic patients (Cutting/Murphy 1990). However, because there was no normal control group in this study, the result is difficult to interpret. A memory bias in depressed patients favoring negative events has been found in some studies (Lloyd/Lishman 1975). This may possibly contribute to the preponderance of negation in their language production. In summary, most of the abnormalities of depressed patients found for lexical or semantic variables appear to be related to effects of the general complexity or amount of effort required for the task. The question, if there is a semantic retrieval problem in depression, however, must be clarified in further studies.
5.
Fluency and Speech Disruptions
Past descriptions of language in depression stressed the point that these patients talk rarely or say almost nothing at all, in contrast to manic patients (Wernicke 1906). Newman/ Mather (1938) characterized the speech in depression as having a slow tempo, frequent pauses and hesitations, slow initiation of response and short length of the response. In contrast, the speech of manic patients differs in the initiation of the response, which is described as rapid, and in the length of the response, which is described as long (see also Lorenz/Cobb 1952). The topic of fluency has been mentioned above in conjunction with word finding problems of depressed patients. Fillmore (1979) discusses fluency as one dimension of individual differences regarding competency in the use of one’s language. The reduction of the basal amount of language production is seen by some researchers as a symptom of psychomotor retardation in depression. They therefore consider such factors as pause times, for example, to be quantification variables of retardation (s. below). The basal amount of language production may be considered — according to this approach — as an underlying variable, which can be assessed by many of the fluency parameters more or less reliably. 5.1. Basal Amount of Language Production 5.1.1. Elicited Language Samples In speech of depressed patients the pauses between words seem to be prolonged. In view of this finding, researchers usually analyze sequences of automatic speech. Zuberbier (1957) for example, had her patients produce a series of la, la .... She noticed a slowing for the last 5 items. Furthermore there are several data about counting times in depression — the patients counting from 1 to 10 ‚at their own speed’. Table 52 .1. shows the results for studies involving this paradigm. In most investigations only few patients have been studied. It has been found, that the pause time is almost twice as high in depression as compared to normal controls, as well as compared to patients in an euthymic state, that is, after recovery. However, this seems not to hold for bipolar patients in the depressed state (Hoffmann/Gonze/Mendlewicz 1985). It should be mentioned, that two of the studies tried to investigate manic patients as well, but it
52. Pathology of Language Behavior in Affective Psychoses
Study
Szabady 1976 Greden 1980 Greden 1981
Godfrey 1984 Hardy 1984 Hoffmann 1985
Nilsonne 1988
Depression Diagnosis-Criteria N Age Medicated 4 22—56 yrs. RDC 7 42—82 yrs. nonmed. RDC Unipolar 24 57.2 yrs. Bipolar 12 52.3 yrs. DSM III 5 DSM III 16 22—74 yrs. nonmed. RDC 6 unipolar 10 bipolar 21—71 yrs. nonmed. RDC 28 26—63 yrs.
517
Pauses Depress.
Remission
Controls
4.28 (1.49) 4.20 (3.14)
1.75 (0.54) 2.05 (0.80)
0.95 (0.71)
3.44 (3.03) 3.13 (2.73) 4.72
1.94 (1.05) 2.19 (1.48) 2.08
1.87 (1.13)
4.10
2.79
(1.48)
(1.11)
Comment
2.66 Corr. with retardation
3.36 (1.21) 1.47 (0.79)
1.74 (0.67)
3.1 (0.4)
2.9 (0.4)
Corr. with simple react. time, and retardation
Table 52.1: Pause times in counting (Nine intervals from 1 to 10) (sd) seemed to be almost impossible to have these patients perform this task properly (Greden/ Carrol 1980; Godfrey/Knight 1984). Correlational analyses have shown a relation of pause duration to measures of psychomotor retardation in the depressed state and also in the course of recovery. In addition, neuroleptics do not appear to alter pause times (Szabady/Bradshaw/Gazner 1980). Reading times were found to be affected as well as the pause durations in depressed patients (Zuberbier 1957; Darby/Hollien 1977; Nilsonne 1987). Darby/Hollien (1977) and Newman/Mather (1938), found neither a strong relation between the state of the patients and the reading time nor specificity regarding the differentiation between psychiatric diagnostic groups. The effect of sedative drug effects on pauses in reading was noted by Hargreaves/Starkweather/Blacker (1965).
5.1.2. Language Production in an Interview Situation The language production in an interview is dependent on many complex factors. In the language production of an interview, the proportion of speech of the depressed patient is reduced (Ellgring 1976; Rehm 1987, negative finding Rutter 1977). Monologue material from interview situations has been most often analysed for fluency parameters. The word per minute count obtained in several studies is shown in Table 52 .2 . There are important differences regarding the exclusion of speech pauses. In the Klos/Ellgring study (1984), for example, only the time for the utterances was analysed, and dialogue material has been analysed, so that a slightly higher count results. Reischies (1988) found a significant correlation between the word per
IV. Pathologies of Language Use in Psychiatric Disorders
518
Study
Sample
Weintraub 1967
10 min
Hichcliffe 1971 Klos 1984 Gottschalk 1986
5 min 53 yrs. 5 min
N Age 45
Depression
Remission
Control
Comment
104.8 (30.8)
124.8 (35.5)
Exclus. longer pauses
19
101.6
123.4
16 55.6 yrs. 29 37 yrs.
140.1 (38.8) 103.2
179.8 (33.9)
Exclus. pauses male 112.2 female 94.6
Table 52.2: Words per minute in an interview situation (uninterrupted speech sample) minute count for one minute to the global cerebral blood flow (r = 0.59). The corresponding counts of words per minute were in accordance with the reported data: 112 .04 (sd 42 .2 0) for the depressed state and 12 8.82 (sd 38.64, t = 1.98) for the remitted state of 2 8 patients, which have been investigated two times. As would expected, manic patients show an increased amount of language production (Newman/Mather 1938; Stoddard/ Post/Bunney 1977), assessed as words per minute (Lorenz/Cobb 1952). The amount of language production has been shown to be quite stable for an individual person (see Goldman-Eisler 1968) and to be related e. g. to personality factors like extraversion (Scherer 1979 a). It varies, however, with the emotional state, especially anxiety, which is an common element of the depressive syndrome (Benton/Hartman/Sarason 1955; Pope/Blass/Siegman/Raher 1970; Murray 1971; Siegman 1978). Here the evaluation of the importance of the topic in the communicative situation may be mentioned. Manic patients usually feel as though they were contributing important topics to the conversation. It is even difficult to interrupt their speech (Newman/Mather 1938). In contrast, part of the psychopathology of depression is that the depressed patients think, they have nothing important to say. The possible role of cognitions like this in the explanation of the amount of language production seems to have not yet been systematically studied. Because an imbalance of cholinergic and adrenergic effects in the brain of depressed patients has been postulated (Janowsky/ElYousef/Davis/Serkerke 1972 ), the findings of decreased talkativeness after psychopharma-
cological interventions (e. g. the application of physostigmine, a central cholinergic drug, Bowers/Goodman/Sim 1964), and conversely increased talkativeness after an adrenergic stimulant amphetamine (Griffith/Stitzer/ Corker 1977) are especially relevant. Furthermore frontal lobe damage can lead to less spontaneous language production (Stuss/ Benson 1986), possibly in relation to an abolic state. The importance of such factors, which may influence verbal fluency, for the affective psychoses has not been studied in detail. 5.2. Speech Disruptions There are grammatical and non-grammatical explanations for the discontinuation of speech (Miller 1973). Nongrammatical pauses are of more interest in the language behavior of depressed and manic patients. Reasons for non-grammatical pauses can be intrusions, stuttering, slips of the tongue, corrections and incompletion as well as omissions (Mahl 1956). The frequency of these classes of disruptions, which are related to affects like anxiety (Mahl 1956; Mahl/Schulze 1964; Glaister/Feldstein/Pollack 1980), seems to be not systematically investigated in conjunction with affective psychoses. Bouhuys/MulderHajonides van der Meulen (1989) identified a factor of fragmentation of speech. The Pauses between speakers and the duration of vocal activity were included in this factor. The pauses between utterances have been found to be reduced in depression. Zuberbier (1957) reported a mean pause duration of 2 .2 2 sec, versus 0.98 in controls, Klos/Ellgring (1984) 1.76 in depression and 1.05 sec. in the remitted state.
52. Pathology of Language Behavior in Affective Psychoses
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The latency from the end of an utterance of the interviewer to the utterance of the depressed patient is prolonged (Renford 1986; Nilsonne 1988), which might be an effect of a general increase in behavioral response latency, reported by Libet/Lewinson (1973). Nongrammatical pauses can also be caused by cognitive activity, e. g. thinking about the continuation of the phrase (Miller 1973). Because depressed patients suffer from a disorder of decision (Corvin/Peselow/Feenan et al. 1990) with a tendency to decide more cautiously, a prolonged time for decisions may contribute to the fragmentation of speech and to the global reduction of language production. Since the reverse seems to be true for mania, the quick response of manic patients (Newman/Mather 1938) may be related to their altered decision behavior (Corvin/Peselow/Feenan et al. 1990).
Andreasen, N. C. & Pfohl, B. (1976). Linguistic analysis of speech in affective disorders. Archives of General Psychiatry, 33, 1361—1367. Benton, A. L., Hartman, C. H., & Sarason J. G. (1955). Some relation between speech behavior and anxiety level. Journal of A bnormal and Social Psychology, 51, 295—301. Bouhuys, A. L. & Mulder-Hajonides van der Meulen, W. R. (1984). Speech timing measures of severity, psychomotor retardation, and agitation in endogenously depressed patients. Journal of Communication Disorders, 17, 277—288. Bowers, M. B., Goodman, E., & Sim, V. M. (1964). Some behavioral changes in man following anticholinesterase administration. Journal of Nervous and Mental Disease, 138, 383—389. Bucci, W. & Freedman, N. (1981). The language of depression. Bulletin of the Menniger Clinic, 45, 334—358. Corvin, J., Peselow, E., Feenan, K., Rotrosen, J., & Fieve, R. (1990). Disorders of decision in affective disease: An effect of ß-adrenergic dysfunction? Biological Psychiatry, 27, 813—833. Cutting, J. & Murphy, D. (1990). Preference for denotative as opposed to connotative meanings in schizophrenics. Brain and Language, 39, 459—468. Darby, J. K. (1981). Speech and voice studies in psychiatric populations. In J. K. Darby (Ed.), Speech evaluation in psychiatry. 253—284. New York: Grune/Stratton. Darby, J. K. & Hollien, H. (1977). Vocal and speech patterns of depressive patients. Folia Phoniatrica, 29, 279—291. Darby, J. K., Simmons, N., & Berger, P. A. (1984). Speech and voice parameters of depression: a pilot study. Journal of Communication Disorders, 17, 75—85. Diagnostic and statistic manual of mental disorders, 3rd edition (revised) (1987). American Psychiatric Association, Washington. Ellgring, J. H. (1976). Kommunikatives Verhalten im Verlauf depressiver Erkrankungen. In W. H. Tack (Ed.), Bericht über den 30. Kongreß der DGfPs. 190—192. Göttingen: Hogrefe. Emery, O. B. & Breslau, L. D. (1989). Language deficits in depression: comparisons with SDAT and normal aging. Journal of Gerontology, 44, 85—92. Faber, R. & Reichstein, M. B. (1981). Language dysfunction in schizophrenia. British Journal of Psychiatry, 139, 519—522. Fillmore, C. J. (1979). On Fluency. In C. J. Fillmore, D. Kemper, & W. S.-Y. Wang (Eds.), Individual differences in language ability and language behavior. 85—101. New York: Academic Press. Frommer, J. & Tress, W. (1989). Merkmale schizophrener Rede. Eine vergleichende Untersuchung
6.
Conclusion
As with all other disturbances of information processing in psychiatric diseases, there are several components or stages of the language system, which can be interfered with. This aspect would include the metabolic parameters of the disease, for example. On the other hand, there may be also a direct effect of an underlying dimension of psychopathology, like psychomotor retardation or the inability of depressed patients to invest effort for a task. A third possibility is, that a language variable is altered as a physiological expression of an extreme affective state (like grief, anxiety). In this case, which may be true for some prosodic variables, it would be not justified to regard these aspects of the language behavior as abnormal. Further investigation of this problem is necessary. In depression as well as mania the interaction of disease factors with the language system seems mainly to occur at the possible multiple stages controlling fluency of language production.
7.
References
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beiden nonverbalen vokalen Sprachparameter Stimmlage und Stimmlagenmodulation bei stationären depressiven Patienten unter einer antidepressiven Therapie. Dissertation, Psychiatrische Klinik, Freie Universität Berlin. Wernicke, C. (1906). Grundriß der Psychiatrie (2nd Edition). Leipzig: Thieme. Whitman, E. N. & Flicker, D. J. A. (1966). A potential new measurement of emotional state: A preliminary report. Newark Beth-Israel Hospital, 17, 167—172. Wykes, T. & Leff, J. (1982 ). Disordered speech: Differences between manics and schizophrenics. Brain and Language, 15, 117—124. Zuberbier, E. (1957). Zur Schreib- und Sprechmotorik der Depressiven. Zeitschrift für Psychotherapie und Medizinische Psychologie, 7, 239—249. Zwirner, E. (1930). Beitrag zur Sprache der Depressiven. Journal der Psychologie und Neurologie, 41, 43—49.
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53. Thought Disorders and Language Behavior in Schizophrenia
1.1. The Distinction between Language and Thought
plicated by certain considerations. We may present the problem succinctly by comparing the production of utterances as analogous to typing a manuscript from a text previously dictated onto an audio tape. If the finished typescript has significant deviations from normal patterns of utterance, there are several possible explanations: — The typescript is a faithful transcript of a deviant text. — The typing process is faulty, and has transformed a normal text into a deviant typescript. — Both of the above have occurred in combination.
The diagnosis of schizophrenia is significantly dependent upon the characteristics of the language utterances that the patient produces. It is by listening to the language utterances of the patient that the clinician concludes that the patient is delusional, that the coherence of his thought processes is disturbed, that his emotional experience is anomalous, that he is experiencing hallucinations, and so forth. However, the process of inferring disturbances of inner psychological states from overt utterances, spoken and written, is com-
The problem that we face is created by the fact that we have access only to the typescript (i. e. the utterance); we cannot listen directly to the tape (i. e. the thought). Hence we are faced with the problem of differentiating between language disturbance and thought disturbance on the basis of a source text in which both may be compounded. At the heart of the matter is the question of whether or not language and thought may be conceptually and operationally differentiated from each other.
1. 2. 3. 4. 5. 6. 7.
1.
Introduction The Description and Quantitative Measurement of Schizophrenic Utterance Language and Motor Behavior Associational Processes Memory and Language A Model of Schizophrenic Utterance: The Association Activation Hypothesis References
Introduction
53. Thought Disorders and Language Behavior in Schizophrenia
There is an additional complication to be considered. Thought disorder has been considered by many authorities to lie on a continuum with normal thinking. This was the case with Schneider, with Freud in his references to the “psychopathology of everyday life”, with Beringer (192 6) and with Kraepelin. It is not widely known that Kraepelin (1906) studied disturbances of language in dreams in order to understand the same phenomena as he encountered them in the clinic. He drew the material mainly from his own dreams, keeping a record of his own “dreamlanguage” for a period of more than 2 0 years. Dream material has been a common source of inference about the possible nature of psychotic disorder. Later in this chapter we shall look at one of the few recent studies to use this in a laboratory study. One of the implications of the view that thought disorder is best understood as an exaggeration and elaboration of normal thought processes is that it is thereby rendered less likely to be specific to a particular psychosis. Writing about thought disorder, Kurt Schneider commented “... the thinking does not connect adequately with what has preceded it, so that for the investigator the various thoughts stand side by side as they are expressed, apparently unrelated. It is true that with schizophrenics this is a common fashion of speech and thought. Milder degrees of incoherence are not uncommon among normal people. There are those who are naturally scatterbrained and incoherent, and others who become so when in upsetting situations or when drunk and delirious. However important these thought disorders may be for the theoretical definition of the nature of schizophrenia, they do not hold much weight in practice as diagnostic features. The milder degrees which occur in ambiguous cases are far too difficult to pin down as unmistakable schizophrenic symptoms” (Schneider 1959, 99; our italics, translation slightly changed by the authors).
1.2. Strategies of Inference As we cannot get at the thought of the patient in intelligible verbal form, we are compelled to turn to other strategies. Chief amongst these has been the comparison of characteristics of the language of schizophrenic patients with that of another diagnostic group. This approach is intended to establish that there are reliable phenomena associated with the presence of an entity labeled ‚schizophrenia’. However, as the diagnosis of schizophrenia (as well as that of other psychiatric
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disorders) is heavily influenced by the verbal behavior of the patient, there is a dangerous element of circularity in this approach. The problem lies in the fact that such research may simply ‚discover’ differences that were used (consciously or not) by the clinician to determine the diagnosis in the first place. In this sense it may be telling us as much about the way that the clinician has been trained to diagnose as it does about the nature of the pathological phenomenon itself. While there is some value in the development of quantitative measures of the phenomena that the clinician had already assessed more loosely through clinical judgment, this value ultimately resides in its potential for research into the relationship of these measures to other nonverbal aspects of the patient’s behavior. Additional methodological issues should be mentioned here. Much credence is given to the view that schizophrenia is heterogeneous. That is to say, that there are subtypes of schizophrenia, each having unique features, and each sharing something in common with the other types. It is this common factor (whatever that may prove to be) that justifies our use of the single noun ‚schizophrenia’, at least for the time being. However, the selection of research subjects on the basis of a common diagnosis of schizophrenia necessarily entails the risk that samples of patients will not only be heterogeneous with regard to their clinical pictures, but also with regard to their performance on laboratory tests. This being the case, attempts to establish a common psychopathology in schizophrenia through the technique of comparison with non-schizophrenic samples is a blunt instrument. Unless the investigator has happened to have hit upon the common pathology, it is highly likely that some portion of a sample of schizophrenics will not exhibit the differences that have been hypothesized to distinguish them from non-schizophrenics. The ultimate solution to this problem lies in the conduct of large-scale comprehensive studies of schizophrenic samples, directed toward the discovery of clusters of symptoms and of laboratory responses that differentiate reliably and repeatedly within the population of schizophrenics generally. Failing this, the next best tactic is to seek to relate differences within samples of schizophrenic patients on one set of measures with differences in another set of non-overlapping measures. The discovery that, for example, the average memory performance of a group of schizophrenics is lower than the average
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performance of other kinds of patient, is less informative than studies that relate individual differences within the schizophrenic sample to differences in memory efficacy. In this article we shall review the state of current knowledge that is the outcome of this strategy. In order to set about this task, we must first consider the problem of the description and quantitative measurement of language utterances. With this done, we shall then turn to look at the relationships between these measures and measures of memory, motor behavior, attention and other non-verbal events. Each of these will be examined in the context of methods that have been employed in the study of normal behavior, and for which we have a reasonable understanding of the processes that are involved.
2.
The Description and Quantitative Measurement of Schizophrenic Utterance
Bleuler (1950) gave emphasis to the significance of language as a reflection of the processes that he believed to be fundamental to the psychopathology of schizophrenia. He hypothesized that disturbances of the associational processes formed a crucial part of the inner core of the pathology. His clinical illustrations are, however, necessarily in the form of the overt utterances of the patient. Thus: Olive oil is an A rabian liquor-sauce which the A fghans, Moors and Moslems use in ostrich farming. The Indian plantain tree is the whiskey of the Parsees and A rabs. The Parsee or Caucasian possesses as much influence over his elephant as does the Moor over his dromedary. The camel is the sport of Jews and A rabs Barley, rice and sugar cane called artichoke, grow remarkably well in India. (Bleuler 1950, 15) Bleuler’s own comment on this kind of example was: “Of the thousands of associative threads which guide our thinking, this disease seems to interrupt, quite haphazardly, sometimes single threads, sometimes a whole group, and sometimes even large segments of them. In this way, thinking becomes illogical and often bizarre”. (1950, 14) Bleuler, of course, employed vivid clinical instances to demonstrate his theoretical points. However, the progress of scientific understanding of clinical phenomena depends upon the development and application of objective quantitative measures to clinical material, and the construction of laboratory tests
that make this approach possible. Research investigations into the phenomena of schizophrenic utterance have typically employed two kinds of description and/or measurement — ratings and tabulated counts. They have also varied between seeking to describe an utterance by noting what is m i s si n g from it, versus seeking to describe and measure what is p r e s e n t in the utterance. Examples of the former include assessments of the ‚incoherence’, the ‚lack of grammatical structure’ or the ‚unpredictability’ of the utterances that are being examined. It will be at once apparent that this approach runs into significant conceptual difficulties. An utterance may be incoherent in many different ways. We find incoherence in the utterances of certain kinds of aphasic patient, utterances by normal individuals speaking in a language in which they are not fluent, utterances made by somebody who is speaking while trying to listen to somebody else speaking in the background and so on. Fine-grained analysis of the positive characteristics that are present in these various kinds of incoherence may reveal substantial differences between them; more to the point, these analyses may suggest hypotheses about the processes that produce them, processes that will be different in each case. Global judgments of attributes such as incoherence may be useful for certain kinds of crude initial clinical assessment (such as deviant versus normal), but are unlikely to be fruitful in suggesting the specific pathological processes that are at work in each case. 2.1. Descriptive Features of Schizophrenic Utterance Descriptions of the anomalies of schizophrenic utterance have pointed to certain recurring characteristics. These characteristics are p r e s e n t in the utterances; their presence frequently gives rise to the global characteristic of reduced coherence that has been mentioned above. They have been summarized by one of us (Maher 1983) as follows: (a) Repetition of Units: The repetition of words or phrases in ways that are not typically found in normal utterances. For example: I fancy chocolate eclairs, chocolate eclairs donuts, I do want some syrup, a tin of golden syrup ... (Critchley 1964, 361). Repetition may occur at the level of syllables as well as words or phrases. Thus the example: Das ist vom Kaiserhaus, sie haben es von den Voreltern, von
53. Thought Disorders and Language Behavior in Schizophrenia
der Urwelt, Frankfurt-am-Main, das sind die Franken, Frankfurter Würstchen, Frankenthal, Frankenstein. (Mittenecker 1951, 366) (b) Associative Intrusions: Schizophrenic utterances are sometimes marked by the inappropriate intrusion of words that are associated with some elements of the utterance, but that are out of place in the utterance itself. Examples: My mother’s name was Bill ... and coo? (Chaika 1974); a patient of Bleuler, when listing her family members: Father, son ... and Holy Ghost (Bleuler 1950). These associations may be in the form of klang (rhyming) associations, punning associations or of associations that are connected to the utterance elements in a normal manner. (c) Punning: Some intruding associations appear to be connected to an alternative meaning of one of the words in the utterance, thus giving the intrusion the semblance of a pun or play on words. Example: To Wise and Company [A department store] If you think that you are being wise to send me a bill for money I have already paid I am nowise going to do so unless I get the whys and wherefores from you to me. (Maher 1983, 8) (d) Object chaining: In English-speaking patients there is a tendency to terminate sentences with a series of noun objects, many of these seeming to be chains of association. Example: I have no way of knowing how much differences of opinion different editors, politicians, historians, sexologists, astrologers or theologians might have to say ... (Maher 1983, 9) As will be seen later on, the critical stimulus for the associative chain does not appear to be the noun object as such; rather it appears to be the component that occurs at the end of the sentence — a feature that is influenced by the normal patterns of the language in which the utterance is made. 2.2. Empirical Studies of Schizophrenic Utterance We may now turn to reports of research in which the characteristics of schizophrenic utterance have been compared with those of other groups, using quantitative measures. 2.2.1. Repetition Several investigators have studied the incidence of repetition in the utterances of schizophrenic patients. A thorough review of these studies is provided by Cozolino (1983). We
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may summarize and update the issue briefly here. (a) The Type-Token Ratio: One measure of repetition uses the single whole word as the unit, computing the ratio of different words per segment of language as an index of repetition at the word level. Thus in the sentence immediately preceding this one there are thirty-one words. However, the word as appears twice, the word of appears three times, the word word appears twice, the four times, and repetition twice. Hence there are twenty-three different words. Division of this by thirty-one gives us a ratio of 0.74. This is the Type-Token Ratio (TTR). Token here means word, and Type means different word: The more repetitious the utterance, the lower the ratio. — While differences in patient samples and in the method of eliciting language utterance have complicated the interpretation of the literature, the general tenor of the fourteen studies reviewed by Cozolino is that schizophrenic patients have lower TTRs (i. e., are more repetitious) than controls. While the differences tend to be small, the direction of the findings is consistent. Schizophrenic patients without concurrent thought disorder (NTD) produce TTRs similar to those of control subjects, the lower values being found in patients with thought disorder (TD). Subsequent studies include work by Maher/Manschreck/Hoover/Weisstein (1987) and Manschreck/Maher/Celada et al. (1991) who report lower TTRs for TD schizophrenics than for other groups. In the first of these reports the investigators applied the concept of specifity/sensitivity developed by Anthony/ LeResche/Niaz et al. (1982 ). Using a cut-off TTR of < 0.64, the technique correctly identified 60% of the schizophrenics, correctly rejected 60% of the non-schizophrenics, but created 40% false positive and 40% false negatives respectively. These values are marginally improved when a TTR of < 0.61 is used to distinguish TD schizophrenics from others. — These investigations make it clear that TD schizophrenics are reliably more repetitious than other schizophrenics or other types of psychiatric patient. However, the differences are insufficiently great to permit their use in the clinical assessment of individual cases. (b) Syllable Repetition: Mittenecker (1951; 1953) investigated repetition in the speech of schizothymic and non-schizothymic normal German subjects. He counted the repetition of syllables rather than words, reporting that repetition was greater in the schizothymic
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sample. He proposed that the processes that give rise to repetitions are present in the potential patient before they become manifest in the morbid state. There do not appear to have been any replications of this rather interesting finding. (c) Phrase Repetition: While units such as words or syllables may appear intuitively to be the components of chains of utterance, everyday observation suggests that phrases may act as units, and hence may be relevant to the investigation of repetitions. Maher/ Manschreck/Hoover/Weisstein (1987) analyzed the distribution of two-word and threeword phrase repetitions in the utterances of their subjects. They found that schizophrenics differed very significantly from non-schizophrenic patients in their production of phrase repetitions of both kinds. They also reported that immediate sequential perseveration of single words in the utterances differed significantly between their comparison groups. Individual repetitions scores correlated significantly with certain kinds of thought disorder as assessed by the Schedule for Affective Disorders and Schizophrenia (SADS) of Spitzer/ Endicott (1978). Specifically, rated scores on Derailment, Logic, Understandability and Poverty of Content were positively correlated with the various indices of repetition. 2.2.2. Object-Chaining The appearance of chains of object nouns in the utterances of schizophrenic patients was first reported by Maher/McKean/McLaughlin (1966). Object chaining is measured by computing the ratio of object-nouns to subject nouns in each sentence. Thus in the example given in Paragraph 2 .1. (d) above there is one subject-noun (I) and six object nouns, editors, politicians, historians, sexologists, astrologers, theologians, giving a ratio of 6.0 in that particular case. This measure was termed the OSR (object — subject ratio). In the Maher et al. (1966) study, TD schizophrenic patients produced a mean OSR of 1.40, while NTD schizophrenics produced a significantly lower mean OSR of 0.78. A replication by Manschreck/Maher/Celada et al. (1991) produced OSRs as follows: TD schizophrenics 1.2 6; NTD schizophrenics, 0.79; normal controls, 0.89. The first mean was significantly higher than the oher two. These data essentially replicate the original findings. 2.2.3. Predictability Several techniques have been developed for the measurement of the predictability of the
patient’s utterance. The most common is the so-called ‚Cloze’ technique (Taylor 1953) in which portions of a transcript of the patient’s utterance are eliminated systematically (every fifth word is a common standard). These mutilated texts are then given to a panel of normal readers, who are asked to fill in the omissions with their best estimate of the missing words. — A second technique, developed by Rutter/Draffan/Davies (1977), involves rearranging the order of the sentences spoken by the patient, normal readers then being asked to arrange them in the order in which they think that they were spoken. Both of these measures may be seen as measures of the coherence or internal organization of the utterance. They tell us what the text lacks, but do not give us a fine-grained analysis of the components of the text that make it incoherent.
3.
Language and Motor Behavior
Relatively little effort has been put into the study of the relationship between motor anomalies and language behavior in schizophrenia, including the motor aspects of language utterances themselves. We begin with the latter question. 3.1. Motor Aspects of Schizophrenic Speech Beattie/Butterworth (1979) report that in normal speech words of either low predictability in context (redundancy) or of low frequency in the language are preceded by longer pauses than are words of high redundancy or frequency. Low frequency words tend to be of low redundancy in most contexts, but statistical separation of their effects showed them to be independent. Maher/Manschreck/Molino (1983) investigated this relationship in schizophrenic patients. The redundancy of individual words was established via the Cloze procedure, word frequency from standard sources, and pause length by computerized measurement techniques. In this study NTD patients showed the normal relationship, but TD patients did not. Pause length seems to be related to the time taken for lexical access (related mainly to word frequency), and to the attentional load placed upon the listener by the occurrence of elements with high information load (low redundancy elements). Thus the pathological processes here may involve impairment in either or both of these factors. Silverman (1972 ) performed an overall analysis of the pause-time to speech-time ratio
53. Thought Disorders and Language Behavior in Schizophrenia
in schizophrenic utterances and found greater pause times in chronic schizophrenics than in other patients. This ratio is closely related to simple speech rate. Some studies have failed to find significant difference between normal speech rates and those of schizophrenics. Hart/Payne (1973) did, however, report negative correlations between the severity of other symptoms and the speech rate of schizophrenics. 3.2. Motor Behavior The clinical literature contains abundant descriptions of motor pathologies in schizophrenia. A good general review of these is to be found in Manschreck (1983). However, the quantitative laboratory study of motor behavior and its relationship to language pathology is relatively uncommon. This seems to be due in part to the difficulties that beset the measurement of voluntary motor behavior; it is also due to the absence of any coherent model of schizophrenic pathology from which the relations of language and motor behavior might be postulated. Systematic work has, however, been recently reported by Manschreck, Maher and their colleagues. Manschreck (1983) provides a detailed review of these studies, the main elements of which can be summarized here. An initial study (Manschreck/Maher/Ader 1981) examined the relationship of the TTR, TD (measured by the SADS), and motor anomalies assessed clinically in different samples of psychiatric patients. A highly significant negative correlation (— 0.59) between the TTR and motor anomalies was found. Motor anomaly scores for TD schizophrenics were significantly higher than for NTD patients. Relationships between specific TD elements and motor anomalies were also high. Thus: Poverty of Content 0.78; Impaired Understandability 0.71; Disturbed Logic 0.61. All coefficients were significant beyond the .01 level. — These studies demonstrated under reasonably well controlled conditions that clinically assessed motor anomalies in schizophrenia are correlated with clinically assessed thought disorder, and with quantitatively measured repetition in language utterance. While this research was promising, it was constrained by the limited reliabilities associated with clinical assessment. The need for quantitative measurement of all variables remained unfilled. Accordingly, a subsequent investigation turned to the measurement of simple motor
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behavior. This required the patient to tap a key at the same rate as a series of audible clicks produced by an electronic signal generator. Several different rates were employed. Accuracy of the response at each rate was measured as (a) the actual mean interval produced by the patient, and, (b) the variability of the response as measured by the standard deviation around the mean interval. By these definitions a perfect score would be one in which the mean interval was the same as that of the auditory stimulus, with a standard deviation of zero. At rates between 40 beats per minute (bpm) and 80 bpm, there were marked differences between schizophrenic patients and normal and other psychiatric controls. Comparison of laboratory motor performance and clinical assessment of motor anomalies indicated a significant relationship, the correlation being — 0.53, better performance being associated with fewer clinical anomalies. From this we may reasonably conclude that the two methods — laboratory and clinical assessment — are fundamentally reflecting the same disordered motor process. A third step in this investigative sequence turned to the association between quantitative measures of language and quantitative measures of motor behavior. Correlation of the TTR with motor tapping accuracy produced a significant coefficient of +0.35, i. e. lower rates of word repetition in speech are associated with greater accuracy in generating a rhythmic motor response. At a later point in this paper we shall comment on the relevance of rhythmic motor movements for the understanding of schizophrenic pathology. Meanwhile it may be helpful to note that the generation of automatic responses of any kind depends upon the capacity to utilize predictabilities in sequences of environmental stimuli. As predictabilities are by definition redundancies, the role of impaired redundancy utilization may be of some interest to us.
4.
Associational Processes
Bleuler, as we have seen, emphasized the loosening of “associative threads” in the discourse of schizophrenics. While the terminology is striking, the clinical phenomena of schizophrenic utterance suggest not so much that some “thread” has been “loosened”, but that strongly linked associations have intruded into the thread of intended speech — this thread being ordinarily organized not in an
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associational manner, but in terms of an intended plan of utterance. Paradoxically, it is as if the threads of association are too strong and tight rather than weak and loose. Contemporary cognitive science has found it useful to conceptualize associations as n e two r k s. Any given element in memory may be seen as the hub of a network of related stored elements. These elements may be in the form of words, visual icons, sounds, etc. Activation of an element by external stimulation produces activation of other elements in the network. The elements that are affected by s p r e a d i n g a c t i va t i o n do not ordinarily enter consciousness, and appear to be rapidly inhibited by the sequential activations produced by serial stimulation from the environment. Evidence for the activation of networks comes from several sources. One of the most important contemporary techniques used to detect activation is the method of l ex i c a l d e c i s i o n, or s e m a n t i c p r i m i n g. The subject faces a computer screen and is presented with a verbal stimulus — a single word — the ‚prime’. After a brief exposure it is replaced with a second string of letters, the ‚target’. These may constitute a word or a non-word, i. e. a random string of letters. The task of the subject is to decide whether or not the target is a word. This decision is signalled by pressing one of two keys as quickly as possible after recognition has taken place. The dependent measures are the accuracy of the identification and the speed with which this is made. Many studies have established that when the prime and target are associated, recognition takes place more quickly than when they are not associated. This gain in speed of recognition is termed fa c i l i t a t i o n. Facilitation is interpreted as evidence that associates to the prime have been activated by the appearance of the prime, and that this leads to more rapid recognition because the task requires only an automatic matching of target with a limited number of activated network elements. Lack of association between prime and target, on the other hand, means that activated associations to the prime must be inhibited, and that recognition must involve searching a large lexicon of possible words for a match to the target. Clearly, individuals whose facilitation gains are larger than those of others may be regarded as having unusually high levels of activation of their associational networks. Given the general hypoth-
IV. Pathologies of Language Use in Psychiatric Disorders
esis that schizophrenic patients are subject to associational intrusion, it is reasonable to predict that they will produce superior facilitation to that of normal controls. First reports of the use of this technique (Maher/Manschreck/Hoover/Weisstein 1987; Manschreck/Maher/Milavetz et al. 1988) report that TD schizophrenic patients showed facilitation that was superior to NTD schizophrenics, to unipolar depressed patients, and to normal controls. This is, of course, highly consistent with the proposition that thought disorder is a consequence of hyperactive associational processes. A replication by Kwapil/Hegley/Chapman et al. (1990) employed a somewhat different recognition technique. After the recognition threshold was calibrated for normal controls and schizophrenic patients, the target words to be recognized were presented in a degraded fashion by the random elimination of pixels from the screened representation of the words. Subjects could systematically restore portions of the word until they reached a level at which they could correctly identify the target. Associated words were recognized at lower thresholds than nonassociated words. With this technique the investigators repeated the finding of superior facilitation in schizophrenics. As they did not divide their patient sample on the basis of thought disorder, it is not possible to replicate that particular component of the original reports. In a study of normal subjects Spitzer/Mamelak/Stickgold et al. (1991) employed the lexical decision technique to test the hypothesis that REM sleep will be characterized by greater activation of associational processes. There is, of course, a long-standing history of comparisons between dreams and psychopathological states, notably schizophrenia. It would, of course, be a mistake to simply equate schizophrenic phenomena with those found in dream states. Nonetheless, the plausibility of the belief that associations are hyperactive in both suggests that facilitation in a lexical decision task given immediately upon being awakened from REM sleep should be greater than that found in the normal daily waking state. In the study by Spitzer/Mamelak/Stickgold et al. (1991) subjects were presented with the lexical decision task under three conditions. Normal waking, awakened from non-REM sleep and awakened from REM sleep. The REM condition produced superior facilitation compared to the other two conditions.
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These latter two conditions did not differ between themselves. As performance on the non-associated pairs was not different between conditions, it is clear that all of the effects may be properly ascribed to the facilitation produced by the associated condition. This study has the added value, in the context of the present chapter, of demonstrating the presence in normal subjects under special circumstances of a process that appears important in pathological subjects. Two other aspects of these studies are important. The pairing of associated prime and target is done on the basis of word association norms, the assumption being that for most subjects the norms will adequately define the network of associations that will be activated. As this is only normatively likely, and will not be true for all individuals in the sample, the lexical decision technique probably underestimates the facilitation that might be gained were the prime-target pairings made on the basis of the previously established associations of the individual patients. A second more important consideration is the fact that the presence of a psychopathological impairment is here demonstrated by superior performance, rather than by the more common tactic of demonstration by deficient performance. Deficient performance may always be explained as due to lack of motivation, medication effects, fatigue or other non-specific factors, unless these are all carefully controlled — which is almost never the case. This makes it important to develop tasks in which what is usually an impairment becomes an advantage, thereby permitting the testing of hypotheses without the problem of non-specific disruptive factors. The lexical decision task presents many opportunities to advance our understanding of the associational processes of patients and normal subjects alike. We may expect to see increasing use of it for these purposes.
5.
Memory and Language
The study of memory and language in schizophrenia is vulnerable to confounding due to the extensive reliance that is placed on verbal report in studies of memory. Verbal data that suggest a deficiency in memory may therefore simply reflect a deficiency in formulating the retrieved contents of memory into adequate verbal form. There are some solutions to this problem. One is to vary the conditions under which memory for verbal material is elicited,
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assuming that the disruptive effect of language disorder per se is constant across conditions. The other is to seek evidence of deficiency in performance on non-verbal memory tasks, and then to correlate this with measures of language disturbance. We shall confine ourselves to this kind of study in this chapter. General reviews of memory functioning in schizophrenia may be found in Koh (1978), Braff (1991), and Neufeld (1991). 5.1. Contextual Constraint and Memory in Schizophrenia Miller/Selfridge (1950) demonstrated some years ago that items from lists of words would be recalled in increasing numbers as the lists increasingly resembled sentence-like sequences. The more the list approximated to a normal language sequence, the greater the number of words available to immediate recall. This effect has been shown to be robust across several languages (e. g. Maher/Skovengaard 1988): As word sequences in normal sentences have transitional probabilities between individual words greater than is the case for random word lists, it is assumed that these enhance the detection and storage of the elements of the list. The technique uses lists in which the words are of equal frequency, so that vocabulary knowledge does not affect recall. Lewisohn/Elwood (1961) reported that schizophrenics were less able to recall language texts of low contextual constraint than were control comparisons. Maher/Manschreck/Rucklos (1980) employed the MillerSelfridge technique to study the relationship between context effects in memory and language and thought disorder. Thought-disordered schizophrenics were significantly less able to profit in memory from increasing contextual constraint than were comparison groups of NTD schizophrenics, normals and depressed patients. This finding reminds us again of the difficulty that thought disordered patients have in any task in which performance is facilitated by redundancy. 5.2. Primacy and Recency Effects Items in lists presented to be memorized tend to be learned, and to be available for recall before learning is complete, in a pattern in which items presented early in the list or late in the list are learned sooner than those in the middle of the list. These are referred to as the primacy effect and the recency effect respectively. Studies of these effects in schiz-
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ophrenic patients have produced conflicting results. Some studies report no difference between schizophrenics and controls (Berg/Leventhal 1977; Mungas 1983). Other have reported reduced primacy (Oltmanns 1978; Frame/Oltmanns 1982 ), while one has reported reduced recency (Koh/Kayton 1974). The capacity to retain early items in a list suggests that the organization of verbal material into chunks is the underlying process. Grossberg (1982 ) suggests that this process is dependent upon stability of attentional input; it is likely therefore to be impaired in persons whose attentional processes are unstable. With these considerations in mind, Manschreck/Maher/Celada et al. (1991) investigated primacy and recency effects in schizophrenics, depressed patients and normal controls, using the Miller-Selfridge lists. No difference in recency effects was discovered. However, substantially reduced primacy was found in the schizophrenic group, with less severe but significantly reduced performance in the middle segment of the list. Within the schizophrenic sample, reduced primacy was significantly related to inability to gain from context (r = 0.44). Reduced primacy was related to repetition in speech as measured by the TTR obtained from an independent sample of speech (r = 0.54). Comparison of a subset of drug-free patients with those on medication revealed no effect of medication on performance in these tasks. As this now brings to three the total number of reports of loss of primacy effects in schizophrenic memory, it seems reasonable to conclude that this is a reliable phenomenon. 5.3. Backward masking The storage and retrieval of stimulus input involves a rather complex sequence of steps. One of the earliest of these is the process whereby an immediate input activates the peripheral receptor. Thus a visual stimulus activates the retina, an activation that decays over time. The retinal response creates a central event. Both the retinal and the central events continue for some time after the external stimulus has terminated. However, the input of another visual stimulus shortly after the onset of the first stimulus can mask the effect of the first. Thus the brief display of, for example, the letter A , followed rapidly by the letter O placed at the same focal point, can prevent the correct recognition of the A. Intervals of 50 msec. are effective in creating
masking effects in about 50 percent of cases. In one of a series of important studies conducted by Saccuzzo and his associates, (Miller/Saccuzzo/Braff 1979) the data showed that masking effects were more pronounced in schizophrenic patients regardless of the presence or absence of thought disorder. This suggests that this defect in information processing is a trait rather than a fluctuating state. As language disorders in schizophrenic patients are related to thought disorder, and rise and fall in state-like fashion, it seems probable that excessive vulnerability to masking effects has little explanatory power in relation to the language deficits of schizophrenics. This conclusion is buttressed by reports that similar vulnerabilities have been found in bipolar and in unipolar psychotic patients. As it does not appear to be specific to schizophrenia, it seems to be of greatest interest in its potential relationships with either medication effects or with some general slowing of the information processing systems in psychosis.
6.
A Model of Schizophrenic Utterance: The Association Activation Hypothesis
Any model designed to account for the phenomena of schizophrenic utterance must explain certain kinds of data. What must be explained are not only the bases of the utterance anomalies themselves. The findings from memory, lexical decision, motor activity and so forth must be plausibly connected together, at least in broad outline. Examination of the findings summarized here suggest that the model must encompass: — The inability of the patient to benefit from predictabilities in sequences of events to which a response must be made. This includes the inability to generate predictabilities to improve response patterns that must be made by the patient. — The range of specific language anomalies that are present to clinical observation. — The many other kinds of anomaly that have been reported repeatedly in the clinical literature. These include distractibility, difficulties in filtering out external and internal stimulation when trying to focus on a limited field of conscious experience, difficulties in forming abstract categories or concepts.
53. Thought Disorders and Language Behavior in Schizophrenia
In our view, it is useful to consider a broad general model along the following lines. We begin with the principle that adaptive behavior involves the utilization of predictabilities in sequences of events, i. e. r e d u n d a n c i e s. These must be exploited where this is useful, but must be ignored when circumstances require it. In simple terms this means that an organism surviving in a world of predators and prey must learn to recognize critical sequences in the environment. The shadow of the hawk that presages the attack that will follow must lead the sparrow to become motionless, Pavlov’s dog must learn that the sound signal will be followed by food, if the adaptive salivary response is to be made in an effectively anticipatory fashion. In language, the formation of associations between commonly co-occurring words or phrases is a useful automatic mechanism. Associations are formed by repetitious pairing, a pairing that occurs naturally in the social habitat, but which is created systematically in the laboratory. Natural pairings give rise to transitional probabilities as they create a cumulative base upon which we may expect one element to be followed, predictably, by another. The priming effect that leads to the quicker recognition of an associated word may be seen as an advantageous process, one that makes the recognition of normal communication easier. However, a counter-process of discrimination requires that the exploitation of redundancies be adjusted to the c o m p l ex o f circumstances (i. e. the context) in which the behavior is occurring. A simple response to a single element in the environment will be maladaptive if the context has not been inspected to determine whether a modified response is more appropriate. The process of discrimination sometimes requires the inhibition of the most common response in favor of a less common but more effective response. This principle has been beautifully demonstrated in the classic paper by Chapman/Chapman/ Miller (1964) in which schizophrenic subjects exhibited an inability to inhibit high probabilities when the context called for the low probability response to be made. From this point of view, the utterance of a coherent sentence requires that activated normal associations to each word be inhibited to prevent their disruptive intrusion into the planned utterance. They will be permitted to ‚intrude’ only if they are consistent with the plan of the utterance. These associations may
531
intrude in various forms, including simple repetition of a previously uttered segment, the chaining of associations as in object chaining or enumeration, clang associations, tangential or derailed segments due to the simultaneous activation of association networks to both meanings of multiple meaning words — which produces the ‚punning’ effect already described, etc. The intrusion of these elements is hypothesized to be particularly likely at those points in an utterance at which the attentional demands of the speaking or writing task are minimal — as for example at clause and sentence boundaries. Object nouns tend to be placed most often at the end of sentences uttered in English, hence the phenomenon of associative chaining presents itself as object-chaining. Associational intrusions do occur in normal speech with some frequency, but generally in ways that are congruent with the context and intent of the discourse; hence, they do not disrupt the plan of the utterance, but escape notice and do not create comprehension difficulties. Schizophrenic failure to be influenced effectively by the context of utterances, including their own, is assumed in this model to be not so much a positive failure of a mechanism responsible for adaptation to such influence but to reflect instead the overriding of this by an unusually strong degree of activation of associations. We have already examined the data from lexical decision studies, including data from normals awake and awakened from sleep, schizophrenics and depressed patients. These data support the notion that associational processes are activated more vigorously in patients with concurrent utterance anomalies than in other groups, and is thus consistent with the hypothesis. The data from studies of memory and of motor behavior point again to impairment in the use of redundancies, and the relationship of this impairment to the presence of anomalies of language utterance — especially repetition. We have, as yet, no clear hypothesis as to the probable etiology of this impairment, other than to suggest strongly that the defect is neuropsychological in nature. Given the steady accumulation of evidence pointing to possible frontal lobe involvement in schizophrenia, it would not be surprising to find that language and other cognitive anomalies will prove to be associated with measured anomaly in frontal lobe structure and/or function. However, the data are only suggestive and this matter is still very much open.
IV. Pathologies of Language Use in Psychiatric Disorders
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Furthermore, the fluctuating nature of the language symptoms suggests that the most immediate underlying etiological factors are themselves of a fluctuating type. Finally, the probability of the heterogeneous nature of schizophrenic disorders suggests that assumptions of unitary etiologies and unitary patterns of language disturbance are unlikely to provide a comprehensive model for the understanding of empirical results. In the immediate future, several questions for research can be identified. These are: (1) The determination of the internal patterns of language disorder within the presumably heterogeneous group of schizophrenic patients who bear this diagnosis. Multivariate analysis of reliable, quantitative data seems to be the appropriate strategy here. Equally important is the determination of longitudinal patterns in these anomalies. (2 ) The determination of the correlations between identifiable patterns of language disturbance, measurements of brain structure and function, and identifiable, quantitatively measured, patterns of disturbance in other non-verbal functions. (3) The fine-grained analysis of the processes of associational activation in patients and controls. Specifically the determination of the duration of activation of associations, the role of transitional probabilities between words in limiting associational links in normal subjects, the effect of diurnal fluctuation and other threats to longitudinal stability in these measures. (4) The study of verbal patterns in the utterances of family members of patient probands. (5) The effect of neuroleptic treatments on the nature and duration of verbal disturbances. We believe that progress in our knowledge of psychopathology will be made more rapdily by the use of reliable, ratio-scale quantitative measures of performance that are minimally dependent upon ratings made on the basis of clinical judgment. These latter approaches are suitable in the early stages of scientific research, but are severely limited in their usefulness in the investigation of the most significant questions that human abnormality poses to us.
7.
References
Anthony, J. C., LeResche, L., Niaz, U., von Korff, M. R., & Folstein, M. F. (1979). Limits of the “Mini-Mental State” as a screening test for dementia and delirium among hospital patients. Psycho-
logical Medicine, 12, 397—408. Beattie, G. W. & Butterworth, B. L. (1979). Contextual probability and word frequency as determinants of pauses and errors in spontaneous speech. Language and Speech, 22, 201—211. Berg, P. A. & Leventhal, D. D. (1977). The effect of distractor strength against the rate of item presentation on retention in schizophrenia. British Journal of Social and Clinical Psychology, 16, 147—152. Beringer, K. (192 6). Denkstörungen und Sprache bei Schizophrenen. Zeitschrift für Neurologie und Psychiatrie, 103, 185—197. Bleuler, E. (1950). Dementia præcox or the group of schizophrenias. (Originally published 1911), New York: International Universities Press. Braff, D. L. (1991). Information processing and attentional abnormalities in schizophrenic disorders. In P. A. Magaro (Ed.), Cognitive bases of mental disorders. 262—307. New York: Sage Publications. Chaika, E. (1974). A linguist looks at “schizophrenic” language. Brain and Language, 1, 113—118. Chapman, L. J., Chapman, J. P., & Miller, G. A. (1964). A theory of verbal behavior in schizophrenia. In B. A. Maher (Ed.), Progress in experimental personality research. Vol. 1. 49—77. New York: Academic Press. Cozolino, L. J. (1983). The oral and written productions of schizophrenic patients. In B. A. & W. B. Maher (Eds.), Progress in experimental personality research. Vol. 12. 101—152. New York: Academic Press. Critchley, M. (1964). The neurology of psychotic speech. British Journal of Psychiatry, 110, 353—364. Frame, C. & Oltmanns, T. F. (1982 ). Serial recall by schizophrenic and affective patients during and after psychotic episodes. Journal of A bnormal Psychology, 91, 311—318. Grossberg, S. (1982 ). Studies of mind and brain. Holland/Boston: Reidel. Hart, D. S. & Payne, R. W. (1973). Language structure and predictability in overinclusive patients. British Journal of Psychiatry, 123, 643—662. Koh, S. D. (1978). Remembering verbal material by schizophrenic young adults. In S. Schwartz (Ed.), Language and cognition in schizophrenia. 55—99. Hillsdale, N. J.: Erlbaum. Koh, S. D. & Kayton, L. (1974). Memorization of unrelated word strings by young non-psychotic schizophrenics. Journal of A bnormal Psychology, 83, 299—310. Kraepelin, E. (1906). Über Sprachstörungen im Traume. [On disturbances of language in dreams]. Leipzig: Engelmann.
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Kwapil, T. R., Hegley, D. C., Chapman, L. J., & Chapman, J. P. (1990). Facilitation of word recognition by semantic priming in schizophrenia. Journal of Abnormal Psychology, 99, 215—221. Lewisohn, P. L. & Elwood, D. L. (1961). The role of contextual constraints in the learning of language samples in schizophrenia. Journal of Nervous and Mental Diseases, 133, 79—81. Maher, B. A. (1983). A tentative theory of schizophrenic utterance. In B. A. Maher & W. B. Maher (Eds.), Progress in experimental personality research. Vol. 12. 1—52. New York: Academic Press. Maher, B. A., McKean, K., & McLaughlin, B. (1966). Studies in psychotic language. In P. J. Stone, D. C. Dunphy, M. S. Smith, & D. M. Ogilvie (Eds.), The General Inquirer. Cambridge, Mass.: MIT Press. Maher, B. A., Manschreck, T. C., Hoover, T. M., & Weisstein, C. C. (1987). Thought disorder and measured features of language production in schizophrenia. In P. Harvey & E. Walker (Eds.), Positive and negative symptoms in psychosis: Description, research and future directions. 195—215. Hillsdale, N. J.: Erlbaum. Maher, B. A., Manschreck, T. C. & Molino, M. (1983). Redundancy, pause distributions and thought disorder in schizophrenia, Language and Speech, 26, 191—199. Maher, B. A., Manschreck, T. C., & Rucklos, M. E. (1980). Contextual constraint and the recall of verbal material in schizophrenia: the effect of thought disorder. British Journal of Psychiatry, 137, 69—73. Maher, B. A. & Skovengaard, J. (1988). Contexutual constraint: a Danish language replication of Miller-Selfridge with methodological improvements. Scandinavian Journal of Psychology, 29, 194—199. Manschreck, T. C. (1983). Psychopathology of motor behavior in schizophrenia. In B. A. Maher & W. B. Maher (Eds.), Progress in experimental personality research. Vol. 12. 53—99. New York: Academic Press. Manschreck, T. C., Maher, B. A., & Ader, D. N. (1981). Formal thought disorder, the type-token ratio and disturbed voluntary motor movement in schizophrenia. British Journal of Psychiatry, 139, 7—15. Manschreck, T. C., Maher, B. A., Celada, M. T., Schneyer, M., & Fernandez, R. (1991). Object chaining and thought disordered speech. Psychological Medicine, 21, 443—446. Manschreck, T. C., Maher, B. A., Milavetz, J. J., Ames, D., Weisstein, C. C., & Schneyer, M. L.
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(1988). Semantic priming in thought disordered schizophrenics. Schizophrenia Research, 1, 61—66. Miller, S., Saccuzzo, D. P., & Braff, D. L. (1979). Information processing deficit in remitted schizophrenics. Journal of A bnormal Psychology, 88, 446—449. Miller, G. & Selfridge, J. (1950). Verbal context and the recall of meaningful material. American Journal of Psychology, 63, 176—185. Mittenecker, E. (1951). Eine neue quantitative Methode in der Sprachanalyse und ihre Anwendung bei Schizophrenen. Monatsschrift für Psychiatrie und Neurologie, 121, 364—375. Mittenecker, E. (1953). Perseveration und Persönlichkeit. Zeitschrift für Experimentelle und A ngewandte Psychologie, 1, 5—31. Mungas, S. (1983). Differential clinical sensitivity of specific parameters with the Rey auditory verbal learning test. Journal of Consulting and Clinical Psychology, 55, 848—855. Neufeld, R. W. J. (1991). Memory in paranoid schizophrenia. In P. A. Magaro (Ed.), Cognitive bases of mental disorders. 231—261. New York: Sage Publications. Oltmanns, T. (1978). Selective attention in schizophrenic and manic psychosis: the effect of distraction on information processing. Journal of A bnormal Psychology, 87, 212—225. Rutter, D. R., Draffan, J., & Davies, J. (1977). Thought disorder and the predictability of speech. British Journal of Psychiatry, 131, 67—68. Schneider, K. (1959). Clinical psychiatry (transl. by M. W. Hamilton/E. W. Anderson). New York, London: Grune and Stratton. Silverman, G. (1972 ). Redundancy, repetition and pausing in schizophrenic speech. British Journal of Psychiatry, 122, 407—413. Spitzer, M., Mamelak, A., Stickgold, R., Williams, J., Koustaal, W., Rittenhouse, C., Maher, B. A., & Hobson, J. A. (1991). Semantic priming in a lexical decision task on awakenings from REM-sleep: Evidence for a disinhibited semantic network. Sleep Research, 20, 131. Spitzer, R., & Endicott, J. (1978). Schedule for A ffective Disorders and Schizophrenia (SA DS). New York: Biometric Research, New York State Psychiatric Institute. Taylor, W. L. (1953). “Cloze” procedure: A new tool for measuring readability. Journalism Quarterly, 30, 415—433.
Brendan A. Maher, Cambridge, Mass. (USA)/ Manfred Spitzer, Heidelberg (Germany)
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54. Linguistic Aspects of Language Behavior in Schizophrenia 1. 2. 3. 4. 5.
1.
Linguistic Deviations in Schizophrenic Speech Systematic Studies of Naturally Occurring Schizophrenic Speech Experimental Studies Conclusions References
Linguistic Deviations in Schizophrenic Speech
1.1. Introduction No domain of mental life is immune to schizophrenia. Thought, affect, perception and beliefs can all be altered, thereby challenging the very human essence of the person suffering from this disorder. Even with such a wide range of signs and symptoms, abnormalities of language behavior have long been considered the hallmark of schizophrenia (Bleuler/ Perrault 1911/1950). These language alterations make it harder, and at times impossible, for the listener to discern the communicative intentions of the schizophrenic speaker (Hoffman/Kirstein/Stopeck/Cicchetti 1982 ). While the effects on the listener are fairly clear-cut, the nature of the language alterations themselves is much harder to determine. Certainly the c o n t e n t of what a schizophrenic has in mind to say may render the communicative intentions of the speaker more obscure; his thoughts, affects, perceptions and beliefs, are, at times, confused, complex, and bizarre, and may be difficult to express in words. The central question for this article, however, is the following: Are there specific ‚linguistic deviations’, defined as violations of linguistic rules and constraints, which obscure the comprehensibility of schizophrenic speech and are independent of the content, deviant or not, of what the speaker has in mind to say? This question has considerable empirical importance insofar as there is now evidence suggesting that at least some schizophrenics suffer from some sort of dominant hemisphere disturbance (Flor-Henry 1976; Morstyn/ Duffy/McCarley 1983; Coffman/Andreasen/ Nasrallah 1984; Crow/Ball/Bloom et al. 1989) which could impair linguistic abilities. 1.2. Typology of Linguistic Deviations As is the case for many other classes of lin-
guistically disturbed speakers, the irregularities produced by individuals suffering from schizophrenia are highly diverse in nature. Some schizophrenics produce words that do not belong to the conventional lexicon. This may reflect an alteration of a lexical morpheme, e. g., (1) he is a grassical person (Hoffman/ Sledge 1983, 157), or a deviation in phonetic construction: (2) he still had fooch with teykrimez, I’ll be willing to betcha (Chaika 1974, 261). A more common type of lexical deviance occuring in schizophrenic speech corresponds to acceptable lexical morphemes inappropriately attached to an affix (Lecours/Vanier/Clément 1976). Examples of these construction, which are referred to as ’derived morphemic paraphasias’ (Lecours/Vanier-Clément 1976), are: (3) attain vigoration and strength (Hoffman/Sledge 1984, 150); (4) stated not necessarily factuated(Vetter 1968, 5; quoting Maher 1966). — In addition, some schizophrenics are prone to the inappropriate coupling of two lexical morphemes, a construction that has been referred to as ‚composed morphemic paraphasias’ (Lecours/Vanier-Clément 1976), e. g., (5) lie-truths (Bleuler/Perrault 1911/1950, 150). — Schizophrenics can also demonstrate wordfinding problems that result in inappropriate insertion of lexical elements in syntactic frames. A ‚mild’ example is: (6) He owns a store on Fifth Avenue, and that’s never mentioned because that is his sidek i ck (intended: s i d e - l i n e; Hoffman/ Sledge 1988, 97). A more ‚severe’ error in word selection produced by a schizophrenic patient inserts a noun into the verb slot of the sentence structure: (7) fish school in their own communities (Hoffman/Sledge 1988, 97). — Schizophrenic patients, moreover, also produce paragrammatical segments, i. e., utterances in which word order and/or word combinations deviate from acceptable syntactic forms. One example, which includes a derived
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morphemic paraphasia, at least approximates grammatical English: (8) That’s why, you know, the fact there was no stigmatism (sic) attached to that clearly explained in the record why you were put back (Hoffman/Sledge 1984, 154). A much more deviant segment typifies what, in psychiatric terms, is referred to as ‚wordsalad’: (9) The honest bring-back-to-life doctors agents much take John Black out through making up design meaning straight neutral underworld shadow tunnel (Chaika 1977, 466; quoting Lorenz 1961). — Finally, schizophrenics demonstrate difficulties in organizing and sequencing sentences to express a coherent message. I refer to these difficulties as ‚pragmatic” insofar as: (i) they do not involve specific linguistic rules that govern sentence generation, and (ii) the degree of deviance experienced by the listener can be altered by changing the verbal and non-verbal context of the segment (cf. art. 53 and art. 56). In summary, patients with schizophrenia demonstrate a wide spectrum of difficulties in word construction, selection, and sequencing which qualify as departures from conventional linguistic rules and constraints. Discovering the nature and significance of these linguistic abnormalities could yield important clues regarding the neurocognitive basis of schizophrenia. 1.3. Schizophasia as a Subtype of Schizophrenic Language Behavior An important paper by Chaika (1974) discussed a particularly severe class of linguistic deviance produced by certain schizophrenics whereby the communicative intentions of the speaker are almost entirely hidden. She invokes the term “schizophasia” for this language behavior, and argues that this special subclass of schizophrenic utterances are very similar to jargonaphasia (cf. art. 55). Chaika suggests that schizophasia may therefore also be the product of some organic disturbance of the brain. A reply to this position was provided by Lecours/Vanier-Clément (1976), who agreed that schizophasia does exist, that it can yield practically all manifestations ordinarily associated with jargonaphasia, but stressed that this syndrome is relatively rare among schizophrenic speakers. This was confirmed in a
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recent study by Hoffman/Sledge (1988), who examined randomly selected speech segments produced by eleven schizophrenics and only found one such speaker who produced segments whichin any approached the level of incomprehensibility described by Chaika. This particular patient produced example (7) (cf. above); the complete utterance containing this segment is as follows: (7a) Interviewer: Tell me about school? (the question posed in the context of asking the patient about her childhood, the question therefore intending to refer to her experiences going to school) Patient: School? Well there are schools of play and schools of fish, mostly you see fish school, people edumacating (sic) themselves, you see, sea is one thing and education is another. Fish is school in their community, that’s why the community of man stands in the way of the community of the sea, and once they see the light of sunny sunshine then they will let it be (see also Hoffman 1986, 507). Besides the paraphasic phonemic transformation, edumacating, (7a) demonstrates other features characteristic of schizophasia which were stressed by Chaika (1974) and, later, Lecours/Vanier-Clément (1976). These features include a preoccupation with too many semantic features of a particular word (re: the different uses of school), and production of words according to phonological features (see, sea, be) rather than according to topic. Lecours/Vanier-Clément (1976) argued that these forms of word play are not at all characteristic of jargonaphasia. When considered along with derived and composed morphemic paraphasias, which suggest intact though poorly regulated lexical generation abilities, word play in schizophasic speech raises the question of whether deviance is intentionally generated. Thus, Lecours/Vanier-Clément opposed Chaika’s position by arguing that schizophasia reflects intact speech production abilities molded to deviant thought rather a primary impairment in language production per se. It should be added that schizophasia occurs primarily in the more advanced stages of schizophrenic illness, and generally is associated with prolonged periods of social isolation and functional deterioration (Hoffman/Sledge 1984; Kirov 1985). Chronic social isolation, sustained alienation from other human beings, coupled with bizarre ideation,
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may, over time, cause the schizophrenic to volitionally disregard the constraints of ordinary language. Under these conditions, the interpersonal communicative goals of speech may be usurped by a kind of verbal game where language is molded to the bizarreness of the speaker’s own ideas regardless of its communicative value to others. On the other hand, extremely chronic schizophrenic illness may be accompanied by the final stages of an as yet uncharacterized neurodegenerative process that could procedure a true aphasic syndrome. Moreover, just because schizophasia reflects word play that seems somehow willful by no means rules out the possibility that other types of linguistic deviance produced by the same speaker (e. g., certain paraphasias and paragrammatisms) are the unintended result of impaired speech production abilities. Thus the intentionality of schizophasic speech remains an open question. 1.4. Fromkin’s Challenge Besides the intentionality issue raised by Lecours/Vanier-Clément (1976), another noteworthy challenge to Chaika’s hypothesis was provided by Fromkin (1975), who noted that the speech of normal individuals is often deviant as well (cf. art. 2 and art. 5). The following are typical examples of the kinds of slips of the tongue and other utterance irregularities that all of us, to some degree or other, are prone to: (10) soul hecond path (intended: whole second path; Fromkin 1975); (11) in a manner of speakingly (intended: in a manner of speaking; Fromkin 1975). Chaika herself provides a representative sample of “nonproficient” writing by an “ostensibly normal college student”: (12) Generalizations have no place in terms of different opinions insofar as the discussion of heros or any other topic ... (Chaika 1977), and the verbal excesses of political speechmaking: (13) In temperance due I don’t see any reason why two men can’t proceed as popular as ever both in themselves as a duocratic and as a demoncratic premise ... (Chaika 1977; quoting Laffal 1965). On the basis of segments such as these, Fromkin argued that the speech irregularities
IV. Pathologies of Language Use in Psychiatric Disorders
produced by schizophrenics are not specific to this disorder but reflect the imprecision of speech generation that all of us, to some degree or other, are vulnerable to. — Chaika (1977) responded to Fromkin by arguing that the deviance contained in schizophasic speech can be distinguished from the speech errors produced by normals insofar as the latter are readily decipherable in terms of communicative intent while the former are not. This position is questionable, however, because Chaika had already defined schizophasia so that it represents only the more extreme forms of deviance produced by schizophrenic speakers. It is likely that the most extreme forms of speech irregularities produced by normal speakers, even though extremely rare, could also be fairly incomprehensible. There may, however, be another characteristic of speech irregularities produced by schizophrenics, besides degree of comprehensibility, that sets them apart from the speech irregularities produced by normal speakers. This is illustrated by deviant speech produced by a schizophrenic man (Hoffman/Sledge 1984). In spite of normal intelligence, he repeatedly generated quite distinctive speech errors, for instance: (14) the communists who have a class-struggle creation and a few seconds later: (15) a creation class-struggles. Examples (14) and (15) both reflected difficulties in generating the noun phrase, creation of (a) class-struggle(s). These errors can be understood as a failure to elaborate a particular type of grammatical structure via proper use of closed class words; here the term ‚closed class’ refers to the stable set of ‚grammatical’ words that each language contains. It is well known that normal speakers can drop closed class words yielding nongrammatical results (Butterworth/Howard 1987). What is unusual is that this particular type of speech error was repeated; this suggests that vulnerability to the speech error was sustained over a period of time. — Another example of a ‚sustained’ vulnerability to a certain type of error for this same patient was referred to earlier: (8) That’s why, you know, the fact there was no stigmatism (sic) attached to that clearly explained in the record why you were put back (Hoffman/Sledge 1984, 154).
54. Linguistic Aspects of Language Behavior in Schizophrenia
Taken in context, this segment seems to discuss the consequences of being left back a grade in school. The target intention corresponds to something like the following (bracketed words need to be added to render the segment completely grammatical): (8a) [It] clearly explained in the record why you were put back ... that’s why, you know, there was no [stigma] attached to the fact that I [was]. Besides the erroneous attachment of an affix to stigma, the relationship between (8) and (8a) reflects the exchange and reordering of actual phrases. Of note is that this deviant segment was followed soon after by another: (16) It’s a long term investment, insurance being one of your soundest investments, which now even you that’s what those brings you know retirement policies and things, that’ll pay you X amount of dollars. This segment can be ‚unpacked’ in a fashion very similar to segment (8), namely as exchanges of phrasal segments, thereby yielding the following, quite ordinary and non-bizarre speech intention: (16a) It’s a long term investment, insurance being one of your soundest investments, which even now [will] pay you X amount of dollars, you know that’s what those retirement policies and things bring. — These speech segments suggest that vulnerability to certain types of error, in particular, deficiencies in grammatical phrasing and exchanges in grammatical phrasing, can be sustained over time in schizophrenia (see also Chaika 1977). Slips of the tongue produced by normal speakers generally do not reproduce a particular structural problem within a matter of moments.
2.
Systematic Studies of Naturally Occurring Schizophrenic Speech
2.1. Introduction The above discussion, which primarily derives from case studies and analyses of isolated speech segments, highlights two important challenges that must be met in order to adequately evaluate and understand the nature of speech irregularities in schizophrenia. The first challenge is objectively determining the frequency of speech errors in schizophrenics
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as a group. The case study discussed by Hoffman/Sledge (1984) suggest that an important factor in differentiating normal and schizophrenic speech errors may be density of these errors within a corpus of speech. The second issue is the ‚severity’ of errors. Chaika defines schizophasia as utterances produced by schizophrenics which are relatively undecodable. However it is clear that errors produced by schizophrenics are often decodeable and correspond to relatively ordinary speech intentions. While these may not correspond to examples of traditionally defined schizophasia, in our experience they represent the majority of speech difficulties among schizophrenics. It may, however, be the case that gradations of error ‚severity’ rather than the simple dichotomy of decodeable vs undecodeable — still could shed light on the nature of schizophrenic speech irregularities. 2.2. Systematic Studies Examining Frequency of Errors In a rigorously conducted study, Morice/Ingram (1982 ) examined the speech of 34 schizophrenics, 11 manics, and 18 normal control subjects. Manics are of considerable interest insofar as they represent another psychiatric disorder with severe symptomatology which also can lead to certain speech alterations (cf. art. 52 ). These are many so-called ‚nonspecific factors’ — e. g., preoccupation with bizarre or troubling thoughts, the effects of medication, and abnormal states of arousal — that can distrub the speech integrity of psychiatric patients. It is reasonable to assume that manics as well as schizophrenics respond to many of these same factors, especially when both of these patient groups are studied in an acutely decompensated state. — Approximately 1000 words of free speech for each subject were included in the Morice/Ingram study, which was then carefully transcribed and subjected to linguistic analysis. Schizophrenics were found to score low, relative to manics and normals, on the percentage of well-formed sentences. Replication studies by Morice/McNicol (1986) and Fraser/King/ Thomas/Kendell (1986) found the total instances of speech errors to be considerably higher in schizophrenics than in manics and normals. A challenge not taken up by these studies is the specification of the severity of instances of deviance. The idea that different errors differ in severity has an intuitive appeal, and
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is motivated by examples given above. Compare, once again, examples (6) and (7): (6) He owns a store on Fifth Avenue, and that’s never mentioned because that is his sidek i ck (intended: side-line; Hoffman/ Sledge 1988, 97); (7) fish school in their own communities (Hoffman/Sledge 1988, 97). The problem in example (6) is that side-kick is a slang term that refers to an animate object, and store is decidely not aminate. The second error reflects the inappropriate use of the noun, school, in the verb syntactic slot. The first error seems somehow less ‚pathological’ than the second, though both reflect ‚lexical selection’ difficulties; the challenge is to find a way to operationalize this differentiation. One strategy for capturing this difference is to acknowledge that (6) has only one obvious correction, namely substituting side-line for side-kick. On the other hand, there are multiple alternative strategies for correcting (7). One correction might be (7b) communities of fishes form schools, Which corresponds to a major reworking of the syntax, while a second, though retaining the syntactic form, drops the word, school: (7c) fish swim in their own communities. This reasoning formed the basis for a later study by Hoffman/Sledge (1988) whereby speech errors were classified according to the relative ambiguity of what the target speech intention seemed to be. For the two examples reviewed above, (6) has only one plausible correction that is consistent with the rest of the segment, while (7) has two or more, some requiring alternations of the surface syntax of the sentence. Therefore (7) should be rated to be more severe than (6). — In this study, speech productions of eleven schizophrenics were compared to that of nine patients with psychiatric disorders other than schizophrenia. Both groups of patients had recently been hospitalized and therefore were acutely ill, and were well matched in terms of age, gender and educational level. Two of the responses were randomly selected for careful transcription and analysis of grammatical deviance. Slang and variations due to local dialect were not scored as deviant. All instances of dysfluency (word or phrase repetitions, word or phrase corrections, false starts) were eliminated from the error corpus. The fact that
IV. Pathologies of Language Use in Psychiatric Disorders
our control group consisted in other psychiatric patients controlled in part those ‚nonspecific’ factors tending to produce speech errors, i. e., anxiety, stress, fatigue, etc. Speech analyses were conducted blind to diagnosis. — An important aspect of this study is that deviance was scored in a way to minimize the effects of ideational bizarreness of certain schizophrenic utterances. To illustrate how this was accomplished, consider the following segment (from Hoffman/Sledge 1988): (17) my family’s sociology. One could assume that (17) is a simple lexical selection error, where the expressive intent of the utterance is something along the lines of my family’s social situation. On the other hand, the phrase might be non-deviant if the speaker was referring to a particular set of behavioral rules governing the social interactions of his family. This ideationally offbeat notion could theoretically be within the realm of what the schizophrenic speaker was attempting to communicate. Consequently, our scoring system considered each putative error in all possible contexts, no matter how bizarre. Only instances of apparent deviance that were non-correctable by all contexts remained scored as errors. — After screening for the effects of ideational bizarreness, each remaining instance of grammatical deviance was classified in terms of whether it involved lexical selection or word order, and along the lines just discussed, the ambiguity of corresponding ‚target’ or intention for each instance of deviance was determined in order to assess error severity. — The major finding was, that schizophrenics produced grammatical deviance at a mean rate of .11 instances per clause while nonschizophrenics produced .045 instances per clause, a difference that was statistically significant at the .02 level. In terms of the type of error, there was a roughly equal number of inappropriate or poorly formed open-class words (nouns, verbs, adjectives, adverbs) among the two subject groups. However there was many more errors involving grammatical morphemes (prepositions, conjunctions, suffixes, etc.) among the schizophrenic patients. The following are two typical examples: (18) That was a decent things to do (intended: thing); (19) We could be wheelchairs (intended: we could be in wheelchairs).
54. Linguistic Aspects of Language Behavior in Schizophrenia
Moreover there was a strong trend in the direction of more severe (i. e., ambiguous) syntactic or combinatorial deviance within the schizophrenic corpus, a difference that was statistically significant at the .05 level. Included among this group of errors was a relatively large number of syntactic blends. Here distinct syntactic structures are inappropriately combined. One such instance precipitated a paraphasia whose intended meaning can be guessed at from its context: (20) I guess we went upstate somewhere I don’t know wirth white people (the speaker, who was schizophrenic, was a black woman recounting a childood memory of attending a summer camp away from her native New York City; intended utterance seemed to be a blend of: I guess we went upstate somewhere — don’t know w h e r e/I guess we went upstate somewhere — I don’t know — w i t h white people). These data suggest that schizophrenics are prone to two types of difficulties when combining words into well-formed syntactic structures, the first reflecting difficulties in elaborating a particular syntactic frame (see examples [7] and [9]), and the second reflecting difficulties in selecting one syntactic frame over another (thereby producing syntactic blends as in example [2 0]; for more extensive discussion see Hoffman 1991). The frequency of these linguistic abnormalities in no way approached that of speakers who are classically ‚aphasic.’ Moreover, in practically all cases grammatical deviance was readily traceable to ordinary speech intentions, thereby not belonging to the class of schizophasia as defined by Chaika (1974). Although normal speakers can also produce syntactic errors of various sorts (Butterworth/Howard 1987; Morice/Ingram 1982 ; cf. art. 2 and art. 5), the abnormally high frequency of syntactic errors in the schizophrenic group seems to be a robust quantitative finding. 2.3. Studies of Syntactic Complexity in Schizophrenia The importance of certain syntactic difficulties in schizophrenic speech is reinforced by studies of sentence structure. Analyses of trancribed spontaneously produced discourse by Morice/Ingram (1982 ), Morice/McNicol (1986), and Fraser/King/Thomas/Kendell (1986) have each demonstrated significant
539
diminutions in syntactic complexity in schizophrenics compared to normals. Aspects of syntactic complexity that were relevant to differentiating schizophrenic and non-schizophrenic speakers included reductions in the number and depth of embedded clauses, the percentage of reduced relative clauses, and the precentage of dependent clauses with whpronouns. These findings suggest that the increased frequency of syntactic errors noted in schizophrenics may in fact reflect some impairment in combining words into complex syntactic structures. 2.4. Syntactic difficulties may alter speech performance at other levels Perhaps a subgroup of lexical generation errors produced by schizophrenics also reflect disruptions at the level of syntactic or combinatorial processes. For instance, the context containing example (1) pertained to the educational pursuits of her boyfriend, suggesting that the underlying conversational intention of the speaker was something along the lines of: (1a) He is a person who studies/enjoys the Greek classics (see also discussion in Hoffman/Sledge 1984). It may be that the speaker was unable to elaborate this complex syntactic structure, but instead could only realize the simpler, (1b) He was a (adjective) person. In this case the nominal phrase, Greek classics would have to be pushed into the adjective position, resulting in (1c) He was a (Greek classical) person, which then becomes condensed into a single word: (1) He is a grassical person. In addition, example (2 0) demonstrates how a paraphasia can be induced by a syntactic blend. Thus the generation of certain nonwords by schizophrenics may be triggered by a primary difficulty in elaborating complex syntactic structures. This hypothesized mechanism still requires the postulation of some impairment in self-monitoring of speech that permits the production of words that do not belong to the lexicon. The hypothesis that difficulties in elaborating syntactic structures could reflexively alter language production at other linguistic levels is supported by another study (Hoffman/Hogben/Smith/Calhoun 1985). Twenty-
IV. Pathologies of Language Use in Psychiatric Disorders
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four schizophrenics and 2 4 non-schizophrenics were given the Hunt test (Hunt 1970), a writing task which requires the subject to utilize complex sentential syntax to combine a set of simple propositions into a complex, extended narrative. An analysis of the rewritten paragraphs showed many more meaning errors in the schizophrenic group compared to the non-schizophrenic group. Relevant to the topic of this chapter is that schizophrenics were much more likely to produce meaning errors when the rewritten proposition assumed a more complex syntactic form, i. e., the passive. This finding held up even when the effects of message complexity was controlled for. We suggested that these data were evidence that syntactic processing was somehow more effortful in schizophrenics and the production of complex syntactic forms distracted the speaker from the meaning of his own speech and writing intentions.
3.
Experimental Studies
The hypothesis that schizophrenia is associated with specific language processing defects has led to a range of psycholinguistic, cognitive, and neuropsychological investigations. 3.1. Sensitivity to Syntactic Structure Two studies of psychiatric patients, one by Rochester/Harris/Seeman (1973) and the other by Carpenter (1976), examined the sensitivity to syntactic structure by embedded click paradigms. Schizophrenics tended to mislocate clicks at clausal boundaries to the same degree as normal subjects, suggesting that the ability to utilize syntactic structure to ‚chunk’ linguistic information into clausal units is intact in these patients. In addition, a study by Miller/Phelan (1980) compared the ability of schizophrenics and normal controls to determine the acceptablity of stimulus sentences which, to different degrees, were ungrammatical. No significant differences were found in the schizophrenics’ ability to detect unacceptable syntax. These three studies thus appear to demonstrate that syntactic abilities during language comprehension remain intact in schizophrenia. While these findings are important, they do not rule out the possibility of deficits specifically in language p r o d u ct i o n in schizophrenics.
3.2. Comparing Schizophrenic and Aphasic Language Abilities Two studies have demonstrated that schizophrenics were superior to aphasic patients in terms of language ability. DiSimoni/Darley/ Aronson (1977) administered a standard battery of tests to schizophrenics and compared their performance to previously collected data using aphasic subjects and other patients with ‚organic’ deficits. They concluded that schizophrenic patients did not demonstrate a classic ‚aphasic’ profile, though some impairments were noted in reading comprehension. Patients whose duration of illness was greater showed a general deterioration in performance, but the authors concluded that this pattern of deterioration most closely conformed with patients demonstrating a generalized intellectual impairment. While these findings are of interest, it should be noted that since a normal group of subjects were not included, one cannot conclude that the performance of schizophrenic subjects was actually in the normal range. Partially supporting the findings of the DiSimoni group is a study by Rausch/ Prescott/DeWolfe (1980). In this study, subjects were requested to restore the order of sets of words derived from scrambled sentences. Aphasic patients performed more poorly than schizophrenics; however, it was noted that schizophrenics tended to produce somewhat more errors than normals, especially when sentences contained both direct and indirect objects. In contrast, three systematically conducted studies have highlighted similarities between schizophrenics and aphasics. Kelter/Cohen/ Engel et al. (1977) requested subjects to sort pictures of animals in order to assess the organization of semantic memory. The hierarchical patterns of sorting behavior were most diffuse for fluent aphasics and schizophrenics, and could be differentiated from the greater clarity of sorting behavior among nonfluent aphasics and normals. In a study by Faber/Reichstein (1981), schizophrenics, patients with affective disorder, and normals were administered the Boston Diagnostic Aphasia Examination. Schizophrenics who had ‚formal thought disorder,’ i. e., demonstrated diminished comprehensibility of their spontaneous speech, showed significant abnormalities compared to the other groups, particularly on the Token Test and the Phrase Repetition Test. These findings were interpreted as demonstrating that a subgroup of
54. Linguistic Aspects of Language Behavior in Schizophrenia
patients with the diagnosis of schizophrenia can show language performance deficits in the range of aphasic patients. Further support for this hypothesis was provided by a later study by Faber/Abrams/Taylor et al. (1983). Speech samples of 14 patients with schizophrenia with formal thought disorder were compared with the speech productions of 13 neurologically impaired patients with aphasia. Transcriptions were given to five ‚specialists,’ including a speech pathologist, two neurologists and two psychiatrists, who were requested to identify the diagnosis of the patient. Three of the five specialists performed better than chance but only one (the speech pathologist) achieved high discriminating ability. These findings were interpreted as indicating schizophrenics can share language abnormalities with aphasic patients, but do not exhibit a classic aphasic syndrome. 3.3. Cognitive Deficits vs Language Deficits A wide range of studies have examined diverse parameters of cognitive functioning in schizophrenia, including selective attention, short-term memory, information filtering and context-sensitivity of perceptual processes; a review of this research as it pertains to language abnormalities in schizophrenia can be found in Schwartz (1982 ). Distracting ideas, preoccupation with certain words, or insensitivity to linguistic context could interfere with the speaker’s ability to hold an appropriate syntactic structure in mind while speaking; this could theoretically lead to at least some of the syntactic problems described above for schizophrenics. On the other hand, it seems very hard to account for many of the paraphasias produced by schizophrenics in terms of a general cognitive defect. Certainly some of word finding problems described above could derive from excessive distractibility or impaired ‚filtering’ of candidate elements of the lexicon (see again example (6) and (7)). On the other hand, one is hardpressed to propose a reasonable account, on the basis of general cognitive deficits, for the production of the types of nonwords in examples (1)—(5). With the exception of certain types of anticipation and transposition errors ordinarily produced by normal speakers (see again Garrett 1975; cf. also art. 5 and art. 7), it is hard to imagine how errors in matching phonetic strings to semantic entities and combining morphemes into words could derive from attentional problems or failures in context-sensitivity of cognitive outputs.
541
4.
Conclusions
There is now considerable evidence that schizophrenic persons tend to produce abnormalities of speech corresponding to specific ‚linguistic deviations’ which are independent of the deviant content of what the speaker has in mind to say (see also a review recently published in German by Dittmann/Fehrenbach/Welsh 1989). The incidence of these speech abnormalities exceeds that of other psychiatric patients and probably normal speakers as well; many of these abnormalities, when considered individually, tend to be more ‚pathological’ than those produced by normal speakers or non-schizophrenic psychiatric patients, though nonetheless are relatively decodeable. On the other hand, these abnormalities, in general, are less ‚severe’ in terms of quantity and type when compared to aphasic speakers; they do not represent impaired ‚linguistic competence’ but do reflect episodic disruptions in the ability to produce wellformed speech. Moreover, a small subgroup of schizophrenics can produce very densely paraphasic and/or paragrammatical speech which is as disordered as aphasic speech; it is not clear if the cause of these more severe linguistic difficulties is some sort of organic lesion or is ‚sociolinguistic’ — i. e., an intentional disregard of the conversational maxim to speak clearly by upholding linguistic rules and conventions. On the other hand, it does seem clear that the more decodeable errors produced by schizophrenics represent episodic deficiencies in speech production which are not obviously creative or intentional. Disruptions in cognition not specific to language processes theoretically could account for some of the speech abnormalities produced by schizophrenics but not the more severe types of lexical difficulties. The nature of brain dysfunction underlying these language difficulties is not known. Recent studies by this author and colleagues suggest that schizophrenics suffer from impairments in tranferring information between different cortical areas (Hoffman/Dobscha 1989; Hoffman/Buchsbaum/Escobar et al. 1991). If this applies to language production processes in schizophrenia, then their linguistic difficulties would reflect periodic breakdowns in the exchange of information between relatively intact language modules. We hope to directly test this hypothesis shortly.
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5.
References
Bleuler, J. F. & Perrault, C. R. (1911/1950). Dementia praecox or the group of schizophrenias. A schaffenberg’s Handbuch. International University Press. Butterworth, B. & Howard, D. (1987). Paragrammatisms. Cognition, 26, 1—37. Carpenter, M. D. (1976). Sensitivity to syntactic structure: Good versus poor premorbid schizophrenics. Journal of A bnormal Psychology, 85, 41—50. Chaika, E. A. (1977). Schizophrenic speech, slips of the tongue, and jargonaphasia: A reply to Fromkin and to Lecours and Vanier-Clément. Brain and Language, 4, 464—475. Chaika, E. A. (1974). A linguistic looks at “schizophrenic” language. Brain and Language, 1, 257—276. Coffman, J. A., Andreasen, N. C., & Nasrallah, H. A. (1984). Left hemisphere density deficits in chronic schizophrenia. Biological Psychiatry, 19, 1237—1247. Crow, T. J., Ball, K., Bloom, S. R., Brown, R., Bruton, C. J., Colter, N., Frith, C. D., Johnstone, E. C., Owens, D. G. C., & Roberts, G. W. (1989). Schizophrenia as an anomaly of development of cerebral asymmetry: A postmortem study and proposal concerning the genetic basis of the disease. Archives of General Psychiatry, 46, 1145—50. Dittmann, J., Fehrenbach, R. A., & Welsh, C. (1989). Morphosyntaktische Abweichungen bei Schizophrenie. Ein Überblick über den Stand der Forschung. Neurolinguistik, 2, 145—173. DiSimoni, F. G., Darley, F. L., & Aronson, A. E. (1977). Patterns of dysfunction in schizophrenic patients on an aphasia test battery. Journal of Speech and Hearing Disorders, 41, 498—513. Faber, R. & Reichstein, M. B. (1981). Language dysfunction in schizophrenia. British Journal of Psychiatry, 139, 519—522. Faber, R., Abrams, R., Taylor, M. A., Kasprison, A., Morris, C., & Weisz, R. (1983). Comparison of schizophrenic patients with formal thought disorder and neurologically impaired patients with aphasia. A merican Journal of Psychiatry, 140, 1348—1351. Flor-Henry, P. (1976). Lateralized temporal-limbic dysfunction and psychopathology. A nnals of the New York Academy of Science, 280, 77—797. Fraser, W. I., King, K. M., Thomas, P., & Kendell, R. E. (1986). The diagnosis of schizophrenia by language analysis. British Journal of Psychiatry, 148, 275—278. Fromkin, V. A. (1975). A linguist looks at “A linguist looks at schizophrenic language”. Brain and Language, 2, 498—503. Garrett, M. (1975). The analysis of sentence production. In G. Bower (Ed.), The psychology of
learning and motivation. Vol. 9. 133—177. New York: Academic Pres. Hoffman, R. E. (1986). Verbal hallucinations and language production processes in schizophrenia. Behavioral and Brain Sciences, 9, 503—548. Hoffman, R. E. (1991). The microgenesis of schizophrenic symptoms. In Hanlon, R. (Ed.), Microgenetic approaches to cognition: A neuropsychological perspective. 133—149. Hillsdale: Lawrence Erlbaum Associates. Hoffman, R. E., Buchsbaum, M. S., Escobar, M. D., Makuch, R. W., Nuechterlein, K. H., & Guich, S. M. (1991). EEG coherence of prefrontal areas in normal and schizophrenic males during perceptual activation. Journal of Neuropsychiatry and Clinical Neurosciences, 3, 169—175. Hoffman, R. E. & Dobscha, S. (1989). Cortical pruning and the development of schizophrenia: A computer model. Schizophrenia Bulletin, 15, 477—490. Hoffman, R. E., Hogben, G. L., Smith, H., & Calhoun, W. F. (1985). Message disruptions during syntactic processing in schizophrenia. Journal of Communication Disorders, 18, 183—202. Hoffman, R. E., Kirstein, L., Stopek, S., Cicchetti D. V. (1982 ). Apprehending schizophrenic discourse: A structural analysis of the listener’s task. Brain and Language, 15, 207—233. Hoffman, R. E. & Sledge, W. (1984). A microgenetic model of paragrammatisms produced by a schizophenic speaker. Brain and Language, 21, 147—173. Hoffman, R. E. & Sledge, W. (1988). An analysis of grammatical deviance occurring in spontaneous schizophrenic speech. Journal of Neurolinguistics, 3, 89—101. Hunt, K. W. (1970). Syntactic maturity in schoolchildren and adults. Monographs of the Society for Research in Child Development, 35, 2—67. Kelter, S., Cohen, R., Engel, D., List, G., & Strohner, H. (1977). The conceptual structure of aphasic and schizophrenic patients in a nonverbal sorting task. Journal of Psycholinguistic Research, 6, 279—303. Kirov, K. (1985). Long-term study of schizophasic patients. Psychopathology, 18, 226—229. Laffal, J. (1965). Pathological and normal language. New York: Atherton. Lecours, A. R. & Vanier-Clément, M. V. (1976). Schizophrenia and jargonaphasia: comparative description with comments on Chaika’s and Fromkin’s respective looks at “schizophrenic” language. Brain and Language, 3, 516—565. Lorenz, M. (1961). Problems posed by schizophrenic language. A rchives of General Psychiatry, 4, 603—610. Maher, B. A. (1966). Principles of psychopathology. New York: McGraw-Hill.
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Miller, W. K. & Phelan, J. G. (1980). Comparison of adult schizophrenics with matched normal native speakers of English as to “acceptability” of English sentences. Journal of Psycholinguistic Research, 9, 579—592. Morice, R. D. & Ingram, J. C. (1982 ). Language analysis in schizophrenia: Diagnostic implications. A ustralian and New Zealand Journal of Psychiatry, 16, 11—21. Morice, R. D. & McNicol, D. (1986). Language changes in schizophrenia: A limited replication. Schizophrenia Bulletin, 12, 239—251. Morstyn, R., Duffy, F. H., & McCarley, R. W., (1983). Altered P300 Topography in schizophrenic. Archives of General Psychiatry, 40, 729—734.
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Rausch, M. A., Prescott, T. E., & DeWolfe, A. S. (1980). Schizophrenic and aphasic language: Discriminable or not? Journal of Consulting and Clinical Psychology, 48, 63—70. Rochester, S. R., Harris, J., & Seeman, M. V. (1973). Sentence processing in schizophrenic listeners. Journal of Abnormal Psychology, 82, 350—356. Schwartz, S. (1982 ). Is there a schizophrenic language? The Behavioral and Brain Sciences, 5, 579—626. Vetter, H. (Ed.) (1968). Language behavior in schizophrenia. Springfield, Illinois: Thomas.
Ralph E. Hoffman, New Haven, Connecticut (USA)
55. Glossomania and Glossolalia in Schizophasia and their Linguistic Kinships to the Jargonaphasias 1. 2. 3. 4.
1.
Schizophrenic Speech Schizophasia Schizophrenic Speech, Schizophasia, and Jargonaphasia References
Schizophrenic Speech
In 1911, Eugen Bleuler combined the greek word for “split”, “schizo”, with the greek word for “mind”, “phrenia”, (also in “phrenology”). He needed this expression to refer to a form of d e m e n t i a, a dreadful disorder of t h o u g h t which first manifests itself relatively early in life (‘ d e m e n t i a p r a e c ox’). Bleuler originally used the plural form of his new term. But, as the basic clinical manifestations of his “schizophrenias” were observed to remain constant irrespective of epochs and societies (Cancro 1983), and as evidence suggesting an organic substratum was repeatedly found (Weiner 1983), schizophrenia has come to be perceived as a single nosological entity. If only because of its ‘hallucinatory’ dimension, the mental status of schizophrenics causes repercussions throughout their behavior, overt speech included. Insofar as particular speech manners are thus inherent to schizophrenia, the notion of ‘schizophrenic speech’ is pertinent from the phenomenological point of view. As a matter of fact, clinicians do agree that episodes of unconventional speech-behavior represent an easily recognized sign of schizophrenia. Nonetheless,
the linguistic characterization of schizophrenic speech remains imprecise; it has not yet been the object of explicit interpretations by psycholinguistic theories of cognition. Thus, although seemingly straight forward, diagnosing schizophrenia based on speech behavior continues to depend on largely overlapping, anecdotal, impressionistic clinical parsing. The unclarity as to exactly what makes up schizophrenic speech is reflected in the myriad of terms used to describe it: ‘poverty of speech’ (‘laconic speech’), ‘poverty of content of speech’ (‘poverty of thought’, ‘empty speech’, ‘alogia’, ‘verbigeration’, ‘negative formal thought’), ‘pressure of speech’, ‘distractible speech’, ‘tangentiality’, ‘derailment’ (‘loose associations’, ‘paralogia’, ‘flight of ideas’), ‘incoherence’ (‘word salad’), ‘illogicality’, ‘clanging’, ‘neologisms’, ‘word approximations’ (‘metonyms’), ‘circumstantiality’, ‘loss of goal’, ‘perseveration’, ‘echolalia’, ‘blocking’, ‘stilted speech’, ‘self-reference’ (Andreasen 1979 a). Not unexpectedly given the richness and diversity of the above lexicon, the single nosological entity known as schizophrenia is said to encompass “18 subtypes of thought disorders” (Andreasen 1979 b, 132 8). According to Andreasen (1979 a), the epitome of one of these subtypes, “poverty of content of speech”, is the following quotation (1). (1): “Many of the problems that I have ... are difficult for me to handle or to work on because I am not aware of them as problems which upset me
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personally. I have to get my feelers way out to see how it is ... I am, I think, becoming more aware that perhaps, on an analogy, the matter of some who understand or enjoy loud rages of anger ... The same thing can be true for other people and I have to kind of try to learn to see when that is true and what I can do about it.”
From a clinical point of view, this type of behavior might be compared to that of braindamaged subjects with Einfallsleere “lack of ideas” (Bay 1964); that is, with the particular form of verbal jargon occasionally observed — as illustrated in (2 ) — in patients with transcortical sensory aphasia (Lecours/Osborn/Travis et al. 1981). (2 ): “C’est assez compliqué, hein. ... Ça devient assez compliqué de ... de tirer ça ... J’arrive à faire que le total arrive à faire un certain bien ... et qu’on arrive à arriver à ... à avoir des ... des marchandises.” [It is quite complicated, eh. ... It becomes quite complicated to ... to draw that. ... I manage to do that the total manages to do something good ... and that we manage to manage to ... to have some ... some merchandises.]
2.
Schizophasia
According to Porot (1975), Kraepelin coined the term ‘schizophasia’ at the turn of this century, to denote episodes of deviant speech behavior coexisting with conventional speech abilities. Furthermore, to the best of my knowledge, no convincing documents exist that might lead one to understand ‘schizophasia’ as being a synonym for ‘schizophrenic speech’. On the contrary, cautiousness would rather lead one to consider schizophasia as specifying at least two forms of unconventional speech behavior, ‘glossomanic schizophasia’ and ‘glossolalic schizophasia’, which can be observed in certain psychotic subjects. Both can be utterly spectacular but nowadays neither can be said to represent a frequently observed clinical phenomenon (perhaps as the result of the addition of potent drugs to our current ‘therapeutic’ arsenal). In g l o s s o m a n i c s ch i z o p h a s i a the linguistic components of utterances — whether phonemes, words or more complex units — are selected and combined on the basis of phonological or semantic kinships rather than by docile compliance to a given topic. In contrast, g l o s s o l a l i c s ch i z o p h a s i a can be defined as entirely or nearly entirely neologistic discourse-like speech.
2.1. Glossomanic Schizophasia Glossomanic speech can be fluent and abundant. Like Wernicke’s jargonaphasia, it can require only minimal participation from the interlocutor. Some first perceive its most striking characteristics to be at the level of word-like entities, although its essence, as I have just indicated, is probably best isolated at sentence level. In the present context, wordlike entities will be referred to as ‘neologisms’ (Lecours 1982 a) and discussed under three subheadings, ‘derived morphemic deviations’, ‘composed morphemic deviations’, and ‘abstruse neologisms’. Attempts at a characterization of aberrations at the sentence level will be made under three further subheadings, ‘full glossomaniac utterances’, ‘antonymic doublets’, and ‘virtuosity’. 2.1.1. Derived Morphemic Deviations In this (morphologically constrained) type of glossomaniac production, the monolingual speaker associates legitimate roots and bound morphemes in line with the word derivation rules inherent to his or her native language, therefore creating, as in (3) to (6), neologisms with an obvious semic potential. (Except for (17), (2 5) and (2 6), all of the examples of glossomanic schizophasia quoted in this chapter were produced by the same psychotic subject in the course of a long interview made in Lausanne by Professor Gil Assal (Lecours/ Nevert/Ross 1981).) (3): prefix + ‘page’ [page-boy] + suffix ⇒ “apagé” [one who is being made a page-boy], idem ⇒ “apageant” [one who makes someone else a page-boy], idem ⇒ “apagement” [the fact of being made a page-boy]; (4): prefix + ‘capitale [capital city] ⇒ “acapitale” [without a capital city]; (5): ‘douane’ [custom] + suffix ⇒ “douanerie” [custom system]; (6): ‘logarithme’ [logarithm] + suffix ⇒ “logarithmie” [logarithmic system].
Interestingly, one patient with Wernicke’s jargonaphasia has been reported to produce — as illustrated in (7) — numerous deviations of this type (Lecours/Lhermitte 1972 ), although his lexical root selections were far more limited and the semic potential of his neologisms far less transparent than in the case quoted above. (7): Root(s) + suffix(es) ⇒ “C’est pas le /fɔrs-jal/ habituel. ... Je ne suis pas des /burs-jεl/ personnels. ... les /prɔm-yr/ que j’ai promus. ... Mon /sɔld-aʒ/ s’emploie différemment.” [it is not the usual /fɔrs-
55. Glossomania and Glossolalia in Schizophasiaand their Linguistic Kinships to the Jargonaphasias
jal/. ... I am not from the personal /burs-jεl/. ... the /prɔm-yr/ whom I promoted. My /sɔld-aʒ/ is to be employed differently.]
2.1.2. Composed Morphemic Deviations In addition to combining morphemes in an unconventional way, the glossomanic speaker might also associate at least two legitimate open-class words in line with the word composition rules inherent to his or her language. In this way the speaker creates, as in (8) to (11), a second form of neologism with an obvious but usually perplexing semic potential: (8): ‘quart’ [quarter] + ‘cinquième’ (fifth] ⇒ “quartcinquième” [quarter-fifth]; (9): ‘été’ [summer] + ‘hiver’ [winter] ⇒ “été-hiver” [summer-winter]; (10): ‘jour’ [day] + ‘nuit’ [night] ⇒ “jour-nuit” [daynight]; (11): ‘ouvre’ [open] + ‘ferme’ [close] ⇒ “ouvreferme” [open-close].
To the best of my knowledge, this type of behavior is not congruent with the clinical picture of any type of jargonaphasia. It should be emphasized, however, that replacement of a word by a potential antonym is a form of ‘semantic paraphasia’ often observed in Wernicke’s jargonaphasia. 2.1.3. Abstruse Neologisms Whereas both derived and composed morphemic deviations have a recognizable semic potential, abstruse neologisms, phonologically constrained word-like entities, have no semic potential other than that which may perhaps be gleaned from the context. As (12 ) and (13) demonstrate, the abstruse neologisms of schizophasic glossomania can take part of their phonological components from previous utterances in the immediate context, and they can comprise morpheme-like components, especially affixes. These two features are also characteristic of the neologistic productions of a number of brain-damaged patients with Wernicke’s jargonaphasia (Lecours/Osborn/Travis et al. 1981; cf. art. 16). (12 ): “Je fais mon classement des ‘soudocheries’ (/sudɔʃri/) d’où je viens ... C’est pestilentiel, vous savez, cette soude (/sud/) ... du duché (/dyʃe/) ou de communale ...” [I make my classification of the /sudɔʃri/ from where I come ... It stinks, you know, this bicarbonate ... of the dukedom or commune ...] (13): “... en perdant la maîtrise de sa classification, en allant dire des grossièretés. ... C’est une espèce de maladie, de ‘grossiomige’ (/grosjomiʒ/)”. [... by
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loosing the mastery of one’s classification, by being gross in speech. ... It is a kind of disease, of / grosjomiʒ/.]
An essential difference between the abstruse neologisms of schizophasic glossomanics as opposed to those of Wernicke’s jargonaphasics is that the former — but never the latter — will, as in (14) [where the speaker answers a question about the meaning of /grosjomiʒ/ (13)], are in no way anosognosic with regard to such utterances and will discuss and justify them if requested to do so. [This is in line with Bleuler’s (1966) teachings about the neologisms of psychotics although it contradicts Chaika’s (1974) assumptions.] (14): [Concerning /grosjomiʒ/:] “Oui, C’est une espèce de bête. Voilà! C’est un terme que j’ai créé, que j’ai fait, comme ça pour ... pour donner une petite base personelle, privée. Voilà!” [Yes, it is a kind of beast. That’s it! It is a term which I have coined, which I have created, just like that, in order to ... to provide a small personal, private basis. That’s it!]
2.1.4. Full Glossomanic Utterances As mentioned above, glossomanic characteristics can be observed not only at the phonological and lexical level, but also at the sentence level. Glossomanic schizophasia owes its name to a form of utterance that is apparently generated along more playful though rule-governed lines. As indicated above, such rules require sentence production to be guided, according to conventional syntactic constraints, by (paradigmatic) phonological similarities and/or potential semic kinships between individual words and word-like neologistic entities rather than by an intention to formulate an immediately sharable phrastic message. The ‘game’, which is not unlike one of Andreasen’s (1979 a) “18” subtypes of thought disorders [i. e., “clanging”,], can be mostly phonological, as in (15) and (16), or mostly semantic, as in (17) [quoted from Chaika (1974)], but it usually is both, as in (18): (15): “C’est comme ça que les vieux faisaient les fondations. Ou bien de cause (/koz/) : un /kozam/, un /klozam/, /glozan/. Vous comprenez? Et, à ce casier, on a un savoir de Lausanne (/lozan/).” [It is this way that the ancients built foundations. Or else of cause: a /kozam/, a /klozam/, /glozan/. You understand? And, in this bin, one has a knowledge from Lausanne]; (16): “Et alors, il y a des joues (/ʒu/), jours (/ʒur/), des j’ouvre (/ʒuvr/)-ferme qui sont ...” [And then, there are some cheeks, days, some ’ I open-close which are ...];
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(17): “My mother’s name was Bill ... and coo? St. Valentine’s Day is the official startin’ of the breedin’ season of the birds. All buzzards can coo. I like to see it pronounced buzzards rightly. They work hard. So do parakeets”; (18): “Mais oui, à cette organisation de travail, il y a donc des plans d’heures et un calendrier du plan de secondes, de minutes, d’heures, d’horlogerie et d’orâge. Vous appelez ça des heures-âges, d’où des tonnes-âges qui, de l’âge du début d’un certain âge, par rapport au calendrier ...” [Yes indeed, to this organization of work, there are thus draughts of hours and a calendar of the draught of seconds, of minutes, of hours, of clock-making and of gold-age. You call that hour-ages, hence ton-ages which, from the age of the beginning of a certain age, by reference to the calendar...]
In exceptional cases, certain brain-damaged subjects with transcortical sensory aphasia occasionally produce, as in (19), sentences that would qualify as semantic glossomania. Likewise, as in (2 0), subjects with Wernicke’s jargonaphasia may produce, within a same context, sequences of formally related abstruse neologisms. When viewed out of context, such neologisms are somehow remindful of phonological glossomania (Lecours/Vanier 1976). (19): “... on s’est aperçu que, partout ailleurs, ils ont mis des petits colporteurs — literally: ‘collar bearer’ — et ils ont pu, avec un veston ... avec un manteau colporté ...” [... we realized that, everywhere else, they posted little peddlars and they were capable, with a jacket ... with a peddled mantle ...] (2 0): “... ces gens qui étaient à la /kɔmi/ ... au ... au /glasrɔ/ ... au /kɔmorɔ/ ... /kɔrokomuit/ ...” [... those people who were at the /kɔmi/ ... at the ... at the /glasɔ/ ... at the /kɔmorɔ/ ... at the /kɔrokɔmuit/ ...]
2.1.5. Antonymic Doublets The extreme and therefore ‘pathognomic’ (although probably not qualitatively different) form of ‘full glossomanic utterance’ on the sentence level, which cannot be grouped among any type of jargonaphasia resulting from focal brain damage, is the one simultaneously expressing a given notion and its opposite. This kind of utterance can be based on pairs of words, of phrases, or of more complex speech entities. The simplest way of creating an antonymy is by blending part of the phonemic components of two words with potentially opposite meanings [such as ‘smig’ for ‘small + big’ (fictious example)]. Two blends of this sort, which have the advantage of illustrating the fact that schizophasics will occasionally challenge phonological legality, a type of behavior so deliberate that it prob-
IV. Pathologies of Language Use in Psychiatric Disorders
ably is incompatible with the very notion of aphasia are quoted in (2 1) below. Another way of building an antonymic doublet would be to attach antonymic affixes to the same root [as in ‘unuseful’ (fictious example)]. As in (9) to (11) above, as well as in the first part of (2 1) below, such ‘self-contradicting’ neologisms can also be created through composition, or else, as in (2 2 ) to (2 5), through more complex syntagmatic procedures, i. e., by incorporating antonymic words or phrases to the context of a same sentence: (2 1). ‘froid’ + ‘chaud’ ⇒ “froid-chaud” /frwa-ʃo/ ⇒ “/fʃowa/” ⇒ “/frʃowa/”: “De froid-chaud ou de chaud-froid. De /fʃowa/. Ils ... Ils parlaient comme ça, les anciens. Ils disaient: Un /frʃowa/”. [Of coldhot or of hot-cold. Of ‘chotld’.They ... They talked like that, the ancients. (This assertion is strikingly in line with Freud’s (1910) astonishing beliefs about the origins of language.) They said: a ‘cohotld’.] (2 2 ): “Et alors, je commence la première classification: ça me fait un homme sain et un homme fou.” [And then, I begin the first classification: this makes me a healthy man and a crazy man.] (2 3): “Lorsqu’on fait un siècle, il y a toujours un début et une fin ... Toujours, le premier jour du siècle correspond au dernier jour de la fin du siècle ... Le vrai calendrier est différent du faux.” [When one makes a century, there is always a beginning and there is an end ... Always, the first day of the century corresponds to the last day of the end of the century ... The true calendar is different from the false one.] (2 4): “Un bureau ambulant, un cadavre vivant ... où de la terre glaise a formé, de dessus aux bases classificatrices de dessous...” [A walking desk, a living cadaver ... where clay has formed, from above to the classificatory bases of under ...] (2 5): “Je voudrais bien avoir de nouveau un bon nombre d’années pour me retrouver dans l’âge de la jeunesse.” [I really wish I could be a great deal older anew so that I might find myself again in the age of youth.] (From Schmidt/Perrot (1976)).
2.1.6. Virtuosity Schizophasic speakers do not only combine opposing units of speech to form antonymic doublets, they will occasionally combine entire phrases and use them like single nouns, [for instance, see “des j’ouvre-ferme” (16)]. Indeed, production of this sort — which should obviously be considered syntactic virtuosity rather than dyssyntaxia — can, as illustrated in (2 6; the only example of ‘ s ch iz o g r a p h i a’ quoted in this chapter), become quite spectacular in cases such as the one reported by Levy-Valensi/Migault/Lacan (1931). Probably the most staggering glossomanic utterances are those in which — as in (2 7), (IPA transcriptions are provided in
55. Glossomania and Glossolalia in Schizophasiaand their Linguistic Kinships to the Jargonaphasias
Figure 55.1) — cascades of words and wordlike entities stemming from a few paradigmatically associated roots are attached to antonymic affixes until nearly all possible combinations have been exploited within a single set of consecutive sentences (Figure 55.1). (2 6): “Je fais de l’âme est lasse à toujours vous servir. ... Si vous voulez faire le tant l’aire est belle qu’il la faut majorer de faits, c’est que vous êtes ... ... faire un beau maitrisez-moi.” [I make some the-soul-isweary because I always serve you. ... If you wish to make the so-beautiful-is-the-area-that-one-has-toraise- it-up-with-facts, it is because you are ... ... to make a beautiful subdue-me.] (2 7): “Pour prendre une pierre, ils l’appelèrent une ‘pierre’ ... la lever et la poser: ils dépierrent à repierrer, n’est-ce-pas? C’est juste: et on les appela dépierra-repierra. On les appela les roches de la roche, de définition. Et ils arrochent des roches. Vous comprenez? Et les deux pierres à deux roches, ça devient des procha. A classement de ... de généralité — n’est-ce pas? — transpositif de pierra es à rocha. Rocha est à ... est à deux pierra mais, à la synthèse des deux, c’est un procha de pierra ou de rocha.” [To take a stone, they named it ‘stone’ ... to lift it up and to put it down: they unstone to restone, don’t they?. It is adequate: and they were named unstoned-restoned. They were named the rocks of the rock, by definition. And they arock some rocks. You understand? And the two stones to two rocks, they become strocka. In a classification of ... of generality, right, transpositive of stona is to rocka. Rocka is to ... is to two stona but, at the synthesis of the two, it is a strocka of stona or of rocka.]
Figure 55.1 Clearly, the glossomanic schizophasic is one who should be taken at his or her word (rather than sentence). Although paradigmatic and syntagmatic constraints are respected throughout his or her enigmatic discourse, when they are not exaggerated, they somehow undermine their supposed intention, namely conventional sharing of ideas. Indeed, one retains the impression that glossomaniac behavior sometimes qualify as a
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variety of ‘hyperphasia’. 2.2. Glossolalic Schizophasia Just as some of the few who are believed to be episodically possessed by a devil, as well as otherwise healthy Pentecostal believers merely under the week-end influence of the Holy Ghost (Samarin 1972 ), certain psychotics will, on occasion, spew endless neologistic utterances (Cénac 192 5). Bobon (1947), reported that such patients may resort to several different ‘tongues’. This was the case of the psychotic subject whose ‘English temperament’ is quoted in (28). (2 8) “/azumba bεRgεs koRo bRubjεR paRa bRazja mnεRges keRɔkoRo bRubjεR mizœ pRiz aRakaska RœkaRœ bRazjε mnεRgεs keRakɔRo. ... azaRa kuRu bRubjεr paRa bRasja minεRgεs keRœkuRu bRubjεR mizœ pRiz aRakaska RœkaRœ bRasja minεRgεs kaRœkuRu bRubjεR mizœ pRiz aRakaska RakaRa bRazja minεRgεs kεRokoRu bRubjεR mesi./” Glossolalic schizophasia occurs in the form of asemantic although prosodically invested perseverative monologues in which (a) the tonic accent of the speaker’s mother tongue can be replaced by another and (b) the speaker’s regional accent can be attenuated. In the productions of the monolingual glossolalist, phonemes are those of the mother tongue but their relative frequency is grossly modified. The overall impression is that of a phonologically, lexically, and syntactically impoverished ‘foreign’ language (Lecours 1982 b). Although such speech is very uncommon and thus far has been observed exclusively in polyglot elderlies (Lecours/Osborn/Travis et al. 1981; Perecman/Brown 1981), glossolalia can, as illustrated in (2 9), occur as a form of Wernicke’s jargonaphasia. Both glossalic schizophasia and glossalic aphasia are not far from the segmental point of view but they differ in that the latter represents residual behavior, takes the form of a dialogue with an interlocutor and, to some extent, retains conversational prosody, whereas the glossolalia of schizophrenic subjects occurs episodically (that is, it coexists with a capacity for conventional speech production), takes the form of monologues, and assumes one form or another of stereotyped prosody (Lecours, 1982 b). (2 9) “/s dikte di tR dRikdedeRe digœRe dis tis tilavε kloRe œ le dø tRke ditibε dœRe disœ te kotegoRe dil kdeteRe. ... a wi dœ vilεbRiʃ ʒe la lãbεtɔRi de dεl lãtetεRœme di katedɔRe e œ e εlzekute εlmœpurimakte tã tutse dœgRedœgRε dis gy lateRe digeloteRe./”
IV. Pathologies of Language Use in Psychiatric Disorders
548
3.
Schizophrenic Speech,
Schizophasia, and Jargonaphasia As demonstrated above, schizophasia can have certain linguistic features in common with one form or another of fluent aphasia. However, whereas evidence of malfunction of at least one of the mechanisms of language production is always manifest in the former, it is evidence of exalted function, for instance, exaggerated but accurate use of word derivation or normalization rules, that one observes in the latter (Lecours/Vanier 1976). Whether or not schizophasia should be considered as a manifestation of schizophasia or of another form of psychosis remains an open question. At any rate, schizophasics, glossomanics in particular, can give proof of such mastery of rule-governed language that one can hardly conceive of their behavior as being a manifestation of focal brain damage involving the speech area [as suggested by Chaika (1974)]. On the other hand, I see no reason to exclude the possibility that a more subtle organic dysfunction, as in certain types of intoxication, might influence brain activities in a manner such that certain linguistic constraints are magnified to the detriment of the natural outcome of human language abilities, that is, conventional communication. As a matter of fact, the main difference between spectacular schizophasia and certain forms of literary creation (cf. art. 8) is that the former appears to be exclusively founded on formal and/or semic kinships between words and/or word-like entities, whereas the latter is both founded on such kinships a n d topic-guided (sharable). Author’s note: The author’s research is funded by the “Conseil de la recherche médicale du Canada” and by the “Fonds de la recherche en santé du Québec”.
4.
References
Andreasen, N. J. C. (1979 a). Thought, language and communication disorders: I. Clinical assessment, definition of terms, and evaluation of their reliability. A rchives of General Psychiatry, 36, 1315—1321. Andreasen, N. J. C. (1979 b). Thought, language and communication disorders: II. Diagnostic significance. A rchives of General Psychiatry, 36, 1325—1330. Bay, E. (1964). Principles of classification and their influence on our concepts of aphasia. In A.V.S. de Reuck & M. O’Connor (Eds.), Disorders of Language. 122—142. London: Churchill.
Bleuler, E. (1966; translation from the 1911 German edition). Dementia Praecox or the Group of Schizophrenias. New York: International Universities Press. Bobon, J. (1947). Trois langues artificielles d’origine ludique chez un paraphrénique hypomaniaque. Journal belge de neurologie, 47, 327—395. Cancro, R. (1983). History and overview of schizophrenia. In H. I. Kaplan & B. J. Sadock (Eds.), Comprehensive Textbook of Psychiatry (Volume I). 631—643. Baltimore: Williams & Wilkins. Cénac, M. (192 5). De certains langages créés par les aliénés: Contribution à l’étude des glossolalies. Thèse de doctorat (Médecine), Paris: Université de Paris. Chaika, E. O. (1974). A linguistic looks at schizophrenic language. Brain and Language, 1, 257— 276. Freud, S. (1910; 1964 translation). The antithetical meaning of primal words. In J. Strachey (Ed.), The Standard Edition of the Complete Psychological Works of Sigmund Freud, Volume XI. 155—161. London: Hogarth. Lecours, A. R. (1982 a). On neologisms. In J. Mehler, E. C. T. Walker, & M. Garrett (Eds.), Perspectives on Mental Representations. 217—247. Hillsdale: Erlbaum. Lecours, A. R. (1982 b). Simulation of speech production without a computer. In M. Arbib, J. Marshall, & D. Caplan (Eds.), Neural Models of Language Processes. 345—367. New York: Academic Press. Lecours, A. R. & Lhermitte, F. (1972 ). Recherches sur le langage des aphasiques: Analyse d’un corpus de néologismes (notion de paraphasie monémique). L’encéphale, 61, 295—315. Lecours, A. R., Nevert, M., & Ross, A. (1981). Langage et pensée du schizophase. Confrontations psychiatriques, 19, 109—144. Lecours, A. R., Osborn, E., Travis, L., Rouillon, F., & Lavallée-Huynh, G. (1981). Jargons. In J. Brown (Ed.), Jargonaphasia. 9—38. New York: Academic Press. Lecours, A. R. & Vanier, M. (1976). Schizophasia and jargonaphasia: A comparative description with comments on Chaika’s and Fromkin’s respective looks at schizophrenic language. Brain and Language, 3, 516—565. Levy-Valensi, J., Migault, P., & Lacan, J. (1931). Ecrits inspirés: schizographie. A nnales médico-psychologiques, 89, 1—26. Perecman, E. & Brown, J. (1981). Phonemic jargon. A case report. In J. W. Brown (Ed.), Jargonaphasia. 177—257. New York: Academic Press. Porot, A. (1975). Manuel alphabétique de psychiatrie. Paris: Presses Universitaires de France.
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Samarin, W. J. (1972 ). Tongues of Men and A ngels. New York: MacMillan. Schmidt, P. & Perrot, M. (1976). A propos d’observation de troubles du langage dans la schizophrénie. A nnales médico-psychologiques, 134, 708—714.
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Weiner, H. (1983). Schizophrenia: Etiology. In H. I. Kaplan & B. J. Sadock (Eds.), Comprehensive Textbook of Psychiatry (Volume I). 650—680. Baltimore: William & Wilkins.
André Roch Lecours, Montréal, Québec (Canada)
56. Communicative Behavior in Schizophrenia 1. 2. 3. 4. 5.
1.
Introduction Description of Deviances Conditions of the Occurrence of Deviances Summary References
Introduction
In analyses of schizophrenic speech, different concepts of ‘communication’ are often used. The target of this article are approaches which view communication as an actual communicative exchange aimed at achieving mutual understanding. There is general consent that at least with some schizophrenics the actual communicative exchange is at times difficult (Rühmke 1941; Wyrsch 1946), and that the cause of this ‘mis-communications’ must be examined. In tackling the problem the majority of investigations focuses on the schizophrenic’s contribution to communication. That is, difficulties of communicative exchange are construed as being generated either by the schizophrenic’s difficulty to produce understandable utterances or by his/her difficulty to correctly understand the adequate utterances of his/her healthy partners. It is assumed that the difficulty in understanding schizophrenic utterances is brought about by inherent features of content (Faria/Figueira 1989; Rosenberg/Tucker 1979) and/or form (van Belle 1987; Chaika 1982 ; Cohen 1978; Cohen/Camhi 1976; Cohen/Nachmani/ Rosenberg 1974; De Decker/Van Campe 1989; Hoffman/Kirstein/Stopek/Cicchetti 198 2 ; Penn 1987; Rochester/Martin/Thurstone 1977). Conversely, a schizophrenic recipient’s difficulty in understanding his/her partner is based on the schizophrenic’s deficient speech perception (Lawson/McGhie/ Chapman 1964). In contrast, very few investigations focus on components of the communicative exchange itself, nor do they conceive of difficulties as at least dyadic problems
of mutual understanding (Blakar 1984; van de Craen 1989). — Obviously, one must first pinpoint the key constituents of successful communication before one can locate the source of miscommunication in schizophrenic discourse and/or actual communicative exchange. With regard to the investigations under review successful communication on the one hand is narrowly conceived of as a contextfree understanding and of making oneself understood as a product of an individual achievement, and, on the other hand a conception of a mutually satisfactory process of interpretation which is determined by communicative intentions relevant to the given situation (Dittmann 1991; Fischer 1987; Leodolter 1975; Wróbel 1990, 2 1 ff). In the following an attempt is made to show with regard to each of these perspectives (a) how the basic communicative difficulties are described as specific deviances, and (b) what is known about the conditions under which they occur in which type of (schizophrenic) person.
2.
Description of Deviances
2.1. Difficulties in Speech Production In an empirical approach (Rutter 1979) raters’ achievements in reconstructing the original discourse structure from a randomized set of clauses are quantified. Performance which is based on intuitions about language rather than on explicitly defined features of utterances is worse when raters are confronted with clauses from a schizophrenic’s (vs a healthy person’s) text. — In other approaches the analyses are based on explicitly described linguistic (Faria/Figueira 1989; Harvey 1983; Jones 1977; Rochester/Martin/Thurstone 1977; Schmidt-Knaebel 1983; Tress/Pfaffenberger/Frommer 1984; Wróbel 1990), specifically pragmatic (van Belle 1987; De Decker/ van Campe, 1989), and logical (Hoffman/Kir-
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stein/Stopek/Chicchetti 1982 ; Lincourt 1981; Nöth 1976; Werner/Levis-Matichek/Litowitz 1975) devices for the construction of meaning in discourse. Forms of deviation are determined against these types of backgrounds. — Qualitative and quantitative aspects of the well-defined devices of cohesion and reference (Halliday/Hasan 1976) are determined by trained analysts. These aspects lead to the finding that compared to healthy persons schizophrenics, especially those with a thought-disorder (TD) produce discourse which is characterized by cohesive weakness and unclear reference (Rochester/Martin/ Thurstone 1977; Rochester/Martin 1979). Relations between propositions (Hoffman/Kirstein/Stopek et. al. 1982 ), and of semantic recurrence between units (e. g. paragraph, theme, topic) which hierarchically structure a text (Nöth 1976) are modelled in a global fashion by determining an individual degree of acceptability (Nöth 1976) or a score of deviation (Hoffman/Kirstein/Stopek et al. 1982 ). The findings that schizophrenics’ scores of deviation systematically differ from the scores of non-schizophrenic psychotics (Hoffman/Kirstein/Stopek/Cicchetti 2 198 ) and of manics (Hoffman/Stopek/Andreasen 1986) have to be judged against critical evaluations of the algorithm of description (Beveridge/Brown 1985; Käsermann 1989). The approaches mentioned so far describe aspects of the understandability of schizophrenics’ discourses originating from an actual dialogue (usually a partially-structured interview with a staff member). It is noteworthy, however, that the descriptions do not encompass the healthy partner’s actual achievement in understanding his/her schizophrenic interlocutor. — In experimental investigations of the specifically referential communication (Cohen 1978; Cohen/Camhi 1976; Cohen/ Nachmani/Rosenberg 1974) a (schizophrenic) speaker is instructed to produce a clue which allows a hearer to identify the referent (one of the objects or words, usually synonyms, of a pair of stimuli). Comprehension is defined as proportion of a hearer’s correct selections of the intended referent and is usually determined outside of an actual situation of communication. Compared to healthy persons schizophrenics show a reduced performance as communicators but not as recipients. The significance of this paradigm with regard to an understanding of schizophrenia is disputed (Neale/Oltmanns/Harvey 1985). — The given approaches describe the understandability of
IV. Pathologies of Language Use in Psychiatric Disorders
schizophrenics’ discourse with regard to its objective informational effectiveness. An alternative view is the conception of verbal oddities as having the function of metacommunicative commentaries about the actual communicative situation (von Block 1979; Dieckmann/Dittmann 1989; Schmidt-Knaebel 1983; Werner/Levis-Matichek/Litowitz 1975): Hiding this function by not being clearly marked as such or entailing contradictory messages makes these utterances hard to understand (Käsermann 1988; Nöth 1976). 2.2. Difficulties in Speech Perception Schizophrenics’ difficulties in understanding utterances of their healthy partners is known from first person accounts (Chapman 1966; Freedman 1974; McGhie/Chapman 1961). While the schizophrenic’s problem of producing understandable utterances is thought to stem from his/her failure at providing information necessary for the reconstruction of meaning, his/her difficulty in understanding is equated with his/her not being able to use information given in utterances. One type of information mediating meaning in discourse is the predictability within clauses (modelled by different word order approximations; Miller/Selfridge 1950) which schizophrenic listerners cannot use fully according to results of an experimental investigation (Lawson/ McGhie/Chapman 1964). However, it can be shown (Rochester 1973; Rochester/Harris 1973) that schizophrenics’ reduced performance as listeners is not primarily based on a disability in processing syntactic information but rather on an impaired processing of primary sensory data. — The analyses reviewed in sections 2 .1. and 2 .2 . are characterized by the assumption that the difficulties experienced in communicative interaction with schizophrenics are based on the latters’ deficient productive and perceptive treatment of syntactic, semantic, referential, propositional, and pragmatic (van Belle 1987; De Decker/ van Campe 1989) aspects of language. Findings are interpreted mainly as an expression of the schizophrenic individual’s problems with language and/or information-processing, and seldom as an expression of a schizophrenic individual’s problems with communication. In comparison the communicative exchange as such is not a target of investigation (with the exception of Schmidt-Knaebel 1983). However, it is certainly topicalised theoretically either by proposing an algorithm used for describing speech oddities as a model
56. Communicative Behavior in Schizophrenia
of the (healthy) listener’s interpretive difficulties (Hoffman/Kirstein/Stopek 1982 ), or by reflecting the possibility of speech oddities as being dependent on an interpersonal failure (Andreasen 1979; Nöth, 1976; Rochester/ Martin/Thurstone 1977). However, at least the latter has been rejected as quite improbable (Rochester 1978) on the basis of results concerning paraverbal aspects of schizophrenics’ linguistic performance (Rochester/ Thurstone/Rupp 1977). — The controversy is unlikely to be solved within a framework capturing a primarily communicative phenomenon in terms of individual achievements and deficits. Even those findings about the schizophrenic individual’s ability to decenter or to take another’s perspective based on anecdotic (Wróbel 1990) or experimental evidence (Harrow/Lanin-Kettering/Miller 1989; Kreitler/ Schwartz/Kreitler 1987; Strober 1979) gathered outside an actual communicative context, are of limited value in testifying for or against the interpersonal-failure-thesis, because in these settings the interpersonal situation as a variable itself is neglected. 2.3. Failures of Communicative Exchange Investigations of problems of communicative exchange with schizophrenic persons are aimed either at aspects of enduring patterns of communication (Doane/Goldstein/Rodnick 1981; Vaughn/Leff 1976) or at features of the actual communicative interaction. — The attempt to locate difficulties of communicative exchange with schizophrenics in an ongoing conversational situation is based on the assumption that an adequate and satisfactory communicative process between interlocutors presupposes shared meaning or a contract, respectively (Rommetveit 1974; Swartz/Swartz 1987), processes of convergency (Alberti/Käsermann 1983), a cooperative endeavor (Grice 1975) in general (Buckingham jr. 1982 ; De Decker/van de Craen 1987; Käsermann 1983; Leodolter 1975), and, a cooperative endeavor aimed at organizing turn-taking (Schlatter/Käsermann 1991), respectively. Blakar (1973) proposes a method for investigating communicative interaction between interlocutors proceeding from presuppositions which by experimental induction are made to differ between participants. It can be shown, that parents with a schizophrenic offspring when conversing with each other (Blakar/Paulsen/Solvberg 1978; Blakar/ Valdimarsdottir 1981) as well as when conversing with the schizophrenic communicate
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less efficiently and more egocentric about a given problem than do healthy dyades or triades (Mossige/Pettersen/Blakar 1979). Leodolter (1975) examined the characteristics of informations given in answering questions and distinguishes four types of dialogues with schizophrenics. Käsermann (1983; 1986; 1987) analysed adjacency pairs (Sacks/Schegloff/Jefferson 1974) and tried to determine the effect of the expected or non-expected request-reply exchange on the course of conversation. She proposed two types of algorithms to grasp expected and non-expected courses of interaction (Käsermann 1983; 1987). With regard to a schizophrenic’s contribution to conversation the latter allows for discriminating types of deviations from a cooperative communicative behavior. This method of description can also be expanded to encompass the quality of the healthy partners’ cooperation (Käsermann/Altorfer 1989). Within the framework of single case studies, it can be shown that differences in cooperation between healthy and schizophrenic interlocutors cannot be interpreted meaningfully without taking into account variables like overall goals of conversation and distribution of knowledge (Käsermann 1991). — The analysis of signals used to organize turn-taking (Duncan/Fiske 1977; Schlatter/Hänni 1989) show that a substantial proportion of so-called incoherences (Andreasen 1979) in a schizophrenic’s utterances occur as a function of the healthy partner’s refusal to take over the speaker’s role (Schlatter/Käsermann 1991). This approach expands the description unit from two- to three-turn sequences. This allows for a type of analysis which systematically corroborates the impression (Schmidt-Knaebel 1983) that the healthy partner’s backchannels or hearer signals acting as a substitute for an adequate substantial utterance may lead to oddities in the schizophrenic’s communicative behaviour. These findings contrast with evidence from a two-turn-sequence analysis where the healthy partner’s backchannels are interpreted as strategically adequate to keep conversion going (van Bijsterveld 1987). — With possible exceptions (Doane/West/Goldstein et al. 1981; Miklowitz/Strachan/Goldstein et al. 1986; Goldstein 1987) investigations of enduring patterns of communication do not focus on features of actual communicative interaction with a schizophrenic person but look at communicative styles of his/her relatives. Occurrence and frequency of specific
IV. Pathologies of Language Use in Psychiatric Disorders
552
message types (critical, hostile or positive remarks, emotional overinvolvement, warmth: Vaughn/Leff 1976; Leff/Vaughn 1985; criticism, intrusiveness, guilt induction, support: Doane/West/Goldstein et al. 1981) are registered. It is shown that a familial style of communication characterized by negative message types (e. g. criticism; emotional overinvolvement) is systematically related to occurrence (Doane/West/Goldstein et al. 1981) and course (esp. risque of relapse) of the schizophrenic condition (Vaughn/Leff 1976). — The manner of construing aberrations has major methodological implications. Aberrations constituted inductively by comparing the achievements of schizophrenics and (healthy) controls are not independent from specific features (of the situation, of the investigated persons) and limitations on sampling procedures of that investigation. As a consequence replications of given results are very rare. In contrast, the use of categories which define oddities as deviations from implicit (Dawson/Bartolucci/Blum 1980) or explicit standards (Swartz/Swartz 1987), especially the standards of linguistic or logic correctness (e. g. Rochester/Martin/Thurstone 1977; Rochester/Martin 1979) create descriptions which are independent of features of the actual situation. This independence forms an indispensable prerequisite for answering the following question (Chaika 1981; Lakoff 1981; Lecours/Vanier-Clément 1976).
3.
Conditions of the Occurrence of Deviances
Generally speaking the conditions determining speech deviances cannot be isolated conclusively, neither by investigations proceeding without well-defined types of deviance, nor by single cases studies, not by investigations operating with unspecified samples of schizophrenics and controls. 3.1. Features of the (Schizophrenic) Subjects under Investigation The question as to which schizophrenics show a given speech production deviance has been investigated with regard to the distinctions between process vs reactive (Putterman 1975), acute vs chronic (King/Fraser/Thomas/Kendell 1990; Thomas/King/Fraser/Kendell 1990), and, thought-disordered (TD) vs nonthought-disordered (NTD) conditions. The results suggest that within schizophrenia sub-
groups may be distinguished on the base of their respective productive achievements. It is a matter of controversy, however, whether cohesive weakness found in TD schizophrenics is specific for that subgroup or can also be found in TD manics (Harvey 1983; Harvey/Brault 1986; Schonauer/Buchkremer 1987; Villegas i Besora 1989; Wykes/Leff 1982 ), and NTD schizophrenics compared to NTD manics (Bartolucci/Fine 1987). Basic problems connected with a non-tautological definition of the TD-NTD distinction have been discussed by Andreasen (1979), Chaika, (1982 ), Dittmann (1991), and Rochester/Martin (1979); (cf. art. 53). It seems likely that deviances specific for schizophrenia or for one of its subgroups can only be found if sampling procedures take into account additional nonlinguistic criteria (Andreasen/Tsuang/Canter 1974; Hoffman/Stopek/Andreasen 1986; Küfferle/Lenz/Schanda 1985), or if deviances are described more precisely on a morphosyntactic level (Dittmann/Fehrenbach/Welsh 1989; Fraser/King/Thomas 1986; King/Fraser/ Thomas/Kendell 1990; Morice/Ingram 1982 ; Thomas/King/Fraser/Kendell 1990; cf. art. 54). In the reviewed investigations of difficulties in speech perception distinctions of subgroups are not made, and controls are healthy persons. — Investigations of failures of communicative exchange make clear that the communicative style found in families with a schizophrenic offspring prone to relapse (Doane/Goldstein/Rodnick 1981) is also present in families with a bipolar manic (Miklowitz/Goldstein/Nuechterlein et al. 1988), and, therefore is not specific for schizophrenia. 3.2. Features of Communicative Situation The important fact that specific deviances can only be observed intermittently is sometimes not acknowledged at all (Tress/Pfaffenberger/ Frommer 1984) or it is interpreted as a direct expression of the phasic nature of linguistic (Chaika 1982 ) and/or information-processing impairments in schizophrenics (Rochester 1978). By drawing attention to the infrequent occurrence of the specific variety of cohesive weakness found even for TD schizophrenics, however, a perspective biased towards interpreting observed deviances in terms of schizophrenic individuals’ deficits may be a point of discussion (Rosenbaum/Sonne 1983). With regard to speech production it can be shown that all, TD, NTD, and healthy persons react to a variation of speech contexts (cartoon
56. Communicative Behavior in Schizophrenia
description, narrative, interview) with a differential use of types of cohesive devices (Rochester/Martin 1979; Villegas i Besora 1989). — No investigations of conditions determining the occurrence of deviances of speech perception exist. — Most of the investigations of situational conditions leading to deviances are in some way or other related to focussing on failures of communicative exchange. As these analyses often operate with deviances that have not been properly defined or stem from few case results, they have, at best, an exploratory character. The actual occurrence of deviances as a function of topic and/or style of conversation is described in the form of an anecdote (Leodolter 1975; Seeman/Cole 1977) or systematically investigated (Käsermann 1986; Rutter 1977; Shimkunas 197 2 ; Spring/Briggs/Cozolino/ Mannuzza 1982 ). There is evidence that deviances occur more frequently in interviews where topics distressful for the schizophrenic are pursued (Käsermann 1986; Shimkunas 2 197 ; Spring/Briggs/Cosolino/Mannuzza 1982 ) and where the schizophrenic’s interlocutor behaves in a conversationally invasive manner (Käsermann 1986). When the schizophrenic does not react in this manner then the selection of topics must not have disturbed him/her (Rutter 1977). — An important though not easily tangible condition of the occurrence of deviances seems to be the (restricted) quality of interpretation of the schizophrenic’s (metacommunicative) conversational contribution (Schmidt-Knaebel 1983). — The actual effect of a specific communication style on the on-going conversation is investigated with regard to families with either a schizophrenic or a manic offspring: While both diagnostic groups show similar nonverbal signs of stress they can be discriminated on the base of their verbal coping strategies (Altorfer/Goldstein/Nuechterlein et al. 1990). — The set of variables which certainly play a role but as a rule are not controlled in studies dealing with schizophrenics’ impaired production and perception may be conceived of as instances of emotionally distressful conditions of conversation. In recent models of schizophrenia (Gjerde 1983; Zubin/Spring 1977) schizophrenics’ vulnerability to emotional stress manifested in speech deviances is construed as exclusively determined by the individual’s disease. Alternatively, it has been proposed that higher-order communication variables like asymmetric and dominant characteristics of exchange may be introduced as interactionally effective medi-
553
ating factors (Käsermann 1988; 1990; Szasz 1974). — Deviances cannot only be conceived of as reactions to specific conditions but also as instruments used by the schizophrenic in a goal-directed manner. The instrumental use of oddities is known from investigation of impression-management (Braginsky/Braginsky 1967; More/Malony 1982 ). In a single case study it has been shown that the frequency of some types of deviances changes as a function of the schizophrenic’s partner being diverted from pursuing a distressful topic by their occurrence (Käsermann 1986). — Therapeutic endeavors make use of both the dependence of the occurrence of deviances on specific conditions as well as their instrumental use by trying to modify existing contingencies through communicative interventions during actual communicative exchange (Cohen/Florin/Grusche et al. 1973; Florin/ Cohen/Meyer-Osterkamp 1973; Liberman/ Teigen/Patterson/Baker 1973; Mace/Webb/ Sharkey et al. 1988; Swift/Magaro/Antonitis 1977).
4.
Summary
The review emphasizes the fact that difficulties of communicative exchange with a schizophrenic person are approached from two different angles, namely the monologic, and the dialogic one (Foppa 1987). The seeming disparity between these two perspectives (Dittmann 1991) may vanish readily if one considers (a) that the methodological core of each investigation should be created by a precise and replicable description of oddities as deviations from linguistic, logical, and/or conversational standards, and, (b) that such descriptions are the necessary prerequisite of probing into conditions which control the occurrence of a well defined phenomenon. A valid explanation of deviances presumes that their occurrence may be predicted on the base of knowledge about their relevant determinants.
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ization in mute schizophrenics. Psychological Reports, 41, 575—580. Szasz, T. S. (1974). Language and humanism. The Humanist, 34, 25—30. Thomas, P., King, K., Fraser, W. I., & Kendell, R. E. (1990). Linguistic performance in schizophrenia: A comparison of acute and chronic patients. British Journal of Psychiatry, 156, 204—210. Tress, W., Pfaffenberger, U., & Frommer, J. (1984). Zur Patholinguistik schizophrener Texte. Der Nervenarzt, 55, 488—495. Vaughn, Ch. & Leff, J. (1976). The measurement of expressed emotion in the families of psychiatric patients. British Journal of Social and Clinical Psychology, 15, 157—165. Villegas i Besora, M. (1989). The failure of communication in schizophrenic thought disorder. Communication and Cognition, 22(2), 191—202. Werner, O., Levis-Matichek, G., & Litowitz, B. (1975). An ethnoscience view of schizophrenic speech. In M. Sanchez & B. Blount (Eds.), Sociocultural dimensions of language use. 349—380. N. Y.: Academic Press. Wróbel, J. (1990). Language and schizophrenia. Amsterdam: John Benjamins Publishing Company. Wykes, T. & Leff, J. (1982 ). Disordered speech: Differences between manics and schizophrenics. Brain and Language, 15, 117—124. Wyrsch, J. (1946). Ueber die Intuition bei der Erkennung des Schizophrenen. Schweizerische Medizinische Wochenschrift, 46, 1173—1176. Zubin, J. & Spring, B. (1977). Vulnerability — A new view of schizophrenia. Journal of A bnormal Psychology, 86, 103—126.
Marie-Louise Käsermann, Bern (Switzerland)
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V.
Pathologies and Disorders of Language Development
57.
Landmarks in Children’s Language Development
1. 2. 3. 4. 5.
1.
Introduction The Development of Linguistic Competence The Development of Communicative Competence Some Closing Words References
Introduction
The speed and course of normal language development are enormously variable, yet there are certain landmarks that all children pass on their way to becoming competent speakers of their native languages. The purpose of this chapter is to describe those landmarks and to provide an approximate timetable for their achievement. The goal is to describe ‚what’ children acquire and ‚when’ they do so. Issues of ‚how’ children acquire what they do fall outside the scope of this chapter. Thus this chapter is not a review of theories of language development, although some discussion of theoretical issues is necessary where the appropriate description of what the child has acquired is at issue. The first and largest section of this chapter describes the course of the development of linguistic competence with separate treatments of phonological, lexical, and grammatical development. Semantic development is not discussed as a separate topic, but the meanings of children’s words and sentences are discussed in the sections on lexical and grammatical development, respectively. The second section adds to this account of children’s mastery of their language, brief summaries of the development of the ability to communicate intentions and the development of the discourse skills required to use language for communication.
2.
The Development of Linguistic Competence
2.1. Phonological Development 2.1.1. Production 2.1.1.1. Prespeech Phonological Development The first perceptible landmark in the development of speech sounds occurs at around 6 to 8 weeks of age when the infant starts to coo. Before that the infant’s vocal repertoire consists of cries, burps, sneezes, and other vegetative sounds which, like speech, require the vocal cord to vibrate and air flow to be stopped and started, but which bear no obvious resemblance to the sounds of speech. The coos that 8 week old infants produce sound like long, single-segment vowels, although careful analysis reveals the presence of some consonantal elements as well. Infants coo when they appear contented and, particularly, when they are engaged in social interaction. Between approximately 2 and 8 months of age, the vocal repertoire of the infant expands and the infant gains increasing control over the use of that repertoire. Cooing noises are concatenated in long, multi-segment series, laughter appears, the variety of vowel and consonantal sounds produced increases, and finally — toward the end of this period — these emerging features are produced together in increasingly long and complex combinations sometimes termed marginal babbling. Squealing, growling, and a variety of ‚friction noises’ are also characteristic of infant vocalizations during this period (see Stark 1986 for a more complete summary of early phonological development). The second major landmark in phonological development is the appearance of canonical babbling, which occurs sometime between 6 and 9 months of age. Canonical babbling is distinguished from the vocalizations that preceded it by the presence of true syllables.
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The definition of canonical babbling is highly technical (i. e., in terms of multiple acoustic parameters such as frequency resonance, intensity, rate of formant transition, and others (Oller 1986)), but the appearance of canonical babbling is obvious to the listener because of the clear syllabic quality of the infant’s sounds, typically produced in reduplicated series of the same consonant-vowel combination such as [dada] or [n3 n3 n3]. Canonical babbling is not produced by deaf infants, and thus this landmark appears to be the first development that distinguishes the vocal development of hearing children from that of deaf children (Oller 1986). The appearance of canonical babbling is followed by a period of variegated babbling in which new consonants and vowels are added to infants’ repertoires, and consonantvowel and consonant-vowel-consonant syllables are combined in series. Although some prosodic features may be present in infants’ productions from the time of marginal babbling, if not earlier (Crystal 1986), once prosody is added to these strings of non-reduplicated babbles infants sound as though they were speaking — until close attention reveals that what is being produced is the melody of language, but not the words. By 8 months the prosodic contours of babbling sequences may begin to show the specific influence of the prosodic characteristics of the target language (Crystal 1986, de Boysson-Bardies/Sagart/ Durand 1984 ), but the consonant and vowel repertoires of children at this stage seem consistent across children acquiring different languages (Vihman 1988). Children seem to vary in both the extent to which they produce these word-less intonation patterns and how long they persist at this. Some children spend months in this expressive jargon phase, and many children continue to produce long strings of jargon after producing their first words. Next, and more so for some children than others, there is a transitional phase between babbling and the appearance of the first identifiable word. During this period children produce sound sequences, or sound plus gesture sequences, which seem to have consistent meanings for the child, but the meanings of these sequences are not derived in any obvious way from the target language. These sequences have been variously labelled protowords (Bates 1976), sensori-motor morphemes (Carter 1979), quasi-words (StoelGammon/Cooper 198 4 ) and phonetically
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consistent forms (Dore/Franklin/Miller/Ramer 1976). Their use tends to be tightly bound to particular contexts and/or pragmatic functions. Studies of the phonetic characteristics of vocalizations during this transitional period suggest that there are commonalities among children acquiring the same language and also that children’s sound repertoires have been influenced by the phonological properties of the target language (Vihman 1988). In the vocalizations of children acquiring English, single syllables are most common, and some disyllabic units are produced. Among consonants, stops (e. g., [b] and [d]) are the most frequent, nasals (e. g., [m] and [n]) and fricatives (e. g., [f] and [đ]) are present but rarer, consonant clusters are infrequent. Central vowels (e. g., [⋀], [3], [æ]) are more frequent than high vowels (e. g., [i], [u]). (See Vihman 1988 for a more complete description). 2.1.1.2. Phonological Development During Early Language Development Sometime within a few months before or after their first birthdays, children reach the landmark that ends the period of prespeech phonological development — they produce their first words. These first words make use of the same sound repertoires that were evidenced in children’s late babbling and transitional forms. Even at the 50-word vocabularly mark (around 18 months) sounds that appeared in early babble are among the more frequently used, and many sounds are not yet produced. In children acquiring English, for example, [m], [b], and [d] are consistently present as initial consonants in their 50-word vocabularies, and [θ], [đ], [1], and [r] are consistently absent (Leonard/Newhoff/Meselam 1980). However, there is also considerable variety across children in the phonemes in their first 50 words. Normative inventories of the phonemes in the speech of American children at different ages have been collected by Templin (1957) and Sander (1972). However, several factors limit the usefulness of such norms as descriptions of phonological development (Menyuk/ Menn 1979). First, the likelihood that a sound will be articulated depends on the sound’s position in the word and on the neighboring sounds in the word, and these factors affect different sounds differently. For example, fricatives tend to be produced first in wordfinal position; stops tend to be first produced in word-initial position. Second, there are in-
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dividual differences in the course of phonological development, although the nature and extent of these differences is a matter of some controversy (Stoel-Gammon/Cooper 198 4 , Ferguson/Farwell 1975, Goad/Ingram 1987). And third, there is good evidence of crosslinguistic variability in the course of phonological development. According to Pye/Ingram/List (1987) children acquire first those distinctions which are most relevant in their language, and relevance in the target language is the most important determinant of the order of acquisition of phonemes. A more useful way to try to describe phonological development is in terms of the kind of understanding of the phonological system children appear to have at different points in development, although there is not agreement on what this description should look like. The most widely held view is that children initially use the whole word as a single, unanalyzed phonological entity (Ferguson/Farwell 1975). Analysis into small units that can be recombined (i. e., phonemes or features) occurs later. The evidence for this is that there is a lack of phonological consistency across different words in children’s early productive vocabularies and also that sometimes children initially articulate words well, and then the phonological quality of their productions later declines. This apparent regression is seen as evidence that the child’s whole-word approach has been supplanted by a phonological system that is not yet adultlike. An alternative view of phonological development is that children’s phonological systems operate over distinctive features from the start and that development consists of learning the contrasts relevant in the target language (Ingram 1988). The argument for this view is the claim that, when looked for properly, there is phonological systematicity to be found in children’s early productions. Hence, the disagreement hinges on methodological considerations involved in arriving at children’s phonological inventories. Both these views of phonological development converge in identifying 18 months or the achievement of a 50-word productive vocabulary as a major landmark in phonological development. Some significant change in children’s phonological systems seems to occur at this point that allows children to learn new words much more quickly than before and that therefore contributes to — if not fully explains — the spurt in children’s vocabularies which occurs at this time. As de-
V. Pathologies and Disorders of Language Development
scribed by Menyuk/Menn/Silber (1986) the change that occurs is the development of a system that maps phonemes in the target language to sounds within the child’s more limited repertoire, thus allowing the child to approximate most one or two syllable words after only a few hearings. Many of these mapping rules (often termed processes or patterns) are common across children (at least within a language). These common patterns give young children’s speech characteristic features such as reduplication (e. g., bottle — [baba]), substitution of stops for fricatives and cluster reduction (e. g., sandwich — [taewis], and substitution of glides for liquids (e. g., rabbit — [wæbIt]) (Dale 1976). (See Ingram (1986) for a comprehensive discussion of the common phonological processes in children acquiring English). In addition to the patterns that are common across children, there are also individual differences and even marked idiosyncracies in the patterns that children develop (Fey/Gandour 1982). And there are strategies other than the application of patterns that children may adopt when confronted with a new word in the target language. Children may avoid acquiring new words that use sounds that are not in their repertoires (Schwartz/Leonard 1982), or they may assimilate a new word to either another similar-sounding word in their lexicons or to a preexisting whole-word sound pattern (termed a canonical form). Some children seem to modify all new words to fit a small set of canonical forms, and for others the use of a few canonical forms coexists with a more elaborate system of phonological patterns. These individual differences and exceptions notwithstanding, the development of these patterns is a major change in children’s phonological systems and their emergence is the last major landmark in phonological development. The rest of normal phonological development consists of the gradual lessening of reliance on these patterns as children’s articulatory abilities develop. By the age of 4 years children’s phonological systems are usually close to that of adults with only a few sounds still causing trouble. Normally, children sound adult-like by the age of 6 to 7 years. 2.1.2. Phonological Development in Perception and Comprehension It is well established that prelinguistic infants are able to discriminate between sounds
57. Landmarks in Children’s Language Development
which differ in terms of features that mark phonemic contrasts in many of the world’s languages. In experimental tasks in which discrimination is assessed using changes in infants’ heart rates, sucking, or attention, infants as young as 1 to 4 months have shown discrimination of consonants based on differences in voice onset time and place of articulation, discrimination among several vowel contrasts, and discrimination of glides and liquids (Eilers 1980). Infants also show sensitivity to intonation and stress cues (Eilers 1980). Some of these discriminatory capabilities appear to be innate, but there also appears to be some learning taking place during the prelinguistic period as evidenced by effects of the target language on speech sound perception in infants as young as 6 to 8 months (Eilers/Gavin/Oller 1982), although there is controversy surrounding this claim (Jusczyk/ Shea/Aslin 198 4 , Eilers/Oller/Bull/Gavin 1984). The fact that two sounds are discriminable to infants does not mean that two words that differ in that feature will be understood by children to be two different words with different meanings. Children as old as 24 months age of 4 (Grunwell 1986). 2.2. Lexical Development 2.2.1. Production 2.2.1.1. Early Lexical Development Sometime around their first birthdays most children produce their first recognizable word. This event is a major landmark in language development, but it does not seem to represent any discontinuity in children’s internal representations of language. Like the protowords that preceded them, children’s first words tend to be context bound. For example, more might be used only as a request and not to comment on recurrence and no might be used only to indicate refusal (Gopnik 1988). This sort of word use suggests that the child’s mental representation of the word is that it is what one says to accomplish particular pragmatic ends, rather than that it is a label for a referent or a symbol for a more abstract meaning (Bates/Benigni/Bretherton et al. 1979, Dromi 1990, Gopnik 1988). Labels for people and things typically appear after the first context-bound words, but they tend to be less frequently used or less numerous in children’s early vocabularies. However, there are individual differences in this, with
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fail to treat as phonemic, contrasts that are perceptible to prelinguistic infants (Barton 1978, Menyuk/Menn/Silber 1986). The particulars of when different phonemic contrasts are acquired in word perception are subject to disagreement over the appropriate method for testing their acquisition (Barton 1975, Garnica 1973). Even the relationship between the development of comprehension and production is unclear. Ingram (1989) has suggested that the course of phonological development in production depends on preceding developments in comprehension, and some production errors seem due to perceptual difficulties. On the other hand, some production errors seem to be more the result of motor difficulties (Vihman 1988), and certainly there is good evidence that comprehension of a contrast in the speech of others does not guarantee accurate production of that same contrast (Butler 1920/1980). Children seem to have mastered the phonemic contrasts in their language by 4 years (Menyuk/Menn/Silber 1986), but metaphonological knowledge and skills such as those involved in counting the number of segments in a word, in rhyming, and in appreciating puns develop after the some children producing more object labels from the start (Nelson 1973). A third word type, which typically appears later than either context-bound words or labels and which probably depends on cognitive developments that are not necessary for the use of these other two word types, are words with relational meanings such as gone — used to indicate disappearance, or no — used to indicate failure. Initially, for most children, the rate of vocabulary acquisition is relatively slow. Reported average rates of vocabulary acquisition between the first word and the achievement of the 50-word mark vocabulary range from 8 to 11 words per month (Benedict 1979, Goldfield/Reznick 1990, Nelson 1973). Also, during this early period of lexical development newly-learned words are not necessarily permanent additions to children’s productive vocabularies. Sometime around 18 months, but ranging from 15 to 24 months, children achieve a productive vocabulary of 50 words (Benedict 1979, Goldfield/Reznick 1990, Nelson 1973). Reaching this point in lexical development or reaching the age of 18 months — it is not clear whether age or productive vocabulary is the best indicator — represents the second major landmark in lexical development and does seem to reflect some underlying change
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in children’s linguistic systems. At this point many children show a marked increase in the rate at which they acquire new words — to an average rate of 22 to 37 words per month (Benedict 1979, Goldfield/Reznick 1990) — and words acquired after this point tend to be permanent additions to children’s vocabularies. An average difference in ease of word learning between children who are on either side of the 50-word vocabulary mark or 18 months of age has also been demonstrated experimentally (Lucariello 1987, Oviatt 1982). What appears to change lexical development at this point is a newly-developed ability to learn names for things. The word spurt is not a spurt in the acquisition of all kinds of words, rather it is a spurt in the acquisition of object labels (Goldfield/Reznick 1990). The occurrence of this spurt seems to depend on the convergence of several factors. As already suggested (see 2.1.1.2.), phonological development may play a part. There are also several proposals of cognitive prerequisites to the naming explosion including the development of the notion that things are members of categories (Gopnik/Meltzoff 1987), the development of the cognitive ability to break events down into nameable components (Nelson/Lucariello 1985) and the achievement of the insight that things have labels (Dore/ Franklin/Miller/Ramer 1976, Stern/Stern 1907). In addition, having a mother who plays labelling games may be helpful if not necessary (Goldfield/Reznick 1990). At the 50-word point in lexical development, children’s vocabularies are typically described as consisting primarily of nouns or object labels, with verbs or actions words constituting a smaller proportion of children’s vocabularies; modifiers and words which express affective states or serve social functions make up the remainder (Benedict 1979, Gentner 1978, Snyder/Bates/Bretherton 1981). First nouns typically include words for food, clothing, animals, body parts, household items involved in children’s daily routines, and people (Clark 1979). Several sources, however, call into question the view that nouns predominate in early vocabularies. Children learning languages in which the verb is more salient in the surface structure of sentences than it is in English have been reported to acquire verbs at an earlier age than do children learning English (Clancy 1985, Gopnik/Choi 1990). Also, the extent to which nouns dominate at the 50-word vocabulary
V. Pathologies and Disorders of Language Development
mark varies across children as a function of the individual differences in the early tendency to acquire labels vs. social function words. And Lieven (1990) has suggested that nouns dominate early vocabularies when children have mothers who play labelling games with them. (Lieven, E. V. M. (1990). Remarks made in the workshop “Non-referential children: slow or different?” Fifth International Congress for the Study of Child Language. Budapest.) Thus the current view of what is normative may be biased by the predominance of first-born, middle class children as subjects of child language research. A separate question from what sort of words young children have in their productive vocabularies is what sort of meanings children have for the words that they use. Even once words no longer have the limited contextbound meaning of children’s very first words, the meaning representations that children have may be different from the meanings of those words in adults’ lexicons. Narrower meanings are reflected in the underextension of words — such as using water only to refer to water in a glass. Broader meanings are reflected in overextensions — such as using the word dog to refer to any four-legged animal or using the word Daddy to refer to any adult male. Although such overextensions are commonly reported, the phenomenon of overextension may be more salient to the listener than it is pervasive in children’s word use. Most of children’s early words are not overextended. Rescorla (1980) reported on the basis of 6 children whom she followed from 12 to 18 months that 33% of word uses were overextended but that only a few different words accounted for a disproportionate share of those overextensions. The bases of overextensions seem to be many, including perceptual similarity to the original word referent (e. g. dog for wolf), functional similarity (e. g., hat for a shirt stuck on someone’s head) and contextual association (e. g., a child pointing to his father’s briefcase and saying Daddy). Where overextensions occur, there is disagreement concerning the extent to which these overextended uses reveal children’s overgeneral representations of word meanings or reflect a communicative strategy that is forced by the child’s limited vocabulary (Huttenlocher/Smiley 1987, Hudson/Nelson 1984 ). As children acquire more differentiated vocabularies, for example words for animals other than dog, overextensions decline (Rescorla 1980).
57. Landmarks in Children’s Language Development
2.2.1.2. Later Lexical Development Less research attention has been given to the course of productive lexical development after the age of two years, although it is clear that changes take place in the size of children’s vocabularies, the content of children’s vocabularies, and possibly the ease with which new words are acquired. In terms of size, Templin (1957) estimated that children have vocabularies of approximately 8,000 words by 6 years and approximately 18,000 words at 8 years. In terms of content, children acquire new types of words that encode meanings and/or serve syntactic functions that are absent in the speech of younger children. For example, children add adverbs, syntactic connectives, and terms that indicate temporal and causal relations to their vocabularies (Bloom/ Lahey/Hood et al. 1980, French/Nelson 1985, Scott 1984 ). In terms of the process of acquisition, Rice (1990) has suggested that starting at age 3 years, and increasingly thereafter, children become better at picking up new words (particularly object labels) from incidental exposure in context. There are also late-appearing errors in children’s word use such as the production of novel verbs (e. g. unstraighten meaning to bend) or verbs used in novel ways (e. g., Don’t comb me baldheaded) that appear to reflect that lexical development consists of changes in children’s understanding of lexical principles — not just the acquisition of increasing numbers of lexical items (Bowerman 1985). 2.2.2. Comprehension Children understand words in their language before they produce any, and it seems to take children less time to learn new words for the purpose of comprehension than to learn new words that are used in production. There are anecdotal reports of children as young as 5 months selectively responding to words (Vihman 1988). In her longitudinal study of eight children, Benedict (1979) found that children attained comprehension vocabularies of 20 words at ages ranging from 10 to 16 months. The average rate of growth in comprehension vocabulary during this period was 22 words per month. Comparison of these figures to comparable figures for the development of productive vocabulary reveals that comprehension vocabulary not only precedes productive vocabulary but also develops more rapidly even after productive language begins. In addition to the differences in the times
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of onset and rates of lexical development in comprehension and in production, there are several other asymmetries between children’s comprehension vocabularies and the vocabularies they use in productive language. The most obvious asymmetry is in size. Children’s comprehension vocabularies are larger than their productive vocabularies at every age tested (Benedict 1979, Goldin-Meadow/Seligman/Gelman 1976). Comprehension and production vocabularies also differ in content. Benedict (1979) and Goldin-Meadow et al. found that there were proportionately more verbs in children’s comprehension vocabularies than in their production vocabularies, perhaps, as Gentner (1978) has suggested, because communication works adequately with a minimal verb vocabulary. As noted before, however, the cross-linguistic generality of the later acquisition of verbs is suspect. Overextensions of word meanings, which is one of the most noted characteristics of early word use, occurs little, if at all, in comprehension (Kay/Anglin 1982, Chapman/Thompson 1980, Fregmen/Fay 1980, Huttenlocher 1974 ). Thus, the picture of early vocabulary development is one of greater competence in comprehension than in production, although occasionally children have underextended representations of word meanings or use words only in specific situations thereby appearing more competent than they really are. The relation between comprehension and production for later-acquired terms is different. That picture is captured well in French/ Nelson’s (1985) treatment of the development of words that indicate relational meanings. Terms that express relations between propositions, such as if, or, but, and so forth, were correctly used in children’s spontaneous speech as early as age 3, despite the fact that children failed to show full command of all the contrastive meanings of these terms in experimental tests of comprehension even years later (e. g., French 1988). Bassano/ Champaud (1989) report similar findings for the French connective même. One possible explanation for the discrepancy between the production and comprehension data is that children can use not-fullyacquired terms correctly by using them in memorized routines that are imitated from adult speech, such as brush your teeth before you go to bed. However, most of the utterances in French and Nelson’s data base seem more likely to be children’s own productions because they are things adults are unlikely ever to have said. Utterances that are factu-
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ally incorrect are perhaps the clearest examples of utterances that are unlikely to be imitations (e. g., ... a waiter comes, and if he sees us, he tells us what I, what I, what us, what what I want here.) French and Nelson’s explanation for children’s ability to produce relational terms before they demonstrate full competence in comprehending relational terms is that young children can display competencies in the supportive context of describing familiar events that they are unable to display in typical experimental settings. 2.3. Grammatical Development 2.3.1. Production 2.3.1.1. The Emergence of Grammatical Structure in Children’s Speech The first time children combine two words or a single word plus a bound morpheme (such as adding a plural -s to a noun) in one utterance, they have reached a major landmark in their productive speech — the beginning of grammar. This landmark is typically reached around 18 to 24 months and only after children spend several months talking in single word utterances. Although the beginning of grammar is a significant landmark, it is not always an obvious one. Some children — typically those who produce long strings of jargon — produce utterances longer than one word by inserting one clear word into what is otherwise an incomprehensible babble sequence. Most children have at least some multiword phrases in their repertoires that have been memorized as unanalyzed wholes and that therefore do not reflect the development of the ability to combine words (Peters 1986). (Iwant and Idon’tknow are examples of unanalyzed wholes that are common in children’s early language.) To further complicate matters, all these phenomena may exist simultaneously so that one child’s 2-word utterances may include some rote-learned wholes, some filler + word combinations, and some truly productive word combinations. Some children seem to make heavy use of rote learned phrases, and the distinction between a word-by-word, analytic approach to language acquisition and a wholistic, gestalt approach to language acquisition is a major dimension of individual difference (Peters 1983). For some children grammatical development begins with a clear 2-word stage that may last for several months, and for other children the 2-word stage is brief and
V. Pathologies and Disorders of Language Development
barely identifiable as a separate stage preceding the next landmark — the production of utterances with 3 or more words. The first 2-, 3-, and 4 -word utterances that children produce can be characterized as word-order correct (typically declarative form) sequences of words from the major grammatical categories of nouns, verbs, and adjectives, with few grammatical functors such as articles, prepositions, auxiliaries, and noun and verb inflections. Pronouns are frequent in the early word combinations of some children and rare in the speech of other children (Bloom/Lightbown/Hood 1975). Children’s first sentences are frequently described as telegraphic because of their similarity to the style adopted by adults when writing telegrams in which each additional word carries a cost. Only the high information bearing words are included; inflections and words whose main functions is to mark grammatical structure are omitted (Brown/Fraser 1963). (This similarity to adults’ telegrams is limited to the grammatical structure of utterances. The content of children’s early multiword utterances, unlike that of telegrams, tends to be context bound.) The telegraphic quality of children’s early word combinations has been reported in studies of children acquiring a variety of languages. However, children seem to acquire inflectional systems earlier in the course of language development if their language has a rich and regular inflectional system (Berman 1986). And children acquiring Turkish, which has a highly regular, rich, and perceptually salient inflectional system, have been reported to produce inflected forms prior to combining words (Aksu-Koc/Slobin 1985). The appearance of 3-word utterances in children’s speech is a major landmark in the course of grammatical development because it is at about this point that most children begin to add grammatical morphemes to their sentences. Children appear to follow relatively similar courses of early morphological development — albeit at varying rates. In his widely-known longitudinal study of Adam, Eve, and Sarah, Brown (1973) found that the orders of acquisition of some of the grammatical morphemes of English were very similar in the development of these three children, and the general sequence that he found was largely replicated in a cross-sectional study of children’s spontaneous speech (de Villiers/de Villiers 1973a). These sources suggest, for example, that the present progressive verb inflection (-ing), the plural noun inflection (-
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s), and the prepositions in and on are among the first-acquired grammatical morphemes. Auxiliaries (i. e., the is in is going and the have in hav e been) are the latest acquired. In these studies, a grammatical morpheme was considered to have been “acquired” when it was used in 90% of obligatory contexts. However, when grammatical morphemes first appear they may not be used equally across all syntactic contexts, but instead their use may be limited by semantic factors. For example, when -ing first appears it is not used with all verbs but only with verbs that describe durative, non-completive action, and this sort of semantic constraint on the use of verb inflections has been found in children acquiring languages other than English (Bloom/Lifter/ Hafitz 1980). Another syntactic development, which typically begins around the time the first grammatical morphemes appear, is the development of the linguistic means for marking negation and asking questions. As Tager-Flusberg (1989) describes, children tend to first express negatives in utterances like Not sit down and to express questions in forms like Where Daddy go? Later, children use more advanced, but still not adult-like, forms such as I no want book and What she is playing? Children use adult forms of negatives and questions fairly late in syntactic development — at least in English — because these sentence forms depend on the acquisition of auxiliaries, and auxiliaries are among the last grammatical functors to be acquired. After the development of grammatical morphemes and the development of different sentence forms is well under way, the next grammatical development is the appearence of sentences that contain more than one clause. The order of appearance of complex constructions in spontaneous speech (based on Bowerman 1979, Brown 1973, Limber 1973) appears to be first object complement constructions (e. g., I see you sit down), followed by wh- embedded clauses (e. g., Can I do it when we go home?), followed by coordinating and subordinating clause structures. Children produce complex sentences with and as the coordinating conjunction first (e. g., You play with this one and I play with this). Subordinate clause structures, such as clauses introduced with before, after, because, and so on, appear later with the order of appearance of particular conjunctions depending in part on the complexity of the concepts that they encode (Bloom/Lahey/Hood et al. 1980).
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Complex sentences first appear in children’s speech around the age of 2½, and children use most of the major types of complex constructions by the age of 4 (Bowerman 1979, Limber 1973). Probably for this reason, it is frequently asserted that children have essentially mastered the grammar of their language by the time they are 4 years old. However, there is good evidence that a further landmark is reached at 5 years when children begin to use grammatical devices to organize cohesive text. According to Karmiloff-Smith (1986), what changes at 5 years is not so much the forms children produce, but the way in which the forms are used and the internal linguistic representation of these forms. For example, pronouns are present in the speech of 2 and 3 year olds, but at that age the function of pronouns is only deictic, that is, to refer to a particular extralinguistic referent. For 2- to 3-year-old children, each utterance is a unit unto itself — its content and structure constrained only by the need to make the utterance match its nonlinguistic referent. It is only at age 5 that children start to connect sentences in discourse. Therefore, only at this time do pronouns come to be used anaphorically, that is, to refer to a referent in a prior utterance. 2.3.1.2. Meanings Expressed in Early Grammatical Speech The semantic content of children’s early multi-morphemic utterances is limited. In their early speech children talk almost exclusively about the here-and-now, and even at 3 years mention of absent or imaginary events is rare (Sachs 1983). In addition, children express a limited number of relational meanings in their first word combinations. Brown (1973) proposed a list of 8 semantic relations that he claimed accounted for the majority of meanings that children acquiring a variety of languages express in their first 2-word utterances. That list included relations between agents and actions (e. g., Daddy sit), actions and objects (e. g., Driv e car), agents and objects (e. g., Mommy sock), actions and locations (e. g., sit chair), entities and locations (e. g., toy floor), possessors and possessions (e. g., my teddy), entities and attributes (e. g., crayon big), and demonstratives with entities (e. g., this telephone). (See also Bloom/Lightbown/Hood 1975 for a description of the semantic/syntactic relations in early combinatorial speech). When children begin to pro-
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duce 3- and 4 -word utterances, according to Brown, their utterances consist of combinations of these 2-term relations — with the redundant term mentioned only once (e. g., agent and action combined with action and locative yields an utterance such as Daddy sit chair). As children’s syntax develops there is an increase in the proportion of their utterances that express 3- and 4-term relations. 2.3.1.3. Measuring Grammatical Development As children acquire the grammar of their language, their utterances become increasingly complex, and this complexity results in the utterances becoming increasingly long. Because children seem to follow similar courses in adding complexity, the average length of children’s utterances (counted in morphemes) has been widely used as a measure of syntactic development. Children with similar mean utterance lengths (MLUs) have been found to be similar to each other in other grammatical properties of their speech including the grammatical morphemes used and the phrasal and clausal structures used — up to an MLU of 3.0 (Rondal/Ghiotto/Bredart/Bachelet 1987). According to Brown (1973), MLU is a better predictor of the grammatical properties of children’s speech than is age, and a timetable of grammatical development described in terms of MLU is more accurate than one described in terms of age. Brown used MLU as the basis for defining five stages of syntactic development. That stage terminology, somewhat modified subsequent to Brown’s original proposal by Brown and others (de Villiers/de Villiers 1973 b, Miller/Chapman 1981) is widely used in the child language literature. The stages and their associated MLU intervals (based on Miller/Chapman 1981) are as follows: Early Stage I MLU = 1.0—1.5, Late Stage I MLU = 1.5—2.0; Stage II MLU = 2.0—2.5, Stage III MLU = 2.5—3.0, Early Stage IV MLU = 3.0—3.5, Late Stage IV and Early Stage V MLU = 3.5—4 .0, Late Stage V MLU = 4 .0—4 .5. The major accomplishment of Stage I is the beginning of combinatorial speech, and the major accomplishment of Stage II is the beginning of morphological development. Sentence modalities (i. e., negative and question forms) begin to develop during Stage III, and complex sentences begin to emerge at Stage IV and continue to develop during Stage V. Based on Miller/Chapman’s (1981) analysis of normally-developing American middle-
V. Pathologies and Disorders of Language Development
class children, the age ranges during which approximately two thirds of children can be expected to reach these stages are as follows: Early Stage I, 16—26 months; Late Stage I, 18—31 months; Stage II, 21—35 months; Stage III, 24 —4 1 months; Early Stage IV, 28—4 5 months, and Late Stage IV to Early Stage V, 31—50 months. However, the usefulness of MLU as a general index of grammatical development has been challenged by empirical findings that the power of MLU to differentiate among children at different levels of grammatical development is limited (Klee/ Fitzgerald 1985), and the premise underlying the use of MLU as an index of grammatical development does not apply to children whose multi-morphemic utterances consist largely of a repertoire of rote-learned wholes. 2.3.2. Comprehension The relation between comprehension and production in grammatical development echoes the relation between comprehension and production that was found for lexical development. That is, early developments occur receptively before they appear in production, but complex constructions first appear in children’s spontaneous speech years before children demonstrate solid mastery in comprehension. In a task in which very young children can demonstrate sentence comprehension merely by looking longer at a videotaped event that matches a sentence than at a carefully controlled, but mismatched event, Hirsh-Pasek/Golinkoff (in press) have demonstrated that 17-month-old one-word speakers are sensitive to meaning carried by word order (e. g., they discriminate between Cookie Monster’s tickling Big Bird and Big Bird’s tickling Cookie Monster) and that 28-montholds are sensitive to the distinction between the transitive and intransitive meanings of verbs (e. g., they discriminate between Big Bird is turning Cookie Monster and Big Bird is turning with Cookie Monster). Using more conventional methods, other researchers have also found that one-word speakers understand the meanings in multiword utterances, although in these cases there was no controlled test of meaning distinctions marked solely by syntax (Huttenlocher 1974 , Sachs/ Truswell 1978). Children who were just beginning to combine words have shown evidence of understanding word-order marked meanings (de Villiers/de Villiers 1973b), and telegraphic speakers have been found to be more responsive to commands that included
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grammatical morphemes than to commands that were more like the speech the children were producing themselves (Shipley/Smith/ Gleitman 1969). In some circumstances 17month-old girls, but not boys, have demonstrated understanding of the common-proper noun distinction marked only by the presence or absence of an article (e. g., a biff to indicate one of a class of items vs. Biff to indicate a particular item) (Katz/Baker/Macnamara 1974). This picture of early comprehension of basic aspects of grammar before those grammatical devices appear in spontaneous speech contrasts with the results of studies of the comprehension of later-appearing grammatical structures. With respect to comprehension of complex sentences, the literature presents a complicated and not always consistent picture of children’s abilities (Bowerman 1979). Two conclusions seem relatively clear: First, children employ a variety of strategies for interpreting complex sentences before children are capable of full analysis of the linguistic structures. For example, children interpret the order in which events are mentioned in a sentence to indicate the order in which those events occurred. This works for interpreting sentences such as John played before Mary sang, but it yields misinterpretations of sentences such as John played after Mary sang or Before Mary sang, John played. Second, how children interpret complex sentences is highly dependent on the nature of the experimental tasks that are employed. Reviewing studies of the comprehension of a variety of complex forms in different languages, Karmiloff-Smith (1986) concluded that children reach another landmark in language development at the age of 8 when their performance on comprehension tasks becomes consistent and unshakable, no matter how unnatural and contrived the experimental task. Karmiloff-Smith describes this landmark as the achievement of the capacity to cope with language abstractly. At that point children can process sentences without the support of the normally-present extralinguistic and discourse contexts.
3.
The Development of Communicative Competence
3.1. Overview Children who have acquired the sound system, the vocabulary, and the grammar of their language have acquired a system for express-
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ing meaning in a sequence of uttered sounds. The most obvious manifestation of this accomplishment is that children communicate with other people by talking. In the last section of this chapter we briefly discuss the course of the development of the communicative functions to which language is put and the development of the discourse skills involved in talking to others. 3.2. The Development of Communicative Functions Children produce vocalizations and other behaviors that have the effect of communicating before children acquire language. The cries and coos that infants produce can be interpreted by adults as signals of infants’ internal states. However, these signals — at least initially — are reflexive, and their communicative value depends on adults’ inclination to interpret these signals. A landmark in communicative development appears to be reached at 8 to 10 months when children start to use combinations of vocalizations, eye gaze, and sometimes touch for the purpose of gaining help in obtaining objects (Harding/ Golinkoff 1979, Sugarman-Bell 1978). Exactly what sort of intentions these behaviors indicate is a matter of some dispute. Shatz (1983) and Shatz/Watson O’Reilly (1990) have argued that these prelinguistic behaviors and even the seemingly communicative behaviors of 1- and 2-year-olds are evidence only that children know that they can fulfill their own goals via others. Children do not have truly communicative intentions, that is, intentions to share ideas, until they have developed an understanding of the mental states of others — typically not before 3 years. However, a less restrictive definition of communication is more common, and those adopting a more liberal stance with respect to attributing communicative intent to young children have identified multiple communicative functions served by children’s prespeech vocalizations and gestures and by children’s early speech. Chapman (1981) has surveyed the many systems that have been proposed for categorizing children’s communicative intents, and her summary suggests the following description of the course of communicative development: At 8 to 10 months infants use gesture to request objects or activity, to reject, and to comment. Between 9 and 15 months vocalization is added to and eventually replaces gesture as a means for communicating these
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same intentions. During this period from 8 to 15 months the first words typically appear, yet, despite the availability of this means of reference, children’s communicative intentions always pertain to something in the physical context. Between 16 and 22 months, as children’s linguistic skills develop, children start also to express intentions that refer to the discourse itself — they request information, answer questions, and acknowledge prior speech. At approximately 24 months children begin to use language to refer to absent objects and events and to use language imaginatively, as in pretend play. Most descriptions of changes in the functions of child speech after 2 years focus on changes in the discourse functions of speech — for example children learn to query, to answer questions appropriately, to request clarification, and so on. An exception to this is Tough’s (1977) system, which identifies four major meaningdefined functions of language in the speech of 3- to 7-year-old children: Language is used to direct the behavior of self and others, to interpret experience and to reason, to project (i. e. to refer to future events, other peoples’ internal states, and imaginary contexts) and to mediate social relations. Tough’s work focuses more on social class differences in the use of language than on developmental changes. Her controversial proposal is that children from more advantaged backgrounds use language for interpreting and projecting more frequently than do children from less advantaged backgrounds. (See Wells (1977) for a contrary view). 3.3. The Development of Discourse Skill In Western culture, adults interact with infants in formats that have the rough structure of conversation from the time the infant is born (Snow 1977). Very young babies contribute to these interactions by looking at their mothers when the mothers vocalize. However, the turn-taking structure of the early interactions appears to depend on mothers building a conversational structure around their children’s behavior, and it does not reflect interactive skill on the part of infants (Shatz 1983). There is no clear landmark that signifies the child’s entry into conversational participation. Rather, the relative burdens carried by the adult and the child in sustaining conversation gradually become more equal as children develop an understanding that they have responsibilities as conversational participants, as they learn
V. Pathologies and Disorders of Language Development
what is required of them to fulfill these responsibilities in different linguistic contexts, and as they master the linguistic devices for meeting those requirements (Shatz 1983). One-year-old children demonstrate that they know that another speaker’s utterance calls for some sort of response. An early strategy is to respond with action. This strategy is effective in allowing young children to respond appropriately to much of what is typically said to them such as Why don’t you play in the sandbox? and Where are your shoes? However, the unsophisticated basis of such responding is revealed when an experimenter asks a 2-year-old Why don’t you wear shoes on your head? and the child complies rather than answers verbally (Shatz 1978). Although children continue to rely on this action strategy in some circumstances, by 18 months children begin to more reliably respond to talk with talk, particularly in response to where or what questions (Chapman 1981). Before they reach 2 years children also respond differently to different types of utterances. They respond more frequently to questions than to non-questions (Bloom/Rocissano/Hood 1976, Hoff-Ginsberg 1990), and they respond to different forms of question with appropriately different forms of reply (Shatz 1983). Thus 2-year-old children show a rudimentary ability to participate in conversation, but children improve considerably in that ability over the next few years. One salient change is an increase in the length of conversation that children are able to sustain. Brown (1980) estimated that the number of topicallyrelated utterances children can produce in sequence (related either to their own prior utterance or to intervening utterances by adults) changed from an average of less than 1 utterance at MLU = 1.0 to an average of over 20 related utterances at MLU = 3.0 (This range in MLU, and the correlated variability in discourse skill, was found in a sample of 21 children all of whom were 30 months old.) Probably contributing to this increase in the length of conversations children can sustain are increases in children’s abilities both to initiate topics and to produce utterances relevant to the topic under discussion (Bloom/Rocissano/Hood 1976, Foster 1986, Hoff-Ginsberg 1987). The most marked change in children’s discourse that Bloom et al. found during the period from Stage I to Stage V was an increase in the proportion of children’s responses that added new infor-
57. Landmarks in Children’s Language Development
mation that was relevant to the topic of the prior speaker’s utterance. There is also development after 2 years of age in children’s sensitivity to the discourse requirements of different types of utterances as evidenced by increases in the appropriateness of their replies. For example, 2-year-olds commonly respond to why questions as though they were what questions; 3- and 4 -years-olds do so less frequently (Shatz/McCloskey 1984 ). Another developmental change in children’s conversation is the emergence of new linguistic devices for maintaining discourse cohesion. For example, anaphoric use of pronouns to refer to a noun introduced earlier in discourse begins with the use of I at Stage II, and you appears at Stage IV. Auxiliary ellipsis appears at Stage IV or V (e. g., Ellen did. in response to Who came?) (Ervin-Tripp 1978). Thus far we have been describing the developmental changes in how children fill their roles in conversation with an adult. Children also converse with peers from a farily early age. Keenan/Klein (1975), reporting on the early morning crib conversations of a pair of twin boys aged 2½, provide evidence that the children attended to each other’s utterances and produced related responses. However, many of these related responses were not topically related but rather relied on repetition and sound play to maintain discourse cohesion. More truly social conversation among peers seems to emerge around the age of 3, and children improve at sustaining conversation through the school years (Dorval/Eckerman 1984 , Garvey/Hogan 1973, Mueller/ Bleier/Krakow et al. 1977). For example, Garvey/Hogan (1973) found in the free play interactions of previously unacquainted 3½to 5-year-old children that children were able to sustain sequences of talk between 4 and 12 or more exchanges long and that between 21% and 77% of the children’s utterances were contingent on the verbal or nonverbal behavior of others. Why preschoolers are sometimes social in their conversations but sometimes produce talk unrelated to what has preceded it may have in part to do with whether the children share background knowledge. Nelson/Gruendel (1979) have suggested that true dialogue between preschoolers is facilitated when shared knowledge of routines such as planning a meal or going shopping provides a script for their conversation. (See McTear (1985) for a comprehensive description of the development of conversation). Another conversational skill
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that children have is the ability to monitor the conversations of others and to take advantage of opportunities to gain the floor for themselves. The rudiments of this ability can be seen in 2-year-olds’ intrusions into the conversations between their mothers and older siblings (Dunn/Shatz 1989), and that skill continues to develop through the preschool years (Forrester 1988).
4.
Some Closing Words
The goal of this chapter was to paint in broad strokes a picture of the course of normal language development. Of necessity, much that is interesting and important was left out. Nothing was said about language development past the age of 8 years, although the exposure to reading, to writing, and to peer influences that come with entry to school affect all the aspects of linguistic and communicative development that were discussed in this chapter. The discussion of the development of discourse skills concentrated on conversation and ignored the burgeoning research on children’s development of narrative skills. Perhaps the most serious omission for a chapter in a handbook on pathologies of language development is the omission of a full discussion of the range of individual differences in the course of early language development that nonetheless culminate in normal language acquisition. The chapter provided age ranges for the achievement of the landmarks it described, and those ranges can serve as a guide to the range of differences in language development rate that is observed in normal populations. However, normallydeveloping children differ in more than their rates of language development. Children present varied complexes of language capabilities. A metaphor for language development that has been used by several authors is that it is a rope composed of multiple independent but interwoven strands (Peters 1986, Snow 1988, Tager-Flusberg 1988). The aspects of language development that were reviewed in this chapter — phonological development, lexical development, grammatical development, and the developments of communicative intentions and conversational skills — are major strands in that rope. The evidence suggests that children follow relatively consistent orders of development along each strand, but that children vary in the rates at which they progress — not only overall, but on each
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separate strand. Each individual child’s language level at any given point in development is a composite of his or her levels of development on different strands. Using this metaphor, then, individual differences among children result from asynchronies of development along the various strands. I end this chapter with this metaphor in the hope that it helps to bridge the gap between the simplified picture of normative language development that this chapter has provided and the more complex and unique courses of development that individual children follow. Author’s note: I am grateful to JoAnn Buhr, Lucia French, Wendy Leeds-Hurwitz, and Amy Weiss for their thoughtful comments on an earlier version of this chapter.
5.
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Erika Hoff-Ginsberg, Kenosha, Wisconsin (USA)
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58. Definition and Diagnosis of Language Development Disorders 1. 2. 3. 4.
1.
Introduction Decline of the Medical Model The Psychology of Language Development Disorder References
Introduction
The human mind is biologically prepared to learn language — at a predicable age, without formal instruction, and with remarkable rapidity and case. Children begin to combine words into phrases by age two. By age three, they are producing full sentences and learning nine words a day; by age six, they are fluent conversationalists and are using language to think about hypothetical events and absent worlds. This human faculty for language learning is normally robust, but a small group of children, some 3—5% of the population (Stevenson/Richman 1976; Beitchman/Nair/ Clegg/Patel 1986), present a different picture. They are late to talk, have restricted vocabularies, struggle with oral grammar, and are frequently unsuccessful in using language as the tool of thought. Such language problems are seen in children with mental retardation, autism or hearing impairment and are presumed secondary to the neurological and/or metabolic states which underlie these syndromes. Language delays may also occur in the virtual absence of other symptoms of disorder. This condition is known as ‘developmental dysphasia’ or ’specific language impairment’ (SLI) and is discussed in detail in subchapters 61—63, 75. The purpose of this subchapter is to provide an orientation to the broader spectrum of developmental language disorders, focussing in particular on issues related to assessment.
2.
Decline of the Medical Model
2.1. The Model and Clinical Practice Developmental language disorders have been studied for almost two centuries (Weiner 1984 ) with a consequent evolution in diagnostic categories and method. For much of this period, however, the primary investigators were physicians, e. g. the Berlin Sprachärzte Treitel and Liebmann, and the frameworks used to study the disorders were con-
sistently drawn from the medical sciences. In such ‘medical models’, emphasis is placed on differential diagnosis and classification by etiology with the ultimate goal of identifying and describing the underlying condition so that a cure may be found. As practiced in North America, application of the medical model to the diagnosis of language development disorders has meant determining (a) whether a child’s language behavior meets chronological age expectations, and if not, (b) whether the language delay is the result of mental retardation, autism, hearing loss, or specific language impairment. Other conditions, e. g. elective mutism, cerebral palsy, or low vision, are recognized as having implications for language development but are not routinely considered in the diagnostic argument. Standardized language measures are the current most reliable means for answering the first diagnostic question. In order to decide whether a child’s language behavior meets age expectations, the clinician must have normative data on the language performance of children at various ages. At best, these data should come from ecologically valid tasks, administered to large, well-described and representative groups of children. The data should also reflect language knowledge of diverse sorts, have proven predictive value, and be organized so as to indicate variance as well as central tendency. Since the development of normative instruments requires considerable time and expense, it is not surprising that only a few of them meet many of these criteria (McCauley/Swisher 1984 ). Psychometric weaknesses clearly compromise the decisions made from normative data. Even when quantitative criteria are met, clinicians must frequently choose reliability and representativeness over ecological validity. Normative data from spontaneous language samples may eventually remedy that situation, but as yet such data come from modest sized samples (e. g. Miller/Chapman 1981; Rescorla 1989), limited population sectors (Lee 1974 ), and/or earlier times (Templin 1957). Despite these problems, in all but the most extreme cases, only standardized language measures can confirm the presence of a delay in language development and determine the extent of that delay. Having concluded that a language delay exists, the clinician operating from within the
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medical model continues on to make decisions about the condition which underlies this delay. Audiometric testing is used to establish hearing acuity; neurological examination to establish motoric function; intelligence tests, particularly those requiring little or no language, to measure mental abilities; and psychiatric interviews and/or observations to determine the normalcy of the child’s socioemotional development. Informed by these additional data, the clinician assigns the child to one or another diagnostic category. Children with subnormal nonverbal intelligence, normal hearing, and no signs of affective disturbance are diagnosed as ‘mentally retarded’; children with poor auditory acuity are diagnosed as ‘hearing impaired’; children with an early lack of social responsiveness, or inappropriate affect and rigidity are diagnosed as ‘autistic’; children with normal nonverbal intelligence, normal hearing, and normal social relations are diagnosed as having ‘specific language impairment (developmental dysphasia)’. In practice, of course, the decisions are seldom so straightforward. Clinicians frequently find themselves debating the proper category for a child whose language seems poorer than would be expected for the extent of a hearing loss, or whose level of nonverbal intellectual development is lower than age expectations but higher than language levels. It is also increasingly unclear how the child with frank neurological impairment fits into this scheme. Until recently, specific language impairments were presumed to imply neurological dysfunction (Proceedings, 1962). Proof of that dysfunction was useful, but was not considered necessary to the diagnosis given the absence of all other etiological factors and the presence of the language delay itself. This, of course, led to groups of children with widely varying degrees of neurological involvement. Perhaps to minimize this diversity, some researchers now define ‘specific language impairment’ so as to exclude children with known neurological dysfunctions (Stark/Tallal 1981). Incorporation of this shift into clinical practice would require some subdivision of the SLI category. In short, working within the tradition of the medical model, clinicians and scientists have established the major parameters of diagnosis for developmental language disorders and have generated large literatures on topics such as ‘specific language impairment’, ‘language in the retarded’, ‘language in autism’, etc. There are now, however, growing signs
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that the conventional categorical approach to developmental language disorders may no longer be productive (Lahey 1988; Marge 1972). 2.2. Shortcomings of the Medical Model 2.2.1. Lack of Empirical Validity Only one group of researchers to date has reported a validation study for the categorical labels that are traditionally assigned to language disordered children. At Stanford University, Rosenthal/Eisenson/Luckau (1972) used cluster analysis techniques to group 82 language disordered children who had been examined at a suburban medical centre. Thirty two variables derived from medical examinations, EEG, psychological testing, and language testing were involved in the analysis. The researchers’ goal was to compare the resultant clusters with the groupings created by the diagnostic judgements of the centre’s staff, i. e. dysphasic, hearing impaired, apraxic, disarthric, retarded, autistic, maturational lag (organic). In fact, the statistical analysis yielded only two clusters of children, those originally designated as retarded or autistic, and those designated as hearing impaired, dysphasic, or maturational lag (organic). Within these two groupings, children were not reliably different; between the groupings, differences were primarily related to nonverbal intellectual functions, children in the first cluster functioning at lower levels. A further attempt at analysis used a reduced number of variables, two from psychological tests, two from observations of emotional health, and twelve from the medical examination. When applied to data from 138 children, this matrix yielded only one cluster, the retarded/autistic cluster (N = 71) identified previously. Each of the remaining children merged as a ‘group’ of one. Rosenthal and his colleagues conclude that “the original diagnostic categories ... are neither unique nor homogeneous with respect to measurements routinely collected in the course of clinical evaluation” (1972, 135). Since the time of the Stanford study, there have been important refinements in the clinical taxonomy. Autistic children are now routinely designated as ‘high functioning’, i. e. with normal range nonverbal intelligence, or ‘low functioning’. The criteria for autism have also broadened (DSMIII 1980) so as to include children with more diverse and milder disturbances, children who might once have
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been classified as ‘autistic-like’ or ‘language impaired with affective problems’. Children with mental retardation are now more frequently subcategorized by etiology, e. g. organic versus familial (Zigler/Hodapp 1986), and by behavioral profiles, e. g. without or without specific language impairment (Miller 1988). These refinements may make it possible to validate the traditional clinical categories. A very large scale effort to do so is underway. Researchers at six university centres, under the current direction of I. Rapin, have been administering a comprehensive battery of psychological, psychiatric, medical and language examinations to some 500 children with autism, mental retardation, or specific language impairment. The children are being seen longitudinally at both preschool and school ages, with electrophysiological and magnetic resonance imagery data collected at the latter point. There is no doubt that this project will provide rich data on the psychosocial functioning of children with language disorders. Whether it meets its own goal of creating an “empirically based common nosology of higher cortical disorders of childhood” (Rapin 1990) remains to be seen. In the meantime, there is little empirical foundation for use of the medical model in studying language disorders. If children labelled as mentally retarded, for example, are not reliably different in behavior than those labelled as autistic, describing the medical condition of retardation or autism is not likely to explain the behavior, linguistic or otherwise. 2.2.2. Behavioral Syndromes Without Cause Even if clinical categories had sharper boundaries, the traditional framework would still prove disappointing in its failure to address true etiologies. Although the medical model is oriented towards causal conditions, the taxonomy that is commonly applied to children with language disorders refers only to behavioral syndromes, h e a r i n g i m p a i r m e n t being the major exception. If all goes well, behavioral syndromes are early heuristic tools that lead researchers to discover causal states and their cures. In the case of language disorders, however, it seems that the clinical categories have obscured more than they have revealed. M e n t a l r e t a r d a t i o n is now known to result from a large and heterogenous collection of conditions that are metabolic (e. g. PKU), neurological (e. g. anoxia),
V. Pathologies and Disorders of Language Development
physiological (e. g. lead poisoning), or genetic (e. g. Fragile X) in character. With such diversity, the single fact that a child’s language delay is associated with retardation can imply neither cause nor cure. The likelihood of heterogeneity is also a theme in the current literature on a u t i s m (Wing/Attwood 1987), but efforts to establish the organic roots of this syndrome have not yet borne fruit (Prior 1987). Appeals to the condition of autism as an explanation for language delays remain empty. Finally, consider the inclusion of s p ec i f i c l a n g u a ge i m p a i r m e n t or d eve lo p m e n t a l d ys p h a s i a as a diagnostic category within the medical model. As noted in 2.1, the diagnostic criteria for this category have evolved so as to systematically exclude most of the possible etiological factors, i. e. intellectual deficit, affective disorder, sensory or motor impairment, frank neurological insult. We are thus left with the paradox of an ‘etiological’ category which is defined by the absence of causal indices. One recent paper has gone so far as to suggest that the condition has no cause other than the normal distribution of language abilities among individuals (Leonard 1987). In the context of that argument, the promise of the medical model seems particularly hollow. As things now stand, the categories applied in the traditional diagnosis of developmental language disorders seldom refer to single conditions with known etiologies that can be identified and/ or treated. 2.2.3. Absence of Unique Treatments A third shortcoming of the medical model can be found in reports of language intervention with children. A wide variety of treatment programs are in current use by speechlanguage pathologists and educators in North America. They differ in the degree to which they rely on behavioral modification techniques, respond to the child’s spontaneous activity, focus on pre-selected goals, or incorporate family members. They also employ different types of linguistic interaction, from imitative drill to free conversation. Many of the intervention programs have been subjected to controlled tests of effectiveness, and a recent meta-analysis indicates that “the average language disabled child involved in language intervention can be expected to perform better than 85% of [those] ... not receiving language intervention” (Nye/Foster/ Seaman 1987, 350). However, the literature gives no indication that one type of treatment
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is more effective than another for children in a particular diagnostic category. Instead, master clinicians argue that the same principles of intervention apply regardless of diagnosis (Fey 1986; Lahey 1988). 2.3. Contributions of the Model The shortcomings of the medical model indicate that alternate frameworks are needed for the study and treatment of children with language disorders. In developing such frameworks it will be important to maintain the strengths of the traditional approach. These contributions lie in two areas. First, the medical model treated l a n g u a ge b e h av i o r a s a s y m p t o m of some underlying disturbance. Longitudinal studies of children with specific language impairment attest to the wisdom of that stance. Even when these children learn to speak in ways that seem age appropriate, they continue to have trouble with academic tasks such as reading and mathematics (e. g. Aram/Ekelman/Nation 198 4 ; Scarborough/ Dobrich 1990; Stark/Bernstein/Condino/et. al 1984 ). By one interpretation, these data indicate some continuing, if hidden, specific impairment in language functions. It is also possible, however, that the impaired learning mechanisms that underlay the language delay in the first place remain operative and cause later difficulties with analogous tasks. A second contribution of the medical model has been to orient us to the ge n e r a l n a t u r e o f s u ch m e ch a n i s m s. At the foundation of the traditional classification scheme is a set of psychological constructs such as intelligence, emotion, social relationship, and perceptual ability. These global parameters do not suffice to create unique classificatory groups: children with diagnoses of specific language impairment, mental retardation, or autism may all have intellectual impairments; children with diagnoses of autism, specific language impairment, hearing impairment, or mental retardation may all evidence emotional disturbance, and so forth. Nevertheless, these global parameters do draw our attention to the sorts of factors which determine language acquisition and use. 2.4. Conclusions It is time to rethink our commitment to the use of the medical model in studying and treating children with language development disorders. The traditional diagnostic categories have little empirical support, little ex-
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planatory value, and little connection with treatment possibilities or practice. A more useful framework might be one that emphasized psychological states and mechanisms rather than physical conditions, that focused on individuals rather than groups, that stressed description rather than diagnosis, and that aimed towards effective intervention rather than cures. Steps in this direction have been taken by a number of researchers and clinicians over the past two decades. These scholars draw on contemporary linguistic and psychological theories to explain the language behavior of disordered children and to develop therapeutic regimen. At the same time, they use groups of language disordered children as natural experiments for the testing and validation of these theories. The products of this symbiosis will be reviewed in the following sections, again emphasizing issues related to assessment.
3.
The Psychology of Language Development Disorder
This ambitious heading suggests more than will be delivered. It may also offend those who would prefer to see l i n g u i s t i c s mentioned explicitly. However, if we take the term ‘psychology’ in its general sense to include psycholinguistic models, the phrase Psychology of Language Development Disorder captures much of the emergent alternative to a medical model. Clinicians and researchers who work from within contemporary, nonmedical frameworks purpose a somewhat different assessment task than the traditional practitioner. They also use a wider range of assessment procedures and hence have come to new understandings of the nature of atypical language acquisition. 3.1. Assessment Tasks and Procedures The first assessment task within non-medical models is still to decide whether or not a child’s language performance is in accord with chronological age. The second goal is not, however, to determine which condition has caused the delay, but to describe the child’s current language knowledge and the resources he or she will bring to the language learning task. This description is seen as the key to effective intervention (Crystal 1984 ; Fey 1986; Lahey 1988; Lund/Duchan 1988). Standardized measures remain necessary to establish language and/or intellectual delays. They may even be necessary to establish rel-
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ative levels of proficiency in various linguistic and/or cognitive domains. However, informal procedures, including the collection and analysis of spontaneous language samples, are the preferred tools for description (Fletcher 1991). Standardized measures provide reliable performance comparisons, but they usually demand metalinguistic/metacognitive skills, and a close adherence to established task procedures. Moreover, with most normative instruments, children are not free to pursue their own interests or speak their own communicative intents. [Schemes such as Lee’s (1974 ) Developmental Sentence Analysis are the rare exception to this rule.] For these reasons, tests frequently underestimate the knowledge implicit in a young child’s everyday language usage (e. g. Prutting/Gallagher/ Mulac 1975). Yet it is exactly this knowledge which is central to intervention planning. What the child already knows about language influences his or her interpretation of new exemplars and hence determines what will or can be learned (e. g. Clark 1987; MacWhinney 1987; Peters 1983; Pinker 1989). No procedure captures this knowledge better than the systematic observation of spontaneous communication. The scope of this informal analysis will be guided by the clinician or researcher’s theory of language, particularly in regard to the range of pertinent subsystems and their key features. Most investigators will, however, include analyses of the lexicon, sentence patterns (semantic relations, phrase structures, or predicate-argument structures), phonology, morphology, and patterns of use (e. g. speech acts, adherence to conversational postulates, discourse schemes). The descriptive task must also be guided by broader theories of mind and person, since the resources a child brings to language learning include a variety of nonverbal, even nonintellectual, functions and schemes. Standardized tests may be useful, but informed observation of spontaneous play can again reveal much about a child’s real-life conceptual repertoire, attention span, problem solving abilities and social relatedness. Here the nonmedically oriented investigator tries to determine those states and mechanisms which will facilitate or hinder further development. What has been learned in these efforts to study language development disorders from within contemporary, non-medical models of language psychology? Without pretending to be comprehensive, and skirting many of the current theoretical debates, the following ex-
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amples will serve to illustrate the value of this approach. Each section will begin with a brief statement of the basic psychological principle which informed the clinical investigations. 3.2. New Perspectives on Language Disordered Children 3.2.1. Language Knowledge is Abstract and Categorical Psycholinguists are currently debating the nature of the processes which lead to the mental representation of language categories such as Subject. Some prefer to speak of hypothesis testing and rules, some of parameter setting, and others of the emergence of hidden nodes in neural networks. No one seems to be arguing, however, that language schemes are simple records of past behavioral events. Chomsky’s maxim that language knowledge must be abstract to account for the speaker’s productivity is still the consensus view. This principle has influenced our understanding of language development disorders in at least two ways. First, it illuminates the ‘rote’ language seen in certain autistic, retarded or language impaired children. Fay/ Schuler (1980, 78), for example, report a child who said sea scallops to eat whenever he saw a particular type of automobile tail light. Traditional views of such expressions have treated them as bizarre metaphors. However, the contemporary investigator, informed by an understanding of language knowledge as abstract and productive, tells a more interesting story. Children who use expressions of this sort seem to be learning unanalyzed phrases as single lexemes. This hinders their integration into larger systems of categorical rules, and leads to particularistic use (Prizant 1983). A predominance of such forms would greatly restrict abstraction and productivity. The importance of these expressions thus lies not in their lack of conventionality, but in their implications for the developing language system. A second clinical lesson from this principle concerns the phenomena of generalization. Interventionists frequently report that children with language disorders learn new language patterns in therapy but fail to use these patterns outside the lesson. Traditional views would hold that language disordered children somehow fail to generalize their linguistic knowledge. Contemporary investigators, informed by the principle of abstraction, suggest a different interpretation. Such children
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may not have learned an abstract language pattern at all, or at least not one of the expected breadth (Johnston 1988a). Clinicians may help a child to say cow eat, dog eat, baby eat, etc. and believe they are teaching the Noun + Verb pattern, when in reality the child is only learning a local rule for the activity predicate EAT. In such cases, if the child later fails to say things such as doggy run, this behavior would indicate a lack of categorical knowledge rather than some failure to use known forms in new situations. Now that the possibility of under-analysis and lexically-bound ‘rules’ is clear, clinicians are learning to assess productivity before assuming that a disordered child knows a particular language pattern. For example, distributional analysis of various lexemes in spontaneous speech can help determine the extent to which a given word occurs in a variety of linguistic contexts. Such analyses are increasingly possible with the advent of language sample analysis software such as SALT (Miller/Chapman 1985). 3.2.2. Language Knowledge is Multiplex Scholars may disagree over the structuring, autonomy or origins of various linguistic subsystems, but there is no disagreement over the fact that language is comprised of diverse and systematized domains of knowledge. This principle has led to the solution of at least one clinical enigma and the setting of a major research and clinical agenda. The enigma arose out of the literature on children with s p e c i f i c l a n g u a ge i m p a i rment. Throughout the 1970s, a series of research studies reported that these children learned grammatical morphemes, phrase structure rules and certain lexical families in a surprisingly normal fashion. Acquisition of these forms was ‘delayed’, but the order in which they were learned and the developmental errors which occurred were highly similar to the patterns seen in normal children. Many clinicians, however, continued to hold the traditional view that children with specific language impairment used ‘deviant’ language. A resolution to this conflict began to emerge when investigators, informed by the multiplexity principle, proposed that various subsystems of language might be developing with a lack of normal synchrony (e. g. Johnston 1982; Kemp 1983). Subsequent research data confirmed this hypothesis. Earlier studies had focused on separate subsystems and thus in-
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dicated normalcy, but when several domains were viewed simultaneously, the total language system was revealed to be developing in an asynchronous fashion (Clahsen 1989; Johnston/Kamhi 198 4 ; Liles/Watt 198 4 ; Moore/Johnston in preparation). The likelihood of asynchronous language development in disordered children makes the ‘linguistic profile’ a clinical and research necessity. Bloom/Lahey (1978; Lahey 1988) have long argued for broad stroke profiles that contrast a child’s command of language fo r m, c o n t e n t and u s e. It now seems additionally important to elaborate such profiles w i t h i n the formal domain, contrasting competencies in, for instance, morphology, sentence patterns and the lexicon. (See Crystal 1982; Johnston/Ammon/Kamhi 1988; Miller 1982 for illustrative analysis systems.) Given asynchronous development, no single language measure can represent a child’s current knowledge and provide a basis for intervention plans. Moreover, if we assume that ‘dips’ in a linguistic profile reflect some specific deficiency in the underlying learning mechanism, single measures will obscure psychosocial differences among disordered children that could be important for treatment or research. On the other hand, descriptive analyses of language competence in several domains can represent the child’s verbal strengths and weaknesses, and can alert the practitioner to important experiential, perceptual, social and/or intellectual constraints on further learning. In short, recognition of the multiplex nature of language knowledge and subsequent evidence of asynchrony have added linguistic profiles to the assessment agenda. 3.2.3. Language Acquisition is Orderly Detailed accounts of acquisition patterns have revealed an impressive orderliness in the way in which language knowledge develops, both within and across languages. Fine grained analyses have sometimes revealed alternative paths from one knowledge state to the next, but major deviations from the common sequence of surface patterns have proven rare. Researchers differ in their explanations for this orderliness, some emphasizing constraints within the language system, others emphasizing perceptual and cognitive factors or input variables. The normally predictable course of acquisition for a given language most probably reflects an interplay of all of these causal vectors.
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Armed with knowledge of the common patterns, researchers have been able to describe the language acquisition of disordered children in considerable depth. What is most remarkable about these data is the degree to which language ‘disordered’ children have been revealed to be ‘normal’. Mentally retarded children (Abbeduto/Rosenberg 1987), autistic children (Paul 1987), and children with specific language disorders (Johnston 1988b; but see also Grimm 1987) seem to learn language patterns in much the normal order, albeit late and more slowly. Where there is evidence of subsystem asynchronies, e. g. morphological problems for SLI children, vocabulary peaks for retarded children, or pragmatic gaps for autistic children, the normal causal influences can still be seen to be at work. For example, Rom/Leonard (1990) use Hebrew and English data to argue that basic p e r c e p t u a l m e ch a n i s m s may be at the root of failure to master unstressed grammatical morphemes. These researchers also recognize the role of f u n c t i o n a l i t y, i. e. the relative importance of morphology in expressing semantic intent, as do Lindner/Johnston (in press) arguing from German and English data. Analogous arguments pointing to the influence of l i fe ex p e r i e n c e in vocabulary learning and the influence of s o c i ab i l i t y in illocationary choices are made by Fazio/Johnston/Brandl (in press) and Johnston (1985b). Even the truly odd language behavior of some disordered children has assumed a degree of normalcy when viewed through the frameworks of language psychology. Echolalia is a good case in point. Immediate imitation of utterances used to be cited as proof of the bizarre, superficial nature of autistic language. However, such imitation is now know to be linked to language level (Caparulo/Cohen 1983; Howlin 1982), selective (e. g. Paccia/Curcio 1982), often functional (Prizant/Duchan 1981; Tager-Flusberg/ Calkins 1990), and associated with more positive outcomes (Caparulo/Cohen 1983; Howlin 1982). Moreover, it frequently occurs at rates which fall within the range observed for young normal children (e. g. Cantwell/Baker/ Rutter 1978). Imitative language in some autistic children persists longer than is normal, and it may have unusual phonetic veridicality, but it is not generally rote or meaningless. The overwhelming normalcy of language development in disordered populations has revolutionized clinical practice in many countries. Disordered children are now routinely
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assessed by reference to normal ‘stages’ of acquisition (e. g. Crystal/Fletcher/Garman 1976; Johnston/Ammon/Kamhi 1988; Lahey 1988; Miller 1982), and normal data provide the basis for intervention programs in virtually all theoretical camps (Fey 1986, 101—8), the notable exception to this rule being the North American ‘special education’ establishment responsible for schooling. Greater sophistication in applying the normal data will be needed as we learn more about the extent and causes of developmental asynchrony. There may be, after all, no particular merit in replicating normal acquisition patterns if a given disordered child has resources which would allow him/her to forge ahead in particular areas of language competence. Psychological models of language development should continue to provide guidance in this regard. 3.2.4. Acquisition Depends on the Analysis of Exemplars Children learn the language they hear. As they interact with care-givers and peers, children are provided with a stream of utterances which illustrate how to express various intents. Researchers argue as to whether specific features of this ‘linguistic input’ are keys to learning. How important is it for care-givers to talk about events which have already captured the child’s attention? Or to repeat portions of what the child has just said, in a more grammatical fashion? Researchers also argue about the way in which the input data lead to changes in knowledge. Do children store exemplars for pattern induction? Do they compare exemplars to their own inner version of the same utterance? Do they d o anything at all? This, of course, is language psychology’s version of the nature-nurture debate and there is little chance of a single outcome. Even in the absence of conclusions, however, this literature has had a clinical impact by drawing attention to the role of language input. One line of investigation has focused on the nature of the language used by parents of disordered children. As an extension of the folk wisdom which holds that late-talkers merely lack a reason to speak, researchers have wondered whether language disordered children receive normal input. The answer, thus far, appears to be yes. Investigations of parental speech to mentally retarded children (e. g. Rondal 1978), autistic children (Howlin/ Rutter 1989), and children with specific language disorders (Grimm/Weinert 1990; Leon-
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ard 1987) have produced scant evidence to support the view that these children fail to learn because of the language they hear. Instead, parents of such children seem to speak to them in ways which are largely normal for their levels of language competence. The language environment of disordered children does not seem to explain their language delays, but it may nevertheless play a key role in facilitating acquisition. The key to this paradox is the notion of ‘supra-normal’ input. Using psychological reports on ‘motherese’ and cognitive processing, some theorists now argue that language disordered children are ill-equipped to analyze regularities in the utterances they hear and thus require specially crafted input (e. g. Fey 1986, 21, 168—189). In the words of Lahey, “what may be an effective linguistic environment for the child learning language without difficulty may not be effective enough to facilitate language learning in the language disordered child”. (Lahey 1988, 356). Caregivers, teachers and practitioners can assist poor language learners by presenting exemplar utterances at high proportional frequencies, in contexts which clarify meaning. Prosody and discourse can also be manipulated so as to highlight forms that may otherwise go unnoticed, and to illustrate just those linguistic patterns which correspond to the child’s language level and communication needs (Johnston 1985c). Such techniques seem to provide unusually accessible data from which to learn, and have led to accelerated language growth in both normal and disordered children (e. g. Campbell/McNeil 1985; Hoff-Ginsberg/Shatz 1982; Johnston 1988a; Leonard 1975; Nelson 1976; Schwartz/Chapman/Terrell et al. 1985). Caregivers will differ, however, in their facility with the on-line metalinguistic analyses that are required by some of these procedures. This creates a new focus for collaborative assessment as clinicians and caregivers cooperate in determining how and when the language of the home should be altered. 3.2.5. Acquisition is Bound to Cognitive Development This is surely the most controversial of the principles discussed in this chapter, and a point at which psychologists and linguists are likely to diverge. In part, the disagreements are theory based and concern the degree to which language is modularized. However, the debates also stem from a failure to recognize that the relationships between language and
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cognition vary with developmental level and with the aspect of language or cognition being considered (Johnston 1985a). Even for committed cognitivists, the literature in language psychology suggests four different sorts of developmental linkage between language and non-verbal cognition. First, early intellectual development seems to pave the way for language as the infant builds social relationships and learns to think instrumentally. At later ages, cognition can be seen to provide the general mechanisms for language analysis, and the components of meaning for verbal symbols. Finally, language, once learned, seems to be a powerful tool for reflection and problem solving. The first and last of these hypothesized relationships have had particular impact on our understanding of language disordered children. Piagetian accounts of infancy have fuelled numerous studies of the connection between sensori-motor intelligence and language learning. The usual research question has focused on whether or not a particular level or product of intellect is prerequisite to language. To date, the strongest evidence points to the importance of Stage V intelligence: children who have not at least attained the means/ends reasoning, imitation skill, and object-related actions which are characteristic of this Stage do not seem to produce referential speech (e. g. Bates/Benigni/Bretherton et al. 1979; Ingram 1978; Snyder 1978). Research with the mentally retarded indicates that this constraint holds true even at older ages (Kahn 1975). The clinical implications of these findings seem quite clear. Some nonverbal retarded children or low functioning autistic children may not yet be cognitively prepared for language. Others may have achieved a general cognitive level which would support verbal communication, but have specific learning disorders which impede their analysis of the language system. Clinicians familiar with the frameworks of language psychology are now including cognitive assessments to try to distinguish between these two groups of nonverbal children. A second, and quite different, sort of hypothesized relationship between language and cognition has influenced our understanding of specific language impairment. Insights in this case have come from the recognition that language is normally one of the major tools of representational thought (Olson 1975). Studies of visual imagery (e. g. Kosslyn 1980), as well as studies of deaf and SLI children
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(e. g. Furth 1966; Inhelder 1966) have made it clear that language is not the sole path to reflective problem-solving. Language does, however, provide unique resources for propositional reasoning, and it thus seems u nlikely that a person with limited language facility would be fully capable of normal intellectual achievement. How then are we to understand children with specific language impairment? Do they disprove the psychological theory, or have we over-estimated their mental abilities? Research in the last decade supports the latter conclusion. In spite of their normal-range nonverbal IQ, children with SLI have performed less well than their age peers on a wide range of nonverbal cognitive tasks. (See Johnston 1988b for a review.) The exact nature of these deficits is not yet known, but they may stem, at least in part, from limitations in attentional capacity. Johnston/ Smith (1988) found that language impaired preschoolers had difficulty with verbal problem solving even when they could demonstrate knowledge of all of the elements required by the problem space. What they seemed unable to do was to use these resources simultaneously in the service of a particular reasoning task. Data of this sort suggest that the focus in clinical assessment must broaden to include language p e r fo r m a n c e as well as language c o m p e t e n c e. To succeed in language tasks, whether communication or thought, children must know the language system and be able to draw on this knowledge in a reliable and economical fashion. Extending Fletcher’s argument, clinical assessments must gather evidence “not so much from syntax, but from syntax deployed in the language-production process” (Fletcher 1991, 186). This may require new techniques designed to measure a child’s relative degree of mastery with familiar language patterns. 3.3. Summary and Conclusions The renaissance of language psychology in this half of the twentieth century has had a profound impact on our approach to developmental language disorders. Some researchers and clinicians continue to search for firstcauses and cures; they make use of traditional diagnostic categories in the hope that these groupings will point the way to an underlying causal condition. Other researchers and clinicians, however, have abandoned such medical models, and have built a new framework
out of the principles of contemporary psycholinguistics. To greater and lesser degrees, they have moved beyond diagnosis to description. They have become less interested in conditions and more interested in characterizing the child’s current knowledge state and learning mechanisms. When they invoke the traditional categories of developmental language disorder, they do so merely as a convenient shorthand for constellations of psycho-social variables. The purpose of the present chapter has been to explain this shift in orientation, and to illustrate the sorts of assessment questions which have emerged from the frameworks of language psychology: — Is this child intellectually and socially prepared to learn language? — What does this child know about language? and what is he or she likely to learn next? — Which aspects of this child’s language are productive? — How fully does this child control familiar language schemes? — Are there aspects of language which are relatively easy or difficult for this child to learn? — Does this child have intellectual, social or environmental resources which will make it possible to ignore the common acquisition sequences when selecting learning goals? — How and where can language input be altered to facilitate this child’s learning? These questions are no easier to answer than the questions of differential diagnosis, but they seem to have a more direct application to the practice of language intervention. As we learn to answer them, we immediately improve our ability to help language disordered children become effective language users. This is an admittedly practical stance, one in which hopes for a cure have been tempered by the reality of persistent learning deficits. But it is also a visionary stance, one that insists on language as a human birthright.
4.
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Aram, D., Ekelman, B., & Nation, J. (1984 ). Preschoolers with language disorders: 10 years later. Journal of Speech and Hearing Research, 27, 232—244. Bates, E., Benigni, L., Bretherton, I., Camaioni, L., & Volterra, V. (1979). The emergence of symbols: Cognition and communication in infancy. New York: Academic. Beitchman, J., Nair, R., Clegg, M., & Patel, P. (1986). Prevalence of speech and language disorders in 5 year old kindergarten children in OttawaCarleton region. Journal of Speech and Hearing Disorders, 51, 98—110. Bloom, L. & Lahey, M. (1978), Language dev elopment and language disorders. New York: John Wiley. Campbell, T. & McNeil, M. (1985). Effects of presentation rate and divided attention on auditory comprehension in children with an acquired language disorder. Journal of Speech and Hearing Research, 28, 513—520. Cantwell, D., Baker, L., & Rutter, M. (1978). A comparative study of infantile autism and specific developmental receptive language disorder — IV: Analysis of syntax and language function. Journal of Child Psychology and Psychiatry, 19, 351—362. Caparulo, B. & Cohen, D. (1983). Developmental language studies in the neuropsychiatrie disorders of childhood. In K. E. Nelson (Ed.), Children’s language, 423—463. New York: Gardner. Clahsen, H. (1989). The grammatical characterization of developmental aphasia. Linguistics, 27, 897—920. Clark, E. (1987). The principle of contrast: a constraint on language acquisition. In B. MacWhinney (Ed.), Mechanisms of language acquisition. 1—34. Hillsdale, NJ: Lawrence Erlbaum. Crystal, D. (1982), Profiling linguistic disability. London: Edward Arnold. Crystal, D. (1984 ), Linguistic encounters with language handicap. Oxford: Basil Blackwell. Crystal, D., Fletcher, P., & Garman, M. (1976). The grammatical analysis of language disability. New York: Elsevier. DSM III (1980). Diagnostic and statistical manual of mental disorders (Third Edition). American Psychiatric Association, Washington, D. C. Fay, W. & Schuler, A. (1980). Emerging language in autistic children. Baltimore: University Park. Fazio, B., Johnston, J., & Brandi, L. (in press). Relationship between mental age and the development of vocabulary consisting of labels versus relational terms among mildly mentally handicapped children. American Journal of Mental Deficiency. Fey, M. (1986). Language interv ention with young children. San Diego: College Hill.
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Judith R. Johnston, Vancouver (Canada)
59. Neurological Aspects of Language Development Disorders 1. 2. 3. 4. 5.
1.
Introduction Hemisphere Structure Associated Neurological Abnormalities A Critical Period for Language Acquisition? References
Introduction
The allegedly unique potential of humans to develop language is based on the coordinated activity of their cerebral and thalamic/basal ganglia circuitry. The subcortical nuclei are involved in adopting verbal mental set, the
task-specific activation of the cortical language areas (Cambier/Elghozi/Strube 1979, Ojemann 1975) and transducing verbal thought into speech. The cerebrum assumes the major role in language processing. Therefore the neurology of language development is primarily cerebral neurology. It subdivides into the normative and the clinical: How the language area and its connections differentiate in the course of normal brain maturation, and how pathology of early onset — structural, genetic and metabolic disease — compromises this aspect of brain maturation.
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Conceivably, environmental variables (deprivation, stimulation) also affect the differentiation of language circuitry (Bertenthal/ Campos 1987). Spurred by claims for a unique ‘language acquisition device’ in the human brain, much effort has been expended on inquiry into the nature of the neural substrate for language. Neurolinguistics have sought support for the view that language represents a discontinuity, not only in the evolution of communicative systems, but also in the underlying neural hardware. Is the language area a focal dedicated (‘modular’) neural system, and one that cannot be replaced by other areas of brain, at least after an initial ‘plastic’ period, during which true language, transcending mere indexical utterance, is still emerging? Or is a continuity view more defensible; that language cortex is quite variable in location between individuals and readily if not fully replaceable at any age? Neither macroscopically nor microscopically are there any attributes of neuronal morphology, or of neuronal connectedness, that uniquely characterize those areas of cortex that implement language function. This inability to verify modularity of language at the neuronal level may be because wide areas of cortex harbor language potential, and no distinctive language neurohistology exists. Alternatively, what in fact differentiates language from general cognitive cortex has so far eluded observation. In either case, it becomes necessary to adopt indirect means to locate language cortex. One way to do so is through observing the effects of brain damage. Inferences about the neurological substrate of language development can be based on the effects of early damage of the language area. As in adults, given enough cases, it might become apparent which locations when damaged result in impaired language function, and which do not. Such effects can be obscured, however, by the compensatory potential of brain areas that would not in the normal course of events subserve language. This comes to light when the classical language area is damaged early on. In children, language compensation may be complete (Alajouanine/Lhermitte 1965), so that unless the language status is assessed acutely, immediately after the damage is done (which may not be practicable) no deficit is observed. Alternatively, language compensation may be incomplete (St. James Roberts 1981), either
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because the undamaged parts of the brain that compensate were not fully suited to assume language control, or because those that could have were also damaged by the insult. Evidence from pathology derives from cases in which the abnormality preponderantly impacts on language development. It excludes generalized mental retardation. However, certain genetic mental redardation syndromes do have a disproportionate effect on language (Down syndrome, fragile X, Williams syndrome). The chromosomal basis of specific developmental language disorders is discussed by Netley (1983). Yet there is no independent evidence that these pathologies target the classical language area. This may be because, if damage is purely local, it would normally be substantially compensated by the developing brain. Specific developmental language disabilities similarly do not afford evidence of frank left hemisphere damage. These cases often give evidence of genetic transmission, in the form of pedigrees in which language problems are prominent (Ingram 1959). 24 % of his 75 probands had a least one parent with language difficulty as did 23% of their siblings. Similar conclusions were reached by Bishop/Edmundson (1986) and Tallal/Ross/Curtiss (1989). A genetic causation for delayed language development leaves it open whether what is transmitted is a tendency toward rather subtle miswiring, or a risk factor for experiencing insults that induce neuronal dysgenesis at some stage during fetal existence. In normally developing righthanders the left hemisphere is responsible for all aspects of language, except perhaps intonation (prosody) and some higher levels of verbal comprehension, including humor. But in the majority of nonrighthanders, language is bilaterally represented, apparently without loss of efficiency. How does left lateralization of language develop, and what is its functional significance? Evidence on the development of language lateralization can be organized in relation to two competing hypotheses — progressive lateralization (Lenneberg 1967) and invariant lateralization (Kinsbourne 1975). The former conforms to a broad perspective on the emergence of the brain basis of higher mental functions, that exalts both the ‘language acquisition device’ and its lateralization as uniquely human. This is that greater lateralization of the brain basis corresponds to more sophisticated function, of the behavior that is
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represented, both in phylogeny and in ontogeny (Lenneberg 1967). As presented, progressive lateralization generally encourages a ‘discontinuity’ view, granting language special status. No corollary suggestion is made that nonverbal functions, such as those subserved by the right hemisphere, also emerge from a bilateralized base. Such a view would anticipate that lateralization is most marked for the neural representation of the highest level of behavioral control, in the brains of the behaviorally most sophisticated species, and, within a species, in those subgroups and individuals whose brains are most mature and whose behavioral control is most effective. The progressive lateralization hypothesis has spawned a multitude of hypotheses, according to which one would expect incomplete or absent lateralization in nonhuman species, in very young children, in mentally retarded, language impaired, learning deficient and even stuttering humans. Even gender differences among humans have been rationalized under the aegis of this sweeping hypothesis. Correspondingly, it also predicts that any group that deviates from the norm in including a greater proportion of ill-lateralized individuals (notably lefthanders) should evidence a relative language or other cognitive inferiority. New predicitons along these lines continue to be made, even though convincing support has not been forthcoming for this line of reasoning. Progressive lateralization offers theorists a hypothetical process, the shift of language control from both hemispheres into the language ‘dominant’ hemisphere. This process might not yet have evolved in animals that have no language capability and might be unavailable to totally nonverbal humans. It may be delayed in those whose language development lags behind the norm. It may arrest prematurely in those whose language development arrests at a subnormal level. And, of practical importance, if it is slow to develop, or if it has prematurely arrested, then perhaps maneuvers can be devised which would get the lateralization process going again. This would enable the language therapist to bypass the demanding and often thankless task of remediating the language function by working on it directly. This tantalizing prospect contributes intensity to the continuing interest in the progressive lateralization model. In contrast, according to the invariant lateralization hypothesis the origins of language rely on the same general area of brain that
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ultimately controls it in the fully mature individual. Usually this is the left hemisphere, but it can be the right hemisphere, or both hemispheres. In neither minority case does it follow that, in the absence of accompanying brain damage, any inferiority of language function would be expected. If one were to discover that in some language-deficient group, language lateralization is anomalous, this would not, according to the invariant lateralization hypothesis, serve to explain the language deficiency. Progressive lateralization predicts that asymmetries of brain organization should become increasingly evident in those species whose behavioral control is relatively advanced. This expectation conflicts with a wealth of recently acquired information about lateralization of function in mammals (reviewed by Corballis 1989). Asymmetries abound, even in species as behaviorally limited as the rat, and no single organizing principle seems capable of predicting which function will be symmetrically and which asymmetrically represented. In nonhuman primates lateralization exists but has proven relatively hard to demonstrate. Whether lateralization develops in animals according to the progressive or the invariant model appears not yet to have been studied. Potential sources of evidence in humans on the timing and location of the process whereby one hemisphere (almost always the left) assumes control over emerging language function include the following: Structural specializations of the language area or language hemisphere, asymmetries in apparent precursors of language, behavioral and/or psychophysiological asymmetries observable while language is developing, and the relative incidence of language impairment (aphasia) after left versus right cerebral damage.
2.
Hemisphere Structure
Neither direct nor microscopic inspection of the normally developing cerebral hemispheres reveals the site of emerging language. Language-specific neuronal architectonics have not been characterized. The suggestion that the ‘language hemisphere’ has a distinctive shape, in particular a larger temporal planum (Geschwind/Levitsky 1968), led to examinations of the brains of newborns available at autopsy. Both Witelson/Pallie (1973) and Wada/Clarke/Hamm (1975) found significantly more asymmetries favoring the left
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planum temporale. If the larger planum truly marks the language hemisphere, then these findings are consistent with invariant lateralization, given the early stage at which they could be recognized. A test is the nonrighthander, who is often less or even conversely lateralized for language. Obviously such a test cannot be applied to the newborn children studied at autopsy, as they had no opportunity to demonstrate their hand preference. But even among adults, it is not clear that neuroanatomic asymmetries discriminate at a useful level of significance between right and left handers. Asymmetries in question include different slopes of the left and right Sylvian fissures and the right frontal and left occipital prominences that are found in most people (Le May 1976) and are already present in the fetus (Le May 1984). If the above asymmetries are truly related to the language function, one might expect them to be observably modified in cases of language impairment. In general, group differences in the expected direction have been found (e. g. Roberts/Varney/Reinatz/Parkins 1988), though with too many individual exceptions to be of diagnostic use. In some language impaired individuals, language is lateralized to the smaller hemisphere (Pieniadz/ Naeser/Koff/Levine 1983, Ratcliff/Dila/Taylor/Milner 1980). An interesting group difference is a tendency for the temporal plana to be more symmetrical than expected. But rather than implying a diminished and illdeveloped left planum, as Geschwind and Levitsky thought, Galaburda/Corsiglia/Rosen/Sherman (1978) have suggested that it is the right planum that is overly large when the plana are symmetrical, perhaps on account of inadequate neural pruning, leading to miswiring of neurons with detrimental effects on function. Jernigan/Hesselink/Tallal (1987) reported a larger right than left posterior region in six of ten language-impaired children on magnetic resonance imaging. In contrast to the weakly circumstantial evidence that derives from gross morphological asymmetries is the very specific evidence gathered from an admittedly limited number of autopsied cases. Landau/Goldstein/Kleffner (1960) reported a patient with developmental language disorder who had old bilateral infarctions of the Sylvian region and severe retrograde degeneration of both medial geniculate nuclei. This supports the view that bilateral damage is necessary, not only to impair language function but also to preclude
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contralateral compensation. But Cohen/ Campbell/Yaghmai (1989) in their single case of developmental language disorder found only the expected lack of temporal planum asymmetry and a dysgenetic microgyrus in the left insula. The vast majority of language impaired children probably does not suffer from such gross pathology. But microscopic abnormalities have not been ruled out. A limited but growing data base of neurohistological abnormalities derives from cases of developmental dyslexia, a condition which, reading being based largely on access to oral language knowledge (Bertelson 1986) can be considered a subtype of language disorder (Vellutino 1979). Consistent with an early case report by Drake (1968), Galaburda and colleagues have published detailed accounts of microscopic foci of neuronal dysgenesis variably distributed across cerebral cortex of autopsied dyslexics, with a left-sided preponderance of lesions sometimes concentrated in the classical language area (Galaburda/Sherman/Rosen et al. (1987), and leftsided thalamus (Galaburda/Eidelberg 1982). Because this work is so labor-intensive, normal control studies are not yet available, so that there is no assurance of the specificity of this finding. Nonetheless, it is the first available anatomical confirmation of the general conviction that these cases of dyslexia are brain-based, and suggest an origin in mid-trimester, because this is when the affected neurons would normally have migrated to their proper locations. The widespread distribution of the lesions is unexpected were dyslexia a ‘pure’ or highly selective deficit in reading. Instead, it supports studies that highlight the wide range of cognitive deficits that can be discovered in these patients if they are thoroughly studied (e. g. Kavale/Nye 1991, Kinsbourne/ Rufo/Gamzu et al. 1991, Vellutino 1979). A study of regional cerebral blood flow of adult developmental dyslexics had a generally compatible outcome (Rumsey/Berman/ Denckla et al. 1987). On a verbal task, patients exhibited more hemisphere asymmetry than controls. This could be interpreted as reflecting the greater effort they had to invest in the task. But on a line orientation task, generally considered right hemispheric, they also deviated from controls, in exhibiting a reduced anteroposterior gradient in richness of blood flow. This was interpreted as reflecting “a deficit in the ability of frontal systems to respond adequately to cognitive demands” (Rumsey/Berman/Denckla et al. 1987, 1144).
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3.
Associated Neurological Abnormalities
A relatively widespread distribution of neuronal abnormalities may help explain not only the lack of compensation for dysgenesis of the language area, but also the frequent though variable associated presence of miscellaneous nonspecific minor neurological findings. Certainly, dyslexia is not a clearcut deficiency in an anatomically circumscribed cerebral module. An increased incidence of clumsiness has been noted (Sheridan 1973) and perhaps vestibulocerebellar deficiencies (Horek/Shumway-Cook/Crowe/Black 1988). Johnston/Stark/Mellits/Tallal (1981) found that performance in finger recognition, leftright discrimination, rapid and involuntary movements discriminated their language impaired group from controls. Temporal processing impairment has been documented both in language impaired (Tallal/Piercy 1973, 1974 ) and dyslexic (Tallal 1980) samples. Kinsbourne/Rufo/Gamzu et al. (1991) not only found that neuromotor and temporal order judgement difficulties continue to distinguish dyslexics from controls in adulthood, but that some of these performances are quite highly discriminating. Electroencephalographic abnormalities are also relatively frequent in these children (Goldstein/Landau/ Kleffner 1958). 3.1 Behavioral Laterality When individuals listen to speech, speak, or think in words, certain associated behaviors, and certain associated physiological changes can be observed. The observable associated behaviors subdivide into (i) asymmetry in gaze and gesture (output laterality), (ii) asymmetry in the ability to identify verbal material presented by voice, vision or touch depending on whether the message originates to the right or left of the person (perceptual laterality tests), and (iii) asymmetry in the amount of interference between verbal and sensorimotor performance when both are performed simultaneously (dual task paradigms). Also observable are event-related asymmetries in electrophysiological and in metabolic cerebral activity while people are using language. Many behavioral and psychophysiological studies have monitored the laterality of emerging language in the infant and child. A few instances are given below.
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3.2. Infant Laterality Studies The more directly relevant evidence from infants derives from their behavior when exposed to speech. Entus (1977) found that infants aged 22 to 14 0 days could detect transitions from one consonant-vowel word to another more readily at the right than the left ear. Entus used a non-nutritive sucking disinhibition paradigm. Glanville/Best/Levenson (1977) reported similar results using cardiac dishabituation to input to the right ear compared to the left ear. Mac Kain/StuddertKennedy/Spieker/Stern (1983) observed that six month old infants could detect correspondence between voice and lip movements when orienting right but not when orienting left. Segalowitz/Chapman (1980) reported a rightsided ‘stilling’ of the limbs of premature infants of average age 36 weeks when they were exposed to speech, but leftsided stilling when they were exposed to music. The preferred direction of head turning is also affected by the categorical nature of the stimulus. Newborns turned more to the left during musical than during verbal stimulation (Young/Gascon 1990). Less directly, the long recognized rightward bias of infants’ spontaneous head and eye turning lends itself to theories that relate laterality of speech control to preferred direction of orienting (Kinsbourne/Lempert 1980). In support of this point of view, Bates/ O’Connell/Vaid et al. (1986) reported that pointing coordinated with emerging verbal utterance is predominantly righthanded. They suggest that there are ‘cycles’ in the manifestations of hand preference that are determined by competition for left hemisphere resources of the manual and the verbal performance. According to Archer/Campbell/Segalowitz (1988) hand preference, which tends to stabilize between ages 18 and 30 months, bears an indirect relationship to expressive language ability (mean length of utterance), qualified by gender. Electrophysiological evidence further supports the presence of this early asymmetry. For instance, Molfese/Freeman/Palermo (1975) reported higher amplitude evoked potentials in infants to speech sounds from the right, but to music from the left. Gardiner/Walter (1977) found differently lateralized changes in six months old infants’ E. E. G. power spectra depending on whether they were exposed to speech or music. Infant asymmetries such as the above controvert the notion of strict symmetry in the neural provisions for prospective language.
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Because cerebral circuitry is largely immature at this age, they are most readily ascribed to asymmetrical hardwired activating projections from subcortical regions triggered by speech (or some stimulus parameters contained within speech). The asymmetries are inherent in the provisions for the use of cortex for language, not in the language cortex itself. 3.3. Childhood Laterality: Longitudinal Studies The two models make critically different predictions about the effect of age on verbal laterality in childhood. According to the progressive lateralization model, there should be an interaction between age and degree of rightward bias on the laterality test used, because language function is increasingly left hemispheric as the children grow older. According to invariant lateralization, age should not affect the degree of asymmetry, because such verbal behavior as the child is capable of is left lateralized from the start. By the age of three years laterality tests can be administered with meaningful results. It is therefore possible to test not only Lenneberg’s (1967) concept of progressive lateralization in this way, but also Krashen’s (1973) more restricted concept. In accord with Hiscock/Kinsbourne’s (1977) initial study, numerous longitudinal designs have been used with children aged three and over (e. g. Geffen 1978, Hiscock/Kinsbourne 1978, 1980 a, 1980 b, Piazza 1977, White/Kinsbourne 1980). Earlier work had discovered right ear advantages in verbal laterality for still younger children (Ingram 1975, Lokker/ Morais 1985, Nagafuchi 1970). Subsequent work is comprehensively reviewed by Hiscock (1988). The general finding that magnitude of asymmetry remains constant with increasing age is upheld, even for the preschool years, which Krashen had nominated for progressive lateralization in his weakened form of Lenneberg’s hypothesis. 3.4. Hemisphere Equipotentiality When one hemisphere is damaged before, during or soon after birth, the consequences for language function and further language acquisition provide additional information on language lateralization. Contrary to early impressions summarized by Lenneberg (1967), aphasia in children is usually caused by left hemisphere lesions (Woods/Teuber 1978) just as in adults. Of 15 known right handers who
V. Pathologies and Disorders of Language Development
became aphasic as a result of their unilateral lesions, only one was damaged on the right. Several studies indicate that after early left hemisphere damage, language functions may shift to the right hemisphere (Bingley 1958, Penfield/Roberts 1959, Rasmussen/Milner 1977). Such language compensation would be most dramatic when the lesion inactivates the whole hemisphere, rendering within-hemisphere compensation impossible. However, studies of posthemispherectomy patients who have normal intelligence are few, and the conclusion drawn from them that the right hemisphere may support normal verbal intelligence (Aram/Ekelman 1986), but not normal syntactical function (Kohn 1980, VarghaKhadem/Isaacs/Papalelondi et al. 1991), although appealing, are not always confirmed (Ogden 1988) and are subject to numerous confounds and artefacts (Bishop 1988). Group studies of children with less complete early hemispheric lesions do support the view that left sided lesions cause more compromise in verbal learning, reading and spelling than right (Aram/Whitaker 1988), but the large number of individual cases that behave otherwise remains to be explained. Some of the left hemidecorticates studied by Dennis and her colleagues performed syntactical tasks as well as the right hemidecorticates. The hypothesis that the newborn cerebral hemispheres are equipotential for the representation of language cannot at this time be rejected (Bishop 1988). If the hemispheres are equipotential for language in infancy, what nominates the left hemisphere for language processing in most people? According to Lenneberg, it is progressive lateralization. The infant data already reviewed, and the evidence for invariant lateralization, suggest a different answer. In infancy, dedicated cerebrum cannot play a part because most cerebral areas are still immature at this early stage. Yet preverbal laterality exists in infants, and bears a predictable relationship to subsequent language lateralization. This suggests the alternative model that hemisphere lateralization is a consequence of asymmetric activation coupled with verbal input and the adoption of verbal mental set (Kinsbourne/Lempert 1980). The consistently activated area of cortex becomes the language area. The predominantly bilateral organisation of language circuitry in nonrighthanders is thereby explained as due to little or no asymmetry in the relevant ascending activation (Kinsbourne 1980). As long as the activation is topographically consistent,
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deficient language preformance is not expected, even if the language area is quite differently located from the norm. Thus nonrighthanders as a group are not significantly deficient in language or other aspects of cognition (Hardyck/Petrinovitch 1977). Perinatal asphyxia abolishes the newborn’s rightward turning tendency (Turkewitz/Moreau/Birch 1968). Whether this is permanent is not known. But if for any reason ascending activation is diffuse or variable, this might retard the differentiation of language circuitry and result in inferior language function. Inconsistent dichotic and verbal-manual interference patterns observed by Parlow/Kinsbourne (submitted) in severely mentally retarded patients with and without Down syndrome might indicate that these poor language performers do not consistently activate a given cerebral territory when they are verbally active. Even if language does emerge in the same hemisphere as that in which it becomes permanently established, is its organisation within that hemisphere as differentiated initially as in the adult? Satz/Strauss/Whitaker (1990) have reminded us that that invariant lateralization does not imply invariant localization within a hemisphere. Indeed, given the greatly different myelogenetic cycles of different parts of the hemisphere, it would be surprising if the neural substrate of language in the left hemisphere did not change with increasing age. However, clinical evidence of developmental differences in the anatomical basis of the different syndromes of aphasia remains sparse. Ojemann’s (1983) recent findings have cast serious doubt on the classical diagram of posterior-anterior verbal information flow. But one can at least ask whether the broad correspondence between fluent versus nonfluent aphasia and posterior versus anterior left hemisphere lesion holds for children. Fluent aphasia is, for unknown reasons, rare in children. But in four such cases, Van Dongen/Loonen/Van Dongen (1985) did document mid or posterior temporal lesions, rather than the more customary frontally localised lesions in nonfluent aphasia. Much more clinical evidence is needed before a definitive answer to this question can be offered.
4.
A Critical Period for Language Acquisition?
Animal experimentation offers instances in which deprivation of the customary environ-
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ment or experience impairs the emergence of perceptual capabilities if the deprivation is implemented early enough, within a ‘critical period’. The theoretical position that treats emerging language as neurologically comparable to other biologically preprogrammed capabilities (Lenneberg 1967) is inclined to view the apparent ability of young children but not adults to acquire language without explicitly effortful learning as evidence for the concept of a critical period for language acquisition. Thus up to puberty, according to Lenneberg, or at least till five years of age, according to Krashen (1973), children should have an exceptional facility for learning languages. However, learning a first language and learning additional languages are sufficiently different for the comparison between children and adults to be hopelessly confounded. It is not at all clear that children are better language learners than adults under comparable conditions. When children and adults learned a second language, adults performed better (Snow/Hoefnagel-Hohle 1978), even with respect to acquiring the foreign pronunciation (Snow/Hoefnagel-Hohle 1977), an ability which has been claimed to be restricted to children within the ‘critical period’ (Scovel 1969). If, as has often been argued, infants do have a superior ability to utter as well as discriminate phonemes that are not used in the particular language into which they are growing, that early phenomenon is not congruent in timing with progressive lateralization and the alleged critical period. Additional evidence derives from individuals who, on account of abnormal rearing conditions, were precluded from hearing or using language for the initial years of their life. The most thoroughly studied such case, Genie (Fromkin/Krashen/Curtiss et al. 1974 ), did, when finally introduced into a linguistic environment, exhibit some drastic limitations on the type and extent of language learning she could accomplish. A possibility was raised that her left hemisphere was no longer able to subserve emerging language, and a more limited right hemisphere mechanism had taken over. However, it is not at all clear that the right hemisphere is necessarily a limited language learning device, even in the mature nervous system of the adult. Not only is there substantial evidence that the right hemisphere is capable of compensating for language impairment (i. e. aphasia) due to left-sided stroke (Czopf 1972, Kinsbourne 1971), but several individual case reports suggest that this compensation may be effectively com-
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plete (Nielsen 194 6). Additional evidence for the ‘lateral shift hypothesis’ for the brain basis of aphasic speech is reviewed by Code (1987). The increasing evidence for relatively effective right hemisphere compensation for aphasia is in accord with doubts about the assumption that ‘plasticity’ (the recruitment of other areas of cortex to the programming of behavior impaired by a focal cerebral lesion) is greater in the immature nervous system, that is, in children as compared to adults (Robinson 1981). The question as to the extent, if any, to which right hemisphere compensation in language function is limited by the nature of its neuronal hardware awaits the development of a reliable means of diagnosing right hemisphere language in the individual case of aphasia, which can then be appropriately studied. In the meantime, there is still no neurological support for the existence of the allegedly unique and dedicated left hemisphere language acquisition device.
5.
References
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Geschwind, N. & Levitzky, W. (1968). Human brain: Left-right asymmetries in temporal speech region. Science, 161, 186—187. Glanville, B. B., Best, C. T., & Levenson, R. A. (1977). Cardiac measure of cerebral asymmetries in infant auditory perception. Dev elopmental Psychology, 13, 55—59. Goldstein, R., Landau, W. M., & Kleffner, F. R. (1958). Neurological assessment of some deaf and aphasic children. Transactions of the American Otological Society, 46, 122—136. Hardyck, C. & Petrinovitch, L. F. (1977). Lefthandedness. Psychological Bulletin, 84, 405—411. Hecaen, H. (1983). Acquired aphasia in children: revisited. Neuropsychologia, 21, 581—587. Hiscock, M. (1988). Behavioral asymmetries in young children. In D. L. Molfese & S. J. Segalowitz (Eds.), Brain lateralization in children. 85—169. New York: Guilford Press. Hiscock, M. & Kinsbourne, M. (1977). Selective listening asymmetry in preschool children. Developmental Psychology, 13, 217—224. Hiscock, M. & Kinsbourne, M. (1978). Ontogeny of cerebral dominance: Evidence from time-sharing asymmetry in children. Dev elopmental Psychology, 14, 321—329. Hiscock, M. & Kinsbourne, M. (1980 a). Asymmetries of selective listening and attention switching in children. Dev elopmental Psychology, 16, 70—82. Hiscock, M. & Kinsbourne, M. (1980 b). Asymmetry of verbal-manual time-sharing in children: A follow-up study. Neuropsychologia, 18, 151—162. Horek, F. B., Shumway-Cook, A., Crowe, T. K., & Black, F. O. (1988). Vestibular function and motor proficiency of children with impaired hearing or with learning disability and motor impairments. Dev elopmental Medicine and Child Neurology, 30, 64—79. Ingram, D. (1975). Cerebral speech lateralization in young children. Neuropsychologia, 13, 103—105. Ingram, T. T. S. (1959). Specific developmental disorders of speech in childhood. Brain, 82, 450—467. Jernigan, T. L., Hesselink, J., & Tallal. P. (1987). Cerebral morphology on magnetic resonance imaging in developmental dysphasia. Society of Neuroscience Abstracts, 13, 1, 651. Johnston, R. B., Stark, R. E., Mellits, E. D., & Tallal, P. (1981). Neurological status of languageimpaired and normal children. Annals of Neurology, 10, 159—163. Kavale, K. A. & Nye, C. (1991). The structure of learning disabilities. Exceptionality, 2, 141—156. Kinsbourne, M. (1971). The minor cerebral hemisphere as a source of aphasic speech. Archiv es of Neurology, 25, 302—306. Kinsbourne, M. (1975). The ontology of cerebral
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dominance. In D. R. Aaronson & R. W. Rieber (Eds.), Dev elopmental psycholinguistics and communication disorders. 244—250. New York: Academic Press. Kinsbourne, M. (1980). A model for the ontogeny of cerebral organisation in non-right-handers. In J. Herron (Ed.), Neuropsychology of left handedness. 177—185. New York: Academic Press. Kinsbourne, M. & Lempert, H. (1980). Does left brain lateralization of speech arise from right-biased orienting to salient percepts? Human Dev elopment, 22, 270—276. Kinsbourne, M., Rufo, D., Gamzu, E., Palmer, R., & Berliner, A. (1991). Neuropsychological deficits in adults with dyslexia. Dev elopmental Medicine and Child Neurology, 33, 763—775. Kohn, B. (1980). Right hemisphere speech representation and syntax comprehension after left cerebral injury. Brain and Language, 9, 350—361. Krashen, S. (1973). Lateralization, language learning and the critical period: some new evidence. Language Learning, 23, 63—74. Landau, W. M., Goldstein, R., & Kleffner, F. R. (1960). Congenital aphasia: a clinicopathological study. Neurology, 10, 915—921. Le May, M. (1976). Morphological cerebral asymmetries of modern man, fossil man and nonhuman primate. Annals of the New York Academy of Sciences, 280, 349—366. Le May, M. (1984 ). Radiological, developmental and fossil asymmetries. In N. Geschwind & A. M. Galaburda (Eds.), Cerebral dominance: The biological foundations. Cambridge, MA: Harvard University Press. Lenneberg, E. H. (1967). Biological foundations of language. New York: Wiley. Lokker, R. & Morais, J. (1985). Ear differences in children at two years of age. Neuropsychologia, 23, 127—129. MacKain, K., Studdert-Kennedy, M., Spieker, S. & Stern, D. (1983). Infant intermodal speech perception as a left hemisphere function. Science, 219, 1347—1349. Molfese, D. L., Freeman, R. B., & Palermo, D. (1975). The ontogeny of brain lateralization for speech and non-speech stimuli. Brain and Language, 2, 356—368. Nagafuchi, M. (1970). Development of dichotic and monaural hearing abilities in young children. Acta Otolaryngologica, 69, 409—414. Netley, C. (1983). Sex chromosome abnormalities and the development of verbal and nonverbal abilities. In C. A. Ludlow & J. A. Cooper (Eds.), Genetic aspects of speech and language disorders, 179—196, New York: Academic Press. Nielsen, J. M. (194 6). Agnosia, apraxia, aphasia: Their v alue in cerebral localization. New York: Hoeber.
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Marcel Kinsbourne, Boston, Massachusetts (USA)
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60. Psychiatric and Psychological Aspects of Language Development Disorders 1. 2. 3. 4.
1.
Introduction Influences on Normal Language Development Psychosocial Sequelae References
Introduction
A growing body of research exists now to indicate that a variety of psychological factors can interfere with the process of normal language development. The factors which have been implicated range from exogenous influences such as maternal input to endogenous factors like temperament. Other variables which may be relevant, including gender, birth order and twinning are a particularly inextricable mix of exogenous and endogenous factors and these have been referred to by some authors as ‘biosocial’ variables. A great deal of controversy exists about the extent to which psychological and environmental factors can lead to a clinically significant language delay, as well as about the precise circumstances under which this may occur. Certainly some of these factors seem to affect rates of language development but they may not necessarily lead to variations outside the normal range. This article aims to discuss firstly whether the language acquisition process is vulnerable to external influences at all, and if it is what the effects of specific factors might be. The second main focus of this article is on the psychosocial sequelae of language disorders since it is now well-established that a child with a language development disorder will be at increased risk of educational retardation and/or behavioral or psychiatric abnormalities. A review of relevant research is presented together with a consideration of methodological issues and possible causative mechanisms.
2.
Influences on Normal Language Development
The first question to ask is why language development should be vulnerable to any of these factors. Certainly if language-learning involves an unfolding series of robust programmed processes then it might be assumed to be immune from other influences, but such
a completely biologically-determined explanation seems unlikely. What seems more probable is that both inborn and external factors have a role to play but there is heated debate about the relative contribution made by each side of the equation. The behaviorist viewpoint, for example, asserts that all knowledge derives from the environment and with respect to the language-learning task the child hears speech, imitates it and then acquires it through a process of selective reinforcement (Skinner 1957, 29 f). Whilst this approach gives support to the idea that language development is susceptible to external influences it is now generally accepted that processes such as imitation, reinforcement and generalization cannot alone account for all the linguistic changes which occur as children acquire language, although they may well be of value in explaining certain aspects of the process. The nativists, on the other hand, claim that certain linguistic features are innate, providing schemata which the child can apply to the particular language he is exposed to (e. g. Chomsky 1964 ). Whilst making a valid contribution to the debate, this approach is generally seen now as being rather restricted and the more satisfactory accounts are those such as the epigenetic-interactionist viewpoint (Cromer 1981). This aims to provide better incorporation of the roles of inner determinants with environmental factors and asserts that inherent in the human species are a number of unfolding developmental phenomena, some of which may be specifically linguistic, that interact with environmental variables. This approach differs from the nativist viewpoint in claiming not that children are born in possession of particular structures, but rather that structures are built up from an interaction of innate potential with environmental factors. The disputes between linguists and psycholinguists who support the existence of innate language functions and psychologists who do not, have raged for a number of years now and seem likely to continue for some time. Although there is little consensus of opinion about the degree to which external factors can influence language development there is on balance, support for the basic idea that language development can indeed be susceptible to influence from environmental factors.
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The precise nature of the relations between environment and development deserves closer examination, however. Some of the early work in this field took a unidimensional approach asserting that ‘good environments’ facilitate all aspects of development whilst ‘bad environments’ have the opposite effect. The issues are clearly not this simple and for the most part it is now well-established that relations between environment and development are highly specific in two respects. Firstly ‘environmental specificity’, i. e. different aspects of the environment, do seem to differentially influence specific aspects of development (Wachs/Chan 1986), and secondly ‘organismic specificity’ which predicts that the impact of the environment will be mediated by the individual characteristics of the individual child. The child and the environment will exert a dynamic influence on each other and consequently two children may be exposed to similar environmental stimulation but individual characteristics such as sex, temperament and biological vulnerability will contribute to a different outcome for each child. It is vital that the whole issue of effects on language development is considered from a developmental perspective. A child of 3 years, for example, will perceive and assimilate stimuli in a quite different way from an infant of 12 months, and it is because of these changing circumstances that longitudinal research is of particular value in assessing influences on language development. 2.1. Exogenous Factors Turning to the effects of specific factors, one of the basic external influences which human beings are subject to is interaction with other humans and there has been a great deal of interest in the extent to which qualitative and quantitative variations in the child’s social environment can produce measurable differences in linguistic output. Much of this attention has focussed on the effect of maternal input and this topic is considered elsewhere in this volume, but other important bodies of information have been built up from studying children who have experienced a variety of linguistic backdrops, e. g. children who have been maltreated or institutionalized, those with depressed mothers and also hearing children of deaf parents. The most extreme form of these ‘natural experiments’ however are the well-documented reports of children who have been brought up in circumstances of
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extreme isolation where they have been deprived of social contact. These cases are horrific and fortunately rare but they do serve to highlight the important role that social interaction plays in language development. Skuse (1984 ) documents the cases of nine children who were raised in conditions of extreme social deprivation for periods from 2.5 to 12 years. Many of these children had been completely deprived of any contact with other people or with normal language and several had been physically restrained. A number of important findings emerge from the horrific experiences of these unfortunate children. First, it appears clear that severe environmental privation can lead to devastating cognitive and language impairments since these grossly isolated children were without useful language and functioned in the severely retarded range at the time they were rescued. Second, in most cases there was very substantial recovery within a matter of months of the children being placed in a normal environment, clearly demonstrating that the impairments were not due to congenital deficits. That being said, however, there were several children described in the case reports who did not recover after rescue and although it is plausible that unusually severe social isolation can on its own lead to a permanent and irreversible language handicap, it does seem very likely that the children in question may have had additional biological handicaps which complicated their recovery. A related issue, however, is whether the ultimate degree of recovery is influenced by protective factors during the period of isolation (e. g. twins described in one of the case reports had each other for company) or by particular remedial measures afterwards, but as yet there is little data on their importance. What may be of relevance is the suggestion that if language acquisition is to proceed normally then it must be acquired during the first 12 years of life (Curtiss 1981; Lenneberg 1967, 158). Gross deprivation represents one extreme of the quantitative dimension of social interaction but there is evidence that the quality of attention that children receive, particularly from their principal caregivers, also plays an important role in cognitive development (Matas/Arend/Sroufe 1978; Slade 1987). Werner/ Kaplan (1963, 4 2 ff) claim that the motivation to engage in symbolic activity emanates from the desire to share experiences with a social partner and Bruner (1975) takes a similar view arguing that through dyadic interactions
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with the caregiver the child develops linguistic knowledge. This view seems intuitively reasonable and implies that children who lack a responsive social partner will be disadvantaged in their language development. Maltreated children present a useful case for study here since a number of studies have found maltreating mothers to be unresponsive and not encouraging of the sorts of communicative exchanges described as being ideal for promoting language development. In general, neglecting mothers have been found to interact with their children far less than non-neglecting mothers (Burgess/Conger 1978), to provide less verbal instruction about the environment (Bousha/Twentyman 1984 ) and to use more controlling language. (Aragona/ Eyberg 1981). They have also been found less likely than control mothers to initiate play interchanges (Wasserman/Green/Allen 1983). To investigate whether this impoverished communicative environment does actually affect linguistic development Gersten/Coster/ Schneider-Rosen et al. (1986) studied two groups of lower socio-economic status toddlers — 20 who had been legally maltreated and 20 who had not. The children were observed at 25 months in both structured and unstructured play sessions with their mothers, and coders who were blind to the maltreatment status of the children rated their linguistic performance and communicative behavior. Perhaps surprisingly this study found that at 25 months there were no significant differences between the two groups for communicative behavior, although when attachment security was taken into account differences were apparent with the more securely attached toddlers talking more and consistently demonstrating a more elaborate vocabulary and complex use of syntax. The findings of this study imply that maltreatment in itself need not affect language development, although the mother-child relationship as expressed by attachment may well have an influence on rates of development. As discussed earlier, however, it is vital to consider environmental influences in the developmental context. Consequently the same group of researchers repeated the format of the earlier study but with children aged 31 months (Coster/Gersten/Beeghly/Cichetti 1989). These findings were interesting since in contrast to the situation with the younger children there were by 31 months significant differences in the linguistic behavior of the maltreated and nonmaltreated children. There were no dif-
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ferences in receptive language, nor in the total number of utterances, but the maltreated children used less complex syntax and a smaller range of words. They also used fewer descriptive utterances. These studies suggest that maltreatment may interfere with the processes of normal language development, but it is not clear whether the effects show merely in rates of development or whether clinically significant language delays can result. Another factor likely to affect the quality and amount of attention received by a child is the mother’s emotional state. Cox/Puckering/Pound/Mills (1987) found that depression can impair a parent’s ability to interact responsively with his/her child and a number of other studies attest that depressed mothers interact with their children in ways which may prove disadvantageous to their children (Bettes 1988; Davenport/Zahn-Waxler/Adland/Mayfield 1984 ; Egeland/Sroufe 1981). In general, maternal mental disorder seems more likely to cause disturbances of behavior and socio-emotional functioning than to cause any form of cognitive impairment (Rutter 1985 a, b), but there have nonetheless been clinical reports of language delay in young children with depressed mothers. Richman/ Stevenson/Graham (1982, 183), for example, found that maternal depression when children were aged three years was associated with somewhat lower language and reading scores at eight years even when the maternal IQ, social class and current depression were taken into account. Turning to the age of the child when the mother experiences depression this is likely to be influential and research by Coghill/Caplan/Alexandra et al. (1986) suggests that children may be particularly vulnerable to effect during their first year. Children whose mothers had been depressed before they were one year showed cognitive deficits at 4 years whilst concurrent depression had no effect. The mechanisms through which maternal depression can influence cognitive development are unclear and there are probably several mechanisms in operation (Rutter 1990). First, the negative mood experienced by the mothers may lead to more negative affect being expressed towards their infants and they may also be less sensitive and responsive to their children’s needs and cues. Second, it is not clear whether maternal depression in itself is what constitutes a risk factor for cognitive impairment or whether it is the associated factors such as social disadvantage and
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marital distress which so often co-exist with it (Gotlib/Hooley 1988; Rutter/Quinton 1984 ), and more research is needed to elucidate on this issue. It has already been seen from the descriptions of the children raised in conditions of extreme privation that exposure to some sort of language is necessary for language to develop and further data on what happens when children have a restricted linguistic input is provided by studying hearing children raised by deaf parents. The findings are mixed and there has been little recent research but several studies have identified a range of speech/ language problems in such children including articulation and syntactic deficits (Sachs/ Bard/Johnson 1981; Schiff/Ventry 1976). Other writers, however, have concluded, perhaps unexpectedly, that such children have few or no speech or language deficits (Lenneberg 1967, 137; Vernon 1974 ). The information that is needed to interpret these findings relates to whether there are protective factors which allow some children to escape unscathed. An above average IQ is probably one of these but it is unclear how others such as the quality of the mother-child relationship may contribute. All the cases to here concern variations in the quality of the relationship between the child and his/her mother but obviously not all children are brought up within a family, and many are raised in institutions. In the past, high rates of cognitive and language delay were found amongst institutionalised children (Burlingham/Freud 194 3, 13 f; Goldfarb 194 5), but thankfully improvements in the quality of residential nurseries have resulted in these delays no longer being characteristic of institution-reared children (Tizard/Cooperman/Joseph/Tizard 1972; Tizard/Rees 1974 ) carrying the implication that whilst interaction with adults is crucial to language development this need not necessarily take place with the mother. The quality of the institution does appear to be important, however, and in particular variables such as the amount of verbal interaction between staff and children and whether children’s question are answered have been shown by Tizard/Cooperman/Joseph/Tizard (1972) to be systematically associated with variations in the progress of language development. 2.2. ‘Biosocial’ Variables A number of ‘biosocial’ factors have been implicated as having an effect on rates of
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language development and in some instances on the development of language disorders, although it can be difficult to draw conclusions and distinguish between causal mechanisms which have their roots in variations within the social environment and those where a pure biological cause is in action. Gender is an example of such a biosocial factor and many studies of the pathological dimension have found language delay to be about twice as common in boys as in girls (Morley 1965, 54 ; Silva 1980; Stevenson/ Richman 1976). This sex bias is not apparent in all types of language disorder, however, and Bartak/Rutter/Cox (1975) for example found no significant sex difference in children with severe receptive language difficulties. Observations of language development in the normal sphere, rather than from a clinical viewpoint (e. g. Bloom/Lightbown/Hood 1975) have led to suggestions that there is a gender-associated difference in early grammatical style with girls tending to use the referential style (a high proportion of common object names) as described by Nelson (1973) and boys more frequently employing an expressive style (heterogeneous vocabularies containing items from a variety of form classes). Several studies have found the referential style to correlate positively with rates of language development (Nelson 1973; Ramer 1976) but the suggestion of a sex bias in grammatical style is by no means widely accepted and indeed some studies of early language development have failed to find any evidence of gender-related differences in rates of development (e. g. Bates/Bretherton/Snyder 1988, 233; Macaulay 1978). This issue continues to be unresolved. One biological explanation for the sex bias in ultimate pathology may be very early undetected brain damage which for some reason affects the sexes differently, possibly involving testosterone (Geschwind/Galaburda 1985). It may also reflect some sort of genetic mediation and there is evidence that developmental language delays do indeed have a familial loading (Robinson 1987; Tallal/Ross/Curtiss 1989). The genetic hypothesis remains unproven as yet, however. There have also been suggestions that birth order has an effect on language development with first-born and only children having an advantage in verbal intelligence (Douglas/ Ross/Simpson 1968, 129 f) and reading attainment (Davies/Butler/Goldstein 1972, 176 ff; Record/Mc Keown/Edwards 1969). These differences are only small, however, and seem
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unlikely to result in clinically significant language disorder, although in combination with other factors they may play some role. A particularly interesting area of research has been the language development of twins and results are consistent in confirming that on average twins are disadvantaged in their language development when compared with singletons (Conway/Lytton/Pysh 1980; Hay/ Prior/Collet/Williams 1987). Mittler (1970) found that 4 -year-old twins showed an average retardation of six months in their language development and evidence that the disadvantages of the twin situation can have longer-lasting effects comes from research by Johnston/Prior/Hay (1984 ) who found that older twins are more likely than singletons to be delayed in reading skills. In childhood twins have been shown to have a slightly lower verbal IQ than singletons (Record/ Mc Keown/Edwards 1970; Mittler 1970; Johnston/Prior/Hay 1984 ) and there is an indication that some deficit is still present in the older age groups. Rutter/Redshaw (1991) review the possible causes of the language deficit in twins and highlight factors in the social environment. The parents of twins, for example, in common with the parents of large families are faced with a dilemma of having to divide their attention between more than one child with the result that mothers of twins tend to speak to them less and to use less complex utterances when compared with mothers of singletons (Conway/Lytton/Pysh 1980; Lytton/Conway 1977). The possible influences of maternal mental disorder on language development have already been highlighted in this article and mothers of twins have been found to have higher levels of emotional distress than mothers of singletons (Thorpe/Golding/ Mc Gillivray, submitted) with these stresses continuing beyond the twins’ infancy years and still being apparent at 5 years. Several possible contributory factors to the observed verbal deficit in twins have therefore been identified and important evidence that this deficit may well be a consequence of factors in the postnatal environment is presented by Record/Mc Keown/Edwards (1970). They found that twins whose co-twin had died at birth or during the neonatal period had a measured IQ at the age of 11 years that was similar to that of singletons whereas those who had a living co-twin scored significantly lower. Aside from the possible social/environmental causes there is the possibility that bi-
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ological factors are implicated since twins suffer from a higher rate of obstetric and perinatal complications (Watts/Lytton 1981). This possibility warrants further investigation although it should be said that in general obstetric and perinatal factors do not seem to play a major role in language delay (Mittler 1970). The final factor which will be considered under this heading is social class. The whole issue of social class and its influence on language development is a very vexed one but some relationship does appear to exist (Davies/Butler/Goldstein 1972, 92; Douglas 1964 , 152) with the main effect being seen in patterns of language usage (Bernstein 1971, 61 f; Robinson 1980), although there do seem to be some differences in language competence too (Tizard/Hughes/Carmichael/Pinkerton 1983). Social class, however, is a very broad term and it is not clear precisely which specific aspects of social class are relevant. Silva/Fergusson (1980) found that maternal general mental ability, maternal education and training in child development were all associated with the language level of 3-yearolds and these factors may represent some of the relevant factors associated within the term ‘social class’ but there is a clear need for further investigation. 2.3. Endogenous Factors A number of factors from the external environment may impinge on the child’s language development as has been seen already, but it is also important to consider what the child brings to the language-learning process. One aspect of this is temperament. Bates/Bretherton/Snyder (1988) suggest that sociability may be a significant factor in affecting language-learning style so that a child whose primary theme is to be with and be like other human beings is more likely to rely on rote processes in language-learning whilst a child for whom this is less of a primary theme is more likely to take an analytic approach. There is, however, very little research which links temperamental differences with variations in language development and no evidence as yet to suggest that temperamental differences can result in language pathology per se. The possibility remains nonetheless that temperamental differences when combined with other factors may increase the likelihood of a particular child developing a clinically significant language deficit. It should be borne in mind when considering
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the effect of any environmental factor that the interaction between the child and the environment will be bidirectional with each influencing the other. The difficulty lies in uncovering the interrelated mechanisms. To what extent, for example, is the mother influencing the child’s response and conversely does the child have an inherent preference which encourages the mother to respond in a particular way. Many of the findings presented so far are controversial, but there is nonetheless a strong thread running through the research on language development which suggests that interaction with adults is important in facilitating the growth of children’s language. Clearly other factors must contribute to this process, however, and it should not be forgotten that there is a close relationship between language and intelligence and between language delay and low intelligence (Silva 1981).
3.
Psychosocial Sequelae
As well as certain psychological factors being implicated in the development of language disorders it is now well-established that once children have developed a language disorder they are at an increased risk of other psychosocial problems such as educational retardation, behavioral difficulties and psychiatric symptoms. Although there has been a great deal of research in this area it has been difficult to compare studies and often researchers have obtained contradictory results because of methodological differences (Rutter/ Mawhood 1991). There are six main methodological problems which bedevil this field of research. First, the groups studied have been quite heterogeneous in both type and severity of speech/language disorder. Second, the investigations have varied widely in the level of detail on individual diagnosis and the extent to which children with associated handicaps have been excluded. Third, some studies concern clinic samples with unknown referral biases whereas others are epidemiologically based. Fourth, investigations vary in the extent to which data on psychosocial sequelae have been both standardized and detailed. Fifth, studies differ in the degree to which longitudinal data have been available and statistically utilized in an effective manner. The consequence is that few studies separate the effects of transient language delay from those of persistent language impairment.
Sixth, only some of the projects have used control groups or have had general population data that allow estimation of the degree to which the level of psychosocial disorder in the developmental language disorder is truly significantly raised. The initial studies which looked at the associations between language development disorders and psychosocial difficulties were cross-sectional in design. More recently, however, there has been an increasing awareness that the psychosocial sequelae of language development disorders can be long-term and a number of studies have attempted to investigate the relationships between early language functioning and later psychosocial outcome. 3.1. Educational Retardation Taking educational retardation first, numerous studies have documented the finding that children with developmental language disorders have a substantially increased risk for later reading difficulties (e. g. Aram/Nation 1980; Garvey/Gordon 1973; Griffiths 1969; Silva/Mc Gee/Williams 1983). There are six main issues which arise from this finding; (1) whether the scholastic risk is mainly a function of general intellectual impairment or a specific language deficit; (2) whether the risk is specifically for reading difficulties or more generally for a broad range of scholastic problems; (3) which types of speech/language deficit lead to the greatest scholastic risk; (4 ) whether the scholastic risk associated with a specific language disorder differs in degree or pattern from that associated with developmental disorders of non-language functions (such as motor or perceptual skills); (5) related to the last point, whether the risk stems from the fact that language as such is impaired or from neurodevelopmental or cognitive deficits that may underlie the language disorder; and (6) whether the risk applies only when there is continuing language impairment or whether it applies also to transient language difficulties. Taking the first issue, it has been shown that much of the scholastic risk stems from general intellectual impairment, but that nonetheless reading difficulties arise with an increased frequency even when intellectual level has been taken into account (e. g. Debray-Ritzen/Mattinger/Chapuis 1976; Silva/ Mc Gee/Williams 1983). Turning to the issue of whether the scholastic difficulties extend further than reading Aram/Ekelman/Nation
60. Psychiatric and Psychological Aspectsof Language Development Disorders
(1984 ) found that of 16 children with language delay and an IQ in the normal range, two thirds had required special tutoring or had repeated one or more school grades by adolescence and of the 11 with an initial IQ of at least 90, 5 were in the lowest decile for at least one subject out of reading, spelling and mathematics. It is of note that the scholastic difficulties were as evident in mathematics as in the other two areas and there is some evidence to suggest that any reading deficits may apply more to reading comprehension than to reading accuracy (Bishop/ Adams 1990). Furthermore there are suggestions that these difficulties can continue into adult life. In a follow-up into adult life of boys with a developmental disorder of receptive language, and initially normal IQ, Mawhood/Rutter/Howlin (in preparation) found that the majority, as well as having deficits in reading and spelling also had poor mathematical abilities. For the most part research findings indicate that articulation-impaired children are less likely than language-delayed children to experience serious educational problems (Bishop/Adams 1990; Debray-Ritzen/Mattinger/Chapuis 1976; Hall/Tomblin 1978). Some contradictory findings do exist, however, and Crookes/Green (1963) found that reading difficulties were similarly affected in languageimpaired children and in those with pure articulation problems although arithmetical difficulties were greater in the former group. There appears to be no research which has directly compared language disorders with other non-language developmental disorders and it is therefore not known whether the degree and pattern of scholastic risk associated with language disorders is specifically related to language functioning. Nonetheless this seems possible and a relevant finding comes from the Rourke/Strang (1983) study of learning disabled children, which showed that those with reading difficulties tended to have verbal deficits whereas those with mathematical difficulties were more likely to have visuo-spatial deficits. One important issue which many followup studies have not controlled for is whether the language delay is resolved by the time the child starts school. Bishop/Adams (1990), however, in a well-planned study of 8-yearolds found that reading difficulties at age 8 were evident in children where there was a persistent language impairment but not in a comparison group who had also shown a
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clinically significant language deficit at age 4 , but in whom the deficit had recovered by the age of 8. 3.2. Socio-Emotional Behavioral Disorders Taking psychopathological problems next, there are numerous studies which have found significantly higher rates of behavioral problems in children who have developmental disorders of speech and language (e. g. Jenkins/ Bax/Hart 1980; Prizant/Audet/Burke et al. 1990; Silva/Justin/McGee/Williams 198 4 ; Stevenson/Richman/Graham 1985). In a Canadian study Beitchman/Nair/Clegg et al. (1986) found that amongst 1655 5-year olds 11% had a speech/language disorder and on clinical examination 4 8.7% of these showed some psychiatric disorder, particularly attention deficit disorders and emotional disturbances. The most comprehensive investigations, however, have been the Los Angeles series of studies (e. g. Baker/Cantwell 1982; Cantwell/Baker/Mattison 1979). The investigators took consecutive cases referred to a clinic for speech and language disorders and then carried out a full psychometric and psychiatric evaluation on them. Of the first 100 children to be investigated in this way 53 received at least one psychiatric diagnosis including attention deficit disorder, oppositional disorder and anxiety disorders. An important methodological issue affecting comparison between studies is that they have varied greatly not only in their definitions of speech/language disorder but also in their measures of psychopathology and in whether the data is collected by observational or interview method. Nonetheless, taking all the available data into account the main associations between language development disorders and psychopathology seem to be in the domains of anxiety, social relationships and attention-deficit problems rather than in conduct disturbance or antisocial behavior (Rutter/Mawhood 1991). There are few adequate follow-up studies but those available suggest that psychopathological problems tend to increase rather than diminish as children grow older. Baker/Cantwell (1987) in their follow-up of a clinic-based sample found that the proportion with psychiatric disorder rose from 4 4 % to 60%. Whilst a quarter of the sample were without identifiable disorder at the time of initial appraisal and developed disorder subsequently, only 8% of the sample had a disorder when young which resolved during the follow-up period. Mawhood/Rut-
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ter/Howlin (in preparation) in one of the rare follow-ups into adulthood found that amongst boys who had experienced receptive developmental language disorder 70% showed impaired social functioning in adulthood whereas only 35% had shown poor peer relations in early childhood (Bartak/Rutter/ Cox 1975) and 50% in middle childhood (Cantwell/Baker/Rutter et al. 1989). Turning more specifically to the factors which may affect psychosocial outcome, several studies have found that psychopathological problems are more frequent if language delay is accompanied by lower than average intelligence (Baker/Cantwell 1987; Beitchman/Hood/Rochun/Peterson 1989; Silva/Justin/Mc Gee/Williams 1984 ). The findings on whether the type of speech/language deficit affects psychosocial outcome are contradictory, but it seems that if children with a pure phonological problem are at any increased risk this is more likely to result in emotional problems rather than attention deficit disorders (Cantwell/Baker 1977). It has been suggested by Tallal/Dukette/ Curtiss (1989) that the raised incidence of behavioral difficulties in language-impaired children largely reflects neurodevelopmental impairment. They found that at age 4 years descriptions such as ‘clumsy’, ‘confused’ and ‘can’t concentrate’ differentiated languageimpaired children from controls. However in males, ‘cries too much’ and ‘clings to adults’, and in girls ‘withdrawn’, ‘secretive’ and ‘compulsions’ also did so. This is an interesting idea but on balance, and bearing in mind the findings that anxiety and poor peer relations also increase with age it is extremely unlikely that the socio-emotional difficulties consistently found to be raised in individuals with speech/language impairment are simply reflecting direct manifestations of neurodevelopmental impairment. Whether or not the socio-emotional difficulties stem specifically from speech/language impairment per se or more generally from neurodevelopmental or cognitive deficits that may underlie the language delay, however, is another matter. Systematic comparisons with other types of specific developmental disorder are lacking and are much needed. Without them it cannot be known whether the psychopathological risk with language delay differs in severity or type with that associated with, say, the clumsy child syndrome. The reports to here have focused on common psychopathological problems but there
V. Pathologies and Disorders of Language Development
is evidence that at least severe disorders of receptive language are also associated with risks for serious social abnormalities and for later psychoses. Cases of children with developmental disorders of language who show schizophrenic-like psychoses in early childhood have been observed (Mawhood/Rutter/ Howlin in preparation) as have others showing autistic-like social abnormalities (Paul/ Cohen 1984 ). It is well recognized that some cases of schizophrenia are preceded by developmental problems although these are not specifically in language alone (Rutter/Garmezy 1983), but difficulties arise in classifying both the early language disorder and the psychosis. There are probably diagnostic subgroups amongst language-disordered children, but at present little is known about how to identify them. Some promising work was done in this area by Lewis/Mezey (1985), who presented six case reports of individuals who were found on CAT-scanning to have a cavum septum pellucidum together with an unusual combination of developmental abnormalities including language delay in early childhood and the emergence of a paranoid psychosis in late adolescence or early adulthood. This research provided a puzzling but promising lead. Nonetheless, despite the interest it caused, it has yet to be replicated. It is clear from the findings presented here that there are strong associations between developmental speech and language disorders and a variety of adverse psychosocial sequelae. These problems have been demonstrated in adolescence and one of the few follow-ups into adulthood has revealed a common picture of social isolation, a lack of sexual relationships and frequent job changes (Mawhood/Rutter/Howlin in preparation). What is much less well understood however, are the mechanisms which result in these sequelae. There is little research to help in answering this question but Howlin/Rutter (1987) suggest several possibilities which need consideration. It may be assumed that no one mechanism is likely to explain all the psychopathological associations but each may offer an answer for different varieties of language disorder. First, it is possible that in some cases there are common antecedents which can account for both the language delay and the associated psychopathology. Many of these factors have already been discussed in the first section of this article and include temperamental difficulty, neurodevelopmental impairment, family disadvantage, psychosocial
60. Psychiatric and Psychological Aspectsof Language Development Disorders
deprivation and low IQ. It is plausible that some of the attention deficit disorders seen in language impaired children stem from an underlying neurodevelopmental disorder rather than from language difficulties as such. If this is the case, then they should be equally common in non-language disorders. A second potential mechanism is that speech/language disability may predispose to social or emotional problems because of the child’s difficulties in communication or because language oddities increase the risk of social rejection. It could be hypothesized that the stressful social outcome of language impairment may lead to the raised incidence of anxiety disorders found as sequelae. Third, the scholastic problems that frequently follow language delay may create their own risks as a result of the stresses associated with educational failure (Yule/Rutter 1985). Fourth, the social impairments found in early childhood (Siegel/ Cunningham/van der Spuy 1985) may constitute an intrinsic part of the language disorder, with both the language delay and the social impairment stemming from some underlying specific cognitive deficit. This mechanism may be useful in explaining why severe disorders of receptive language can show highly persistent social deficits. Finally, the language delay and the later psychopathology may be different manifestations of the same constitutional liability. This may be the case, for example, in the links between early developmental delay and the emergence of schizophrenia in late adolescence or early adult life. Adequate data to test these competing alternative explanations is lacking, and if the necessary progress is to be made, future research needs to be carefully designed to allow for some comparability between studies. In particular, prospective longitudinal research would be of immense value (see Rutter/ Mawhood 1991 for review). The most urgent needs for future research in this field are to identify which children are most at risk of developing adverse psychosocial sequelae, and also to clarify which factors, if any, can protect them against this process. Perhaps the most basic question is whether the psychosocial outcome of these children is due to inescapable factors within themselves, or whether it can be accounted for by the intervention of external variables.
4.
References
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Lynn Mawhood, London (United Kingdom)
Children with Specific Language Impairment (Developmental Dysphasia): Linguistic Aspects Introduction Characteristics of Dysphasic Children Patterns of Language Behavior and Development Information Processing Problems References
Introduction
In this chapter I will discuss what characteristics I think distinguish dysphasic or specif-
ically language impaired from normally developing children and other children with language disorders, what their language behaviors appear to be, and the relation between these children’s oral language behaviors and the various processing difficulties they have. Although it had long been held that dysphasic children have no cognitive impairment, more recent research indicates that they have information processing difficulties of various kinds (for example, Johnston/Weismer 1983;
61. Children with Specific Language Impairment (Developmental Dysphasia): Linguistic Aspects
Menyuk 1978). It is from this point of view that the cognitive behaviors of these children will be briefly discussed. Before the chapter begins, a brief discussion of how this author will use the term ‚specific language impairment’ or ‚dysphasic children’ is required. There have been a number of terms applied to the children I will be discussing. Over the past five decades, these children have been called functionally impaired, language disordered, language delayed, language learning disordered, language deficient, language deviant, specifically language impaired as well as dysphasic. I think that these varying terms have been applied to that group of children who have marked language problems but no other evident problems. Thus, children within the group are very loosely alike. The primary causes for the differences in the labels given these children may be first, the variability in their language behavior, and, second, the fact that there are probably distinctly different groups of children to which these labels have been applied despite their surface similarity. There are, also, children in this group who are at the very slow end of the continuum of the rate at which normally developing children acquire language, as well as children who show differences from normally developing children in their pattern of development.
2.
Characteristics of Dysphasic Children
The best explanation of who dysphasic children are remains, at present, unattainable. By definition they are children who have suffered CNS lesion either pre-natally, natally or postnatally. This is a logical conclusion rather than one based on hard evidence in most instances. The exceptions, who will not be discussed in this chapter, are dysphasic children who have suffered stroke or brain injury from accident. In these instances it is clear that lesion of the CNS is present. Without such hard evidence, the only reason to suggest that such lesion exists is that there is no other explanation available. There is no evidence of any other physical difficulty. They do not appear to be mentally retarded or hearing impaired but their language development does deviate from the norm. These children come from a wide variety of socio-economic and socio-cultural groups. Thus, there is no reason to believe that their non-normal lan-
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guage development is the result of environmental factors. In summary, these children seem to be like other normally developing children except for their language impairment, and, therefore, it seems reasonable to conclude that this impairment is due to CNS lesion. Outside of known or suspected CNS lesion, dysphasic children are uncharacterizable as a group. That is, there is a vast amount of individual variation in the language behaviors that are manifested by these children. That there is such great variation in their language behavior seems best explained by the possibility (we cannot claim fact) that their behavior is due to a particular type of lesion or structural difference in the CNS. Different dysphasic children have probably suffered different lesions and/or structural differences. Again, these lesions or structural differences do not appear to markedly affect other aspects of development outside of language, but they may do so in a subtle manner. Some of the differences in the language behaviors of these children are quite similar to the differences seen in adult dysphasics. Dysphasic children may have primarily linguistic output difficulties or input difficulties, reminiscent of Broca’s and Wernicke’s adult aphasics. One factor, then, that varies among these children is whether they have a production or comprehension deficit or both. Other dysphasic children show subtle and minimal differences from that of normally developing children, and are, therefore, very different from adult aphasics. Other dysphasic children have great difficulty in processing and producing language in the way that normally developing children do, and these differences are quite marked. Another factor, then, that varies amongst these children is degree of involvement. As stated, some of these children are severely involved and others are minimally involved. Still another factor that appears to lead to large differences among these children is the age at which the purported lesion occurs. Although there is a great deal of argumentation about what the duration of the socalled ‚critical period’ is, there is agreement that age of lesion is a very important factor in outcome. Thus lesion suffered before age two (pre-natal and natal injury are included in this period) or before age five years or prepuberty (there are varying views about what is the ‚critical period’), apparently affects the degree to which the behavior manifested re-
V. Pathologies and Disorders of Language Development
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sembles that of adult aphasics (Wittelson 1977), and, in fact, whether symptoms of language disorder are severe or not. By definition, all the children in the group to be discussed have, presumably, suffered pre-natal or natal lesion. Therefore, many of them should have only subtle signs of language problems. The fact that some have very evident language disorders indicates that very early lesion, depending on timing in fetal development, site and extent, can nevertheless have a marked and also lasting effect. Still another factor which might bring about variation within this group of children is the experiential one. As stated, these children come from various SES and socio-cultural groups, and may, therefore, have received different kinds of treatment. In summary, dysphasic children are those who are not mentally retarded or hearing impaired. They have apparent, not overt, CNS lesion in areas which affect language development. However, there are several factors which lead to variation in the language behaviors of the children. These are: 1) lesion site or type which affects comprehension or production of language or both with varying degrees of severity, 2) (compounded by) the fetal age at which lesions were suffered, and 3) (influenced by) SES, socio-cultural background and treatment. The above discussion should indicate how difficult it is to diagnose a child as being dysphasic until other aspects of development have been examined. Those aspects are peripheral hearing and general intellectual ability. Further, in instances of subtle manifestation of language disability, and given our current assessment capabilities, it is almost impossible to diagnose a child as being dysphasic under age three. This is due to the fact that children who are developing language normally may manifest different language development milestones at widely different ages. For example, most children are primarily holophrastic at 18 months and have a small repertoire of productive words (about 50) while some few others are producing two and three word combinations and have well over one hundred and fifty words in their lexicons. Still other children produce very few babbled utterances at 9 to 12 months and do not produce any word approximations by 18 months. These three groups of children are taking markedly different paths in early language development. However, it is not clear that one of these markedly different paths will lead to language disorder, and researchers
are struggling to determine which early behaviors do, in fact, do so. Further, it is only long-term developmental research which will determine which patterns of early language development are, in fact, predictive of later language problems. Such research has yet to be carried out with sizeable numbers of these children. It is clear that one must accept the fact that there are marked differences in the language behavior and patterns of language development among dysphasic children. However, one is left with the problem of describing the nature of these language behaviors and patterns which identify them as being that of dysphasics. An attempt will be made to describe the range of behaviors and patterns of language development from a linguistic perspective that appear to exist in this population of children that seem best described as language disordered.
3.
Patterns of Language Behavior and Development
Traditionally, the language behavior of children with language disorders has been described in terms of comprehension and production difficulties. A larger proportion of dysphasic children have been found to have a language production rather than a comprehension problem. A recent definition of children with specific language impairment is that these children exhibit delays of one year or more in language production and one of six months or more in language comprehension on a set of standard tests of these behaviors (Stark/Tallal 1981). This definition and others seem to suggest across the board delay in the development of all aspects of language comprehension and production. Another possibility exists. It may be the case that particular aspects of components of language are affected to varying degrees in some dysphasic children whereas other aspects are not. To explore this possibility, the results of research examining the language behavior of dysphasic children within specific components of language will be reviewed. Researchers have explored the phonological, lexical, semantactic and discourse behavior and development of dysphasic children. 3.1. Phonology Over the past fifty years there have been many studies of the speech sound production and perception of dysphasic children (for a sum-
61. Children with Specific Language Impairment (Developmental Dysphasia): Linguistic Aspects
mary of early studies see Powers 1957). Views of these children’s phonological abilities were largely based on the results of experiments that sampled the children’s speech only one time or assessed their production and perception on standard tests. Children with articulation and perception problems without any apparent organic cause were said to have ‚functional disorders’. There have been comparatively few naturalistic studies of these children’s phonological development (for example, Magnusson 1983; Schwartz/Leonard/ Folger/Wilcox 1980). As might be expected, the results of the two types of studies are different. The former find differences between normally developing and dysphasic children in speech sound production, and sometimes perception, at the segmental level, within specific lexical items (after all the experiments and tests examined this behavior). Using speech samples obtained with varying amounts of frequency and over varying amounts of time, the naturalistic studies have found similarities between the two groups of children in the phonological processes that can be observed during development. These processes include weak syllable deletion, consonant cluster reduction, backward and forward assimilation, stopping of continuants, vowel and consonant harmony (syllable repetition) plus idiosyncratic realizations chosen by particular children. Although these processes describe the early phonological production of lexical items by both normally developing and language disordered children, they appear later and persist longer in children who are considered language disordered. These differences in findings between the two types of studies may be due to three factors: differences in the manner in which the data were obtained (already pointed to), differences in the ages of the children examined, and differences within the children themselves. As was pointed out earlier, it is difficult to diagnose a child as dysphasic under the age of three. Therefore, some naturalistic studies may have examined some children under age three who are delayed rather than dysphasic. Further, both naturalistic studies and studies using standard tests have found variation among older language disordered children in their speech sound realizations of target sounds, and in the phonological processes used. Some possible and observed patterns of early (below age 5) phonological development in relation to lexical development among
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these children have been described (StoelGammon 1991). Three patterns are suggested. One pattern is delay in both lexical and phonological domains. Another pattern is delay only in ways in which phonological realizations are mapped onto lexical items that are age appropriate. A large number of words are collapsed into a small number of realizations. A third pattern is one of an age appropriate lexicon but of unique phonological realizations of lexical items. Still another possibility is that these realizations vary depending on the linguistic and situational context in which a lexical item is targeted. A study of older dysphasic children (over 5) found that these children’s realizations of speech sounds were very much affected by the contexts in which they were realized (Menyuk 1983). That is, the predictability of the target together with the motivation to succeed in reaching the target had an effect on how closely the child approximated the standard phonological realization of a lexical item. It is apparent that no generalizations about all dysphasic children can be made about their phonological development. The naturalistic studies indicate that phonological development in children thought to be dysphasic at ages two and three years looks very like that of normally developing children only delayed. Interestingly, these same results have been found in studies of children with persistent otitis media during the first three years of life (Paden/Novak/Beiter 1987). This might suggest that the children have less accurate hearing, as is the case with children who have had frequent episodes of otitis media. However, analysis of the segmental errors made by children with early otitis as compared to children with specific language impairment indicates that a greater percentage of children with histories of otitis delete initial consonants, substitute /h/ or glottal stop for consonants, and denasalize, stop and change the place of nasal sounds (Shriberg/Smith 1983). These phonological studies of very young dysphasic children may be concerned with children who are at the extreme end of normal development in terms of language, possibly because of some dampening of their hearing ability. With children over three years of age, who have been identified as being dysphasic, using the criteria described in the previous section, there are very marked differences in their phonological production (Menyuk/Looney 1972) and in their phonological perception (Tallal/Stark 1983). There are also dif-
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ferences among dysphasic children in their pattern of phonological production, ranging from those who produce speech sounds that are so different from the normal patterns that they are unintelligible, to children who produce consistent substitutions in their speech sound realizations that listeners can use to determine what they mean. These children’s perceptual difficulties may be based on the rate at which they can perceive speech sound differences that are of very short duration. Thus, their principal difficulty may be to distinguish between stop sounds. However, these children have also been found to have some difficulty in perceiving the differences between sounds that have their energy at high frequencies, and recent research points to more extensive differences among them in terms of fine-grained speech sound distinction abilities (Elliott/Hannen/Scholl 1989). Within a group containing both language impaired and normally developing children, the language impaired children were correctly identified 80% of the time at ages 6 to 7, and 65% of the time at ages 8 to 11 based on their ability to find just notable differences between /ba/ and /pa/ and among /ba/, /da/ and /ga/. It may be the case that all dyphasic children’s speech perception and production abilities are affected, and that these differences in abilities is the cause of the difficulties these children have in lexical, morphological, and syntactic development. Suggestions of this kind have been made by a number of researchers. It is also possible, however, that some of these children have specific difficulties with lexicon because of phonological difficulties, and others because of semantic difficulty. Some may have problems with syntax because of phonological difficulties and others because of semantactic problems. Some may have problems with connected discourse because of semantactic difficulties and others because of perceptual difficulties. These possibilities will be explored in further sections of this chapter. Some of these children’s morphological difficulties seem to be clearly related to their phonological difficulties. For example, they have been found to be somewhat delayed or extremely delayed in their ability to mark tense on the verb phrase and to mark number and possession on nouns. It has been suggested that the surface information of the morphological markers are an important factor in their causing so much difficulty (Leon-
V. Pathologies and Disorders of Language Development
ard 1990). This is why there are differences between English and Italian speaking dysphasic children in which morphological markers are omitted. Markers that English speaking children have difficulty in acquiring, such as plural, are not omitted by Italian speaking children because in Italian they are marked by a vowel syllable (frequently /o/ or /a/) rather than a bound strident sound (frequently /z/ or /s/). Difficulty with morphological markers may be a product of processing problems not lack of linguistic knowledge. Some markers are more learnable than others because of the ease with which they can be isolated from the word and categorized. Markers that are separate syllables and are composed of comparatively more easily identified speech sound categories (are more perceptually salient) are the markers that are more easily acquired by both dysphasic and normally speaking children. Again, there is difficulty in distinguishing between very slow developers and dysphasic children in their pattern of development of morphological markers, since the bound morphemes that have little phonological information are composed of just those speech sound distinctions that create particular productive and perceptual problems for normally developing as well as dysphasic children, and for children with hearing problems. In a study comparing the reproduction of lexical items in sentences that are and are not composed of stems and bound morphemes (for example, friend versus planned), it was found that children with early histories of otitis repeated the word stems significantly more frequently than the morphological markers on the word stems (Teele/ Klein/Chase et al. 1990). Again, the possibility of differences in hearing may account for the morphophonological problems of some dysphasic children. Findings similar to those in phonological development have been found in studies of the morphological development of very young children with specific language problems. During the period at which both normally speaking children and the language disordered children are primarily producing one to three word sentences both groups of children have similar morphological problems (Lahey/Liebergott/Chesnick et al. 1990) and it is difficult to distinguish between the two groups. When the MLU of both groups of children increases, then more differences between them, in which morphological markers are acquried, can be observed. This may in-
61. Children with Specific Language Impairment (Developmental Dysphasia): Linguistic Aspects
dicate that the dysphasic children have a problem in the amount of memory space they can allocate to the realization of all aspects of utterances, especially if they are having difficulty in encoding some aspects. Under these circumstances morphological markers may be sacrificed for lexical stems. In summary, there appear to be at least two types of phonological problems that can be found among dysphasic children. The first is one of marked delay in the development of the phonological system (perhaps accompanied by delay in lexical development). Thus, phonological processes that are found in the speech of normally developing children can be found in the speech of these children but they appear at a later age and persist over a longer time. Some of these processes are concerned with segmental realization and others with syllabic structure, but in terms of both types of processes, the patterns found are in the speech of both so-called language impaired and normally developing children (Ingram 1989). It is possible that these delays may in part be due to a surface level auditory or speech sound perception problem. This may also be the case for some language impaired children who do not exhibit a lexical but only a phonological delay. There is still another group of children who are much more variable in their speech sound realizations, and markedly differ from normally developing children in the consistency with which they realize sounds and in how far they depart from the target sounds within lexical items in terms of features of segments (Menyuk 1983). Some examples of these differences are the following imitations or spontaneous generations: 1. Imitates See the ship as /uh uh uh/ 2. Generates paper as /maber/ 3. Identifies umbrella as /pel/ It is possible that the basis for these phonological difficulties is a deeper problem having to do with how they process and then organize the acoustic information they receive, or how they map these organizations into speech sound movements. That is, there are children who have only a problem in planning speech sound realizations, and others who have both a perceptual organization and speech sound planning output problem. There is still, at least, one further possibility of variation in the phonological development of children labelled as language disordered. It is possible that the phonological errors made by some children are due to difficulties
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in mapping out target segments and sequences. These children, apparently, have no perceptual problem, only an end organ productive problem. They literally have difficulty in achieving the articulatory targets that they have planned. The assumption is that their underlying phonological representations for both perception and production are quite similar to those of normally developing children. Their phonological behavior has been likened to that of adult dyspraxics. Their speech can be highly unintelligible. Therefore, they are labeled as language disordered.
Fig. 61.1: Representation of causes of phonologi-cal problems and products in groups of languageimpaired children
Figure 61.1 above attempts to capture the possible differences between the four groups of children in terms of the causes for their phonological problems and the products of these problems. In Group I, very slow developers, the problem is one of less accurate perceptual abilities than in normally developing children which affects both phonology and lexicon. In Group II, only phonology is affected by the less accurate perception. In Group III, it is postulated, there are different representations of phonological categories which affects both phonology and lexicon. In Group IV only articulatory movements to achieve phonological targets are affected. 3.2. Semantactic Problems It was hypothesized some years ago that online comprehension and production of utterances involves parallel processing of the categories and relations from each component of the grammar. Thus, each component contributes constant ‚updates’ on the information
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needed in the sequence being generated or comprehended. If this were the case, then, it was hypothesized, the phonological and semantactic components of the language should be affected to the same degree in language disordered children (Menyuk/Looney 1972). It was found that the children with the most severe phonological problems were also those with the most severe syntactic problems. In more recent studies variations in these findings have been observed. In one study it has been found that in 30 speech delayed children, only two thirds of them also display an overall syntactic delay, and only one half display some limitations in their use of phonetically complex morphemes (Shriberg/Paul 1982). In a study employing sentence repetition to assess syntactic and phonological processing, however, it was found that the phonological complexity of the target lexical items disrupted the accuracy of repetition of syntactic structures. Both syllabic complexity and clause embedding contributed to the errors made by the children (Panagos/Prelock 1982). Thus, apparently, some language disordered children exhibit delays or problems with both syntax and phonology, and others have either only phonological problems or only syntactic problems. Yet to be determined is whether or not there is independence between the phonological and semantactic levels of the language in the language production of language disordered children. Such a determination has interesting implications for language processing in general. A possible explanation for the differences in the findings concerning the relation between the two components of the language in language disordered children might lie in the differences among the children in the causes of their phonological and syntactic problems. Children who have difficulty in developing phonological representations of lexical items might also have difficulty in developing the semantactic structures that are governed by these lexical items and exhibit delay in both domains as well as in lexical development. Children who have only speech generation problems need not have difficulties in syntax comprehension, and, therefore, exhibit no delays in these developments. Children who have difficulties in formulating more sophisticated syntactic categories and relations need not have difficulties in phonological representations of lexical items, and only exhibit their problems at a later age. These are all suppo-
V. Pathologies and Disorders of Language Development
sitions. There have been very few studies of the simultaneous morphophonological, lexical and semantactic problems that language disordered children may have. A number of studies have found that dysphasic children have both delays and some differences in their semantactic development. These findings have been based on analyses of language samples obtained from these children at different ages, and on results of experiments that have asked these children to engage in various semantactic tasks such as imitation, acting out commands that have been given orally, generating utterances from observed actions and pictures, generating utterances from a set of words, etc., as well as from standardized tests. The variety of means by which these children’s semantactic production and comprehension have been assessed raise questions about the generalizability of the findings in any particular study. Therefore, the fact that there are similarities in findings is not only surprising but, also, suggests that there are particular semantactic behaviors which can be found in at least some children in this group of children. For example, it has been found that dysphasic children stay at particular stages of the development of this aspect of language that mark reorganizations of semantactic knowledge (Menyuk 1978). Thus, younger dysphasic children are producing SVO sentences without expansion of the noun phrase or the verb phrase for a much longer time than their normally developing peers. They appear to plateau at this stage of development for a number of years. Older dysphasic children are producing simply expanded subject plus predicate sentences, and non-coordinated or embedded sentences for a much longer time than their normally developing peers. They, again, appear to reach a plateau but this plateau may exist for an even longer time than the previous one. Dysphasic children use much fewer different sentence patterns than their age peers, and, also, more frequently produce sentences with syntactic errors (Grimm 1987). Utterances with errors of commission appear after errors of omission. Despite producing sentences of the same length as MLU matched normally developing children, dysphasic children produce fewer propositions per utterance and make more syntactic errors in these utterances (Johnston/Kamhi 1984). Some of these results indicate delays in general and marked delays during certain periods of development. These periods are those
61. Children with Specific Language Impairment (Developmental Dysphasia): Linguistic Aspects
during which one can see significant changes in semantactic structures in, at least, the utterances produced by the child. Thus, the difference between normally developing and dysphasic children in semantactic development seems to be, on the surface at least, the rate at which some productive semantactic structures are acquired. However, there are differences as well. The semantactic errors made by dysphasic children lend support to the notion that there are differences as well as delays in dysphasic children’s development of this aspect of language. First, syntactic errors are a much more frequent occurrence in the sentences produced by three year old and older language disordered children than in those produced by normally developing children of a much younger age. Second, the errors made by the two groups of children appear to be different. For example, Grimm (1987) found that dysphasic German speaking children produce utterances such as the following, whereas normally developing children never do: ein Boot Wasser nehmt ham (a boat water taken have); eine Brust ich sehen hab (a breast I seen have). The way in which these children order elements in phrases, as in the examples above, suggests that the underlying representations for these phrases are different. Fletcher (1991) presents some examples of what he calls formulation errors in the utterances produced by a group of 15 language impaired children in England and Scotland, and they are similar in kind to the German examples above: here they got eyes to me; my mum was take me a picture. Fletcher characterized the syntactic problems of these language impaired children as being in four areas: 1) comprehension (as measured by standard tests), 2) output problems as indicated by maze generation (reformulations and repetitions, and formulation errors), 3) grammatical errors (omission of determiners, auxiliary and copula verbs, agreement errors, and morphological errors) and 4 ) problems in expansion of verb phrases, phrases and sentences (coordinated and embedded sentences). Semantactic problems such as those described by Grimm and Fletcher have been found in many studies of dysphasic children (Menyuk 1988). Variability in semantactic behaviors has also been found. Thus, some language disordered children largely strip their sentences of components other than the subject verb and object, whereas others commit the kinds of errors
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that normally developing children never commit. Fletcher points to four sub-groups with differing types of combinations of problems and strengths in semantactic production and comprehension in this small group of children. Each group in the Fletcher study is obviously composed of a very small number of children, and 6 of the 15 children (4 0%) are not exactly groupable, although 4 of these 6 are similar to established groups. All of the children on whom there are comprehension data have comprehension problems except two. Some studies have found children with only sentence production problems, others have found children with severe production problems and minor comprehension problems, and still others have found that some of these children, although they are comparatively fewer in number, may have more severe comprehension than production problems (Liebergott/Menyuk/Chesnik/Korngold 1988). Three of the four different groups pointed to by Fletcher seem to represent somewhat different levels of input and output processing problems. If one examines the data presented from this point of view, the first group shows difficulties in all the areas of sentence generation described above. A second group shows difficulties in output (mazes and formulation errors) but in no other areas. Group three has output problems and, also, doesn’t expand sentences. If we consider sentence expansion as requiring different abilities than phrase expansion then group 1 has difficulties in developing semantactic categories and mapping these categories into output sequences for both SVO and expanded SVO sentences. Group 2 only has difficulties in mapping categories into output sequences, and group 3 is similar to 2 except that they have additional difficulty in developing the categories for expanded SVO sentences. Thus, some children have difficulty in basic category development and in retrieving these categories (an encoding problem), while others primarily have difficulties in programming out these categories (a retrieval problem). Basic category development is different for single versus expanded sentences, and is probably different for different types of coordination and expansion. That there are similarities within subgroups of these children and differences among subgroups is not surprising, given the initial hypothesis that these children suffer lesion of the CNS but suffer different types
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of lesions and/or structural differences. There is also the developmental factor. That is, children cannot display difficulty with an aspect of language until they have acquired that aspect of language. Thus, studies of dysphasic children when they are aged 3 or 5 years might show only delay, and a similar kind of delay. At later ages, when some of the children have acquired basic categories, and are having difficulty in programming them out than differences might appear. It may also be the case that among the children that have been classified as language impaired are children who are simply at the extreme end of slow language developers but who are developing normally. This same possibility was discussed in the section on phonological development. As stated, studies of language impaired children show both similarities and differences in language behaviors among them. Some similarities among them are the data pointed to initially: the slow start, the plateaus in development at the point at which there are new categories to be developed and old categories expanded. Differences among them are, at least, the rate at which they acquire categories and whether or not they have severe production and mild comprehension problems, or a mixture of the two, or mild comprehension and severe output problems, or only output problems. Differences are usually observed in these children after age five to six years and similarities before this age. Studies of these children’s comprehension of semantactic structures in utterances is quite consistent with the findings concerning production similarities. That is, they have difficulty in acting out sentences that have more than one proposition when they are aged 3 to 5 years (Levy/Menyuk 1975). This seems to be an example of reaching a plateau in comprehension of sentence expansion as well as in production of these expansions. When they are around age 8 they continue to have semantactic comprehension problems (Menyuk/Chesnick/Liebergott et al. 1991). They have difficulties in answering questions about sentences that mark time (before and after) or dependent relations (WH clauses and complements) and have more than one proposition. They have difficulty in judging and correcting sentences that contain semantactic errors, both of phrase and clause construction and of morphological markers. They have great difficulty in filling in missing nouns, verbs and adjectives in simple sentences.
V. Pathologies and Disorders of Language Development
Task
Mean Mean Correct Correct Responses Responses Dysphasic Low Average
Answer Questions 7.32 Judge & Correct 27.48 Fill in Parts 11.07
9.43 36.26 16.14
p value .01 .002 .001
Table 61.1: Semantactic comprehension performance of dysphasic and average normal children on various tasks Table 61.1 compares these children’s and low average children’s performance on these tasks. The low average children in this study were significantly different from normally developing children in their rate of developing language, but were not performing as poorly as specifically language impaired children on standard tests of language performance as well as on the tasks described above. An interesting paper suggests that these children might be classified as “low verbal normal” (Snyder 1987) or, as we have termed them here, at the very slow end of normal development of language. A number of researchers who have examined the development of semantactic metalinguistic abilities in normally developing children (for example, Bialystok 1986; KarmiloffSmith 1986; Menyuk 1983) have hypothesized that acquisition of language knowledge takes place in a number of steps. Roughly, the first step might be intuitive knowledge, then awareness of what is known, and finally automatic application of what is known. The state of knowledge of any particular aspect of language changes over these steps. Intuitive knowledge of a structure is ‚fragile’ or not well established knowledge. Bringing this structure to the level of conscious awareness more firmly establishes knowledge of this structure and makes more rapid retrieval possible. The most mature state of knowledge of this structure is automatic use under all appropriate conditions. This is achieved when retrieval of the structure takes place at an optimal rate. In addition to positing a semantactic input processing problem, and/or an output processing problem, it has been hypothesized that these children have a problem in meta-processing semantactic categories and relations in the language (Menyuk 1991). Thus, their knowledge of semantactic cate-
61. Children with Specific Language Impairment (Developmental Dysphasia): Linguistic Aspects
gories and relations and morpho-phonological categories and relations remains fragile for a much longer period of time than in normally developing children. The reason for these children having difficulty in becoming aware of what they know about language may be due to the ways in which they store representations of their knowledge. Lexical-semantic grammars suggest that lexical items, in particular verbs, and the syntactic structures they can find themselves in are stored simultaneously. Language impaired children may be unable to deal with this kind of storage requirement. When discussing the increasing difficulty that language impaired children have in retrieving morphological markers in increasingly longer sentences, it was suggested that they have limitations on how much they can program out in a single utterance. In discussing their metalinguistic problems it was suggested that they have difficulty in storing certain kinds of representations. In discussing the kinds of errors that were labelled formulation errors, it was suggested that these children’s underlying representations of phrases and clauses might be different. The first two suggestions are concerned with how these children process language information, but the last is concerned with the grammars of language they develop. There is a very real difference in these two types of explanations. Except for the formulation errors pointed to, most of the evidence points to processing differences rather than underlying grammar differences. Various hypotheses have been presented to account for the particular kinds of difficulty and delays dysphasic children have in semantactic competence. These explanations include differences in the learning strategies they use, memorial problems, cognitive differences, and as discussed earlier, phonological problems. In addition to putting forth main causes for semantactic problems, some researchers have suggested that there are various subtypes of semantactic problems that these children have, and that these subtypes are due to different causes for the problem. These possibilities along with others will be discussed in the final section of this chapter. 3.3. Lexical Development Given the findings of both phonological and semantactic delay and difference in dysphasic children, it would seem highly likely that these children would have problems in lexical ac-
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quisition. Their difficulties in preception and production of phonological segments and sequences would make acquisition of stable phonological representations of lexical items a problem. There is now data which indicates that this is substantively the case (Schwartz/ Leonard/Frome Loeb/Swanson 1987). It has been found that when language impaired children are in the process of acquiring new lexical items, they appear not to take advantage of the phonological segments that are already in the lexical items they have acquired to add new lexical items containing these segments. To account for this finding, the researchers hypothesize that the children have either a motor output mapping problem or a difficulty in formulating stable phonological representations. Lexical meanings are often derived from the linguistic and situational contexts in which they are used. If a child has difficulties in semantactic processing, these should lead to problems in development of lexical meanings as well. However, the bases for problems in lexical acquisition would be quite different in kind from those suffered by children with phonological representation and retrieval problems, and this difference should be exhibited in both spontaneous speech studies and in confrontation naming experiments. That is, phonological errors should occur in the first instance and hesitations and substitutions should occur in the second instance. There have been comparatively fewer studies of the lexical development of these children than there have been of other aspects of language. The studies that have examined lexical problems and development in dysphasic children have come up with findings that are similar to those in studies of phonology and syntax. There are a group of studies which indicate that lexical development in language disordered children is much like that of normally developing children and others that have found differences. For example, one study found that the inappropriate word extensions found in the speech of language disordered children were quite comparable to those found in the speech of normally developing children at the same linguistic level (Chapman/Leonard/Rowan/ Weiss 1983). This finding suggests that language impaired children are acquiring and structuring their productive lexicons in ways that are similar to those of normally developing children. The language disordered children in this study were aged 2;8 to 3;4 years.
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When the spontaneous speech of older language disordered children is examined, differences rather than similarities are found. The spontaneous speech samples of 7 to 12 year old language disordered children were compared to those of normally developing children, and it was found that there were a significantly greater number of reformulations and word substitutions (German 1982). It, again, may be the case that at least two different populations were being assessed in the studies cited above. The language disordered children in the first study may be at the very delayed end of normal development while the children in the second study might, indeed, be language disordered. The other possibility is that the children in the first study were too young to manifest differences as well as delays in language development. Difference has been a consistent finding in the studies that have examined the ability of language disordered children, as compared to normally developing children, to rapidly retrieve lexical items under the conditions of confrontation naming. The question that arises is whether or not these children have difficulty in acquiring lexical items as well as retrieving them. The answer to the question appears to be that they do when the data from confrontation naming studies is examined. In one such study (Fried-Oken 1987), it was found that language disordered children produced significantly more errors that were unrelated to the pictured items than did normally developing children. This was the case when both first and second responses were examined. This indicated that there was a significant difference between the two groups in the number of pictured items that could be named. The language disordered children simply had a smaller lexicon. Outside of suggesting that there may be two groups of children in studies of dysphasic children’s acquisition of lexicon, as stated above, language disordered children may, initially, have an encoding problem because of their inability to accurately encode the phonological representation of a lexical item. Later, they may have a lexical acquisition problem because they may have limited access to semantic properties (Menyuk 1988). In contradiction to this notion, there is reason to think that there are, indeed, different subtypes of lexical encoding problems in this population initially, as was stated at first. When the spontaneous speech samples of 7 to 12 year old dysphasic children were ex-
V. Pathologies and Disorders of Language Development
amined, two groups could be found. One group was significantly different from normally developing children in the number of different words produced. The researcher suggested they had a “productivity” problem. The other group was significantly different in terms of the number of reformulations and substitutions produced (German 1987). If the second group of children had difficulty in encoding the semantic properties of lexical items rather than in acquiring lexical items, then they would exhibit difficulties in retrieval that reflect semantic errors. This is what they did rather than exhibiting gaps or errors unrelated to target items. It is this kind of evidence which supports the notion that there are two different kinds of lexical problems that dysphasic children exhibit, delay and difference. A number of studies have examined the rapid autonomic naming of language learning disabled children or those with reading problems (Wolf 1984 ). In these kinds of studies behaviors similar to those of language disordered children in confrontation naming tasks and in studies of their spontaneous speech have been found. There are differences in the latency, accuracy and types of responses produced by these two groups of children as compared to the responses of normally developing children. The two types of errors most frequently produced by normally developing children are semantic field errors (for example, knife for fork) and semantic/perceptual errors (for example, skirt for dress). The most frequent errors produced by language disordered children are 1) circumlocutions (for example, it’s to dig with for shovel), 2) comments unrelated to the pictured items or 3) no response at all. The latter two findings simply suggest that the language disordered children have fewer lexical items. The frequent circumlocutions these children respond with under all conditions (in spontaneous speech as well as confrontation naming and rapid autonomic naming) suggest that the semantic features of the lexical items that are acquired by language disordered children may be organized in a manner that is different from that of normally developing children. Functional features specific to a lexical item rather than generalizable perceptual features may be the primary organizers for the language disordered children. This could mark both a delay and a difference in the acquisition of semantic features for lexical items. It has been concluded that functional features,
61. Children with Specific Language Impairment (Developmental Dysphasia): Linguistic Aspects
which are, however, used to generalize, are acquired first by normally developing children. There is a great deal of argument about whether or not this is the case, with some researchers presenting evidence that it is, and other researchers presenting contradictory evidence (Menyuk 1988). The differences between normally developing and language disordered children in acquisition of semantic features for lexical items may lie in the normally developing children acquiring a much greater variety of feature types for different lexical items, and in their ability to make a greater number of generalizations using these features. It is interesting to note, along these speculative lines, that syntactic class of lexical items has a more marked effect on the lexical acquisition of normally developing children than on language impaired children. In a study comparing the lexical learning of young (aged 2;8 to 4 ;2) children it was found that normally developing children learned object words better than action words. This was markedly less the case for language impaired children (Leonard/Schwartz/Chapman et al. 1982 b). Finally, patterns of lexical development in these children may be similar to patterns of semantactic development. There may be plateaus reached in lexical development when
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the nature of the next set of lexical items to be acquired is more complex, just as plateaus in semantactic development occur when the next stage involves a serious complication in the structures to be acquired. There are few data to support such an hypothesis. These few data indicate the following. First, word frequency does play a role in the lexical retrieval problems of language disordered children. Less frequent words are more difficult for them to retrieve than more frequent ones (Liebergott/Menyuk/Chesnick et al. 1988). Of course, this is true of normally developing children as well but with dysphasic children the problem is more marked and lasts a longer time. For example, in the study cited above (Liebergott et al. 1988) it was found that letter and number naming was significantly less accurate than object naming for language impaired, low average and average children. However, there were significant differences between the language impaired children and the other two groups of children that persisted over the three years of the study. The rate of naming letters by the three groups of children over the period of the study is shown in Fig. 61.2 below. As can be seen, the mean rate of naming score increased for most of the children over the period of the study because more of the
Fig. 61.2: Differences in rate of letter naming by language impaired (low), low average (middle) and average(high) children at three points in time
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letters were being named by the low average and average children. This was not true for the language impaired children who seemed to reach a plateau in their letter naming ability. This notion that lexical development becomes markedly slower as more complex words are to be acquired is further supported by the fact that lexical development continues to be slow in language impaired children over the school years. One of the most stable measures of lexical comprehension difficulties in language impaired children are word comprehension tests. Differences between language impaired and normally developing children on these measure can usually be observed from 3 to at least 18 years. The second kind of data to support this hypothesis is that language impaired children have particular difficulty with lexical items and phrases that have more than one meaning. There has been at least one study which indicated that interpretation of metaphor is different in pre-adolescent children with histories of early language difficulties as compared to those without such histories. In these children only differences in metaphorical interpretation can be observed. There are no differences between them and normally developing children on a standard test of literal lexical comprehension (Nippold/Fey 1983). In summary, the studies of lexical acquisition in dysphasic children indicate that there may be at least two patterns of lexical acquisition within the groups of children called language impaired. One pattern appears to be very similar to that observed in lexical acquisition in normally developing children, only delayed. It was hypothesized that the primary cause of the lexical delay in these children may be their inability to form stable phonological representations for lexical items. This slows down their rate of acquisition of new lexical items but the way in which the semantic properties of these items are encoded does not seem markedly different. Another group of children are also slow in lexical acquisition but their difficulties seem to stem from an inability to organize semantic features of lexical items in a categorical way, and in the limitations of the feature types acquired. In spontaneous speech and in confrontation and rapid autonomic naming tasks these children circumlocute and use substitute lexical items such as thing or that. Often these circumlocutions contain references to the functions of the target item. This seems to
V. Pathologies and Disorders of Language Development
suggest that these children more easily store the functional features of lexical items, and then have difficulty in adding perceptual, syntactic and associative features. Their retrieval difficulties may stem from the limited number and types of semantic features they have for lexical items. If the speed of lexical accessing is a function of the number of different routes that have been laid down for reaching a lexical item, then the longer latency of their responses in spontaneous speech and in experimental tasks might be accounted for. 3.4. Pragmatics Over the past decade there has been a heightened interest in the pragmatic development of dysphasic children. This was partially a function of heightened interest on the part of linguists in this aspect of language. However, it was primarily due to the fact that those concerned with the language behavior of these children came to the conclusion that communication, not sentence processing, should be the focus of their attention. There have been three principal strands in the recent research in this area. One of the strands is examination of the language disordered child’s ability to tell or retell stories. Another strand has been examination of these children’s ability to generate different types of speech acts and engage in communicative interaction with various partners. A third and less frequently examined strand has been these children’s concepts of the conditions for communicative interaction. There is yet another strand, how parents communicate with their language impaired children, but much of this research sheds little light on the nature of the interactions. The emphasis is on input. Pragmatic knowledge involves knowing what language to use under which circumstances. Thus, both knowledge of the communicative rules of one’s culture and the rules of the language is required. Simultaneous processing of the situation (social and physical) and of the language that is being exchanged is required in using pragmatic knowledge. Thus, there should be a sizeable amount of strain imposed on the dysphasic child in communicative interaction situations as compared to sentence, lexical and phonological processing situations. However, unlike structural processing situations, there is a great deal of contextual support (visual and affective) which should help the language disordered child.
61. Children with Specific Language Impairment (Developmental Dysphasia): Linguistic Aspects
There are several factors that might play a role in whether or not dysphasic children have pragmatic problems. A primary factor appears to be whether or not the dysphasic children in the study do or do not have a comprehension problem. Another factor is the complexity of the communicative act that is being examined. A third factor is the conditions under which communication is being examined at what age. For example, if one looks at early speech acts such as commands and compares MLU matched language impaired and normally developing children, one might find no differences, since commands can be generated with single words marked with the appropriate intonation. Thus the complexity of the communicative act should play a role in studies examining this knowledge in language disordered children. The results of the research are varied not only in terms of which strand was examined in a particular study, but also which aspects of each strand have been examined. The research carried out thus far, as in the case of lexical development, has been quite limited in terms of amount and the broadness of the questions asked. There have been a few studies of the development of speech acts in language impaired children. In one study of young language disordered children (approximately 3 years) and normally developing children (approximately 2 years), the functions of utterances in a speech sample were examined. It was found that the language impaired children were similar to normally developing children in terms of the frequency of utterances serving most functions (Leonard/Camarata/ Rowan 1982 a). Naming was more frequent in the normally developing children, and answering in the language impaired children. The two groups were the same in terms of the different lexical items that were used to serve the communicative functions of language at this young age. Performative and presuppositional skills of these two groups of children was examined in another study. Again the children were young (the normally developing children were 1;4 to 2;1 years and the language impaired 2;8 to 4 ;2), and again speech samples were used. It was found that the two groups were similar in their use of imperative and declarative performative use, and similar in their tendency to encode changing versus static situational elements (Rowan/Leonard/Chapman et al. 1983). Thus, their use of speech
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acts, and what they selected to talk about (topics) were similar. The findings are somewhat different when the ability of language impaired and normally developing children to comprehend and produce requests are examined. These abilities in language disordered children aged 3½ to 9 years were examined in role play and free play situations in a paradigm similar to that used with normally developing children (Prinz/Ferrier 1983). It was found that in role play direct requests predominated and indirect requests only increased slightly in older children. The researchers suggest that the language impaired children were at a pragmatic level in requesting that was 2 or more years behind their normally developing peers. It was not until 5½ to 6½ years that the children could discriminate between requests on the basis of politeness. These results indicate that more complex speech acts might impose greater strain on language impaired children. The form of indirect or more polite request in English is usually auxiliary or modal permuted questions (Can you give me that one?). In another study the ability of language learning disabled and normally developing children, in grades 1 through 4 , to deliver bad news was compared (Pearl/Donahue/Bryan 1985). In such a situation, both the speech acts used and how they are used (taking into account the perspective of the other) are involved in being tactful. As might be expected, the younger children (grades 1 and 2) were rated as being less tactful than the older children. The language learning disabled children were rated as being less tactful than the normally developing children. The experimenters raise the question of why this was the case. It was not clear from the results of the study whether the language learning disabled children were having problems in generating the linguistic structures necessary to convey tact or whether they were unable to take the perspective of the other. In another study of the ability of these children in grades 2, 4 , 6 and 8 to engage in referential communication, these same experimenters conclude that language learning disabled children have syntactic deficits that limit their ability to engage in successful communications. Although the latter two studies had as subjects language learning disabled children rather than dysphasic children, one might hypothesize that the syntactic problems of the orally language impaired children would be even more prominent. The results of studies
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of young language impaired children suggest similarity, albeit delay, in speech act development. The study of indirect requests and the studies of language learning disabled children suggest that very real barriers exist in these children’s abilities to comprehend and produce speech acts that require semantactic structures that are more complex. There is little evidence to suggest that these children have impoverished notions of what communication is all about and are incapable of taking the perspective of the other. This latter conclusion is reinforced by the findings of a study examining the conversational performance of language impaired and normally developing children who are the same age and younger than the language impaired children (Fey/Leonard 1984 ). In this study, the language impaired children and their normally developing age peers were aged 4 ½ to 6 years. The younger normally developing children were aged 2;11 to 3;5 years. The children engaged in conversation with an adult, a peer and a younger child. It was found that the language impaired children were similar to normally developing children in all aspects of their conversational interaction except that they generated fewer internal state questions, had shorter MLUs and shorter mean pre-verb lengths. They were better than the younger children in the normally developing group in adapting their language to the age of their conversational partner. These data reinforce the notion that the communication problems of dysphasic children are probably due to their semantactic difficulties and not problems about the requirements of communication interaction. However, in a study of somewhat older language disordered children (between the ages of 5;6 and 6 years, the findings were very different. The language disordered children ignored and responded inappropriately to requests more frequently than normally developing children. Their responses were, occassionally, contrary to facts or unrelated to expected information (Brinton/Fujiki 1982). These findings suggest that language disordered children do have difficulties in acquiring the requirements of conversational exchange. However, the contradictory findings might be due to all the factors discussed in the review of studies of other aspects of language. Namely, 1) there might be true differences in the nature of the problems in pragmatics that different dysphasic or language disordered children have, due to underlying
V. Pathologies and Disorders of Language Development
neurological differences, or 2) they might experience difficulties in the acquisition of the kinds of knowledge required in the more sophisticated components of an aspect of language and, thus, exhibit a plateau in development. Unfortunately, the longitudinal and across components of language data needed to determine whether one or two is the case are missing. Evidence from other studies of the conversational interaction of dysphasic as compared to normally developing children, however, support the notion that there are at least two groups of children within the population in terms of the development of competence in communicative interaction. The ability of language disordered children of varying ages (4 ;0 to 6;2 years) to mark new versus old information in conversation was examined. It was found that over half of the language disordered children pronominalized more often than control children of ages 1;11 to 2;10 years. These language disordered children also demonstrated a proportionately different combination of language features for their MLU (Skarakis/Greenfield 1982). These findings suggest that there is a group of language disordered children who develop more sophisticated ways of marking new and old information in conversation despite the fact that their MLU remains the same as much younger normally developing children, and a group who do not. The former group of children appear to have an output problem. The latter might have an input problem. Another study (Craig/Evans 1989) examined the turn exchange characteristics of the conversations between language impaired children and adults, and age and MLU matched normally developing children. The language impaired children in this study were aged 8;8 to 13;11 years. Since there were only five language impaired children in the study, the behavior of individual children was examined closely. It was found that there were qualitative differences in terms of turn errors, interruptions, interactive attention, responsiveness and turn switch times among the SLI children. Children with reduced receptive skills had more difficulties. These data suggest that children who have problems in encoding information in conversational exchanges have more difficulties in responding and in responding appropriately than children who have retrieval problems. This, of course, makes sense. There have been, by now, many studies of the narrative generation and, more fre-
61. Children with Specific Language Impairment (Developmental Dysphasia): Linguistic Aspects
quently, recall abilities of dysphasic children. Most of the dysphasic children in these studies range in age from about 7 to 14 years. Therefore, unlike research in other aspects of language, only older language disordered children are included. For the most part, these studies indicate that language disordered children generate and recall fewer propositions and even episodes than normally developing children but, on the whole, maintain the structure of the narrative. There are, however, some differences in narrative processing that some researchers have found, and they are interesting. The language disordered children do not differ in factual recall but do so in terms of relations linking the critical parts of the story together (Merrit/Liles 1987). The language disordered children exhibit poorer use of cohesive conjunctions (Liles 1987). There are some language disordered children who show temporal inversions and transformations in their recall of stories, and their patterns of recall and story construction are atypical of children of that age (Johnston 1982 b). With these latter children the suggestion was made that they were having comprehension difficulties. Their narrative organization is poorer, and they are poorer in their use of cohesive categories and personal reference. They are equal in their responses to verbatim questions but differ from normally developing children in their ability to answer questions about the structure of the narrative (Liles 1985). Even when they recall a story, they have more problems with inferential questions (Crais/Chapman 1987). The data on story recall and generation indicate that there are, again, possible differences within the population of dysphasic children in this ability. There are those who order story episodes in the manner of normally developing children and those who do not. Those who do not, apparently, have comprehension problems. Thus, there are children in the population who generate less and recall less than normally developing children and others who do the latter, and, also, generate and recall in a different manner than normally developing children. These difficulties in recall are probably related to the differences observed in the ability of language disordered children to answer inferential as compared to verbatim questions and to recall linking structures across the story. There have been differences observed in these children’s ability to generate a variety of conjunctions and cohesive devises which is, presumably, unrelated
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to semantactic abilities. This suggests that at least some of these children have not acquired the sophisticated structures necessary to make discourse connected. This might be considered a particular pragmatic disability. Finally, in a study of these children’s judgement of the adequacy of communicators it was found that they behaved like younger children, and could not accurately judge who was at fault in a poor communication situation (Meline/ Brackin 1987). In summary, some dysphasic children have difficulty in recall of discourse in terms of the amount to be recalled but not in the structure of recall, while others have difficulty in both. They converse in many ways like their peers when they are young but then have greater difficulties in adequate communication when they are older. They behave like their younger normally developing peers when metacognizing about the adequacy of the communication situation. They are, again, both delayed and different in their pragmatic development just as they are both delayed and different in other aspects of language development. Whether they appear to be delayed or different depends on the age at which their behavior is sampled and the conditions under which they are sampled. There appears to be a relation between comprehension difficulties and differences as well as delays in pragmatic development.
4.
Information Processing Problems
The question that has arisen most frequently about dysphasic children and adults has been whether or not their language problem is due to some cognitive deficit or a specific language impairment. With dysphasic children the question has been asked in varying ways: 1) are they behind their age peers on Piagetian tasks?, 2) do they have a perceptual or conceptual problem? and 3) what is the nature of their memory problems? The answers that have been obtained to these questions do shed some light on possible relations between these children’s information processing difficulties and their language problems. The answer to the first question is, as usual, mixed. When comparing language disordered children with their MLU and age matched peers on haptic recognition, water level and classification tasks, it was found that they were better than their MLU peers on all tasks and worse than their age peers on one task, the haptic recognition task (Kamhi 1981). When comparing these same groups of chil-
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dren at a younger age on symbolic play, it was found that the language disordered children were more advanced than their MLU matched group in terms of the number of their play schemes but below age expectations. These data do not clarify the question but do cause serious doubt as to whether disabilities on Piagetian tasks cause disabilities in language development. The findings vis-a-vis haptic recognition might be related to oral motor problems in some dysphasic children but it is clear that not all dysphasic children have such problems. The answer to the second question is also, apparently, mixed. As indicated in the section on phonology studies, the claim has been made that the auditory perpectual problems of these children are the bases for these children’s developmental language problems. A group of language disordered and normally developing children’s profiles on the Leiter scale were compared (Johnston 1982 a). Both groups of children did better on the perceptual tasks than on the conceptual. However, among the 16 language disordered children, 2 showed marked disparity between performance on the two types of tasks with performance on the perceptual always better. Four did better on the conceptual tasks than the perceptual. Still another study found no differences between the non-linguistic concept formation abilities of mental age matched language disordered and normally developing children’s abilities (Kamhi/Catts/Koenig/ Lewis 1984). There are a number of studies that have found differences between language disordered children and their normally developing peers in terms of the rate at which they can encode and then retrieve information (Menyuk 1988). These problems in the rate at which information can be encoded may not be limited to auditory or linguistic information. For example, it has been found that language impaired children can decide whether two geometric arrays are similarly ordered when they are parallel and when they are rotated. There were no differences between them and their normally developing mental age peers in the accuracy of their performance or in the training needed to learn the task. The only significant difference was the mean response time of the groups. The accuracy of the identification of visual, auditory and crossmodal stimuli by language impaired and normally developing children was examined (Tallal/Stark/Kallman/Mellits
V. Pathologies and Disorders of Language Development
1981). The stimuli were presented in varying amounts and rates, and the children were aged 5 to 9 years. It was found that the language impaired children made significantly more errors than normally developing children when more than 2 item sequences were presented, or the stimuli were presented rapidly regardless of modality. The older language impaired children made twice as many errors with auditory than with visual stimuli. For the younger language impaired children the modality made no difference in error rate. These data suggest that language impaired children have a limit in the rate at which they can process all types of stimuli. The fast fading nature of auditory stimuli make such stimuli a particular problem for these children. The rate at which information can be encoded and then retrieved may be a function of the strategies used to process information. These children appear to have less effective strategies than normally developing children, or do not use the strategies they have under stressful conditions such as information overload. Both capacity and strategy differences may bring about the behaviors observed. It is possible that children who show a delay in development are those who have the strategy but cannot use it under all the required circumstances. Children who showed differences in the pattern of their development may be those who have not developed the strategies necessary to encode the information as it increases in complexity. Throughout the discussion of these children’s development of the varying aspects of language two things have been emphasized. The first is that a number of these children are apparently at the very delayed end of normal development while others appear to have particular problems in learning new aspects of language that present a marked change in the complexity of stuctures, and still others exhibit differences in their pattern of language behavior and development. It is possible that the first group of children has difficulty in encoding auditory information accurately or rapidly anough to categorize it. The second group of children may have difficulty in developing the categories into which various classes and relations belong once those categories and relations reach a certain level of complexity. The third group of children may have difficulties in developing categories and relations at any level. The three groups of children have information processing problems but the nature of their problems varies.
61. Children with Specific Language Impairment (Developmental Dysphasia): Linguistic Aspects
There is certainly the possibility that there are other causes that might account for these children’s language difficulties than those outlined above. There may also be differences among them in their patterns of language development and use not pointed to in this discussion. Future research may determine these causes and differences. However, unless this research includes long term developmental studies of all components of language in the same dysphasic children it is doubtful that more complete answers about causes and differences will be obtained.
5.
References
Bialystok, E. (1986). Factors in growth of linguistic awareness. Child Development, 57, 498—510. Brinton, B. & Fujiki, M. (1982). A comparison of request-response sequences in the discourse of normal and language disordered children. Journal of Speech and Hearing Disorders, 47, 57—62. Chapman, K., Leonard, L., Rowan, L., & Weiss, A. (1983). Inappropriate word extensions in the speech of young language disordered children. Journal of Speech and Hearing Disorders, 48, 55—61. Craig, H. & Evans, J. (1989). Turn exchange characteristics of SLI children’s simultaneous and nonsimultaneous speech. Journal of Speech and Hearing Disorders, 54, 334—347. Crais, E. & Chapman, R. (1987). Story recall and inferencing skills in language learning-disabled and non-disabled children. Journal of Speech and Hearing Disorders, 52, 50—55. Elliott, L., Hannen, M., & Scholl, M. (1989). Finegrained auditory discrimination in normal children and children with language learning problems. Journal of Speech and Hearing Research, 32, 112—119. Fey, M. & Leonard, L. (1984 ). Partner age as a variable in the conversational performance of specifically language-impaired normal-language children. Journal of Speech and Hearing Research, 27, 413—423. Fletcher, P. (1991). Evidence from syntax for language impairment. In J. Miller (Ed.), Research on child language disorders: A decade of progress. 169—188. Austin, TX.: Pro-Ed. Fried-Oken, M. (1987). Qualitative examination of children’s naming skills through test adaptations. Language, Speech, and Hearing Serv ices in Schools, 18, 206—216. German, D. (1982). Word-finding substitutions in children with learning disabilities. Language, Speech and Hearing Serv ices in Schools, 13, 223—230. German, D. (1987). Spontaneous language profiles
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of children with word-finding problems. Language, Speech, and Hearing Serv ices in Schools, 18, 217—230. Grimm, H. (1987). Developmental dysphasia: New theoretical perspectives and empirical results. The German Journal of Psychology, 11, 8—22. Ingram, D. (1989). Phonological disability in children, 2nd ed. London: Cole & Whurr. Johnston, J. (1982 a). Interpreting the Leiter I. Q.: Performance profiles of young normal and language disordered children. Journal of Speech and Hearing Research, 25, 291—296. Johnston, J. (1982 b) Narratives: A new look at communication problems in older language-disordered children. Language, Speech and Hearing Services in Schools, 13, 144—156. Johnston, J. & Kamhi, A. (1984 ). Syntactic and semantic aspects of utterances of language impaired children: The same can be less. Merrill Palmer Quarterly, 30, 65—86. Johnston, J. & Weismer, S. (1983). Mental rotation abilities in language disordered children. Journal of Speech and Hearing Research, 26, 397—403. Kamhi, A. (1981). Non language symbolic and conceptual abilities of language impaired and normally developing children. Journal of Speech and Hearing Research, 24, 446—453. Kamhi, A., Catts, H., Koenig, L., & Lewis, B. (1984 ). Hypothesis testing and nonlinguistic symbolic abilities in language-impaired children. Journal of Speech and Hearing Disorders, 49, 169—176. Karmiloff-Smith, A. (1986). From meta-process to conscious access: Evidence from children’s metalinguistic and repair data. Cognition, 35, 95—147. Lahey, E., Liebergott, J., Chesnick, M., Menyuk, P., & Adams, J. (in press 1990). Variability in the use of grammatical morphemes: Implications for understanding language impairment. Applied Psycholinguistics. Leonard, L. (1990). Some rival accounts of morphological deficits in specific language impairment: A crosslinguistic study. Paper presented at the Fifteenth Annual Boston University Child Language Conference, Boston, October. Leonard, L., Camarata, S., Rowan, L., & Chapman, K. (1982 a). The communicative functions of lexical usage by language impaired children. Applied Psycholinguistics, 3, 109—125. Leonard, L. Schwartz, R., Chapman, K., Rowan, L., Prelock, P., Terrell, B., Weiss, A., & C. Messick (1982 b). Early lexical acquisition in children with specific language impairment. Journal of Speech and Hearing Research, 25, 554—564. Levy, C. & Menyuk, P. (1975). Cognitive and linguistic skills of children with normal and deviant language development. Paper presented at the American Speech, Language and Hearing Associ-
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ation Annual Convention, November, Washington, D. C. Liebergott, J., Menyuk, P., Chesnick, M., & Korngold B. (1988). Language processing abilities and reading achievement in children. Mini-seminar presented at the Annual Convention of the American Speech, Language and Hearing Association, November, Boston. Liles, B. (1985). Cohesion in the narratives of normal and language disordered children. Journal of Speech and Hearing Research, 28, 123—133. Liles, B. (1987). Episode organization and cohesive conjunctives in narratives of children with and without language disorder. Journal of Speech and Hearing Research, 30, 185—196. Magnusson, E. (1983). The phonology of language disordered children: Production, perception and awareness. Travaux de L’institut de Linguistique de Lund, C W K Glerup. Meline, T. & Brackin, S. (1987). Language impaired children’s awareness of inadequate messages. Journal of Speech and Hearing Disorders, 52, 263—270. Menyuk, P. (1978). Linguistic problems in children with developmental dysphasia. In M. Wyke (Ed.), Dev elopmental dysphasia. 135—158. London: Academic Press. Menyuk, P. (1983). The role of context in misarticulations. In G. Yeni-Komshian, J. Kavanaugh, & C. Ferguson (Eds.), Child phonology, Vol. 1. 211—228. N. Y.: Academic Press. Menyuk, P. (1988). Language dev elopment: Knowledge and use. Glenview, II.: Scott Foresman/Little Brown College Division. Menyuk, P. (1991). Metalinguistic abilities and language disorder. In J. Miller (Ed.), Research on child language disorders: A decade of progress. 387—398. Austin, TX.: Pro-Ed. Menyuk, P., Chesnick, M., Liebergott, J., Korngold, B., D’Agostino, R., & Belanger, A. (1991). Predicting reading problems in at risk children. Journal of Speech and Hearing Research, 34, 893—901. Menyuk, P. & Looney, P. (1972). Relationships among components of the grammar in language disorder. Journal of Speech and Hearing Research, 15, 395—406. Merrit, D. & Liles, B. (1987). Story grammar ability in children with and without language disorder: Story generation, story retelling and story comprehension. Journal of Speech and Hearing Research, 30, 539—552. Nippold, M. & Fey, S., (1983). Metaphoric understanding in preadolescents having a history of language acquisition difficulties. Language, Speech, and Hearing Services in Schools, 14, 171—180. Paden, E., Novak, M., & Beiter, A. (1987). Predictors of phonologic inadequacy in young children prone to otitis media. Journal of Speech and Hearing Disorders, 52, 232—242.
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Panagos, J. & Prelock, P. (1982). Phonological constraints in the sentence production of language disordered children. Journal of Speech and Hearing Research, 25, 171—177. Pearl, R., Donahue, M., & Bryan, T. (1985). The development of tact: Children’s strategies for delivering bad news. Journal of Applied Dev elopmental Psychology, 6, 141—149. Powers, M. (1957). Functional disorders of articulation-symptomatology and etiology. In L. Travis (Ed.) Handbook of speech pathology. 707—768. N. Y.: Appleton-Century-Crofts. Prinz, P. & Ferrier, L. (1983). Can you give me that one?: The comprehension, production and judgement of directives in language impaired children. Journal of Speech and Hearing Disorders, 48, 44—54. Rowan, L., Leonard, L., Chapman, K., & Weiss, A. (1983). Performative and presuppositional skills in language disordered and normal children. Journal of Speech and Hearing Research, 26, 97—106. Schwartz, R., Leonard, L., Folger, M., & Wilcox, M. (1980). Early phonological behavior in normal speaking and language disordered children: Evidence for a synergistic view. Journal of Speech and Hearing Disorders, 45, 357—377. Schwartz, R., Leonard, L., Frome Loeb, D., & Swanson, L. (1987). Attempted sounds are sometimes not: An expanded view of phonological selection and avoidance. Journal of Child Language, 14, 411—418. Shriberg, L. & Paul, R. (1982). Associations between phonology and syntax in speech delayed children. Journal of Speech and Hearing Research, 25, 536—547. Shriberg, L. & Smith, A. (1983). Phonological correlates of middle ear involvement in speech delayed children: A methodological note. Journal of Speech and Hearing Research, 26, 293—297. Skarakis, S. & Greenfield, P. (1982). The role of old and new information in the verbal expression of language disordered children. Journal of Speech and Hearing Research, 25, 462—472. Snyder, L. (1987). Defining language disordered children: Disordered or just “low verbal” normal. University of Denver, Denver, Colorado. Unpublished manuscript. Stark, R. & Tallal, P. (1981). Selection of children with specific language deficit. Journal of Speech and Hearing Disorders, 46, 114—122. Stoel-Gammon, C. (1991). Issues in phonological development and disorder. In J. Miller (Ed.) Research on child language disorders: A decade of progress. 255—266. Austin, TX.: Pro-Ed. Tallal, P. & Stark, R. (1983). Speech perception of language delayed children. In G. Yeni-Komshian, J. Kavanaugh, & C. Ferguson (Ed.), Child phonology, Vol. 2. 155—172. N. Y.: Academic Press.
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Tallal, P., Stark, R., Kallman, C., & Mellits, D. (1981). A reexamination of some nonverbal perceptual abilities of language impaired and normal children as a function of age and sensory modality. Journal of Speech and Hearing Research, 24, 351—357. Teele, D., Klein, J., Chase, C., Menyuk, P., & Rosner, B. (1990). Otitis media in infancy and development of intellectual ability, school achievement, and speech and language at age seven years.
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Journal of Infectious Diseases, 162, 685—694. Witelson, S. (1977). Early hemisphere specialization and interhemisphere plasticity: An empirical and theoretical review. In S. Segalowitz & F. Gruber (Eds.), Language dev elopment and neurological theory. 303—319. N. Y.: Academic Press. Wolf, M. (1984 ). Naming, reading, and the dyslexias: A longitudinal overview. Annals of Dyslexia, 34, 87—115.
Paula Menyuk, Boston, Massachusetts (USA)
62. Children with Specific Language Impairment (Developmental Dysphasia): Perceptual and Cognitive Aspects 1. 2. 3. 4. 5.
1.
Introduction Perceptual Aspects Conceptual and Representational Aspects The Search for Causal Factors: Conclusions and Future Directions References
Introduction
Language is arguably the most complex of all human behaviors. Normal language development involves the integration of sensory and physical mechanisms; perceptual, cognitive, and linguistic processes; and social, motivational, and psychological factors. Deficiencies in one or more of these components will place a child at risk for delayed language development. Language disorders that can be directly attributed to one or more of these predisposing peripheral or central impairments are often considered to be resulting symptoms of a more pervasive disorder. Such disorders include mental retardation, hearing impairment, severe emotional disturbance, and frank neurological dysfunction (Tallal 1988). Mentally retarded children, for example, are not considered to be primarily language impaired. Children with specific language impairments have significant difficulty acquiring language that cannot be attributed to any of the obvious causes mentioned above. Variously referred to as developmentally aphasic, dysphasic, language impaired, or language disordered, these children acquire language more slowly than their peers and often continue to have difficulty with spoken and written language throughout the developmental
period into adulthood. The existence of a pure or uncontaminated group of language disordered children has intrigued theorists and researchers. Why should children with normal intelligence, intact speech and hearing mechanisms, and a supportive language learning environment have difficulty acquiring language? Four accounts of the bases of specific language impairment or developmental dysphasia have received considerable attention during the past 25 years. The four accounts have attempted to link language delays with deficiencies in (a) auditory processing, (b) a conceptual/representational processes, (c) neurological functions, and (d) the child’s communicative environment. Other chapters in this volume will discuss the neurological aspects of language disorders (cf. art. 59) and patterns of interaction and communication involving children with specific language impairments (cf. art. 68). The present chapter will focus on perceptual and conceptual/representational aspects of language disorders.
2.
Perceptual Aspects
Normal language learning and conceptual processing requires the effective functioning of a variety of perceptual mechanisms. These mechanisms include not only those that are bound to specific senses, such as vision and audition, but also attentional and memory processes that span the senses. A large body of literature has examined auditory processing abilities in children with developmental dysphasia or specific language impairment (SLI). During the 1960’s and 1970’s, there were a number of claims that auditory pro-
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cessing deficits accounted for SLI children’s difficulty learning language (e. g., Eisenson 1966; Lowe/Campbell 1965). As Leonard (1987) has pointed out, the meaning of the term ‘auditory processing’ varied from investigator to investigator. Studies included any one or more of the following abilities: auditory discrimination, sequencing, memory, and synthesis. SLI children often performed more poorly on these tasks than same-age normallanguage children. Lowe/Campbell (1965) are generally credited as being the first investigators to examine auditory temporal processes in SLI children. They compared eight SLI children who ranged in age from 7 to 14 years to a group of age-matched normal language (NL) children on two tasks: a ‘succession’ task which required the child to decide whether the stimuli presented were one or two sounds and a temporal order task which required the child to judge which of two sounds were presented first. The stimuli were two different 15 ms pure tones, 4 00 and 2200 Hz. In the succession task, the SLI children judge that the two sounds were one at an average inter-stimulusinterval (ISI) of 35.8 ms compared to 18.5 ms for the NO group. This difference was not statistically significant. On the temporal order task, however, the SLI children needed an average of 357 ms (range 55—700 ms) compared to 36.1 ms (range 15—80 ms) for the NL children to achieve the same average level of performance (75% correct). This dicrepancy was highly significant, leading Lowe and Campbell to conclude that impaired temporal ordering ability might be a major contributing factor to the language impairment in SLI children. Rees (1973) pointed out three serious problems with Lowe and Campbell’s study and other sequencing experiments conducted up to this point. First, she argued that the conclusions from these studies assumed that pure tones were processed in the same manner as speech sounds. Second, she noted that the use of verbal stimuli to assess perceptual abilities presented a possible confound of low-level auditory processing abilities and higher-level linguistic abilities. The impairment in temporal processing abilities might be one manifestation of the higher-level language impairment. Rees’ final point was that no attempt had been made in these studies to establish a positive correlation between the extent of the auditory sequencing disorder and the degree of language impairment.
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2.1. The Work of Tallal and Colleagues The work of Tallal and her colleagues over the past 20 years has provided considerable data that directly addressed Rees’ concerns. In the initial studies by Tallal/Piercy (1973 a, b), the first two concerns were addressed. Instead of using pure tones, nonverbal acoustic stimuli were synthetically generated to match the acoustic properties of steady-state speech sounds. These sounds did not match the acoustic spectrum of any specific phoneme. The experimental paradigm, referred to as the repetition method, used minimal verbal instructions and incorporated a training procedure to insure that children understood the task. In the first study (Tallal/Piercy 1973 a), 12 SLI children (ages 6;9 to 9;3) were compared to same age NL peers. The children were presented two different 75 ms tones (100 and 305 Hz, ISI = 4 28 ms) and taught to respond to each tone separately by pushing one of two panels for one tone and the other panel for the other tone. The children were then taught to respond to each of the four two-tone sequences presented (1—2, 2—1, 1—1, 2—2) by pushing the panels in the appropriate order. After being trained in this manner, the children were tested on the same two-tone sequences using 12 different ISIs ranging from 8 ms to 4,062 ms. The NL children performed significantly better than chance level for all 12 ISIs. SLI children did not perform better than chance at ISIs less than 305 ms. Similar findings were obtained when the task was changed to a same/different format in which children had to push one panel when the two tones were the same and the other panel when the two tones were different. In a second experiment with the same subjects, Tallal/Piercy (1973 b) varied the duration of the tones and the modality of stimulus presentation. Seven different ISIs were used ranging from 8 ms to 4 28 ms. Four durations were examined: 75, 125, 175, and 250 ms. The SLI children performed below the level of NL children for all ISIs below 150 ms for the 75 and 125 durations. When the tone duration was 175 ms, the SLI children performed more poorly than the NL children only when ISIs were less than 15 ms. No group differences were found for the 250 ms tone. The same procedures were used next to compare each group’s ability to process visual stimuli consisting of light flashes of two dif-
62. Children with Specific Language Impairment (Developmental Dysphasia): Perceptual and Cognitive Aspects
ferent shades of green. Children were tested at several ISIs ranging from 30 ms to 4 28 ms. No significant group differences were found for any of the ISIs. Based on the findings from these two studies, Tallal and Piercy suggested that SLI children have difficulty processing auditory information that is presented at a rapid rate. The time available for processing appeared to be critical for adequate performance. In a subsequent series of studies with a different sample of children, Tallal/Stark/ Kallman/Mellits (1980, 1981) sought to validate and extend the findings from the initial studies. Subjects in these studies were 36 SLI children from 5 to 9 years of age and 38 age matched peers. The auditory stimuli were the same 75 ms tones used in Tallal/Piercy (1973 a). The visual stimuli were changed from the earlier study. Slides of two nonsense letters were presented as light flashes 75 ms in duration. ISIs of 10, 70, and 500 ms were used in all tasks. Both groups performed similarly on the discrimination task. On the sequencing task, the NL children performed better than the SLI children at all ISIs in both modalities. The poor performance of the SLI children for the visual modality was inconsistent with previous findings (Tallal/Piercy 1973 b). Tallal et al. (1981) suggested that age differences in the subject populations may explain the differences. Only the younger SLI children (5and 6-years olds) performed poorly on the visual tasks. The other children, who were approximately the same age as the children in the previous study, performed poorly only in the auditory modality. Tallal/Stark (1981) examined the ability of the same children to discriminate other types of verbal stimuli (e. g., [da]—[ta], [dab]— [dæb], [sa]—[sta]). For each contrast, the children heard a random list of syllables and had to press a response panel when one of the syllables was heard. No response was required for the other syllable. The SLI children performed more poorly than the NL children on three stimulus pairs: [ba]—[da], [da]—[ta], and [da]—[ʃa]. As Leonard notes (1987, 16), what is interesting about this finding is that brevity of acoustic cues did not have the same effect for all stimuli. The SLI children were able to distinguish between [ε] and [æ] even though they were only 4 0 ms in duration. These findings led Tallal/Stark/Kallmann/ Mellits to conclude that the rate specific deficit in processing auditory information in-
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cludes the processing of linguistically meaningful stimuli when these stimuli contain brief acoustic cues that are followed in rapid succession by other acoustic cues. Bernstein/Stark (1985) reported the results of a four-year follow-up study of the children who participated in the 1980/81 studies. Fourteen NL and 29 SLI children were retested. The children now ranged in age from 8 to 12 years. The tasks (discrimination, sequencing, and serial memory) and stimuli ([ba] and [da]) were the same ones used in the earlier studies by Tallal/Piercy (1973 a, b). Both groups of children performed at the same levels on the various tasks. Only one SLI child failed to meet the p < .001 criterion for sequencing with the longest ISI. The findings from this study clearly indicated that SLI children’s perceptual abilities improved with age. However, the extent of development was unclear because the tasks were too easy for both groups of children. The ceiling effects on the tasks made it impossible to consider the relationship between perceptual abilities and language impairment in older SLI children. The SLI children might perform below age level on more advanced perceptual tasks. Importantly, the data support the conclusion that early perceptual deficits do not preclude subsequent language development. 2.2. Relating Perceptual Skills to Measures of Speech and Language The studies discussed thus far have addressed two of the three concerns raised by Rees (1973, 1981). Her third concern was that researchers had not established a positive relationship between the extent of the auditory processing deficit and the nature or extent of the language impairment. Tallal/Stark/Curtiss (1976) addressed this concern by comparing the speech production abilities of the SLI and NL children in the Tallal and Piercy studies. Speech proficiency was evaluated by having these children name pictures of objects and nonsense syllables. The SLI children were found to make many more errors on stop consonants and consonant clusters than on vowel and nasal sounds. Because the SLI children had the most difficulty on sounds containing rapid acoustic changes, Tallal/ Stark/Curtiss concluded that auditory processing limitations were responsible for the speech errors. In a more recent study, Curtiss/Tallal (1991) examined the relationship of higherlevel language abilities to performance on the
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auditory processing tasks. Subjects were 67 SLI children, 57 age-matched peers, and 32 language-matched peers who were followed for five years beginning at age four. Measures of language included the receptive and elicited production tests from the CYCLE (Curtiss/ Yamada 1988). The receptive tests consisted largely of sentence-picture matching items. The production task used a sentence-completion format. To examine the relationship between nonlinguistic sequencing impairments (poor performance on the temporal processing task) and language acquisition, items from the CYCLE were organized into two separate clusters: a + sequentially-cued (+ sc) cluster in which word order uniquely signalled grammatic and thematic role and a — sequentially-cued (— sc) cluster in which ‘key formatives’ cued roles and relations. The + cluster consisted of reversible SVO sentences, such as The girl is pushing the boy vs. The boy is pushing the girl. In these sentences, word order provides the only cue to the relationship between the noun phrases and the verb. The — sc cluster included attributive, stative, and negative sentences, such as The ball is big vs. The ball is little and Here the boy is pulling the wagon but here the boy is not pulling the wagon. The key finding was that the SLI children performed significantly worse on the + sc cluster than on the — sc cluster. The agematched normals consistently performed better than the SLI children and showed no difference in performance levels for the two clusters. Performance on the nonverbal sequencing tasks and the + sc cluster was moderately correlated at years 2 (.4 9) and 3 (.39) of the study. Based on these findings, Curtiss and Tallal suggest that a nonlinguistic sequencing impairment may impact directly on the processing of linguistic structures when the sequential order of linguistic elements uniquely signals important grammatical or semantic information. 2.3. Other Research on SLI Children’s Perceptual Abilities Tallal and her colleagues have not been the only investigators who have examined the perceptual abilities of SLI children. In this section, selected studies from other researchers are reviewed. Tomblin/Quinn (1983) questioned whether SLI children’s poor performance on the rapid processing tasks might be the result of factors other than an inherent deficit in temporal
V. Pathologies and Disorders of Language Development
resolution ability. In their study, 10 NL children (ages 5 ; 8 to 6 ; 9) were administered the repetition task five times over a 5—7 day period. As expected, the children performed better on stimuli with longer ISIs. However, the children also performed better across the session. The finding that temporal processing abilities improve with experience led Tomblin and Quinn to suggest that poor performance on the task may be caused by limited experience, attention, or the inability to use appropriate processing strategies. Some recent studies by Elliott and her colleagues have been more successful than Bernstein/Stark (1985) were in identifying perceptual problems in older SLI children. In a longitudinal study, Elliott/Hammer (1988) presented a set of finegrained auditory discrimination tasks to 21 SLI and 21 NL children over a three-year period. At the beginning of the study, the children averaged 7 years of age. The SLI children were all enrolled in a classroom for language-learning problems. Over the three years of the study, the SLI children consistently performed more poorly than the NL children on the Peabody Picture Vocabulary Test (Dunn/Dunn 1981), The Token Test for Children (DiSimoni 1978), and the Templin-Darley Screening Test of Speech Articulation (Templin/Darley 1969). No other information was given about the specific nature of the children’s language problem. All the children were reported to have normal intelligence. The stimuli were two continua of CV stimuli [ba—pa] and [ba—da—ga]. For [ba—pa], a five formant, eight item continuum that varied in VOT from 0—35 ms was created. For [ba—da—ga], 13 items were created, each having five formants. With these stimuli, it was possible to determine the smallest acoustic differences (‘just noticeably differences’ JNDs) that could be discriminated. On every trial, two syllables were presented sequentially with a 500 ms ISI. Subjects had to make samedifferent judgments by pushing one of two response buttons. The JNDs for the SLI children were nearly always larger than those for the NL listeners in each year of testing. The differences tended to be statistically significant for the VOT continuum, but not for the place-of-articulation continuum. Based on these findings, Elliott and Hammer concluded that SLI children continue to have auditory discrimination problems past the pre-school years and also continue to exhibit speech and language problems.
62. Children with Specific Language Impairment (Developmental Dysphasia): Perceptual and Cognitive Aspects
Leonard (1989) has recently used crosslinguistic comparisons of Italian, Hebrew, and English speaking SLI children to support the relationship between rapid auditory processing deficiencies and specific linguistic deficiencies. He begins by noting that the most striking aspect of SLI children’s language is their extraordinary difficulties with grammatical morphemes (e. g., Johnston/Kamhi 1984 ; Johnston/Schery 1976). These morphemes include inflected forms, such as the past tense, possessive, and plural, and function words such as articles and auxiliaries. Although SLI children consistently have trouble with grammatical morphemes, some morphemes cause less problems than others. The irregular past tense and present progressive -ing emerge only slightly below MLU expectations. Using Pinker’s (1984 ) learnability theory, Leonard suggests that SLI children have difficulty acquiring grammatical morphemes that have low ‘phonetic substance’ and do not have difficulty with grammatical morphemes that do not have low phonetic substance. Low phonetic substance is defined as “monosyllabic consonant segments and unstressed syllables, characterized by shorter duration than adjacent morphemes, and, often, lower fundamental frequency and amplitude” (Leonard 1989, 186). Leonard goes on to argue that the perceptual characteristics of low phonetic substance morphemes closely resemble the characteristics of acoustic stimuli that SLI children have difficulty processing. Leonard also martials evidence from the speech production literature. He argues that final consonant deletion and weak syllable deletion that are common in the speech of SLI children also support the low phonetic substance explanation. Leonard next attempts to show how Pinker’s theory can explain the difficulty SLI children have with other language forms and structures. He suggests that the difficulty SLI children have with morphemes may impede their ability to parse sentences and thus develop new phrase structure rules. Leonard acknowledges, however, that this explanation is weak. He also notes that the definition of low-phonetic substance is simplistic because once a certain absolute duration is reached, relative duration may not be important (193). 2.4. Evaluation The large body of literature documenting the below age-level performance of SLI children
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on rapid processing tasks is compelling. The studies by Tallal and her colleagues as well as other investigators have shown that compared to age-matched peers, SLI children have difficulty perceiving and producing information rapidly in time. The poor performance of the SLI children on visual tasks suggests that the processing deficit is not specific to auditory input (see Elliott/Hammer/Scholl 1990, for the alternative view). The “neural timing deficit,” as Tallal (1988, 164 ) recently refers to it, accurately predicts (a) performance on the nonverbal and verbal serial memory tasks, (b) the pattern and type of speech production and perception errors, (c) the degree of receptive language impairment, and (d) classification of specific language impairment. Despite the overwhelming evidence suggesting that a timing deficit provides a sufficient explanation for a specific language impairment, many remain unconvinced that such a deficit can account for the extent and nature of the specific language impairment (Johnston 1988; Leonard 1987; Rees 1981; Tomblin 1984 ). The problem lies not in the data or methodology of the studies, but with the bottom-up information processing or specific abilities models that provide the theoretical backdrop for most of the studies discussed in this section. An assumption that underlies these studies is that there are fundamental perceptual and memory processes that are necessary for, but independent of, language learning (Tomblin 1984 ). That is, language usage and learning depends on a set of component auditory perceptual abilities that are arranged in some serial, bottom-up, fashion. The perception and processing of sensory information is viewed as passive and unaffected by situational factors, knowledge states, and previous experiences of the individual. The counterclaim is that perceptual and memory processes do not function independently of knowledge states and other conceptual processes. Several contemporary theories of language processing emphasize the complex interactions that occur among structural mechanisms, cognitive processes, knowledge states, and environmental forces (see Bohannon/Warren-Leubecker 1988). Piagetian (constructionist) notions that emphasize the active role the child plays in organizing and making sense of the world have become an important component of current accounts of language learning (e. g., Ingram 1989). There is a rich experimental literature demonstrating the ef-
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fects higher-level language abilities have on speech perception (Pisoni 1978; Rees 1981). In the same vein, short-term memory abilities are known to increase when the individual is able to relate the information to previous knowledge or experiences (e. g., Chi 1976; Huttenlocher/Burke 1976). There are at least two other significant problems with perceptual explanations of specific language impairment. The first stems from the fact that normally developing children younger than 4 ;6 cannot perform the Tallal tasks (Tallal 1976). Four and half-yearold NL children, however, have quite sophisticated language abilities. By this age, they produce many complex sentence structures and use a wide range of grammatical morphemes (Ingram 1989). Given that young NL children have sophisticated language abilities and cannot perform the processing tasks, one must seriously question what successful performance on Tallal’s tasks means for language learning. The perceptual processing abilities of young NL children are apparently sufficient to comprehend and produce quite sophisticated language forms. The second problem directly follows. In Leonard’s words: “... we cannot lose sight of the fact that, although normal children improve across time in their performance on auditory processing tasks, there has been no serious attempt to explain language development on the basis of developing auditory skills” (Leonard 1987, 22). Leonard’s point here is that in order to draw causal connections between perceptual deficiencies and language impairment, there needs to be some theorizing about how particular developments in auditory skills impact on the acquisition of specific linguistic forms and structures. Such theorizing would make specific predictions, for example, about what kinds of perceptual developments precede the acquisition of first words, word combinations, canonical word ordering (SVO), complex sentences, and so forth. Interestingly, as discussed earlier in this section, since Leonard wrote these words, he has made a serious attempt to relate SLI children’s problems with grammatical morphemes to the acoustic characteristics (i. e., low phonetic substance) of these forms. Some of the problems with the ‘low phonetic substance’ hypothesis have already been discussed. The most serious problem, as pointed out by Leonard himself, is that the hypothesis does not account well for SLI children’s prob-
lems with other language forms and structures. The hypothesis also does not account well for the continued difficulty older SLI children have with these forms. Despite having heard these forms millions of times and being able to recognize them in reading, older SLI individuals still use them inconsistently in their speech (Tomblin 1990). In light of these concerns, the most optimistic interpretation of the data is that perceptual limitations account for protracted acquisition of selected language forms such as grammatical morphemes. However, the perceptual deficit does not account well for continued problems with these language forms (e. g., through childhood and adolescence) nor does it account well for other language problems. The most pessimistic interpretation of the data is to argue that all the findings merely establish a strong correlation between rapid perceptual processing and a specific language impairment. The relationship between these perceptual skills and language is not unidirectional (i. e., from perception to language), but interactive and reciprocal, with a language deficit rather than a perceptual deficit being the primary or initial problem. That is, the higher-level language deficit causes poor performance on certain perceptual processing tasks. Although the perceptual deficit is secondary to the language deficit, it can adversely affect subsequent language development.
3.
Conceptual and Representational Aspects
By definition, SLI children exhibit a significant discrepancy between language abilities and nonverbal performance scales of intelligence, such as the Leiter International Performance Scales (Arthur 1952), the WISC, and the Columbia Mental Maturity Scale (Burgemeister/Blum/Lorge 1972). SLI children’s age-level performance on nonverbal intelligence tests initially discouraged investigations of cognitive abilities in areas not tapped by the intelligence tests. The assumption was that SLI children would show agelevel performance in other cognitive measures, as long as the verbal component was minimized. Dissatisfaction, however, with perceptually-based explanations of specific language impairment led researchers to look for cognitive-based explanations for the impairment. Two articles first published in 1973,
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one by Rees and the other by Morehead and Ingram, were the first to suggest that SLI children might suffer from a more general cognitive impairment. Rees (1973) did not speculate what the nature of the cognitive deficit might be, but Morehead/Ingram (1973) suggested that SLI children might be deficient in symbolic representational abilities. The theoretical justification for Morehead and Ingram’s suggestion is found in Piagetian views of language development. According to Piaget (e. g., 1952), language emerges as part of a more general symbolic function — a function defined as the ability to represent symbolically an external event or object in its absence. This view led researchers to look for parallels in the development of language and other symbolic behaviors in NL and SLI children. Early studies with NL children (e. g., Bates/Benigni/Bretherton et al. 1979; Nicolich 1977) found relationships between developments in language and nonlinguistic symbolic behaviors such as means-ends relations and symbolic play. Subsequent studies involving SLI children (e. g., Johnston/Ellis Weismer 1983; Kamhi 1981; Roth/Clark 1987; Savich 198 4 ; Terrell/Schwartz/Prelock/Messick 1984 ) have found that SLI children do not perform as well as NL peers on measures of symbolic play and mental imagery. The SLI children generally performed better than language-age matched peers on these measures. In the sections to follow, representative studies in these two areas will be reviewed. 3.1. Symbolic Play Lovell/Hoyle/Siddall (1968) are generally credited as being the first researchers to investigate symbolic play abilities in SLI children. They compared 10 SLI and 10 children (ages 3;4 to 4 ;8) using Lunzer’s (1959) adaptation and interaction play scales. No differences in symbolic play were found in the 3year-old children. The play activities of the 4 -year-old SLI children were more concrete, less cooperative, and less organized than the age-matched NL children. A significant positive relationship was also found between SLI children’s MLU and the amount of time they spent in symbolic play. Terrell/Schwarz/Prelock/Messick 4 (198 ) gave the Symbolic Play Test (Lowe/Costello 1976) to 15 SLI (ages 2;8 to 4 ;1) and 15 NL children (ages 1;4 to 1;10) matched for language age. Both groups were at the singleword level. The SLI children exhibited signif-
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icantly higher symbolic play skills than the younger NL children. Roth/Clark (1987) compared the symbolic play and social participation of six SLI (ages 5;1 to 7;10) to eight NL children (ages 2;8 to 3;0) matched for MLU (M = 3.3 morphemes). Play behaviors were assessed using three measures: (a) the Scale of Social Participation in Play, (b) the Symbolic Play Test, and (c) a modification of Lunzer’s Play Scale. Compared to the NL children, the SLI children showed significant deficits in symbolic, adaptive, and integrative play behaviors. The SLI children also exhibited significantly more nonplay and less solitary and parallel play than their NL peers. 3.2. Mental Imagery The earliest reports of a connection between mental imagery and language came from Piaget’s colleagues Inhelder (1966) and de Ajuriaguerra (1966; cited in de Ajuriaguerra/ Jaeggi/Guigard et al. 1976). De Ajuriaguerra et al. found that 17 SLI children (ages 4 ;3 to 10;10) had difficulty with imagery tasks that involved analyzing the movement of a projected shadow. Kamhi (1981) compared the performance of 10 SLI children (mean age 4 ;11, mean MLU 4 .82) on six Piagetian tasks to groups matched for MA and MLU. On five of the tasks, the SLI children performed comparably to the MA-matched group. On the sixth task, Haptic Recognition, the SLI children performed significantly worse than the MAmatched group, but significantly better than the MLU-matched children. Not coincidentally, this task, which involves blindly feeling geometric forms and then pointing to the corresponding shape from a visual array, was the only one that clearly required mental imagery. Johnston/Ellis Weismer (1983) used a mental rotation task to investigate mental imagery abilities. Subjects were shown drawings of pairs of linear arrays of geometric forms and asked to push one of two buttons corresponding to same or different. Arrays were presented parallel or with the right hand array rotated either 4 5, 90, or 135 degrees. Subjects were six first-grade and six third-grade SLI children and age-matched controls. A significant linear relationship between degree of rotation and reaction time was taken as evidence that children in all groups used imagistic processes. SLI children did not differ from NL children in accuracy of judgment and the
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number of training trials required, but they did respond more slowly. These findings led Johnston and Ellis Weismer to conclude that SLI children have difficulty generating, maintaining, and/or interpreting mental images rather than difficulty transforming images. Savich (1984 ) compared the performance of 18 SLI and age-matched NL peers (ages 7;6 to 9;6) on five imagery tasks. The SLI children were less successful than their age peers on all five tasks. For example, they had difficulty predicting the position of a ‘snail’ on a circular path, the position of fold lines on paper squares, and the configuration that best represented the assembly of a set of shapes. 3.2.1. Evaluation As Johnston (1988) noted in her summary of the symbolic play and mental imagery research, the search for an underlying symbolic representational deficit seems to have paid off. SLI children consistently perform more poorly than NL peers on symbolic play and mental imagery measures. Correlations between performance on these tasks and measures of language (particularly receptive measures) generally have been moderate and significant (Savich 1984 ). In addition, Johnston pointed out that relative performance levels of verbal and nonverbal symbolic abilities are exactly in line with what would be expected for two cognitive systems that share a common symbolic feature, but differ in other aspects. In other words, verbal abilities have been reported to be better than nonverbal symbolic abilities (Roth/Clark 1987), equivalent to them (Terrell/Schwartz 1983), and worse than them (Kamhi 1981; Savich 1984 ). The data are thus consistent with the view that the linguistic impairment in SLI children reflects a more general deficit in symbolic representation. Although the data support the symbolic representation hypothesis, the explanatory adequacy of this view has been questioned in recent years. Johnston (1988) raises the possibility that SLI children’s symbolic deficits may reflect a more pervasive cognitive limitation that affects both symbolic and nonsymbolic aspects of mental activity. In other words, there are other cognitive limitations that may provide better explanations for the data. Johnston did not speculate what the nature of these limitations might be, but several possibilities will be considered in subsequent sections of this chapter.
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A related problem with the symbolic deficit view is that it implies that there is one symbolic representational process. Many cognitive processes are involved in symbolic tasks, however, including, encoding, storing, integrating, interpreting, and retrieving information. To say that a child has a deficient symbolic function fails to specify where the actual breakdown may occur. Concluding that a general symbolic deficit underlies a specific language impairment thus has little explanatory adequacy. A final problem with the symbolic deficit view is that the degree of symbolic deficit found in SLI children does not account well for the extent and type of linguistic deficiencies demonstrated by SLI children (Kamhi 1981). This is because on most symbolic tasks, SLI children perform more poorly than agematched peers, but better than younger normal children with comparable language abilities. Clear structural parallels between nonlinguistic symbolic skills and SLI children’s language problems also have rarely been shown. For example, what is the relationship between language and the ability to anticipate mentally the future position of a snail? Although some would argue that claims were never made about structural parallels, the lack of such parallels further detracts from the explanatory adequacy of the view. 3.3. Hierarchical Planning One alternative explanation for SLI children’s difficulty with verbal and certain nonverbal tasks has been offered by Cromer (1981, 1983). He suggests that a central planning mechanism is necessary in order to convert thoughts and intentions that are not temporally ordered into events that occur in real time. He refers to this as a hierarchical planning ability and suggests that this ability may be crucial both for the organization of incoming stimuli in perception and for the production of behavior (1983, 145). Cromer (1983) cites research on SLI children’s sense of rhythm to support his view. Kracke (1975), for example, found that 12 years-old receptively disordered SLI children performed significantly worse than NL or deaf peers identifying rhythmic sequences presented verbally and tactilely. In contrast to the NL and deaf children who processed the patterns in a Gestalt manner as wholes, the SLI children processed the rhythms element by element. Cromer suggests that an impairment of a more basic hierarchical planning
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ability may underlie SLI children’s rhythmic problems. In Cromer’s (1983) study, he studied hierarchical planning using a construction task adapted from Greenfield/Schneider (1977). In the first task, children were shown a line drawing of a symmetrical tree structure and asked to copy the figure. In the second task, children were shown a completed 3-dimensional mobile built from plastic straws and asked to duplicate it. Subjects were five severely receptively impaired children (ages 9;6 to 16;4 ) diagnosed as having acquired aphasia with convulsive disorder, seven children diagnosed as having a primary expressive language impairment (ages 8;5 to 12;10), 12 profoundly deaf children, and 12 NL children matched for age to the disordered children. All the subjects performed within normal limits on a performance IQ test. On both tasks, the performance of the two groups of SLI children were treated as one group because task performance was comparable. The measure of hierarchical planning was the number of shifts in construction from one subunit to another. Shifts that involved crossing from one side of the figure to the other were given a double weighting. A chain or sequential strategy resulted in a zero score. The most interrupted strategy — shifting every time — resulted in a score of 25. On both tasks, the SLI children obtained significantly lower scores than both their deaf and NL peers. Although Cromer is careful to make no claims about a direct parallel between language and action, he does argue that it is difficult to imagine how a severe deficit in hierarchical planning could fail to affect language. Unfortunately, Cromer fails to specify the nature of the language deficits one would expect to result from such a disability. One might speculate that individuals with a hierarchical planning deficit would exhibit some difficulty producing well-organized spoken and written narratives, event descriptions, and related discourse forms. 3.3.1. Evaluation Cromer’s notion of a hierarchical planning deficit is provocative, despite its lack of specificity. The finding that many SLI children had difficulty on the two tasks clearly indicates that something is amiss. Why is it that these children could not create a hierarchically organized representation of the drawing and the mobile? The difficulty may not be in
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planning, which Cromer defines as the conversion of sequential events into real time events. Rather, the difficulty may lie in the actual construction of a hierarchically organized representation. SLI children’s representational systems may be organized more sequentially than those of NL children. Although Cromer makes it a point to disclaim direct parallels between language and action, the specific impact a hierarchical planning deficit would have on language needs to be addressed. Future studies are needed that attempt to find parallels between such a deficit and particular linguistic deficiencies. 3.4. Hypothesis Testing Current views of language acquisition suggest that children learn language through a process of formulating and testing hypotheses about specific conceptual domains and linguistic rules (e. g., Slobin 1979). Deficient hypothesis-testing abilities, therefore, might play some role in explaining developmental language disorders. Researchers have examined this possibility by observing SLI children’s performance on various concept formation and discrimination-learning paradigms. In a typical experiment, children view a series of cards each displaying two geometric shapes. One of the forms contains the correct hypothesis (e. g., large, small, circle, or square). On each trial, children point to the form containing their current solution to the problem. Periodic feedback allows the children to evaluate and modify their hypotheses. ‘Blank-trial probes’, in which no feedback is provided, enable the experimenter to determine the child’s hypothesis, the assumption being that the child will maintain a hypothesis if no feedback is provided. Children could use simple object hypotheses (problem solutions are always of this type), alternation hypotheses (left/right, right/left), position hypotheses (left or right), or no hypothesis. Four studies of this general type have been conducted with mixed results (Ellis Weismer 1991; Hoskins 1979; Kamhi/Nelson/Lee/ Gholson 1985; Nelson/Kamhi/Apel 1987). Despite the methodological differences across these studies (e. g., age of subjects and feedback given), the data tend to show that SLI children have difficulty solving discrimination learning problems. This difficulty does not, however, appear to be caused by an inability to generate or test hypotheses (Kamhi et al. 1985). SLI children generated the same proportion of simple object hypotheses as NL
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age peers. The two most recent studies by Nelson et al. (1987) and Ellis Weismer (1991) raised some questions about the short-term memory demands of the tasks. Clearly, solving discrimination learning tasks taps many different cognitive processes, not simply hypothesis-testing abilities. The conflicting findings of the two most recent studies indicate that the difficulty SLI children have solving discrimination learning problems has yet to be adequately explained. Another issue concerns the relationship between the explicit, conscious hypothesis-testing abilities employed in discrimination learning problems and the implicit, largely unconscious comparison processes involved in language learning. We might be comparing apples and oranges here; that is, the hypothesistesting processes involved in discrimination learning problems and language learning might be qualitatively different (Johnston 1988). This indeed seems to be the case. Preschool and young school-age normally developing children, whose language is quite sophisticated, are unable to solve the orthogonal problems presented (Kamhi/Nelson/Lee/ Gholson 1985). One would be hard-pressed to make claims for a direct relationship between hypothesis-testing abilities and language learning. SLI children’s deficient problem solving abilities at best reflect some basic cognitive processing inefficiency that affects language learning as well as nonverbal task performance. 3.5. Analogical Reasoning Within the past few years, there has been increasing interest in the development of analogical reasoning in young children. Such reasoning is assumed to represent a central mechanism in learning, transfer, and discovery (e. g., Brown 1989; Sternberg 1985). Analogical reasoning involves applying or transferring existing knowledge (a familiar concept) from a known situation to a novel one, even if the two situations are superficially dissimilar. Analogical reasoning also has a rich history in theories of language acquisition. For example, according to Bloomfield (1933/1961), a grammar is a description of the analogies that hold for a language. More recently, MacWhinney (1978) includes analogy as one of the three central constructs underlying language acquisition. Traditionally, analogical reasoning has been examined by having subjects respond to proportional analogies of the form A is to B
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as C is to D (e. g., Nippold/Erskine/Freed 1988; Sternberg/Nigro 1980). An example of a proportional analogy is Meaning is to semantics as sound is to? Performance on proportional analogies, however, provides little information about the factors that influence analogical reasoning and the processes involved in reasoning analogically. These processes involve (a) learning the solution to the original problem, (b) noticing the correspondence between the known solution and the target problem, (c) retrieving the solution in terms of its general structure, and (d) applying the solution to the target problem (see Gholson/Eymard/Morgan/Kamhi 1987). Only two studies have examined analogical reasoning abilities in SLI children. Nippold et al. (1988) found that 6- to 8-year-old SLI children performed more poorly than NL age peers on three analogical reasoning tasks. However, when differences in nonverbal intelligence were statistically controlled, the group differences on each task disappeared. The tasks used were two proportional analogies and a story problem adapted from Holyoak/Junn/Billmann (1984 ). In the story problem task, transfer performance in both groups of children was not good because only one analog was presented. Only one SLI children and two NL children solved the transfer problem without hints. Kamhi/Gentry/Mauer/Gholson (1990) used the trial-by-trial acquisition procedures developed by Gholson et al. (1987) to compare analogical reasoning processes of 16 SLI children (ages 6;4 to 8;9) and 16 NL children matched for nonverbal MA. All children received two analogs of the Farmer’s Dilemma (Wickelgren 1974 ), that required a specific sequence of seven moves to solve. In this problem, the subject must find a way to get a fox, goose, and corn across a river without anything being eaten. However, only one thing can be taken across the river at a time and the fox will eat the goose and the goose will eat the corn if either pair is left alone. The key move in solving the problem is taking the goose back across the river after it has already been taken across. Two analogs of this problem were created: one involving a lion, pony, and oats and the other a wolf, rabbit, and carrots. The constraints and goal structure of all the problems were similar. Half of the children viewed physical demonstrations of the problems while they heard the verbal presentations of the problems. The remaining children heard only verbal pres-
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entations of each problem. Data consisted of (a) number of trials to reach the acquisition criterion, (b) the number of moves in the transfer task, and (c) trial-by-trial analyses of the proposition represented in the recall protocols. For the acquisition data, the SLI children in the verbal-only condition needed significantly more trials (M = 15) to reach criterion than the other SLI children and the NL children in both conditions (M = 5 trials). No significant differences were found on the transfer task. The analyses of the recall data found that SLI children in the verbal-only condition were less likely to include the key back-up proposition in their recall protocols. 3.5.1. Evaluation The age-level performance of the SLI children in the ‘modeling’ condition can be taken as evidence that analogical reasoning abilities are intact in SLI children. The difficulty they have learning language thus is not likely due to deficient analogical reasoning skills. However, the way in which the problems were presented had a significant impact on SLI children’s problem solving abilities. SLI children’s problem solving abilities decreased considerably when the story analogs were verbally presented without accompanying physical demonstrations. Although the findings are consistent with the notion that SLI children suffer from a verbal processing deficit, the perceptual studies reviewed earlier suggest that it was not the nature of the input (verbal or nonverbal) that determined performance, but the extent to which the input placed demands on SLI children’s processing system (Stark/Tallal 1988). Input that occurs rapidly in time, such as speech, places particularly high demands on processing resources, resulting in a decrease in the quality of memory codes and the likelihood that these memory codes will decay rapidly over time. Of significance here is that SLI children will be at a disadvantage whenever a problem-solving task is presented verbally without accompanying visual support or when a time factor is involved.
4.
The Search for Causal Factors: Conclusions and Future Directions
Reading or writing a review of SLI children’s perceptual and cognitive strengths and weaknesses is bound to leave one feeling somewhat
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unsatisfied. This is because no single factor (perceptual or cognitive) or obvious combination of factors can explain the extent and nature of a specific language impairment. Failure to find the primary causal factor(s) has led some researchers and clinicians to question the value of continued research and clinical efforts that address causal issues. Leonard (1987) has made the most compelling arguments to-date about the inadequacy of causal research. In the final section of his critical review of causal research, he noted that “accounts of specific language impairment fall short not only because they fail to identify the proper cause of this condition, but also because they assume that the condition is one for which a tangible cause must exist” (Leonard 1987, 30). At one level, all of the studies reviewed in this chapter have attempted to identify a contributing factor or possible cause of specific language impairment. Although some factors seem to have more explanatory adequacy than others, no factor by itself can explain the extent and nature of SLI children’s language impairment. This leads most writers to speculate that SLI is caused by a variety of factors. Leonard, however, views the cause of SLI children’s language limitations as “simply the product of the same types of variations in genetic and environmental factors that lead some children to be clumsy, others to be amusical, and still others to have little insight into their own feelings” (Leonard 1987, 31). Leonard’s view draws on Gardner’s (1983) theory of multiple intelligences in which seven different kinds of intelligence are proposed. If the language delay is viewed as normal variation rather than a disorder or deficit, one effectively eliminates the need to search for a cause. In other words, there can be no cause for the disorder if there is no disorder. This view leads Leonard to the logical conclusion that research efforts in search of causal factors will not be high-yield enterprises. There is a certain appeal to Leonard’s view: By embracing it, we prevent future researchers from expending large amounts of time and resources searching for underlying causes that do not exist. There is, however, a more optimistic view of the causally-oriented research reviewed in this chapter. Johnston (1991), for example, points out that the claim that most SLI children are normal is not the same as the claim that the condition has no cause. Just because there is normal variation
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in an ability does not mean the cause of the variation is of no interest. Some researchers are presumably interested in the neurological correlates of exceptional musical ability. The same holds true for language variation. As Johnston notes, even if we agree with Leonard that the primary cause of specific language impairment is variations in genetic and environmental factors, we can still wonder about the causes of these variations. Why do these children have difficulty learning to talk? Aram (1991) proposes four reasons why it is important to know about why SLI children have difficulty learning language. First, there is the level of science to which we want our profession to aspire. Without explanatory power, she argues, ours is a dead-end science, with the risk that we might become a deadend profession. Second, there is our clinical responsibility to parents of SLI children. Most parents want to know why their child has a language impairment. Aram asks, “How long can a profession continue to say We don’t know to the questions that prompt their consultation?” (Aram 1991, 86). Aram’s third reason is that the identification of causal factors has major implications for intervention programs. Finally, there is the issue of prevention. Aram argues that only through understanding ‘why’ can we have an impact on preventing specific language impairments. If we act as if causation does not matter, is unknowable, or is simply the inevitable result of a normal distribution, we will be unable to prevent future generations of children from having specific language impairments. Aram concludes her short paper by noting that we do know something about the causes of specific language impairment. Johnston (1991) makes a similar point in arguing that we should abandon ‘etiological’ jargon because it has connotations of pathology and primary cause, and attempt to identify the mental processes and mechanisms that influence success in the language acquisition task. If the research on SLI children’s perceptual and cognitive abilities is viewed in this light, we can reason that language learning requires (a) the ability to perceive and produce rapidly presented information, (b) the ability to generate, maintain, and interpret symbols, (c) the ability to organize information hierarchically, and (d) a variety of reasoning processes. Although these claims are by no means earth-shattering, they do represent progress. The weakness of the work, according to John-
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ston, is not in the direction it takes, but in its infancy. Johnston finds no fault with the general research strategy that (a) compares the performance of SLI and NL children on various linguistic and nonlinguistic tasks, and (b) makes inferences about the mental abilities that are causally linked to language learning based on the patterns of performance found. What all researchers seem to agree about, however, is that the basic research strategy needs to be refined. Aram (1991) sees particular promise in using sophisticated neuroimaging techniques, such as MRI and PET to determine whether there are subtle differences in brain morphology and/or activity in SLI children. Another promising avenue of research addresses the genetic bases of specific language impairment (e. g., Lewis/Ekelman/ Aram 1989; Tomblin 1989). Johnston (1991) suggests three refinements in future research efforts. First, we need to explore more complex patterns of association. Most research, she notes, has primarily tried to link language learning to another single mental ability, such as the symbolic function or perception of rapidly presented events. But simple causation models, as Hubbell (1981) has pointed out, do not adequately capture the complex biological and environmental interactions that underlie developments in language throughout the developmental period. Future studies need to examine the reciprocal causation effects that occur among maturing perceptual, cognitive, linguistic, and social abilities throughout the developmental period. Second, we need to figure out how to formalize and operationalize promising mental constructs. For example, there should be other ways to measure hierarchical planning ability than using 3-dimensional mobiles. Or, as Johnston notes, there is currently no experimental task to evaluate the construct of ‘extracting regularities’, which has been suggested as a possible weakness in SLI children. Johnston’s third refinement is that we need to break down familiar constructs, such as language, into their component parts. Instead of looking for associations between generic notions such as language learning ability and other mental functions, we need to look for associations between discrete language subskills and nonverbal competencies. Leonard’s cross-linguistic research discussed earlier is an example of the kind of research needed. Another promising avenue of research is to compare SLI children’s processing abilities
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to those of children with different developmental disabilities. For example, Ludlow/ Cudahy/Bassich/Brown (1983) evaluated perceptual processing abilities in SLI children and children with attentional deficits who had no history of language learning problems. She found that the children with attentional deficits also had difficulty perceiving rapidly presented information, suggesting that poor auditory perception might cause language delays only when it is accompanied by other specific cognitive deficiencies. Another example is research my colleagues and I have conducted with young school-age SLI children and reading disabled children without a history of language impairment (Kamhi/Catts 1986; Kamhi/Catts/Mauer et al. 1988). In these studies, we compared the performance of these two groups of children on measures of visual imagery, short-term memory, rapid naming, word repetition, and phonological awareness. Our objective in this research was to determine whether SLI and reading disabled children demonstrated similar processing limitations. The findings from these studies revealed more similarities between the children than we expected, suggesting that the spoken language problems in school-age SLI children cannot be explained by limitations in the processes underlying mental imagery, short-term memory, and phonological awareness tasks. If these process limitations were causally linked to the spoken language deficit, the reading disabled children should have had similar spoken language deficiencies. It should be clear from the points made in this chapter that the causal underpinnings of spoken and written language disorders are far too complex to be sorted out by cross-sectional studies in which a particular perceptual or conceptual ability is evaluated. But these studies have served an important function in illuminating the kinds of perceptual and cognitive abilities associated with delayed rates of language learning. As our future research endeavors begin to reflect the refinements discussed in the previous paragraphs, we will develop a better understanding of how perceptual and cognitive abilities affect language learning throughout the developmental period.
5.
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Elliott, L. & Hammer, M. (1988). Longitudinal changes in auditory discrimination in normal children and children with language learning problems. Journal of Speech and Hearing Disorders, 53, 467—474. Elliott, L., Hammer, M., & Scholl, M. E. (1990). Response to Tallal. Journal of Speech and Hearing Research, 33, 617—618. Ellis Weismer, S. (1991). Hypothesis testing abilities of language impaired children. Journal of Speech and Hearing Research, 34, 1329—1338. Gardner, H. (1983). Frames of mind. New York: Basic Books. Gholson, B., Eymard, L., Morgan, D., & Kamhi, A. (1987). Problem solving, recall, and isomorphic transfer among third-grade and sixth-grade children. Journal of Experimental Child Psychology. 43, 227—243. Greenfield, P. & Schneider, L. (1977). Building a tree structure: The development of hierarchical complexity and interrupted strategies in children’s construction activity. De v elopmental Psychology, 13, 299—313. Holyoak, K., Junn, E., & Billmann, D. (1984 ). Development of analogical problem-solving skill. Child Development, 55, 2042—2055. Hoskins, B. (1979). A study of hypothesis testing behav ior in language disordered children. Paper presented at the Annual Convention of the American Speech-Language-Hearing Association, Atlanta. Hubbell, R. (1981). Children’s language disorders. Englewood Cliffs, NJ: Prentice-Hall. Huttenlocher, J. & Burke, D. (1976). Why does memory span increase with age? Cognitiv e Psychology, 8, 1—32. Ingram, D. (1989). First language acquisition: Method, description and explanation. Cambridge: Cambridge University Press. Inhelder, B. (1966). Cognitive development and its contribution to the diagnosis of some phenomena of mental deficiency. Merrill-Palmer Quarterly, 12, 299—319. Johnston, J. (1988). Specific language disorders in the child. In N. Lass, L. McReynolds, J. Northern, & D. Yoder (Eds.), Handbook of speech-language pathology and audiology. 685—715. Philadelphia: B. C. Decker, Inc. Johnston, J. (1991). The continuing relevance of cause: A reply to Leonard’s ‘specific language, impairment as a clinical category’. Language, Speech, and Hearing Services in Schools, 22, 75—80. Johnston, J. & Ellis Weismer, S. (1983). Mental rotation abilities in language disordered children. Journal Speech and Hearing Research, 26, 397—403. Johnston, J. & Kamhi, A. (1984 ). Syntactic and semantic aspects of the utterances of language-
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impaired children: The same can be less. MerrillPalmer Quarterly, 30, 65—85. Johnston, J. & Schery, T. (1976). The use of grammatical morphemes by children with communication disorders. In D. Morehead & A. Morehead (Eds.), Normal and deficient child language. 239—259. Baltimore: University Park Press. Kamhi, A. (1981). Nonlinguistic symbolic and conceptual abilities of language impaired and normally developing children. Journal of Speech and Hearing Research, 24, 446—453. Kamhi, A. & Catts, H. (1986). Toward an understanding of developmental language and reading disorders. Journal of Speech and Hearing Disorders, 51, 337—347. Kamhi, A., Catts, H., Mauer, D., Apel, K., & Gentry, B. (1988). Phonological and spatial processing abilities in language- and reading-impaired children. Journal of Speech and Hearing Disorders, 53, 316—327. Kamhi, A., Gentry, B., Mauer, D., & Gholson, B. (1990). Analogical learning and transfer in language-impaired children. Journal of Speech and Hearing Disorders, 55, 140—148. Kamhi, A., Nelson, L., Lee, R., & Gholson, B. (1985). The ability of language disordered children to use and modify hypotheses in discrimination learning. Applied Psycholinguistics, 6, 435—451. Kracke, I. (1975). Perception of rhythmic sequences by receptive aphasic and deaf children. British Journal of Disordered Communication, 10, 43—51. Leonard, L. (1987). Is specific language impairment a useful construct? In S. Rosenberg (Ed.), Advances in applied psycholinguistics, Volume I: Disorders of first-language dev elopment. 1—39. NY: Cambridge University Press. Leonard, L. (1989). Language learnability and specific language impairment in children. Applied Psycholinguistics, 10, 179—202. Lewis, B., Ekelman, B., & Aram, D. (1989). A familial study of severe phonological disorders. Journal of Speech and Hearing Research, 32, 713—724. Lovell, K., Hoyle, H., & Siddall, M. (1968). A study of some aspects of the play and language of young children with delayed speech. Journal of Child Psychology, Psychiatry, and Allied Disciplines, 9, 41—50. Lowe, A. & Campbell, R. (1965). Temporal discrimination in aphasoid and normal children. Journal of Experimental Child Psychology, 18, 201—212. Lowe, M. & Costello, A. (1976). Manual for Symbolic Play Test. London: National Foundation of Educational Research. Ludlow, C., Cudahy, E., Bassich, C., & Brown, G. (1983). The auditory processing skills of hyperactive, language impaired and reading disabled boys.
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In J. Katz & E. Lasky (Eds.), Central auditory processing disorders: Problems of speech, language, and learning. 163—185. Baltimore: University Park Press. Lunzer, E. (1959). Intellectual development in play of young children. Educational Re v iew, 11, 205—224. MacWhinney, B. (1978). The acquisition of morphophonology. Monographs of the Society for Research in Child Development, 43, (No. 1). Morehead, D. & Ingram, D. (1973). The development of base syntax in normal and linguistically deviant children. Journal of Speech and Hearing Research, 16, 330—352. Nelson, L., Kamhi, A., & Apel, K. (1987). Cognitive strengths and weaknesses in language impaired children: One more look. Journal of Speech and Hearing Disorders, 52, 36—43. Nicolich, L. (1977). Beyond sensorimotor intelligence: Assessment of symbolic maturity through analysis of pretend play. Merrill-Palmer Quarterly, 23, 89—99. Nippold, M., Erskine, B., & Freed, D. (1988). Proportional and analogical reasoning in normal and language-impaired children. Journal of Speech and Hearing Disorders, 53, 440—449. Piaget, J. (1952). The origins of intelligence of children, trans. M. Cook. NY: International Universities Press. Pinker, S. (1984 ). Language learnability and language dev elopment. Cambridge, MA: Harvard University Press. Pisoni, D. (1978). Speech perception. In W. Kates (Ed.), Handbook of learning and cognitiv e processes (Volume 6). 171—203. Hillsdale, NJ: Erlbaum. Rees, N. (1973). Auditory processing factors in language disorders: The view from Procrustes’ bed. Journal of Speech and Hearing Disorders, 38, 304—315. Rees, N. (1981). Saying more than we know: Is auditory processing disorder a meaningful concept? In R. Keith (Ed.), Central auditory and language disorders in children. 94—120. San Diego, CA: College Hill Press. Roth, F. & Clark, D. (1987). Symbolic play and social participation abilities of language-impaired and normally-developing children. Journal of Speech and Hearing Disorders, 52, 17—29. Savich, P. (1984 ). Anticipatory imagery in normal and language disabled children. Journal of Speech and Hearing Research, 27, 494—501. Slobin, D. (1979). Psycholinguistics (2nd Ed.). Glenview, IL, Scott-Foresman. Stark, B. & Tallal, P. (1988). Language, speech, and reading disorders in children: Neurophysiological studies. Austin, TX: Pro-Ed. Sternberg, R. (1985). Beyond IQ: A triarchic theory
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of human intelligence. New York: Cambridge University Press. Sternberg, R. & Nigro, G. (1980). Developmental patterns in the solution of verbal analogies. Child Development, 51, 27—38. Tallal, P. (1976). Rapid auditory processing in normal and disordered language development. Journal of Speech and Hearing Research, 19, 561—579. Tallal, P. (1988). Developmental language disorders. In J. Kavanagh & T. Truss, Jr. (Eds.), Learning disabilities: Proceedings of the national conference. 181—272. Parkton, MD: York Press. Tallal, P. & Piercy, M. (1973 a). Defects of nonverbal auditory perception in children with developmental aphasia. Nature, 241, 468—469. Tallal, P. & Piercy, M. (1973 b). Developmental aphasia: Impaired rate of non-verbal processing as a function of sensory modality. Neuropsychologia, 11, 389—98. Tallal, P. & Stark, R. (1981). Speech acoustic-cue discrimination abilities of normally developing and language-impaired children. Journal of the Acoustical Society of America, 69, 568—574. Tallal, P., Stark, R., & Curtiss, B. (1976). Relation between speech perception and speech production impairment in children with developmental dysphasia. Brain and Language, 3, 305—317. Tallal, P., Stark, R., Kallman, C., & Mellits, D. (1980). Perceptual constancy for phonemic categories: A developmental study with normal and language impaired children. Applied Psycholinguistics, 1, 49—64. Tallal, P., Stark, R., Kallman, C., & Mellits, D. (1981). A reexamination of some nonverbal perceptual abilities of language-impaired and normal children as a function of age and sensory modality. Journal of Speech and Hearing Research, 24, 351—357. Templin, M. & Darley, F. (1969). The TemplinDarley Tests of Articulation (2nd edition). Iowa City, IA: Bureau of Educational Research and Services. Terrell, B. & Schwartz, R. (1983). Object transformation: The linguistic aspect of symbolic play? Proceedings of the Symposium on Research in Child Language Disorders, 4, 127—136. Terrell, B., Schwartz, R., Prelock, P., & Messick, C. (1984 ). Symbolic play in normal and language disordered children. Journal of Speech and Hearing Research, 27, 424—429. Tomblin, J. (1984 ). Specific abilities approach: An evaluation and alternative method. In W. Perkins (Ed.), Language handicaps in children. 27—41. New York: Thieme-Stratton. Tomblin, J. (1989). Familial concentration of developmental language impairment. Journal of Speech and Hearing Disorders, 54, 287—295.
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Alan G. Kamhi, Memphis, Tennessee (USA)
63. Children with Specific Language Impairment (Developmental Dysphasia): Treatment 1. 2. 3. 4. 5.
1.
Introduction The Effectiveness of Treatment The Focus of Treatment Summary References
Introduction
Among the groups of children who exhibit language-learning difficulties is a group that shows normal hearing, normal motor and emotional functioning, and age-appropriate scores on nonverbal tests of intelligence. Currently, the most commonly used clinical term for this group (at least in the U.S.) is ‚specific language impairment’, though the term ‚developmental dysphasia’ is also employed. Although the former will be adopted here, the two terms are basically interchangeable. In the decade since Leonard (1981) reviewed the available literature on language intervention with specifically-language-impaired (SLI) children, this area of work has received increasing attention. The purpose of this section is to provide a summary of these recent developments. To facilitate interpretation of the recent work, the section shall be organized as in the earlier review, with subsections added to highlight prominent changes. Although the studies reviewed here should prove to be representative of the work in this area, the relative emphasis placed on certain issues reflects the present author’s own biases. For a review with a somewhat different look, the reader might consult Olswang/ Bain (in press). As in Leonard (1981), the focus shall be on language production (which still constitutes the bulk of the literature on treatment), excluding phonology. The studies included here provided documentation of oral language deficits in the children under investi-
gation. Thus, investigations of learning disabled children, for example, were included only if it could be determined that problems in spoken language constituted part of their handicap. Finally, the review was restricted to studies in which gains could be attributed to treatment with some degree of confidence. Investigations of this type included: (1) the use of a no-treatment control group or a comparison group that received treatment unrelated to the linguistic features of interest; (2) the use of a single-subject design in which experimental control can be demonstrated, such as a multiple baseline or alternating treatments design; (3) the use of statistical estimation to evaluate observed gains relative to those expected from maturation; and (4 ) the use of a nonsense form whose acquisition could not be due to extra-experimental sources.
2.
The Effectiveness of Language Treatment
As the authors of the other sections of this chapter have made clear, children with specific language impairment constitute a heterogeneous population. Even though all of these children display normal hearing, unremarkable emotional development, and ageappropriate scores on nonverbal intelligence tests, they differ from one another in the severity of their language deficit, and in the specific areas of language in which this deficit is most apparent. Unfortunately, a very large percentage of these children continue to have linguistic difficulties throughout childhood and beyond, and are at risk for academic difficulties. Clearly, language intervention is important for these children. However, it must be determined that such treatment is in fact effective.
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If effectiveness is defined as a demonstrable gain in language performance, then clearly language intervention with SLI children is effective. A host of treatment approaches have produced gains of this type. These are discussed below. 2.1. Approaches to Treatment Until the mid 1970s, the dominant treatment approach for SLI children was one that made significant use of elicited imitation. That is, the clinician produces the exact sentence or phrase required of the child, and the child is asked to repeat it. Although imitation-based approaches have consistently resulted in clear language gains by the children, such approaches have not been adopted as frequently in recent years. Olswang/Bain/Dunn/Cooper (1983) made use of elicited imitation to teach new lexical items to SLI children. Other investigators have incorporated imitation into comprehensive intervention programs that include a variety of techniques. For example, Warren/Kaiser (1986) successfully taught SLI children the use of two- and three-word utterances (e. g. boy eat cake) in a program that included picture pointing (e. g. “Show me boy eat cake”), performing the requested action (e. g. “Susan, eat cake”), imitating the target utterance (e. g. “Say boy eat cake”), describing pictures (e. g. “Tell me about this picture”), and describing the actions of others (e. g. “What’s Jane doing?”). Though used less frequently, imitation-based approaches remain an effective alternative for clinicians. A second type of approach involves the use of modeling. The child observes someone (the model) produce examples of utterances containing the linguistic form serving as the focus of training. The child is not asked to imitate the modeled utterances. However, he or she is instructed that the model will be talking in a special way. At this point, specific modeling approaches differ. In some approaches, the child observes only; in others, the child is asked to take turns producing examples of the target pattern once the observation period is over. The majority of earlier studies that employed modeling showed clear gains in language production. More recent studies corroborate these findings. Examples of successful training through some variation of modeling have been reported by Bedrosian/Willis (1987), Johnston/Blatchley/Olness (1990), Skarakis-Doyle/Woodall (1988), and Weismer/Murray-Branch (1989), among others.
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Another type of treatment approach is called ‚incidental language teaching’. This approach resembles the above approaches in that the language targets used for training are preselected by the clinician. However, incidental language teaching is quite different in other respects. It is conducted in a more naturalistic setting, such as free play. The clinician arranges the setting to increase the likelihood that the child will initiate some form of communication. When the child indicates interest in the activity or object in question, the clinician shows attention and, as necessary, provides the child with increasingly specific cues for production of the target form. Natural contingencies are applied to the child’s production of the target. For example, immediately following the child’s successful production of the utterance Iwant block, the clinician gives the child the requested object. Although numerous studies employing incidental language teaching can be found in the clinical literature, only a few have focused on SLI children. However, the results of these investigations leave no doubt that this approach can be effective with these children as well. Examples of studies reporting successful treatment with some variation of incidental language teaching include the works of Olswang/Kriegsmann/Mastergeorge (1982) and Warren/McQuarter/Rogers-Warren (1984). Another approach that requires the child to be the initiator is expansion. This approach has its origins in the literature on normal language development, in which it was reported that mothers often responded to their young children’s telegraphic utterances (e. g. Abby daddy) with a more complete and grammatical rendition (e. g. “yes, Abby is going with daddy”). Relatively few studies have employed the expansion approach with SLI children, and reported language gains have been minimal (Leonard 1981). However, an adaptation of expansion was found to be successful in an investigation by Schwartz/Chapman/ Terrell et al. (1985). In this adaptation, the clinician, rather than the child initiated the communication. For example, in teaching one SLI child locative word combinations, the following interaction was representative: Clinician: Child: Clinician: Child: Clinician:
What’s this? block What’s the block in? truck The block is in the truck
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There are many treatment approaches that differ from one another in certain details but are similar in that they provide the child with concentrated exposure to particular linguistic forms. Leonard (1981) termed such approaches ‚focused stimulation’ approaches. Perhaps the most straightforward example can be seen in lexical training studies (e. g. Leonard/Schwartz/Chapman et al. 1982) in which the clinician introduces a new object during play and says its name several times per session. In other types of focused stimulation approaches, the clinician tells the child a story that contains numerous examples of the target form (e. g. questions containing why), and the clinician and child then act out the story, each taking the role of one of the characters. Brooks/Benjamin (1989) found such a procedure to be quite effective in teaching specific grammatical forms. Other successful uses of focused stimulation can be found in the studies of Culatta/Horn (1982), Leonard/ Schwartz/Allen et al. (1989), McGregor/ Leonard (1989), Olswang/Bain/Rosendahl et al. (1986), Schwartz/Leonard/Messick/ Chapman (1987), Schwartz (1988), and Wing (1990). Many SLI children are enrolled in preschools or classrooms that emphasize language learning. Although special attention is sometimes placed on specific language features that are especially problematic for the child, the goals in settings such as these are usually much broader. Consequently, the language gains made in these settings are often assessed by means of comprehensive tests of language and related abilities. Programs of this type have been shown to be beneficial for SLI children (e. g. Rice/Sell/Hadley 1990, Ripley 1986). 2.2. Direct Comparisons of Treatment Approaches Although several different approaches appear to be effective with SLI children, it is not clear that a single approach will emerge as the procedure of choice across all linguistic features. A meta-analysis conducted by Nye/ Foster/Seaman (1987) seems to support this assumption. These investigators found a large mean effect size for treatment collapsed across type of approach. However, although the mean effect size for certain specific approaches seemed quite high (e. g. modeling), no one approach differed significantly from any other.
V. Pathologies and Disorders of Language Development
Nevertheless, it is reasonable to assume that certain approaches might be more effective than others in teaching specific language material. A number of studies of this type can be found in the literature. For example, Connell (1987) compared the effectiveness of an imitation-based approach and a modeling approach in teaching the use of an invented bound morpheme. Children were taught to add the form -a to nouns to express the notion “part of” (e. g. cata meant “part of a cat”). Connell found that the imitiation-based approach was more successful with the SLI children. (Interestingly, the modeling approach was more effective with a group of normallydeveloping children). Other studies that have compared different approaches for teaching specific language targets include Hughes/Carpenter (1989), McGregor/Leonard (1989), Olswang/Coggins (1984), and Wing (1990). Still another type of comparison pits one variation of a specific approach against another. For example, Weismer/Murray-Branch (1989) compared two types of modeling in teaching forms such as auxiliary is and are, and the nominative case pronoun he. In one version of modeling, no responses from the child were required during the observation period. In the other, the child was given intermittent opportunities to produce examples of the target form. Both procedures proved effective, but the variation that permitted active responding by the child resulted in a slightly more stable pattern of acquisition. Other studies that have compared variations of the same general approach include Olswang/Bain/Dunn/Cooper (1983) and Olswang/Bain/Rosendahl et al. (1986). Just as one might expect certain approaches to be especially effective for teaching particular language targets, one might also assume that certain approaches would be especially well-suited for particular types of SLI children. In fact, earlier work suggested that imitation-based approaches might be the method of choice for SLI children of low ability. However, more recent work by Cole/ Dale (1986) casts doubt on this interpretation. These investigators compared an imitationbased approach and a variation of incidental language teaching. Both approaches resulted in significant language gains, but neither proved superior for SLI children with lower (or higher) ability. 2.3. Generalization and Maintenance Effective language treatment implies more than use of a linguistic feature in a narrowlydefined context. The child must also demon-
63. Children with Specific Language Impairment (Developmental Dysphasia): Treatment
strate the ability to use the feature in new ways. Most investigators do not regard treatment as successful unless, at a minimum, the child is able to use the feature in untrained sentences in a task that resembles the one(s) used during treatment. However, a number of researchers have made the requirement stiffer: The child must use the feature in new sentences during conversational speech. Most studies employing this type of generalization measure have reported positive results (e. g. Connell 1986 a, 1986 b; Olswang/Bain/Rosendahl et al. 1986; Warren/Kaiser 1986; Warren/ McQuarter/Rogers-Warren 1984 ). The study by Hughes/Carpenter (1989) appears to be an exception. Gains made during treatment do not mean very much if they are short-lived, so a number of investigators have made efforts to determine whether the higher levels of performance are maintained. The results are encouraging. For example, in three very different types of intervention studies, Dollaghan/Kaston (1986), McGregor/Leonard (1989), and Warren/McQuarter/Rogers-Warren (198 4 ) all found that SLI children’s performance one month after treatment remained higher than pre-treatment levels. The issue of maintenance is a tricky one for researchers in the area of language treatment because once a language ability becomes relatively well-established, it eludes experimental control. For example, in a study by Hargrove/Holmberg/Zeigler (1986), the children serving as subjects appeared to maintain or even show an increase in the gains made during treatment two months earlier. However, when treatment resumed, followed by an additional maintenance phase, it became clear that the children’s performance was no longer under experimental control. Periods of improvement and no improvement were not closely tied to whether treatment was being provided at the time. Given the seemingly permanent property of language behavior once it is established, researchers wishing to document that gains are attributable to treatment may only be able to do so early in the intervention process. 2.4. Catching Up or Not Losing Ground? The fact that SLI children make gains in treatment that exceed those made without treatment does not necessarily mean than within a few months or years they will be on par with their normally-developing peers. Longitudinal and follow-up studies have
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demonstrated not only that linguistic features emerge at a later age in the speech of SLI children, but the period from emerge to mastery of these features is also protracted. Consequently, without treatment, these children fall even further behind their peers across time. Thus, treatment may actually permit SLI children to catch up, or it may have the more modest effect of allowing the children to begin to progress at a normal rate, so as not to fall further behind over time. Of these two possibilities, the truth seems to fall somewhere in between. On the one hand, studies that make use of standardized tests to assess progress frequently report gains in standard scores and language quotients that are closer to the norm than before treatment began. Such large post-test gains do not appear attributable to a regression toward the mean because they are seen for tests on which the SLI children’s pre-test scores approached or were at the norm, as well as for tests on which the children performed very poorly. Examples of SLI children closing the gap can be seen in the work of Cole/Dale (1986), Rice/ Sell/Hadley (1990), and Warren/Kaiser (1986). The acceleration of SLI children’s learning through treatment notwithstanding, it appears that many children never reach a level of language ability that can be regarded as socially or educationally adequate. Two recent studies illustrate this point. Ripley (1986) reported on 120 children attending a school for SLI children; 90 of these children exhibited problems that extended beyond phonology. Many of these children had attended the school since the age of 7 or 8 years. The children showed very clear gains in verbal IQ scores, with typical increases in the order of 15 to 30 points. However, almost half of these children remained at this special school until the statutory school-leaving age, and the average verbal IQ for the 90 children at exit remained at least one standard deviation below the norm. The second relevant study was conducted by Huntley/Holt/Butterfill/Latham (1988). These researchers examined the abilities of children five years after they had completed a two-year period of language treatment. A small decrease in the children’s verbal IQs was noted following the termination of treatment, but these scores were nevertheless higher than those seen prior to intervention. However, approximately 4 0% of the children did not yet qualify for normal school place-
V. Pathologies and Disorders of Language Development
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ment, or were briefly in a regular school setting but did not succeed. A very real concern for clinicians is to ensure that the gains made by SLI children in treatment include improvement in aspects of language that are important for later functioning (see Damico 1988).
3.
The Focus of Treatment
The last decade has witnessed a significant increase in both the diversity of linguistic features serving as the focus of treatment and in the sophistication with which some of these features have been taught. The former is important because it provides clinicians with a more varied database for serving the heterogeneous population of SLI children. The latter is important because it increases the likelihood that treatment will be directed toward features that play a pivotal role in the child’s language problem rather than on features that are secondary consequences of this problem. Each of these will be discussed below. 3.1. Features of Language Through the 1970s, the great majority of treatment studies dealt with syntax and morphology. These types of features continue to receive attention in the literature, and for good reason: They are perhaps the most vulnerable in the speech of SLI children. Some of the recent studies with this focus include Brooks/Benjamin (1989), Culatta/ Horn (1982), Hughes/Carpenter (1989), Thal/ Goldenberg (1981), and Weismer/MurrayBranch (1989). Yet, the difficulties that SLI children often face in other areas of language warranted treatment research that went beyond the formal aspects of grammar. During the 1980s, work appeared that emphasized the semantic roles served by word combinations (Connell 1986 a; Olswang/Coggins 1984 ; Schwartz/ Chapman/Terrell et al. 1985). However, the most striking developments have occurred in the area of the lexicon (words and their meanings) and in pragmatics (the social use of language). Treatment studies focusing on SLI children’s learning of new lexical items can be divided into two types. The first type is concerned with the goal of increasing the size of the child’s lexicon. Emphasis is placed on establishing an association between the word and its referent, and progress is measured by examining the child’s ability to produce the word when an appropriate referent is pre-
sented. Intervention of this kind has resulted in significant lexical learning on the part of SLI children, as can be seen from the work of Leonard/Schwartz/Allen et al. (1989), Leonard/Schwartz/Chapman et al. (1982), Olswang/Bain/Dunn/Cooper (1983), Olswang/Bain/Rosendahl et al. (1986), Schwartz (1988), and Schwartz/Leonard/Messick/ Chapman (1987). The second type of lexical treatment is designed to facilitate SLI children’s ‚word-finding’ ability, that is, their ability to recall and produce presumablyknown words when needed. This type of treatment is concerned with increasing the children’s knowledge of individual words beyond simple word-referent associations (e. g. pointing out a word’s superordinate category), and with providing the child with strategies for retrieving words from memory. The recent investigations of McGregor/Leonard (1989) and Wing (1990) serve as good examples. The burgeoning literature on teaching pragmatic skills has been no less noteworthy. The communicative behaviors that have been taught to SLI children include: (1) topic initiations referring to past and future events (Bedrosian/Willis 1987); (2) requests for objects and actions (Olswang/Kriegsmann/Mastergeorge 1982); (3) requests for additional information (Dollaghan/Kaston 1986); and (4 ) the use of language for purposes of pretending (Skarakis-Doyle/Woodall 1988). 3.2. Understanding the Interrelationships Although it has always been recognized that language is an intricate system of interrelationships, clinicians working with SLI children have too often had to settle for one of two extremes — either working with single features of language in isolation, or working with a wide range of features without being clear as to how these features are connected. There are some recent signs that this picture is changing. For example, Connell (1986 b) recognized that errors such as them for they in preverb position (e. g. *them like Brenda) may be related to the omission of auxiliary verbs and verb inflections. Specifically, he hypothesized that SLI children showing such errors had not acquired the notion of subjecthood, which requires preverb pronouns of nominative case and verb markers that agree with the preverb noun phrase in number and person. Consequently, he taught pronoun case and certain verb features as a package, and found rather sweeping changes in the
63. Children with Specific Language Impairment (Developmental Dysphasia): Treatment
children’s use of other verb features presumably linked to subjecthood. Another type of study that sheds new light on the interactions within language is exemplified by the work of Johnston/Blatchley/ Olness (1990). These investigators taught two miniature languages to SLI and normallydeveloping children. The unfamiliar nouns in the language referred to fantasy animals that played either an agent or patient role. Unfamiliar verbs were used to refer to the actions that the agent performed on the patient. In addition, a novel suffix was attached to the noun serving as the patient. One of the languages possessed the word order agent + patient + suffix + action, the other action + agent + patient + suffix. The investigators found that the SLI children had a tendency to direct most of their limited resources toward one characteristic of the language (e. g. the perceptually salient suffix that appeared at the end of the sentence in one of the languages) at the expense of another characteristic (word order). Studies of this type can provide valuable information concerning how language material might be organized to promote efficient learning by SLI children.
4.
Summary
Significant progress has been made in language treatment with SLI children. Although it is unlikely that the heterogeneity of this population will ever permit the determination of a single treatment procedure and set of goals to prescribe, it is equally clear that a variety of teaching approaches are effective, for a range of language skills. Gains made during treatment are usually generalized and maintained, and often result in a narrower language ability gap between SLI children and their normally-developing peers. Unfortunately, the long-term language deficiencies seen in some of these children even with treatment make it obvious that much work remains to be done.
5.
References
Bedrosian, J. & Willis, T. (1987). Effects of treatment on the topic performance of a school-age child. Language, Speech, and Hearing Serv ices in Schools, 18, 158—167. Brooks, A. & Benjamin, B. (1989). The use of structured role play therapy in the remediation of grammatical deficits in language delayed children: Three case studies. Journal of Childhood Communication Disorders, 12, 171—186.
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Cole, K. & Dale, P. (1986). Direct language instruction and interactive language instruction with language delayed preschool children: A comparison study. Journal of Speech and Hearing Research, 29, 209—217. Connell, P. (1986 a). Acquisition of semantic role by language-disordered children: Differences between production and comprehension. Journal of Speech and Hearing Research, 29, 366—374. Connell, P. (1986 b). Teaching subjecthood to language-disordered children. Journal of Speech and Hearing Research, 29, 481—492. Connell, P. (1987). An effect of modeling and imitation teaching procedures on children with and without specific language impairment. Journal of Speech and Hearing Research, 30, 105—113. Culatta, B. & Horn, D. (1982). A program for achieving generalization rules to spontaneous discourse. Journal of Speech and Hearing Disorders, 47, 174—180. Damico, J. (1988). The lack of efficacy in language therapy: A case study. Language, Speech, and Hearing Services in Schools, 19, 51—66. Dollaghan, C. & Kaston, N. (1986). A comprehension monitoring program for language-impaired children. Journal of Speech and Hearing Disorders, 51, 264—271. Hargrove, P., Holmberg, C., & Zeigler, M. (1986). Changes in spontaneous speech associated with therapy hiatus: A retrospective study. Child Language Teaching and Therapy, 2, 266—280. Hughes, D. & Carpenter, R. (1989). Short-term syntax learning and generalization effects. Child Language Teaching and Therapy, 5, 202—220. Huntley, R., Holt, K., Butterfill, A., & Latham, C. (1988). A follow-up study of a language intervention programme. British Journal of Disorders of Communication, 23, 127—140. Johnston, J., Blatchley, M., & Olness, G. (1990). Miniature language system acquisition by children with different learning proficiencies. Journal of Speech and Hearing Research, 33, 335—342. Leonard, L. (1981). Facilitating linguistic skills in children with specific language impairment. Applied Psycholinguistics, 2, 89—118. Leonard, L., Schwartz, R., Allen, G., Swanson, L., & Loeb, D. (1989). Unusual phonological behavior and the avoidance of homonymy in children. Journal of Speech and Hearing Research, 32, 583—590. Leonard, L., Schwartz, R., Chapman, K., Rowan, L., Prelock, P., Terrell, B., Weiss, A., & Messick, C. (1982). Early lexical acquisition in children with specific language impairment. Journal of Speech and Hearing Research, 25, 554—564. McGregor, K. & Leonard, L. (1989). Facilitating word-finding skills of language-impaired children. Journal of Speech and Hearing Disorders, 54, 141—147.
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Nye, C., Foster, S., & Seaman, D. (1987). Effectiveness of language intervention with the language/learning disabled. Journal of Speech and Hearing Disorders, 52, 348—357. Olswang, L. & Bain, B. (in press). Language intervention research applied to clinical decision-making. In P. Tallal (Ed.), The neural basis of dev elopmental language disorders. Oxford: Oxford University Press. Olswang, L., Bain, B., Dunn, C., & Cooper, J. (1983). The effects of stimulus variation on lexical learning. Journal of Speech and Hearing Disorders, 48, 192—201. Olswang, L., Bain, B., Rosendahl, P., Oblak, S., & Smith, A. (1986). Language learning: Moving performance from a context-dependent to -independent state. Child Language Teaching and Therapy, 2, 180—210. Olswang, L. & Coggins, T. (1984 ). The effects of adult behavior on increasing language delayed children’s production of early relational meanings. British Journal of Disorders of Communication, 19, 15—34. Olswang, L., Kriegsmann, E., & Mastergeorge, A. (1982). Facilitating functional requesting in pragmatically impaired children. Language, Speech, and Hearing Services in Schools, 13, 202—222. Rice, M., Sell, M., & Hadley, P. (1990). The social interactive coding system (SICS): An on-line, clinically relevant descriptive tool. Language, Speech and Hearing Services in Schools, 21, 2—14. Ripley, K. (1986). The Moor House School remedial programme: An evaluation. Child Language Teaching and Therapy, 2, 281—300. Schwartz, R. (1988). Early action word acquisition in normal and language-impaired children. Applied Psycholinguistics, 9, 111—122. Schwartz, R., Chapman, K., Terrell, B., Prelock,
P., & Rowan, L. (1985). Facilitating word combination in language-impaired children through discourse structure. Journal of Speech and Hearing Disorders, 50, 31—39. Schwartz, R., Leonard, L., Messick, C., & Chapman, K. (1987). The acquisition of object names in children with specific language impairment: Action context and word extension. Applied Psycholinguistics, 8, 233—244. Skarakis-Doyle, E. & Woodall, S. (1988). The effects of modeling upon the verbal elaboration of a language disordered child’s pretend play. Human Communication, 12, 29—35. Thal, D. & Goldenberg, T. (1981). Programming diversity of response: A method for teaching flexibility of language use. Journal of Childhood Communication Disorders, 5, 54—65. Warren, S. & Kaiser, A. (1986). Generalization of treatment effects by young language-delayed children: A longitudinal analysis. Journal of Speech and Hearing Disorders, 51, 239—251. Warren, S., McQuarter, R., & Rogers-Warren, A. (1984 ). The effects of mands and models on the speech of unresponsive language-delayed preschool children. Journal of Speech and Hearing Disorders, 49, 43—52. Weismer, S. & Murray-Branch, J. (1989). Modeling versus modeling plus evoked production training: A comparison of two language intervention methods. Journal of Speech and Hearing Disorders, 54, 269—281. Wing, C. (1990). A preliminary investigation of generalization to untrained words following two treatments of children’s word-finding problems. Language, Speech, and Hearing Serv ices in Schools, 21, 151—156.
Laurence B. Leonard, West Lafayette, Indiana (USA)
64. Acquired Aphasia in Children 1. 2. 3. 4. 5. 6.
Incidence of Childhood Aphasia Ontogeny of Hemispheric Dominance Symptoms of Childhood Aphasia Recovery and Sparing of Function Conclusions References
Childhood language disorders have generally been classified into two types (Freud 1897/ 1968; Ludlow 1980). One type occurs prior to the emergence of language and has been termed developmental or congenital language
disorder. Developmental language disorders may be labeled as being p r i m a r y, when no other sensory or cognitive impairment is present to account for the dysfunction, or s e co n d a r y, when it can be attributed to another dysfunction such as mental retardation or a hearing loss. Developmental language disorders presumably result from nervous system dysfunction (see Ludlow 1980; Swisher 1985), although the specific nature of the nervous system impairment may not always be known. The other type of childhood language disorder occurs after normal language acqui-
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sition has commenced, and has been termed acquired childhood aphasia, or simply childhood aphasia, and is the focus of this review.
1.
Incidence of Childhood Aphasia
The first reports on childhood aphasia (Bernhardt 1885; Clarus 1874 ; Cotard 1868; Freud 1897/1968) appeared shortly after the classic studies of adult aphasia by Broca (1861) and Wernicke (1874 ). Despite the early interest in childhood aphasia, there has been much less interest in childhood aphasia over the years since these first reports. One explanation often given for the relative lack of research on childhood aphasia is that it is considered to be a ‚rare’ disorder. This explanation, though, needs clarification as to whether neural dysfunction that will produce an aphasia in an adult is rare in children, or, given a dysfunction that would produce an aphasia in an adult, aphasia rarely occurs. With regard to the former issue, it is certainly true that lesions frequently producing aphasia in adults such as unilateral cerebrovascular disorders are much less frequent in children. Unilateral lesions do occur, though, and the later issue is of much greater theoretical interest. Cotard (1868), a student of Charcot, was, perhaps, the first to question whether acquired childhood aphasia even existed. He claimed that children with hemiplegia, whichever the side of the lesion, never presented with aphasia, even when the entire left hemisphere was atrophied. This view was soon challenged, however, by Bernhardt (1885), who maintained that aphasia was not rare in children, and that it was a frequent symptom of infantile hemiplegia, even though he considered it to be a transient symptom. In order to investigate the rarity of aphasia given a unilateral lesion, Satz/Bullard-Bates (1981) reviewed the childhood aphasia literature. They selected studies for inclusion in their evaluation based on the following criteria: a) speech was present before the onset of the lesion; b) hand preference was known before lesion onset; c) patients were under the age of 16 at the time of lesion; d) there was evidence that the lesion was unilateral; and e) the presence or absence of aphasia had been assessed after the injury. Of 21 studies, including 929 cases, only five studies met their criteria, including 68 cases (35 of which were right-handed and suffered left hemisphere lesions). Comparing the frequency of aphasia
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in right-handed children and adults following unilateral left hemisphere lesions, Satz/Bullard-Bates found that the percentage of children suffering from aphasia was actually greater than the percentage of adults suffering from aphasia. Table 64 .1 shows a comparison between incidence for childhood aphasia, based on cases of childhood aphasia from Carter/Hohenegger/Satz (1982) and Hecaen (1983), and adult aphasia, from the review by Satz/Bullard-Bates (1981). It seems from these data safe to conclude, then, that children are not less susceptible to aphasia given a unilateral lesion. The rarity of aphasia in children must, therefore, refer to the less frequent nature of unilateral lesions, not less of a likelihood of aphasia following lesions that tend to produce aphasia in adults. Children # of cases 114
Left Hemisphere Lesion Right Hemisphere 78 Lesion Adults # of cases Left Hemisphere 708 Lesion Right Hemisphere 648 Lesion
# of % Aphasics 85 75 11
14
% # of Aphasics 414 58 20
3
Table 64 .1: Incidence of Aphasia after Unilateral Lesions in Right-Handers Adapted from Cater/Hohenegger/Satz (1982), Satz/ Bullard-Bates (1981), and Hecaen (1983).
2.
Ontogeny of Hemispheric Dominance
The incidence of childhood aphasia following unilateral lesions has been of great use in evaluating developmental models of speech dominance. One such prominent model has been advanced by Lenneberg (1967) and has been labeled the equipotentiality hypothesis. “Apparently, there is a period in infancy in which the hemispheres are still equipotential ... during the first two years of life cerebral dominance is not yet well established ... At the beginning of language development both hemispheres seem to be equally involved: the dominance phenomenon seems to come about through a pro-
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gressive decrease in involvement of the right hemisphere” (Lenneberg 1967, 151). Lenneberg, therefore, believed that prior to the first two years of life, cerebral dominance is not well established and that both hemispheres equally participate in language. As the child gets older, according to Lenneberg, dominance is established as the right hemisphere becomes decreasingly involved in language. Much of the development of cerebral dominance was proposed to occur between the ages of two and five, but, he contends, continues to progress until puberty. The concept that the right hemisphere becomes less involved in language with age, resulting in an increase in language asymmetry, has been termed the progressive lateralization hypothesis. Although progressive lateralization is usually attributed to Lenneberg, the idea can be traced to Marie (1922): “The inborn centers which we know (and they are not numerous) are always bilateral and very clearly symmetrical. The motor centers of the limbs, the centers of vision, have their locations in each of the two hemispheres in symmetrical regions ... How can we admit the existence of an inborn center for speech which would be neither bilateral nor symmetrical?” (180; cited in translation by Dennis/Whitaker 1977, 93). “Far from processing a center of speech at birth, each individual must, by his own effort, create one; and it is in the left parietotemporal zone that this occurs. Why? Perhaps simply because the nerve elements of the left hemisphere develop a little before those of the right hemisphere” (181; cited in translation by Dennis/Whitaker 1977, 94). According to Lenneberg’s view, then, one would expect the frequency of aphasia to occur equally often after left and right hemisphere lesions occurring prior to age two, resulting in a greater frequency of aphasia following right hemisphere lesions in children than adults. Since Lenneberg (1967) hypothesized that prior to age 2 the two cerebral hemispheres are equally involved in speech, we would expect that the frequency of aphasia would be equivalent after unilateral left and right hemisphere lesions that occur prior to age two. Penfield/Roberts (1959) reported on the frequency of aphasic symptoms in patients who had cortical excisions for the treatment of
V. Pathologies and Disorders of Language Development
epilepsy before and after age two. We can see from Table 64 .2 that the frequency of aphasia following left hemisphere excisions in children less than two years of age is much greater than following right hemisphere excisions. Ten of the 22 right-handers with left hemisphere excisions showed signs of aphasia whereas none of the 58 patients with right hemisphere excisions showed signs of aphasia. The Penfield and Roberts study, therefore, does not support one of the predictions following from Lenneberg’s model. Early (< age 2) # of # of cases Aphasics Left Hemisphere 22 10 Right Hemisphere 58 0 Late (> age 2) # of # of cases Aphasics Left Hemisphere 157 115 Right Hemisphere 196 1
% 46 0 % 73 0.5
Table 64 .2: Aphasia Onset After Unilateral Lobectomy Adapted from Penfield/Roberts (1959)
Since Lenneberg also hypothesized that the right hemisphere plays a decreasing role in language from ages two through puberty, we would expect that the frequency of “crossed aphasia”, i. e. aphasia resulting from right hemisphere lesions in right-handers, would decrease with age. The incidence of crossed aphasia in studies typically ranges between .4 % (Hecaen 1976) and 4 % (Rasmussen/Milner 1977) in adults, whereas for children estimates range between 7% (Woods/Teuber 1978) and 4 7% (Basser 1962). The greater reported incidence of crossed aphasia in children compared to adults has been taken as evidence for maturation hypotheses of cerebral lateralization; the view that, initially, both hemispheres are involved in language but that the left hemisphere becomes more dominant for language with age. A more critical examination of the literature, however, raises serious questions with regard to the crossed aphasia data in children. For example, the Basser study, which reported the greatest percentage of crossed aphasia in the literature, has been seriously questioned because of the inclusion of subjects with evidence of bilateral lesions (see Woods/Carey 1979).
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In a critical review of childhood aphasia studies, using criteria similar to those found in the Satz/Bullard-Bates report, Carter/Hohenegger/Satz (1982) did not find an increased incidence of crossed aphasia in children compared to adults. Similarly, Hecaen (1983), after adding 30 new cases of unilateral lesions in children to a previous sample (Hecaen 1976), also did not find a significantly greater frequency of crossed aphasia in children. Using the data presented in Table 64 .1 we can estimate the frequency of crossed aphasia in children to be about 14 %. However, this figure includes the cases in the Basser (1962) study, which was criticized for including cases with evidence of bilateral damage. When the cases from the Basser study are excluded, the frequency of crossed aphasia is only 8%, but this figure is still outside the range typically reported for adult aphasia. Carter/Hohenegger/Satz, however, argued that many cases in the childhood aphasia literature are trauma victims, which may have sustained undetected bilateral damage, and, furthermore, that some of the subjects in the literature had not had their handedness adequately tested, which may further contaminate the data with misidentified left-handers. When Carter/Hohenegger/Satz excluded cases of trauma and insufficient testing of handedness, they estimated the frequency of crossed aphasia in children to be zero (although this estimate is based on only four cases of right hemisphere lesions). The Penfield/Roberts (1959) unilateral lobectomy data (see Table 64 .2) also do not show any evidence that the frequency of crossed aphasia declines with age. The incidence data, therefore, do not provide much support for Lenneberg’s equipotentiality hypothesis. It is interesting to note in this context that Lenneberg’s usage of ‚equipotentiality’ differs in a very substantial way from the way it was originally used by Lashley (1921; see Satz/Strauss/Whitaker 1990 for a discussion of this issue). Lashley used the term to refer to the capacity of certain brain areas to mediate functions impaired by damage to other areas of the brain. “The term “equipotentiality” I have used to designate the apparent capacity of any intact part of a functional area to carry out, with or without reduction in efficiency, the functions which are lost by destruction of the whole. This capacity varies from one area to another and with the character of functions involved. It probably holds only
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for the association areas and for functions more complex than simple sensitivity or motor co-ordination” (1964, 25). Notice, therefore, that in Lenneberg’s usage, equipotentiality is used to refer to two or more area’s equal contribution towards a function during normal development. In contrast, in the original usage by Lashley, the term refers to the potential for a brain area to contribute, with or without a reduction in proficiency, to a function previously involving a different brain area. Another critical distinction in the use of the term is that for Lenneberg, the activation would precede any lesion, whereas for Lashley, the activation would follow the lesion. The marked differences in the usage of equipotentiality has led to confusion in the meaning of this concept in the literature. The incidence of childhood aphasia in the literature does not support Lenneberg’s usage of equipotentiality but is not inconsistent with respect to Lashley’s usage. We will reconsider Lashley’s use of equipotentiality when we discuss recovery from childhood aphasia later in this chapter. Kinsbourne/Hiscock (1983) have characterized theories of ontogenetic specialization as either emphasizing change during the lifespan or remaining invariant. Since there has been relatively little support for Lenneberg’s emphasis on change as outlined in his version of the equipotentiality and progressive lateralization hypotheses, the alternative viewpoint, emphasizing invariance, has gained increasing acceptance. The invariance hypothesis roughly states that the left hemisphere is dominant for speech at birth and that the right hemisphere acquires speech only after the left hemisphere is damaged. Since the childhood aphasia data raises serious questions about the symmetrical nature of language early in development, as well as an increasing asymmetry with age, the invariance hypothesis appears to be a reasonable alternative explanation. However, just as there have been different uses of the term equipotentiality, there have also been different uses of progressive lateralization. A less frequent usage of progressive lateralization has been advanced by Luria (1973, 77). “The third fundamental law governing the work of the second brain system ... can be expressed as the law of progressive lateralization of functions, implying their progressive transfer from the primary cortical areas to the secondary and ultimately, to
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tertiary areas ... The left hemisphere (in right-handed persons) has become dominant; it is this hemisphere which begins to be responsible for speech functions, whereas the right hemisphere, unconnected with the activity of the right hands or with speech, has remained subdominant.” Whereas Lenneberg has characterized progressive lateralization as representing increasing asymmetry resulting from a decreased participation of the right hemisphere in language, Luria describes progressive lateralization to be a progressive development of language within the left hemisphere. More specifically, Luria proposed that development within the left hemisphere proceeds from the primary to the tertiary areas within the cortex. Progressive development of the brain from primary to tertiary areas has been supported in a review of anatomical data on cortical development based on studies of myelination, cortical width, and neuronal density by Campbell/Whitaker (1986). There has been a tendency in neuropsychology to focus on the lateral representation of cognitive functions for neurpsychological models of cognition, sometimes at the exclusion of the two other dimensions of the brain (anterior—posterior and inferior—superior). Kinsbourne/Hiscock (1983) remind us that development proceeds along all three dimensions of space; any adequate model of language development will, therefore, need to account for changes in neuropsychological relationships along all three dimensions. Whether the childhood aphasia incidence data fit the models of equipotentiality and progressive lateralization depends on whose definition is used. We have shown that the incidence of childhood aphasia data do not provide much support of Lenneberg’s usage of these terms but they are not inconsistent with either Lashley’s use of equipotentiality or Luria’s use of progressive lateralization. As previously noted, the invariance hypothesis was largely a response to the inability of Lenneberg’s model to fit the childhood aphasia data. However, the invariance model, because it does not allow for ‚change’ is inconsistent with Luria’s model of progressive intrahemispheric development. Furthermore, the invariance model has trouble accounting for the often reported fact that aphasia manifests itself differently in children and adults. Models hypothesizing developmental change in language have usually been used to account for the differing manifestations of childhood and adult aphasia.
The question whether adult and childhood aphasia differ and the ability of intrahemispheric developmental changes similar to those expressed in Luria’s progressive lateralization hypothesis will be the next focus of attention in this chapter. This will be followed by a consideration of the literature on recovery from childhood aphasia and the ability of Lashley’s equipotentiality hypothesis to account for those data.
3.
Symptoms of Childhood Aphasia
One of the issues of greatest debate within the childhood aphasia literature has been to what extent childhood aphasia is similar to adult aphasia. In some trivial sense, of course, childhood aphasia must differ from adult aphasia since the premorbid language system of the child is going to differ from the premorbid language system of the adult. Dennis (1988) even suggests that asking whether children show adult aphasia is the wrong question to ask because it diverts attention from the more critical question whether brain-damaged children differ in their language from non-brain damaged children, a question that might be overlooked if they do not show adult patterns of aphasia. However, the issue of how childhood aphasia might differ from adult aphasia may have important implications for understanding language development. 3.1. Mutism The classic picture of childhood aphasia that has emerged from the early studies and prevailed through much of the twentieth century has been that childhood aphasia is characterized by mutism, reduced initiative for speech, dysarthria, agrammatism, anomia, and an absence of fluent aphasia. One of the distinguishing features of childhood aphasia has been a period of mutism immediately following onset (see e. g. Alajouanine/Lhermitte 1965; Branco-Lefevre 1950). Mutism is considered to be more frequent and longer in duration than with adults. For example, Hecaen (1976) observed that nine of his 15 hemiplegic cases had a duration of mutism ranging from five days to three months. The presence of mutism, though, clearly depends on the location of the lesion. Hecaen reported that 63% of the children in his sample with anterior lesions had mutism, whereas of the children with posterior lesions only 10% had a period of mutism.
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3.2. Hypospontaneity of Speech A reduction of spontaneous speech often follows a period of mutism and is usually of longer duration than mutism. In many cases there may be a very gradual transition from mutism to hypospontaneity of speech. Typically, hypospontaneity of speech has been regarded as part of the motoric, Broca-like aphasia thought to be prevalent in childhood aphasia. Hypospontaneity of speech, however, has also been observed following periods of predominantly fluent signs of aphasia in children (Van de Sandt-Koenderman/Smit/ Van Dongen/Van Hesch 1984 ; Van Hout/Evrard/Lyon 1985). Hypospontaneity has been considered to be one of the hallmarks of childhood aphasia, and has been attributed to dysfunction of an “initiator” of speech associated with subcortical structures (Van Hout/Seron 1983).
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subjects had brain damage prior to the emergence of language. The degree of syntactic dysfunction appears to be positively related to the severity of the injury (Van de SandtKoenderman/Smit/Van Dongen/Van Hesch 1984). 3.5. Anomia
Dysarthria is also a frequent symptom of childhood aphasia (Alajouanine/Lhermitte 1965) but may be mild and transitory (Hecaen 1983). The frequency of dysarthria appears to depend on the age of the child and the location of the lesion; being more frequent in younger children and after anterior lesions of the dominant hemisphere (Hecaen 1983).
Naming impairments in children with acquired aphasia is another frequent symptom of childhood aphasia. Hecaen (1983), for example, reported that 4 4 % of his left-hemisphere sample (15/34 ) had a naming disorder and that it was persistent. Only left hemisphere lesions tend to reliably produce a naming disorder (see e. g. Aram/Ekelman/Rose/ Whitaker 1985; Van Dongen/Visch-Brink 1988; Vargha-Khadem/O’Gorman/Watters 1985), but performance has also been found to be depressed in children with right hemisphere lesions. Aram/Ekelman/Whitaker (1987) suggested that whereas children with left hemisphere lesions have lexical retrieval problems causing naming impairment, in children with right hemisphere lesions naming problems may be due to impulsivity and visual-spatial problems. No association between location of lesion within the left hemisphere and naming impairment has been found (Aram/Ekelman/Whitaker 1987; Hecaen 1983).
3.4. Agrammatism
3.6. Paraphasias
A deficit in syntax has been recognized since the earliest reports of childhood aphasia (Bernhardt 1885). The nature of the syntactic deficit, however, has not been well established. Alajouanine/Lhermitte (1965) maintained that children with aphasia tend to use simplified syntax rather than make errors of syntax as do adults with agrammatism. Dennis (1980) described expressive and receptive agrammatism in a nine year old girl with a left temporoparietal infarct and noted that lower levels of syntactic structure are better preserved. Aram and her co-workers have conducted some of the few systematic studies of syntax in children with aphasia (Aram/Ekelman/ Rose/Whitaker 1985; Aram/Ekelman/Whitaker 1986). They found that syntactic impairments are one of the most reliable differences between children with early left and right hemisphere damage. Whether her results can be generalized to childhood aphasics, though, is unclear because so many of her
Early studies noted the striking absence of paraphasias in children with acquired aphasia. For example, Alajouanine/Lhermitte (1965) and Hecaen (1976) stated that paraphasias were rare. Studies by Van Hout/Evrard/Lyon (1985) and Visch-Brink/Van de Sandt-Koenderman (1984 ), however, maintained that paraphasias are not rare in childhood aphasia. Van Hout/Evrard/Lyon (1985) suggested that the discrepancy between early reports of the rarity of paraphasias and the more recent reports challenging the rarity of paraphasias may be due to several factors: a) that the paraphasias in children tend to be transient and may resolve within days; they may, therefore, have been missed by some investigators, b) since childhood aphasics are generally reluctant to speak, paraphasic errors may be noticed only on formal examination, and c) as Woods/Teuber (1978) suggested, inclusion of children only with hemiplegia in the early studies of childhood aphasia may have biased the sample towards children with anterior lesions.
3.3. Dysarthria
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3.7. Speech Comprehension
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The early studies on childhood aphasia also reported the rarity of auditory comprehension deficits (e. g. Bernhardt 1885). Hecaen (1976), though, noted their occurrence but found that they were usually limited to the acute stages of the disorder. Alajouanine/ Lhermitte (1965) found auditory comprehension deficits in about a third of their patients. These deficits were found to resolve by six months post-onset. Auditory comprehension deficits are most frequently found after left hemisphere lesions (Aram/Ekelman/Rose 1985; Vargha-Khadem/O’Gorman/Watters 1985); but Hecaen (1976) could not find intrahemispheric location to be a factor. Auditory comprehension deficits are most frequently found in cases of Landau-Kleffner syndrome (Cooper/Ferry 1978), suggesting that etiology may be a critical factor in their occurrence.
testing, the location of the lesion, and the nature of the cognitive/behavioral test used. Etiology has also been shown to be a critical variable in studies of childhood aphasia. For example, as previously mentioned, auditory comprehension deficits are much more frequent in children with the Landau-Kleffner syndrome than is the case with other etiologies. Children with closed head injury tend to show ‚subclinical aphasia’ (Sarno 1980) and non-specific linguistic deficits (Ewing-Cobbs/ Fletcher/Levin/Eisenberg 1987), whereas children with cerebrovascular accidents tend to show more specific deficits in the areas of phonology, semantics, morphology, and pragmatics (Dennis 1980). Clearly, future studies will need to take these factors into account if we are to fully understand childhood aphasia. Particular attention will need to be paid to etiology. It may no longer be defensible to group together childhood aphasics of varying etiology.
3.8 Repetition
3.11. Non-fluency
Although the ability to repeat is less frequently noted than other aspects of speech, some studies have reported repetition to be impaired (Hecaen 1976), especially with regard to children showing signs of fluent aphasia (Van Dongen/Loonen/Van Dongen 1985).
Perhaps the greatest debate within the childhood aphasia literature to date has occurred over the issue of non-fluent aphasia in children. As previously noted, earlier studies emphasized the predominance of non-fluent aphasia in childhood aphasia. Some have challenged this characterization and instead argued that this pattern of non-fluent aphasia so frequently reported in the literature is an artifact of: a) some of the early studies including only childhood aphasics with hemiplegia, thereby, biasing the childhood aphasics selected towards those with anterior lesions (Woods/Teuber 1978), or, b) that some of the fluency signs may have been transient and therefore missed by investigators if not examined at a crucial stage following the lesion, or c) that since hypospontaneity of speech is so prevalent, fluent signs may have been missed if not specifically tested (Van Hout/Evrard/Lyon 1985). Since there is no doubt that fluent signs can appear in childhood aphasia, the issue cannot be whether the non-fluent aphasic pattern is invariant, but rather whether fluent aphasia in children is less frequent than in adults (and if so, why?). To question the long-standing view that childhood aphasia is p r e d o m i n a n t ly of the non-fluent type, studies using a large number of unselected childhood aphasics are needed showing that the frequencies of fluent aphasia in children are comparable to those found in adults. To date, most of the studies using a
3.9. Written Language According to Hecaen (1976), written language problems are the most frequent and persistent problems found among children with acquired aphasia. Alajouanine/Lhermitte (1965) reported that written language problems are always present and are more severe than problems of oral language. Of the written language symptoms, writing problems appear to be more frequently found than reading problems (Alajouanine/Lhermitte 1965; Hecaen 1976). 3.10. Pragmatics To date, we are not aware of any systematic studies of pragmatic aspects of language. This is an extremely important aspect of language that certainly deserves more attention. Although it is possible to generate a general picture of the symptoms of childhood aphasia, there are innumerable unresolved issues within this field. Many of the controversies undoubtedly result from the uncontrolled variables across studies including age of the child at the time of the lesion, the age of the lesion, the age of the child at the time of
64. Acquired Aphasia in Children
relatively large number of childhood aphasics, such as those conducted by Hecaen (1983) and Satz/Bullard-Bates (1981) have found that non-fluent aphasia is the predominant type. Many of the more recent studies, while supporting the presence of the fluent variety in childhood aphasia, have not conducted the type of study needed to question the prevailing view. Of the recent studies that have used unselected samples, Visch-Brink/Van de Sandt-Koenderman (1984 ) reported that eight of their 14 children demonstrated paraphasias, but did not report the number who would be classified as fluent, non-fluent, or mixed according to their criteria of rate and mean length of utterance; Van Hout/Evrard/Lyon (1985) reported positive signs of aphasia in 11 of 16 patients, but noted that the positive signs tended to recover faster, “in some cases within a few days”, in children than in adults; and Paquier/Van Dongen (1990), classified only seven of their 4 2 children as fluent aphasics. Several factors complicate the issue of fluency in childhood aphasia. First, as pointed out by Kerschensteiner/Poeck/Brunner (1972), definitions of fluency and nonfluency vary across studies. Agreed upon definitions are, therefore, definitely needed. Second, the clinical picture appears to vary with the age of the onset of aphasia such that the older the child at the time of injury the greater the frequency of fluent signs of aphasia. Third, the location of the lesion is a factor, with posterior lesions more frequently resulting in positive signs (as with adults). Fourth, the time of the examination following the onset of aphasia is important, with the fluent signs tending to appear earlier during the course of recovery (often disappearing days or weeks following the onset of aphasia). While there have been many recent studies demonstrating that fluent signs do appear in some childhood aphasics there have been no recent large scale studies of unselected samples of childhood aphasia that would cause us to reconsider earlier claims that the type of aphasia in children differs from adults, and is predominantly non-fluent in nature. 3.12. Explanation of Childhood Versus Adult Symptoms From the perspective of understanding the development of language, the issue of whether non-fluent aphasia is the predominant form of aphasia in children is less crucial than whether the pattern of aphasia in children
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differs in some way from that found with adults. Given the description of the common symptoms of aphasia in children, there seems to be a number of aspects where the pattern of aphasia in children differs from that found in adults, in addition to the apparently predominant non-fluent nature, including: longer periods of mutism, the predominance of hypospontaneity, the infrequency of auditory comprehension deficits, and more transient paraphasias. Finding a difference between childhood and adult symptoms of aphasia suggests that continued development of language must be taking place between childhood and adulthood, and, thus, would be inconsistent with views of development emphasizing invariance. Such a finding would, though, be consistent with the progressive lateralization hypothesis advanced by Luria (1973), as discussed above. Since Luria proposed that development proceeds from primary to secondary to tertiary areas, it is presumably this aspect of ‚progressive lateralization’ that would ultimately explain any difference between the childhood and adult forms of aphasia. How, then, would progressive lateralization more specifically explain differences between the childhood and adult types of aphasia? According to Campbell/Whitaker (1986), based on anatomical studies of postnatal cortex, maturation proceeds predominantly in an anterior-posterior direction, with structures maturing first in the peri-Rolandic region and later in the occipito-parieto-temporal region. Furthermore, if we assume, as suggested by Goldman and her colleagues (e. g. Goldman 1979; Goldman/Galkin 1978; Goldman/Rosvold 1972), that less mature brain regions are functionally more uncommitted, then injury to such an area would permit greater plasticity and reorganization to occur. The emerging model, therefore, suggests that the typical childhood aphasia pattern, prolonged mutism, hypospontaneity, and non-fluency, should be the result of damage to the more mature, anterior dominant hemisphere areas. The greater plasticity of the posterior areas of the dominant hemisphere, then, would account for the less frequent (and more transient) fluent signs of childhood aphasia, such as fluency, auditory comprehension deficits, and paraphasias, along with the greater recovery from the non-fluent aphasia frequently reported in childhood aphasia. Recent studies have provided support for this model. For example, Ferro/Crespo (1988)
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found that the preponderance of non-fluent aphasias in young adult stroke patients occurred from lesions in the perirolandic and subcortical regions. Similarly, Hecaen/Perenin/Jeannerod (1984 ) reported that most of the symptoms found in childhood aphasia, including the rarer symptoms of auditory and visual comprehension deficits were more common after anterior lesions. They speculated that, “the anterior region of the left hemisphere is more engaged in diverse aspects of language in the child than in the adult, even though the specialization of this region is already fixed for verbal expression” (Hecaen/ Perenin/Jeannerod 1984, 285). Recovery, then, may be the result of intraand interhemispheric mechanisms of reorganization. A more detailed discussion of equipotentiality and mechanisms of sparing becomes even more relevant when we consider the recovery from childhood aphasia in more detail.
4.
Recovery and Sparing of Function
Since the earliest studies of childhood aphasia, it has been recognized that recovery from aphasia in children is much more dramatic than in adults (Bernhardt 1885; Clarus 1874 ; Freud 1897). These early observations have been supported by twentieth century reports as well (Alajouanine/Lhermitte 1965; Basser 1962; Benson 1972; Byers/McLean 1962; Geschwind 1974 ; Guttmann 194 2; Hecaen 1976; Lenneberg 1967; Woods/Teuber 1978). The first major twentieth-century paper was by Guttmann (194 2). This study consisted of 30 unilateral cases of children 14 years and younger, only 10 of which were available for long-term study. Moderate to complete recovery in speech was observed for all but one of the cases. Basser (1962) reported repeated observation data on 30 children, ages 2 to 9 years, who sustained an acute hemiplegia (left = 15, right = 15) after the onset of speech. An initial non-fluent aphasia was observed in most of the cases. In a subsequent evaluation, (3 months to two years after onset), Basser reported significant recovery in all cases. A similar recovery course was reported in a subsequent paper by Lenneberg (1967) for patients ranging from 3 to 18 years. All of the children were aphasic at the initial examination, but only two had a persistent aphasia, both were adolescents when the lesion occurred (ages 15 and 18 years, respec-
tively), whereas for children under the age of 11 at the time of the injury recovery was complete. Alajouanine/Lhermitte (1965) reported on a 1-year follow-up study of 32 children (ages 6—15 years), all of whom were aphasic at initial contact following injury to the left hemisphere. At subsequent testing, 24 of the children had regained “normal or nearly normal language” (659). In contrast, the remaining eight children, most with large cerebral lesions, showed a less favorable course. Byers/ McLean (1962), in a follow-up study of ten children (ages 3—15 years) with unilateral vascular lesions, reported complete restitution of speech function. Hecaen (1976) reported follow-up data on the language status of 17 children (ages 3—19 years) who became aphasic following unilateral left brain injury. Spontaneous recovery was noted in a majority of the cases. However, most of the patients were reported to show long-term difficulties in writing and naming, as previously noted. Woods/Teuber (1978) reported data on 25 aphasic patients who ranged in age from 2 to 15 years at onset. At follow-up testing four years later, 21 of the cases showed spontaneous recovery of speech. In each of these cases, the lesion occurred before 8 years of age. The four cases who remained aphasic ranged in age from 8 to 13 years at the time of the lesion. In a later study of 27 children with predominant vascular injury to the left hemisphere, Woods/Carey (1979) reported nearly complete sparing of speech in those children whose lesion onset was before the first birthday (N = 11). In approximately half of the children who became aphasic post-insult, all (N = 7) recovered speech if their lesion was before 8 years of age. Van Dongen/Loonen (1977) reported aphasia status three years after brain injury in 14 right-handed children who ranged in age from 4 to 14 years at onset. Spontaneous recovery was observed in half of the cases. Unfortunately, it is unclear whether recovery was more associated with lesion onset (i. e. early) or type (i. e. unilateral). Martins/Ferro (1990) examined a number of factors influencing recovery of acquired aphasia in 29 children with unilateral left brain injury after language acquisition. Twenty-two children (76%) recovered completely from the aphasia, as measured by quantitative measures of language ability.
64. Acquired Aphasia in Children
Better recovery was found for vascular and trauma cases than with encephalitis, which, incidentally, is more likely to cause more severe and diffuse brain injury. Interestingly, recovery was closely associated with age at insult, with 100% aphasia recovery in children under age seven. In fact, all of the persistent cases of aphasias were observed in children whose lesions occurred after age 7 years. The importance of age of insult in predicting recovery from aphasia was documented carefully in a study by Vargha-Khadem/ O’Gorman/Watters (1985). The authors measured aphasia and language status in 3 groups of children: 28 patients with left hemisphere injury, 25 with right hemisphere injury, and 15 normal control subjects. Both lesioned groups were also divided by age of insult (Early = prenatal to 5 years, and Late = 5—14 years) and all children were assessed at least 2 years post-insult. With respect to aphasia course, all children in the early left hemisphere group recovered completely and only one child in the older left hemisphere group remained aphasic. With respect to language course, subtle naming difficulties were observed in the early left-lesioned group. However, the impairments were most pronounced for the older left-lesioned group, “... with the pattern being the later the age of acquisition of injury, the more obvious the deficits. This pattern is more evident with respect to naming rather than auditory comprehension deficits and is consistent with the reported finding that there is a relative preponderance of expressive to receptive disorders in acquired left hemisphere injuries” (Vargha-Khadem/O’Gorman/Watters 1985, 692). A final recent study reported aphasia, language and intellectual recovery in 37 carefully diagnosed children with unilateral vascular accidents, 17 left [10 prenatal, 7 post-natal (mean age 5.4 years)] and 20 right [9 prenatal, 7 post-natal (mean age = 6.11); (Riva/Pantaleoni/Milani/Devoti 1990)]. The authors found complete recovery from aphasia in both of the left-damaged groups (virtually all of whom were left-handed and probably pathological left-handers). The weight of the evidence clearly supports the characteristic pattern of faster recovery in childhood aphasia. What remains less clear is the mechanism for the greater sparing of function. Previously, it was mentioned that greater recovery of speech after left hemisphere brain
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damage in children might be facilitated by mechanisms of intra- and interhemispheric reorganization of uncommitted brain areas. The most direct support for an intrahemispheric mechanism of reorganization comes from the seminal report by Lamar Roberts (Penfield/Roberts 1959). This study also provides direct support for interhemispheric reorganization, as well, and the data have been tabulated so as to reflect both outcomes. Table 64 .2 presents the results of aphasia following left-sided lobectomy in nonaphasic adult epileptic patients whose lesion onset was after age two. Inspection of this table shows that 73% of right hemisphere patients became aphasic after operation on the left hemisphere. The incidence of aphasia after a left lobectomy before age two was a much lower 4 6%. The absence of aphasia in the majority of these early lesion onset cases likely reflects the effects of speech reorganization in the right hemisphere after injury to the critical speech zones in the left hemisphere. The mechanism of reorganization is probably facilitated by latent and equipotential structures in the right hemisphere that are activated after injury to the dominant or leading hemisphere. In contrast, the onset of aphasia, which was much less frequent in these early leftsided lesion cases probably reflects, in part, the effects of speech reorganization structures within the injured left hemisphere. As noted above, these posterior structures are hypothesized to represent the substrate for ontogenetically later complex cognitive and linguistic operations (e. g. semantic). The most direct support for an interhemispheric mode of reorganization is based on results using the sodium amytal procedure developed by Juhn Wada (Wada/Rasmussen 1960). The presence of speech arrest in only the right hemisphere, points to an interhemispheric reorganization. However, the presence of speech arrest in only the left hemisphere could reflect an intrahemispheric maintenance or reorganization of speech. The latest review of this literature is by Satz/ Strauss/Wada/Orsini (1988) where four studies are reviewed, representing the few known sources that report parametric data on lesion focus, lesion type, age of onset of damage, handedness and hemispheric speech dominance. The four studies are: (1) Rasmussen/Milner (1977), where the sodium amytal technique was used to assess hemispheric representation of speech, (2) Penfield/Roberts (1959), where
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speech was assessed following left temporal lobectomies, (3) Strauss/Satz/Wada (1990), where the sodium amytal technique was used on 53 consecutive left brain-damaged cases, and (4 ) Orsini (1984 ), where a dichotic verbal listening task was used on 4 0 consecutive children and adolescents with verified left focal seizures. From these studies, patients were classified as being either left hemisphere dominant for speech or atypical, representing either bilateral or right hemisphere dominance for speech. The results are presented in Table 64 .3, which shows the percentage of left versus atypical speech cases by age of lesion onset (Early < 6 years; Late > 6 years). Onset Early Late
Left 107/262 (41%) 377/473 (80%)
Atypical 155/262 (59%) 96/473 (20%)
Table 64 .3: Percentage Speech Type by Lesion Onset across Studies Adapted from Satz (1991)
The results show that early left focal brain injury (before age 6 years) is associated with a dramatic shift from the expected pattern of left hemisphere speech dominance observed in normal populations (approximately 96%) versus the present series (107/262 = 4 1%). Inspection of Table 64 .3 also shows that this difference was due to a dramatic increase in the percentage of atypical speech dominance in the early left brain injury cases (Early = 59%; Later = 20%). Onset Early Late
Left 35/107 (33%) 102/377 (27%)
Atypical 127/155 (82%) 43/96 (45%)
Table 64 .4 : Percentage MLH by Speech Type by Lesion Onset Across Studies Adapted from Satz (1991)
A similar pattern was found for handedness (see Table 64 .4 ). Early left brain damage was associated with a striking increase in the incidence of manifest left-handedness (MLH) [162/262 = 62%] compared to non-braininjured populations (approximately 10%), most of which are accounted for by the atypical group (left = 33%, atypical = 82%). This suggests that the interhemispheric shift in speech was associated with a corresponding shift or alteration in hand preference. This
pattern, however, is not invariant. There were cases of unimodal (speech only) and bimodal (speech and hand) transfer. Furthermore, a bimodal shift was associated with an earlier onset of damage than the unimodal shift and a lower incidence of bilateral speech organization. When cases of interhemispheric versus intrahemispheric speech organization were compared across studies, it was found that time of onset of damage was also associated with type of hemispheric speech organization after left brain injury. In each study, there was a much higher incidence of early damage in cases of interhemispheric reorganization of speech (62% vs. 22%). The most dramatic finding of these studies is that the earlier the left hemisphere dysfunction (i. e. before 12 months), the greater the likelihood of a bimodal interhemispheric reorganization (including a shift in both speech and handedness). Lesions occurring between the ages of 12 and 72 months are more likely to result in either a unimodal interhemispheric shift in speech, a bilateral or less complete form of hemispheric reorganization, or an intrahemispheric maintenance or reorganization of speech. In each of the latter three cases, the likelihood of a corresponding shift in handedness is lower than with lesions occurring before the first birthday, which are more likely to result in a bimodal hemispheric reorganization. It is hypothesized that this latter type of hemispheric reorganization probably accounts for instances of sparing following left hemisphere injury while the former modes of reorganization account for instances of recovery in speech. Unfortunately, it is unclear whether the rate and/or degree of recovery is related to the type of intra- or interhemispheric reorganization. Before concluding this discussion of recovery, let us briefly return to an earlier issue — the uses of the terms equipotentiality and progressive lateralization. The results of research on recovery from childhood aphasia provide further support that Lenneberg’s (1967) use of these terms is inadequate. In addition to finding little support for his notion that the two hemispheres equally contribute to language early in development, the recovery data imply that intra- and interhemispheric mechanisms contribute to the recovery picture, data not accounted for by Len-
64. Acquired Aphasia in Children
neberg’s use of these terms. In contrast, the incidence and recovery data are consistent with Lashley’s (1921) use of equipotentiality (implying that uncommitted brain areas may possess the ability to take on functions normally attributed to another area of the brain that has been damaged) and Luria’s use of progressive lateralization (implying that there are intrahemispheric brain areas involved in speech that develop in a progression from primary to tertiary areas), and therefore, are the recommended use of these terms.
5.
Conclusions
This chapter provides a brief update of the current status of childhood aphasia, focusing primarily on the incidence of aphasia, aphasia type and recovery from aphasia. The incidence data show that childhood aphasia is not rarer than adult aphasia, given a unilateral lesion to the dominant hemisphere. The less frequent nature of childhood aphasia can be attributed to only the less frequent nature of unilateral lesions to the dominant hemisphere in children. The pattern of the incidence data, especially the low frequency of crossed aphasia in children, argue against Lenneberg’s (1967) equipotentiality hypothesis of speech development. However, the original use of equipotentiality as put forth by Lashley is consistent with these data. As was noted by the earliest writers, the type of aphasia typically found in children differs from that found in adults, with the predominant type being the non-fluent variety. It has been clearly demonstrated that all types of aphasia found in adults appear in children, but from even the most recent studies of unselected cases, non-fluent aphasia still appears to be the predominant type. Finding that aphasia manifests itself differently in children than in adults suggests that language representation in the brain undergoes changes during development, and therefore is inconsistent with the invariance hypotheses of language. It has been argued that Luria’s hypothesis of progressive lateralization is more consistent with the data on childhood aphasia. Studies on recovery from childhood aphasia show that recovery of speech is greater in children than adults. Data have also been reviewed that suggest there are intra- and interhemispheric mechanisms of recovery. Although it is beyond the scope of this present chapter, it should be noted that the greater
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recovery of speech in children appears to occur at a cost. There are data suggesting that interhemispheric mechanisms for recovery of speech may ‚crowd-out’ functions normally represented in the right hemisphere (e. g. visual-spatial functions; see Strauss/Satz/Wada 1990 for a discussion of these issues in humans and LeVere/Gray-Silva/LeVere 1988 for a discussion in non-humans). One issue that needs to be addressed is why this type of reorganization takes place after early left brain injury, especially considering that there is no evidence that the left hemisphere allows for comparable reorganization after early right hemisphere lesions (Dennis 1980; Lansdell 1969). Satz/Strauss/Whitaker (1990) suggested that interhemispheric reorganization may be facilitated by the more diffuse representation of functions within the right hemisphere and its slower rate of maturation. If interhemispheric reorganization ‚crowds out’ visual-spatial functions, which are normally represented within the right hemisphere, then it is reasonable to question to what extent more inferential and holistic aspects of language, thought to be represented within the right hemisphere, such as interpretation of familiar phrases (Van Lancker/Kempler 1987), may also be affected by reorganization within the right hemisphere. Similarly, future research should address whether intrahemispheric organization also occurs at a cost, namely at the expense of functions normally found to be represented within the left hemisphere. The study of childhood aphasia has profound implications for our understanding of how language develops, the ontogeny of cerebral lateralization, and plasticity and recovery of function in the nervous system. It should be clear from the preceding review that the results from childhood aphasia studies have significantly shaped the critical questions to be addressed in future research, among them being the mechanisms involved in progressive lateralization, intra- and interhemispheric reorganization, and ‚crowding out‚ of non-speech functions.
6.
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Paul Satz, Los Angeles, California (USA)/ Richard Lewis, Claremont, California (USA)
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65. Language Acquisition and Development with Sensory Impairment: Hearing-Impaired Children 1. 2. 3. 4. 5. 6. 7. 8. 9.
1.
Factors Affecting Language Acquisition Conductive Hearing Loss Prelingual Hearing Loss: Research Questions Oral Language Written Language Lip-Reading Sign Language Acquisition Summary and Conclusions References
Factors Affecting Language Acquisition
Describing the pattern and nature of language acquisition in the presence of a hearing impairment is complex because there are so many variables that can affect the process. Whether the reader’s concern is to understand the impact of a hearing-loss on language acquisition in any individual or to gain a more general view of the process, it is necessary to be aware of the factors involved. These factors include the type and degree of hearing impairment; age of onset and detection; the methods used to treat the impairment, to communicate and educate; the language models available in the home and community; the intellectual and remaining sensory abilities of the child. 1.1. Onset and Incidence of Hearing Loss A hearing loss can be either present at birth or be acquired after birth. The critical factor for language acquisition is whether the loss occurs before, during or after the primary period of language acquisition. Where the loss is prelingual, the effect on language acquisition is most marked. The effects of a loss occurring during development have proved difficult to evaluate although age of onset has been a variable considered in some large-scale studies (Bamford/Mentz 1979). A hearing loss acquired after language has fully developed has little effect on linguistic competence although communication is impaired. — Carrel (1977, 3) states that although worldwide an incidence of more than 1 in 1000 births with hearing loss have been reported, these represent more severe losses. He estimates that a true incidence would be, for the U.S.A., 1 in 200, taking into account milder losses which are more difficult to detect in infancy. An
increase in incidence due to hearing loss associated with middle ear effusion means that 6% of 4 year olds and 3—4 % of 7 year olds are affected (Carrel 1977, 3). 1.2. Degree and Type of Hearing Loss The degree of hearing loss tends to vary with the type and cause of impairment. More severe and profound losses are usually found in sensorineural impairments where the cochlea and auditory nerve are damaged, though mild and moderate losses can also result. Some hearing losses are so profound that the child lacks any appreciable response to sound within the range of intensities and frequencies associated with speech perception. Failure of the conductive mechanism of the middle and outer ear tends to produce losses of mild to moderate degree, especially when resulting from a condition common in childhood, otitis media with effusion, commonly called ‘glue ear’. (This name is derived from the sticky glue-like secretions that form in the middleear and impair its function). The average loss reported is 15—30 dB. (Chalmers/Stewart/ Silva/Mulvena 1989, 22). A conductive loss characteristically affects speech frequencies equally across the speech range (Klein/Rapin 1988). Sensorineural losses tend to be prelinguistic and persist throughout language development. Although some conductive losses are prelinguistic (e. g. Treacher-Collins disease and other hereditary conditions producing malformation of the conductive mechanism), the most common form of conductive loss, due to otitis media with effusion, usually starts in infancy or early childhood and is characteristically transient or fluctuating. — Sensorineural losses vary in the frequencies that are affected. One type of sensorineural hearing impairment affects the higher speech frequencies while hearing in the lower frequencies is preserved so the child may appear to have some intact hearing. Failure to hear consonants, though, means that spoken language becomes unintelligible to the child. Unless audiometry is used to assess hearing across the whole range of speech frequencies, children with high frequency losses can be misdiagnosed as suffering from developmental receptive aphasia (Bishop/Rosenbloom 1987). — The causes of hearing impairment are significant in that some aetiologies are
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frequently associated with additional sensory, motor or intellectual impairments which will further complicate language development (DiBartolomeo/Gerber 1977). While some causes of hearing impairment are being eliminated (e. g. rubella through the immunisation of females of child bearing age) others, especially those associated with preterm birth, are on the increase. It has been estimated that around 50% of congenital hearing losses are due to genetic causes (Carrel 1977) and several different modes of inheritance are involved (DiBartolomeo/Gerber 1977). The high incidence of inherited impairments means that 3—9% (Quigley/Kretschmer 1982, 16) of hearing-impaired children are born to hearing-impaired parents. This has social and cultural implications affecting language acquisition (cf. 1.3.). — Functional hearing ability for language acquisition depends on the level of residual hearing available to the child. In most cases of sensorineural loss the deficit is bilateral although unilateral losses occur. At one time, a hearing loss affecting one ear only was thought to be of little significance because the hearing in the second ear was sufficient for language acquisition. Research suggests, however, that a unilateral loss may affect educational achievement. (Culbertson/Gilbert 1986; Klee/ Davis-Dansky 1986). — Typically, in describing subjects in studies of language acquisition, the degree of hearing loss is indicated by reference to the degree of residual hearing in the better ear. The levels of hearing loss for selected frequencies across the speech range, measured by pure-tone audiometry, are averaged. The resulting value may also be classified indicating the degree of hearing loss: i. e. profound, severe, moderate and mild. However there is considerable variability in the way these terms relate to average decibel values (Conrad 1979, 4 1; cf. Green 1978). As a general guide, losses of below 4 0 dB. are considered ‘mild’, 4 1—70 dB. ‘moderate’, 71—90 dB. ‘severe’, and greater than 90 dB. ‘profound’. This is a crude method of indicating functional hearing ability since it masks differences in thresholds across frequencies which affect the way speech is perceived. Although the degree of impairment strongly relates to measures of language development it does not alone predict either the rate and success of linguistic development or educational achievement (Bamford/Mentz 1979; Conrad 1979, 24 7 ff). — In addition to the factors already discussed, language acquisition depends on measures taken to rem-
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edy hearing loss. Three different types of remediation can be considered but these can only be implemented after the loss has been detected. The age of detection may also affect outcome. The Commission of the European Community (1979) found that only approximately 10% of children born in European Economic Community countries in 1969, with a hearing impairment, had been diagnosed by 12 months and 4 5% were not diagnosed until after 3 years of age. 1.2.1. Medical Treatment Diagnosis and detection are normally considered medical responsibilities. Once a hearing impairment has been diagnosed, treatment aims to correct or improve the functioning of the hearing mechanism. In the past treatment was limited to correcting failures in the conductive mechanism, most frequently due to otitis media with effusion. A variety of measures can be taken to restore the functioning of the middle ear but until the early part of the 1980’s no treatment existed for sensorineural hearing loss. Since that time cochlear implants have been developed to treat sensorineural losses where the cochlea is damaged. This involves implanting electrodes that directly stimulate the auditory nerve. At first these were single channel devices which could only give information on the presence and duration of speech sound but more sophisticated multichannel devices can now give more information about the speech signal. Although a controversial treatment for children with prelinguistic sensorineural loss, some implants have been performed. 1.2.2. Audiological Treatment Audiological treatment aims to provide appropriate amplification to compensate for the hearing loss as early as possible in the child’s development. The amplification provided should be appropriate for the sound characteristics of the environments in which the hearing aid will be used, and the type and severity of loss. Audiological advances include methods of neonatal detection, more reliable infant screening, and assessment of hearing loss which relates more directly to the ability to perceive speech as well as the development and refinement of hearing-aids. Improvements in hearing aids aim to reproduce closely the conditions of unaided sound reception, particularly in conditions where children normally encounter spoken lan-
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guage. Some aids use tactile as well as auditory channels to transmit acoustic information (cf. 6.2.3.). 1.2.3. Educational Treatment Educational treatment reflects advances in medicine and audiology. Earlier detection has led to greater provision for intervention in the prelinguistic period based on parental involvement in early language acquisition and made possible research on prelinguistic development. Improvements in hearing aids has encouraged integration of hearing-impaired children in mainstream education. — The history of research into language acquisition in the prelingually hearing-impaired has been dominated by the controversy concerning methods of communication which favor either oral language acquisition through the amplification of residual hearing and lipreading (oral/aural method), or the acquisition of natural sign language and finger-spelling (manual method). A partial resolution of the controversy followed the introduction of methods of communication which combined oral and manual methods. ‘Pure’ forms of the manual and oral approaches are still used in Britain and the U.S.A., but the predominance of oral approaches has been redressed in the last decade. Newer approaches marry oral/ auditory methods with manual methods in various ways. As a result there are now a variety of communication methods which employ manual means to supplement oral/aural communication: (i) approaches which use the vocabulary of natural sign languages adapted to run simultaneously with spoken language and reflecting the organization of spoken language; (ii) artificial sign languages which have been developed mainly to convey the structure of the spoken language which they accompany. — In English these tend to emphasize the inflectional morphology of the language: (iii) systems that employ hand signals to supply phonetic information not available through residual hearing and lip-reading. There are five main systems of communication in widespread use. S i g n l a n g u a ge s are composed of manual gestures and employ grammars distinct from those of spoken languages. Sign language uses spatial organization to accomplish linguistic and grammatical functions. Sign languages have functioned as a primary means of communication for deaf people for centuries. They are transmitted from one generation to another and vary in form between nations, regions and social
V. Pathologies and Disorders of Language Development
groups. American Sign Language is also known as Ameslan or A. S. L. and British Sign Language as B. S. L. F i n ge r- s p e l l i n g uses a manual alphabet which has 26 handshapes to represent the letters of the written alphabet and allows an exact representation of written English. Different methods of finger spelling employ either one or two hands. Finger spelling usually supplements natural sign and is used for proper names and words for which no sign is available. O r a l/ a u r a l m e t h o d s employ speech for expression and residual hearing and lip-reading for understanding other speakers. Educators who use this method emphasize the early and consistent use of high quality, appropriate amplification and auditory training to optimize residual hearing. Early versions of this method favored specific language and speech training. Modern versions prefer more natural communicative methods that emphasize aural training rather than training in speech, language and lip-reading. To t a l C o m m u n ic a t i o n is variously and loosely interpreted. When first introduced it suggested the use of all means and aids to communication: speech, amplification, signing, finger-spelling, natural gesture, pantomime, reading, writing, drawing pictures. However, there was no specification as to how these means should be combined. It has come to mean simultaneous use of speech with some form of sign and fingerspelling. There are numerous ways in which these combinations can function. There are a number of s i m u l t a n e o u s m e t h o d s used in the U.S.A. and Britain which employ artificially devised sign systems or systems that combine natural and devised signs simultaneously with spoken language. The aim of these systems is to represent the structure of spoken language in signed form. Where English is the spoken language there is usually a means of representing the inflectional system of the language. Pa ge t G o r m a n S i g n S yst e m, S i g n e d E n g l i s h, S i g n i n g E x a c t E n g l i s h and S e e i n g E s s e n t i a l E n g l i s h are such systems. These should be distinguished from the simultaneous use of natural signs with speech where the signs follow spoken language word order. This is known as Signs Supporting E n g l i s h. Cued S p e e ch is a different type of system. It uses eight handshapes in four positions close to the lips. The handshapes and lip patterns together clarify the ambiguities of the phonemes that are present in visual speech reception (cf. 6.1.). It cannot function indepen-
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dently as a manual communication system and assists the use and development of oral language. Although devised for use with English (Cornett 1967) it has been adapted for other languages. 1.3. Sociolinguistic Background The languages used in primary language acquisition with the hearing-impaired are usually determined by the language use in the family home and the immediate social community. Approximately 10% of children are born into families where one or both parents are hearing-impaired. Although language use in the home is not simply determined by the hearing status of the parents, when parents have a prelingual hearing impairment they may use sign language with their children. There may also be siblings and members of the extended family who provide a signing community. Although sign language may be acquired at home, oral language may be used in school and the structure of spoken language will be needed for literacy. Sign language flourishes where the hearing-impaired associate informally. This happens in schools devoted to the education of the hearing-impaired even though oral language is the medium of instruction. Children from oral home environments may acquire a form of sign language by this means. Thus many hearingimpaired children are acquiring language in a bilingual situation. Two different forms of signing may exist in school environments: natural sign language in informal contacts between hearing-impaired children and a form of pidgin sign language used with and by hearing teachers who have learned sign language as adults for classroom use. Language usage is even more complex in the wider deaf community with a continuum between sign language and spoken language. (Lawson 1981). Little recognition of bilingual language acquisition has been made in studies of either oral or sign language acquisition. 1.4. Additional Advantages and Disadvantages Some children with hearing impairment have additional disabilities. The cause of the hearing impairment can also cause visual and intellectual impairments. Most research concerns children with single disabilities since the complexity of multiple disability is hard to untangle and generalizations cannot easily be made. — Variability in linguistic and academic achievement has largely been attributed
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to degree of hearing loss and intelligence. Cognitive abilities such as the form and availability of codes for memory have been shown to be related to success (Bamford/Mentz 1979; Conrad 1979, 247 ff).
2.
Conductive Hearing Loss
A conductive hearing loss results when the capacity to transmit sound to the inner ear from the air is reduced relative to the capacity to transmit sound through the bone of the skull. This occurs when there is damage or malformation of the external ear, the ear drum or middle ear. A variety of conditions lead to conductive hearing loss in childhood but the most prevalent cause in younger children (under 6 years) is middle ear effusion or ‘glue ear’. There are many terms used to denote this condition. These relate to the nature of the effusion which typically changes during the course of the disease. Otitis media is inflammation of the middle-ear, the air-filled space containing the bones that connect the eardrum to the oval window of the inner ear. Normally these bones and the eardrum act as a mechanical transducer for transmitting sound from the ear canal to the auditory nerve ending in the cochlea. If the Eustachian tube is obstructed for any reason, the air in the middle ear tends to be reabsorbed, fluid collects and may then become infected. The fluid reduces the efficiency of sound conduction and this results in a hearing impairment. The condition can be acute and/or chronic. Chalmers/Stewart/Silva/Mulvena (1989, 2) suggest that there is a clear cut clinical distinction between acute otitis media accompanied by pain, with or without ear discharge, and chronic effusions that have hearing impairment as a symptom. Losses due to otitis media are mild, rarely exceeding 4 0 dB. The loss improves when the infection subsides or is treated and the fluid is absorbed or drained surgically. Episodes may recur frequently or the condition may persist. The hearing loss therefore is usually transient. The average duration of episodes is 29—30 days but 9—32% are chronic cases lasting up to 12 weeks. In a small percentage of cases (2—10%) the condition has been known to persist for 1—4 years (Chalmers et al. 1989, 11). Persistent or frequent episodes are most likely to produce an effect on language acquision especially when they occur during the early language learning period. The condition can often predate the onset of language, as
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indicated by estimates of prevalence levels as high as 4 9% in the first year of life and 61% in the second (Klein/Rapin 1988). Given the high incidence of ‘glue ear’ it is likely to coincide with other conditions affecting language acquisition, such as specific language learning difficulties. In Down’s Syndrome and clefts of the hard and soft palate the causes of the otitis media are linked to these conditions. — The critical question is whether in children with no other disability the hearing loss associated with this condition produces sufficient reduction in auditory acuity and exposure to language models to affect language acquisition. A further question is whether there are persistent effects on speech discrimination as a result of this transient loss. If this were so it would lend support to the suggestion that there is a critical period for exposure to speech sounds in the development of the auditory system. 2.1. Research Findings — Early Studies Although the hearing loss associated with ‘glue ear’ is normally equally distributed across speech frequencies, the most vulnerable aspects of speech perception are those associated with low energy consonants in the higher frequencies. Dobie/Berlin (1979) used computer simulation to discover what linguistic information would be lost with a 20 dB. hearing loss. They identified three types of loss: consonants, particularly those marking important morphological distinctions; unstressed words; inflections and intonation contouring. Thus language structure as well as phonology could be affected by losses resulting from ‘glue ear’. These receptive difficulties could also result in delayed development of expressive language forms. Early studies tended to establish an association between early otitis media and later language delays (Holm/Kunze 1969; Needleman 1977). However, there was little consensus on the nature and extent of the effects on language in early studies. 2.2. Methodological Difficulties in Research The shortcomings of these early studies were highlighted by a series of critical reviews. The most influential were by Ventry (1980) and Paradise (1981). These reviews underline the methodological problems that beset research. Paradise lists the methodological flaws identified in early retrospective studies that compared otitis prone and otitis free subjects. First, since onset is often insidious and the
V. Pathologies and Disorders of Language Development
age of onset variable, a hearing loss can go unrecognized unless subjects are regularly tested. The persistence and severity of the hearing loss is also hard to establish without objective measures of middle ear function repeated at regular intervals. Early studies were retrospective rather than prospective and used unreliable reports from medical records and parents for information about diagnosis and history. Subjects were often poorly matched particularly on variables which could affect language development like sex, disadvantage and language learning experiences. Often the hearing at the time of language assessment was not tested. If the loss was present during language assessment the performance would be affected and this would not be a valid or reliable result. Subject samples were often small and unrepresentative. The testing of subjects was not done ‘blind’ so that experimenter effects could operate. Finally, in reporting results there was a selective emphasis on positive rather than negative findings. With some exceptions (Dalzell/Owrid 1976), a distinction between the effects of the untreated loss on concurrent language development and the long-term effects after treatment or recovery were not made. There are other problems in designing research. The effect of a mild intermittent loss will depend on success in detection and treatment which may be related to other indices of advantage and disadvantage such as variations in health care provision. Even where a link between otitis media with effusion and language delay is demonstrated it is difficult to demonstrate that this is causative. 2.3. Recent Research Subsequent research has employed a number of strategies to overcome these difficulties: These include descriptive longitudinal studies (e. g. Brookhouser/Goldgar 1987) where repeated testing was used to identify individuals with middle ear malfunction, the frequency and duration of episodes, and the severity of the hearing deficit. These authors found an association between otitis media and later language delay. Roberts/Sanynl/Burchinal et al. (1986), in a longitudinal follow-up study investigated the relationship between the occurrence of otitis media with effusion during the first three years and subsequent verbal performance and found no evidence of an association between measures. Klein/Rapin (1988), cite a research review of over 50 studies of language achievements in children with
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recurrent otitis media and conclude that the cause-effect relationship between early recurrent otitis media and later cognitive and language impairment remains uncertain. A methodologically rigorous study of a large sample reported by Chalmers et al. (1989, 156) concludes “Deficits in language development, speech articulation, reading, ... first identified at 5 years were found to persist into middle childhood years and were still present at age 11.” However, it should be noted that the effects on language development, even where reported, are relatively mild compared with those which result from a persistent prelingual hearing loss. — Given the variability in outcome in any group of children suffering recurrent otitis media and the high prevalence of the condition it might be a more useful research strategy to identify factors which predict good and poor outcome.
3.
Prelingual Hearing Loss: Research Questions
A prelingual hearing loss is persistent and cannot normally be corrected except through amplification. Current knowledge of the process of language acquisition and the linguistic achievements of the prelingually hearing-impaired is the product of research going back over 50 years or more. Given the variety of approaches, subjects and aspects of language studied there can be no typical picture. Even if additional disabilities and differences in intelligence are ignored there are still a number of factors affecting language development: degree of hearing loss, language medium, age of diagnosis. — The description of language development concerns different aspects of language ability and can be divided into oral (see 4 .) and sign language (see 7.). Competence in written language (see 5.) is a common goal for children from whatever medium of communication is employed. Lipreading (see 6.), although emphasized in oral methods, is an ability developed to some degree by all prelingually impaired. — As well as describing different aspects of language development, studies have varied in their purpose. The research questions have changed over time. — The controversy concerning methods of communication (see 1.2.3.) meant that the purpose of numerous early studies was to evaluate the relative success of competing approaches to communication in fostering language acquisition. Studies tended to
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concentrate on success in lip-reading and written language because poor intelligibility made it difficult to transcribe spoken language. There were also difficulties in comparing oral language competence with sign language because methods of describing and analyzing sign language were lacking. — Until descriptions of sign language and its structure began to appear, research concentrated on children acquiring oral language. Studies on sign language acquisition did not start appearing until the early 1970’s. The spread and development of new combinations of communication methods, implemented in a variety of settings and in different ways, mean that there are many different forms of language acquisition which could be investigated and described. Any attempt to draw a general or comparative picture of current linguistic achievements, in all these communication forms, would be both premature and misleading. — Some studies, carried out in the seventies, of the linguistic achievements of children in oral programmes were proactive in stimulating changes in teaching methods. However, these studies addressed the effects of hearing-impairment on achievement of stages in language acquisition rather than investigating the nature of the process. Crosssectional studies provide no more than a snapshot; to understand the dynamic nature of language acquisition, longitudinal studies are more effective and there have been too few of these. — Most research studies have focussed on language acquisition in children with substantial, moderate to profound sensorineural losses. With the exception of Davis (1986), there have been relatively few studies of children with mild to moderate persistent losses. Nevertheless, these are of importance because they could provide important comparisons with intermittent mild hearing loss already described in section 2. The linguistic achievements of the prelinguistic hearing-impaired cannot be regarded as fixed. Results may change over time reflecting scientific advances, resources and policies which affect age of detection, type and availability of hearing aids, and causes of hearing impairment. Much research has attempted to determine if oral language acquisition is delayed or deviant in the hearing-impaired child but the value and purpose of this effort has rarely been explicitly examined. It was partly motivated by the controversy over methods of communication and language use: the oralists seeking to demonstrate that language acqui-
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sition was merely delayed and not distorted through the perceptual difficulties encountered (see 4 .1.). Others, with different motives, sought to establish that the inherent difficulties in speech perception for the hearing-impaired led to a form of acquisition that is different in character from that of hearing children. This line of enquiry led to questioning whether it is possible to learn a language designed for the auditory system primarily through the visual modality. More sensitivity to the sociolinguistic pattern of language use has encouraged the recognition of the bilingual nature of language acquisition in the hearing-impaired. Studies need to consider the effect that acquiring different languages at different stages of development can have on the form of language acquired. However, not only are two different languages being acquired, but the languages are organized differently; oral language depending on temporal patterning while sign language depends on spatial organization. — Growing awareness of the effect of preverbal experience on the nature of language acquisition and the effects of a communication disability on conversational experience are some recent questions that are being studied. Investigating cognitive models in all aspects of language processing is also a current area of research. The evaluation of technical advances including cochlear implants and vibrotactile aids are of both practical and theoretical significance.
4.
Oral Language
O r a l l a n g u a ge is used to distinguish spoken language from sign language and refers not only to understanding and using speech but to language used for reading and writing as well. References unless otherwise stated are to children in oral language programmes. For an extended review see Mogford (1988). 4.1. Delayed or Deviant? The debate as to whether oral language acquisition is delayed or deviant has been protracted but the nature of this distinction has rarely been discussed in depth. There is general agreement that oral language acquisition is ‘delayed’ if the forms produced are normally immature or if the order in which structures are acquired is similar in the hearingimpaired to hearing children of a younger age. When researchers ask if language is delayed, they want to find out if the language acquisition process for the hearing-impaired
child represents individual recreation of language. It is argued, particularly by supporters of oral approaches, that since hearing-impairment is a peripheral disorder and the cognitive abilities which support language acquisition are unimpaired, the process of acquisition should be similar in character though slower in pace to the hearing child. Critics argue that this ignores the different developmental and social context in which language is acquired when a delay occurs (cf. 4 .2.2.). In addition, the effect of the perceptual difficulties experienced may lead children to develop different strategies for learning and processing language. These strategies will result in hearing-impaired children producing structures not found in hearing children and acquiring the structures of language in a different order. Others argue that the communication methods used mean that the way that oral language is experienced and the interaction in which language is learned are different, which may be reflected in differences in the way language is acquired. — The term ‘deviant’ has been variously defined: to refer to structures inadmissible in adult grammar and not normally found as immature forms; to an atypical order of acquisition; or to an imbalance in elements used compared with hearing children at a similar stage. There is little disagreement that with severe or profound hearing losses acquisition is slow compared to hearing children of the same chronological age. Controversy surrounds additional deviation. The argument has concerned all aspects of language: phonology, syntax, semantics and pragmatics. Whatever the answer to the delayed/deviant debate, descriptions of the nature of oral language development are significant when comparisons are made with the acquisition of natural sign language (see section 7.). 4.2. Prelinguistic Development Early diagnosis facilitates the study of prelinguistic development which can be divided into two areas; (i) prelinguistic vocalization and babbling and (ii) preverbal communication. 4.2.1. Prelinguistic Vocalization and Babbling A study by Lenneberg/Rebelsky/Nichols (1965) established that early vocalization (cooing) emerges even though auditory-vocal models and auditory feedback are unavailable but that hearing plays a role in maintaining and developing early vocalization. Subse-
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quent research suggested that there are qualitative and quantitative differences in the babbling of hearing-impaired infants compared with hearing infants. Although babbling emerges at a comparable age it decreases in frequency in the subsequent period (StoelGammon/Otomo 1986). Smith (1982) also found similarities with hearing infants up to 15 months when labial consonants predominated in samples of hearing-impaired babbling. This suggests that visual cues were beginning to influence vocalizations. The lack of a satisfactory common framework to describe stages in preverbal development has made it difficult to compare studies. Oiler’s (1986) recent framework uses acoustic and perceptual parameters to distinguish early (marginal) and later (canonical) babbling. The latter exhibits most acoustic parameters characteristic of adult speech. Oller recorded marginal babbling in severely/profoundly deaf infants but canonical babbling failed to develop in the first year. He concludes that there are similarities and differences between the vocalizations of hearing-impaired and hearing infants and an auditory handicap delays the development of some properties of syllables that make pre-speech vocalizations appear speech-like to adults. The non-speech like characteristics and infrequency of prespeech vocalizations may be linked to findings that mothers of hearing-impaired children tend to ignore, or talk through, their infant’s vocalizations rather than incorporating them in preverbal exchanges as occurs with hearing infants (Cheskin 1982; Gregory/Mogford/ Bishop 1979). 4.2.2. Preverbal Communication and Early Language Bruner (1975) argued that some aspects of preverbal communication are linked to the emergence of early language. These include vocal imitation of the adult by the child, joint visual attention and turn-taking. Lack of hearing and reliance on the visual channel has been found to delay or interfere with these preverbal abilities. This alters the nature of early language acquisition in that verbal labelling by the infant, which arises out of shared visual attention to objects, is delayed and first words are more likely to concern interpersonal events (Gregory/Mogford 1981). Curtis/Prutting/Lowell (1979) found that some stages of semantic development were passed through before spoken language appeared so that these were not repeated in
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the early verbal period. Gregory/Mogford (1981) also found greater cognitive maturity was reflected in early semantic development in that hearing-impaired children encoded meanings for abstract qualities of size and color earlier than language-matched hearing children. The extended preverbal period has an effect on the language addressed to the hearing-impaired child. Nienhuys/Horsborough/Cross (1985) found that although hearing mothers were able to adapt their language levels to those of the early language of hearing-impaired children they also reduced the complexity of the cognitive content of their language. 4.3. Phonology The development of phonology in hearing children is evident in the development of stable and rule-governed speech forms that gradually approximate to adult speech forms by 4 —5 years of age when the child’s speech is intelligible to adult speaker/listeners. Speech intelligibility is impaired by a hearing impairment (Conrad 1979, 204 ff; Markides 1970). However, it is important to separate phonology from phonetic aspects of speech development. A phoneme is not an acoustic entity but a linguistic abstraction and a way of categorizing the distinctions employed in spoken language. There are two aspects of phonology; the segmental and suprasegmental. The segmental aspect refers to the contrastive system of speech sounds (vowels and consonants); the suprasegmental includes intonation and stress. Phonetic aspects of speech, vocal quality and phonetic accuracy, are affected by the lack of auditory feedback control and auditory access to speech models. The development of phonology, the linguistic element in speech development, concerns the control of segmental and suprasegmental features to make meaningful distinctions. The auditory sense is primarily involved in the acquisition of phonology in the hearing child, although visual cues from articulatory movements also play a part (Dodd 1987). It is possible to develop a mature phonology when visual cues are absent as demonstrated in severe congenital visual impairment, although early development is slower and different due to the absence of lip-read information (Mills 1987). The hearing-impaired child relies more on visual information of articulatory movements to extract the phonological structure of language as the hearing impairment increases (Erber 1974 b). Is it possible to acquire
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the segmental aspects of phonology from the visual channel via lip-reading alone, or is such an ability dependent on the auditory modality? Although lip-reading does not allow the same acuity of speech perception as hearing (see. 6.1.), there is evidence that children with severe and profound prelingual hearing losses can develop knowledge of the phonological structure of their language which can be used in a variety of tasks requiring use of a phonological code. Case studies by West/Weber (1973) and Oller/Kelly (1974 ) found the use of phonemic contrasts and consistent phonological processes which were similar to patterns of phonological development in younger hearing children. Dodd (1976), in a group study of profoundly impaired children 9—12 years, found consistent forms in 85% or more items although all subjects had phonemes missing from their repertoires. These phonemes were those acquired later in hearing children although normally before six years of age. Dodd also found that the rules governing consonant use were similar to those of young hearing children. Other reports indicate considerable delays in phonological development in speech that persist into early adolescence (Abberton/Fourcin/Hazan 1986, 3 ff). Despite the considerable delay in development, there is evidence that where a hearing impairment is so severe as to restrict speech perception almost entirely to the visual modality it is possible to extract rules and regularities of the phonology of the language. Dodd (1987) argues that a stable and abstract system of phonology can be acquired primarily through lip-reading. — Can this abstract knowledge of phonology be employed in a variety of tasks? In hearing children the phonology of a language may also be employed in silent reading, spelling and working memory. Certain metalinguistic tasks employing rhymes and homophones also depend on a knowledge of phonology. Dodd/Hermelin (1977) concluded from a series of studies that hearing-impaired children are able to do tasks requiring phonological coding in ways resembling the hearing, even children who rely entirely on lip-reading for speech perception. This ability was also found in children in a total communication programme (see 1.2.3.) (Dodd 1987). This surprised the researchers who had expected that this group might use a code derived from print or sign rather than lip-reading. It is unclear whether this result was due to the superior language ability of the group in the total communication pro-
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gramme. Not all hearing-impaired children, however, have access to a phonological code. Where this ability is present, there is evidence of greater competence in reading, lip-reading and speech intelligibility (Conrad 1979, 24 4 ). Although a relationship with intelligence can be demonstrated, this ability to use a phonological code is not predicted entirely by either intelligence or hearing loss as it is presently measured. Given the relative lack of sophistication in measuring residual hearing in studies of this kind, it is not surprising that the relationship between the degree and type of hearing has not yet been related to the development of phonology. And although it is possible in an experimental task to demonstrate access to a phonological code through unaided lip-reading, this does not exclude the possibility that some degree of auditory input together with lip-read cues play a part in the acquisition of phonology. 4.4. Syntax The acquisition of the syntax of oral language is the most severely affected aspect of language in the prelingually hearing-impaired. The nature of this impairment has emerged as research methods have grown in sophistication. — Until the mid-1960’s research was largely confined to written language and described structural development which was delayed, simple, stereotyped and inflexible. This approach failed to demonstrate the hearingimpaired child’s developing mastery of the syntactic rules of language or the strategies employed in either comprehension or production of oral language forms in writing and speaking. For a fuller account of this early research see reviews by Cooper/Rosenstein (1966); Swisher (1976). — During the 1970’s, investigators of the development of comprehension and production of spoken language were preoccupied with the delay/deviance dichotomy. Using standardized language tests, it was possible to determine the order of acquisition of the syntactic structures of English in comparison with hearing children. Studies by Presnell (1973), Geers/Moog (1978) and Davis (1977) came to the conclusion that acquisition was not only delayed but also deviant. The children in these studies had hearing losses ranging from moderate to profound. Two other studies (Brown 1984 ; Wilcox/Tobin 1974 ) used small samples of children with less severe losses and reported results suggesting a language delay. In a larger scale study in Britain, Bamford (1979, 73 ff)
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analyzed samples of spoken language for 263 children, aged 8—15 years with hearing-impairments ranging from mild to profound and intelligence levels from I. Q. 64 —150 on the W. I. S. C. performance scale. Samples were analysed using L. A. R. S. P. (Crystal/Fletcher/ Garman 1976, 1 ff), which profiles the structures of English at clause, phrase and word level over seven stages corresponding to normal grammatical development. This study found that development was both delayed and deviant (Bamford/Mentz 1979). For the purposes of the study, ‘deviant’ was defined as uneven distribution of the frequency of structures at word, phrase and clause level. Development was considered delayed because samples were lacking in the recursive features, complex sentences and sentence connectivity expected in hearing children of comparable age. Hearing loss, intelligence and age were positively associated with development while age of onset, age of diagnosis and social class were only weakly associated with outcome. Another large scale investigation (Quigley/ Power/Steinkamp 1977) in the U.S.A., using a specially devised Test of Syntactic Abilities, studied 4 50 children, 10—18 years, from various programmes. A considerable delay in the acquisition of English sentence structures was found: 18 year olds with hearing-impairment were unable to perform as well as 10 year old hearing children. Since the order of acquisition also differed, development was considered to be deviant. In written language, structures were identified that were not used by hearing students. In contrast, the Bamford study of spoken language found few such examples. Bamford/Mentz (1979) suggest that the processes involved in writing may lead to deviant structures or that the bias towards subjects with milder hearing losses in their study accounts for this finding. An important observation made by Quigley/ Power/Steinkamp (1977) was that hearingimpaired children tended to process recursive structures in terms of word order and to treat all sentences as Subject-Verb-Object. Bishop (1983) investigated 79 severely and profoundly impaired children, 8—15 years, and their ability to comprehend structures in spoken, written and signed (artificial) form. Although there was greater difficulty and delay in understanding spoken forms, there was also evidence in the written and signed forms of systematic errors suggesting particular strategies were used for decoding. These strategies involved using the order of mention of
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items and imposing a subject-verb-object interpretation on recursive or embedded structures. Explanations for this linear processing are: (i) that they result from learning temporally ordered material through the visual channel that is primarily adapted for learning spatially organized material; (ii) that it is the product of teaching methods that emphasize particular simple structures at the expense of others; (iii) that there is interference from sign language structure which uses spatial rather than temporal ordering principles in grammar. There have been no investigations of these explanations although similar strategies have been noted in other groups with language disability (Bishop 1982, Quigley/King 1981). 4.5. Semantics Little systematic attention has been given to the study of semantics. What is known comes from three different approaches. Firstly, investigations of lexical semantics began with normative comparisons with the hearing child and established that a delay was evident. It was suggested that some areas of experience might receive greater/lesser lexical representation because of differential sensory experience resulting from the hearing-impaired child’s visual orientation to the world. Further, concepts predicated on auditory experience, those of time and the ordering of events, were considered to give greater difficulty. A second suggestion was that abstract words were fewer than concrete words in the lexicons of the hearing-impaired. Tweney/ Hoeman/Andrews (1975) found, contrary to prediction, that the degree of abstraction in the lexicon was comparable for hearing and hearing-impaired adolescents. Some semantic fields were less well represented, particularly the field connected with words related to sounds. The third approach concerns the development of semantic relations. Comparisons between young hearing-impaired and hearing children matched for stage of language development in structural terms established that hearing-impaired infants exhibited the same semantic functions and communicative intentions but development was delayed (Skarakis/Prutting 1977). — It is sometimes suggested that the hearing-impaired experience difficulty with metaphorical aspects of language. Iran-Nejad/Ortony/Rittenhouse (1981) first established that providing reading material is within the syntactic competence of hearing-impaired children, these children are
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able to select metaphoric titles for simple stories as well as language-matched hearing children, if they are given some practice. This has been interpreted as indicating a difficulty in knowing when to interpret language in a metaphorical way because the ability is only demonstrated in such exercises. 4.6. Pragmatics Since non-verbal elements can supplement oral linguistic forms there appears no reason why uses of language and intentions expressed by hearing-impaired children should be restricted. On the other hand, pragmatic skills are highly dependent on other areas of language development, particularly syntax. Curtis/Prutting/Lowell 1979) found in preschool children, across communicative contexts, that the range of intentions expressed was age-appropriate though the amount of communication and verbal ability to express these intentions was less than in hearing children of a similar age. Schirmer (1985) in contrast found that hearing-impaired children were delayed in using communicative functions. — Conversation is the main vehicle for assessment of pragmatic skills but, unlike other areas of competence, conversational abilities are the product of at least two speakers. The difficulties which oral hearing-impaired children experience in understanding and being understood can alter the character of their conversations as well as the contributions of their conversational partners. Wood/Wood/Griffiths et al. (1982) and Wood/Wood (1984 ) in observing classroom conversations between teachers and pupils communicating orally, noted that teachers exhibited high levels of control which were related to low levels of initiative and shorter conversational turns from the children. Teachers found difficulty in understanding the children and spent turns establishing understanding before a topic could develop. In these investigations and in a subsequent study of dinnertime conversations at home (Bodner-Johnson 1991), it was found that children with severe to profound hearing loss were able to interpret conversational moves and their meaning with few mistakes and to appreciate the obligations placed on them for reply. However, they were less successful in developing conversation and initiating themselves. — Wilbur (1977) investigating another aspect of pragmatics, cohesive devices used in narratives, found that hearing-impaired children had difficulties with the selection of indefinite
and definite articles to indicate new or previously mentioned referents across sentence boundaries. Correct usage depends on the knowledge of the listener and the linguistic context. Wilbur maintains that these devices were used correctly at sentence level, which suggests that the problem was not syntactic but pragmatic; that is knowing when to use these devices. This could be explained by teaching methods which he maintained concentrated on teaching sentence structures and not on connected discourse.
5.
Written Language
An understanding of the hearing-impaired child’s mastery of written forms of language emerged from studies of educational achievement. At first these were attempts to evaluate competing educational programmes so that understanding the pattern of acquisition and the cognitive processes employed was relatively neglected. The difficulties experienced by the hearing-impaired are at first puzzling because access to written language is unaffected by a hearing loss. However, a well developed language system, usually internalized from spoken language use, seems the necessary foundation for reading. The study of the development of reading in the hearingimpaired helps to unravel the complex relationship between mastery of spoken and written forms of language. — Oral language acquisition was first studied through samples of written language because this avoided problems of poor speech intelligibility. Early studies provided descriptions of language produced using sentence length, type-token ratio, the frequency of different parts of speech, and number and types of errors made. Samples from written language were often quoted as well, since these measures failed to characterize the language sufficiently. The terms repeatedly used to describe the language were ‘rigid’, ‘stereo-typed’ and ‘telegrammatic’, the latter term referring to the predominance of ‘content’ as opposed to ‘function words’. As with spoken language, opinions differed as to whether the language described was delayed or deviant. Later studies approached language using linguistically based approaches which give a better description and understanding of the nature of written language of the hearing-impaired (Quigley/Kretschmer 1982, 81 ff for review; Quigley/Montanelli/ Wilbur 1976). At the age of 16—18 years, hearing-impaired adolescents had mastered
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the simpler structures of English in their written language but in some respects their writing differed from Standard English. Difficulties were noted with noun inflections, determiners, and with verb forms, particularly the auxiliary. Few attempts were made to employ complex structures and a preference for subject-verb-object simple sentences was demonstrated. These features probably account for previous findings which described written language as simple, rigid and stereo-typed. 5.1. Spelling Studies of spelling ability (e. g. Hoeman/Andrews/Florian et al. 1976) suggest that this is one linguistic function in which hearing-impaired children are equal to or more advanced than hearing children. Dodd (1979) has suggested that this is the result of access to two routes to spelling: one which uses a visual route and a graphemic code; and the other, phoneme to grapheme correspondence rules which require a speech-based code. However, both Hoeman et al. (1976) and Dodd (1979) found that hearing-impaired children showed fewer errors of a phonetic character compared with hearing children. Dodd argues that some ability to use phoneme to grapheme rules can be demonstrated in children who are orally educated and that lip-reading skills play a part in the ability to use the phonemic route to spelling. Questions concerning spelling are linked with lip-reading and the acquisition of underlying phonological forms of spoken language (see sections 6.2.3. and 4.3.). 5.2. Reading Research, which has used a variety of reading tests, studying children from different educational programmes, has repeatedly demonstrated the difficulty that hearing-impaired children experience in mastering reading. The achievements of school-leavers are disappointing (see Quigley/Kretschmer 1982 for a review). Mastery of written language is highly dependent on the mastery of spoken (oral) language which typically predates the acquisition of literacy. Hearing children map what they read onto what they know about the language: the knowledge of the structure and content of the language and possible messages to be conveyed helping the children to construct understanding from what they are able to recognize in print. The hearing-impaired child, however, is faced with learning both how to recognize what is represented by print and the structure of the language. The diffi-
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culties experienced by the hearing-impaired in understanding oral language in print are similar to those found in understanding spoken language even though the perceptual problems in reading are of course greatly reduced. The nature of the difficulties the hearingimpaired child experiences in understanding written text indicates that the problems of language comprehension experienced in spoken language are not simply or directly the result of difficulty in lip-reading, but are due to the inability to use the structures of oral language as a means of decoding language meaning. Here the debate about different methods of instruction taps some potentially interesting questions. Is it successful communication or the knowledge of the structure of oral language which is most important in learning to read? The mastery of written forms are difficult for children who have not yet mastered oral language structure. However, are children who communicate through sign language more or less proficient at mastering written language? If the problem lies in communication, then children who successfully develop sign language should have fewer problems with the written form and should be faced with a task similar to children acquiring a second language on entering school. Unfortunately, the answer to these questions is not clear cut because reading is not a simple unitary process. Disentangling the effects of language delay on communication, which results in a reduction in cultural understanding and world knowledge from difficulties in the teaching of reading, is one problem. Different abilities are involved at different stages of the learning process. Beginning readers depend on some abilities more than others, for example a linguisticallybased code for recognition of novel words (Hanson/Liberman/Shankweiler 1984 ). Later, with increased experience of print, comprehension will then depend more on ability to use syntactic structures to decode meaning. As has been already discussed, both these abilities are affected by a hearing impairment. In addition, success in learning to read may be affected by teaching methods, the timing of instruction and the suitability of the materials used in the teaching process.
6.
Lip-Reading
The understanding of lip-reading (speechreading) has developed over the last two decades. However, a developmental account of
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its role in oral language acquisition in the hearing-impaired is lacking. (For a detailed review see Mogford 1987). 6.1. The Role of Lip-Reading in Language Acquisition Lip-reading was once regarded as a compensatory visual-perceptual skill developed by the hearing-impaired for speech perception. For the prelingually hearing-impaired child with severe or profound hearing loss, who was acquiring oral language, lip-reading represented the primary means for acquisition even though information about the speech signal from observation of articulatory movements is considerably less than that available from an auditory signal. Lip-read information is limited by distance and poor illumination of the speaker’s face (Erber 1971, 1974 a). Erber (1974 b) concluded that 4 0 English consonant and vowel phonemes produce only 16 discriminable units. In experiments with hearing subjects, Binnie/Montgomery/Jackson (1974 ) and Dodd (1977) showed that, for consonants, place of articulation is best conveyed through vision. However, voicing and manner are largely conveyed through hearing. This implies these features are difficult to detect visually. Erber (1974 b) concluded that the same would be true for hearing-impaired subjects. When a sign language or finger-spelling is used with speech, lip-reading is only one of several forms in which linguistic information is carried. The degree of reliance on lip-reading varies with severity of hearing impairment. While children with mild hearing-impairment make use of lip-read information intermittently, for example, when learning new lexical items, those with more severe hearing losses rely on lip-reading at all times. This places constraints on the management of interpersonal interaction, for the lip-reader needs to visually monitor the face of the speaker. Perception of conversational exchanges can be incomplete because monitoring speakers, in turn, is very difficult. — While lip-reading was regarded as a compensatory skill, the linguistic and cognitive components of the skill were not understood. This was reflected in the variety of methods used to assess lip-reading which often failed to control for the level of general linguistic development of those assessed. Research has now established that auditory experience of speech enhances visual speech recognition and that visual speech cues are used with
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greater skill by the hearing (Dodd 1980). For the hearing, the development of lip-reading is the product of a bi-modal process: distinctions available through audition can serve as a basis for determining the visual distinctions that correlate with acoustic features. For the hearing-impaired, as the hearing loss increases, the degree of reliance on visual speech information through lip-reading can be assumed to increase despite technical improvements in hearing aids and the emphasis in oral programmes on auditory training. As lipreading improves with the degree of residual hearing (Conrad 1979, 186), it seems that for the hearing-impaired also, lip-reading is enhanced through input from two sensory modalities even though the quantity and quality of information from the auditory channel is relatively reduced. 6.2. Lip-Reading Research Lip-reading is defined in different ways by different researchers and hence the abilities measured also vary. For example, lip-reading can be equated either with comprehension of spoken sentences with aided hearing or the ability to recognize phonemes in permissible nonsense words without the use of hearing aids. Often in measuring lip-reading there has been no attempt to control for receptive language ability and so it is not possible to separate difficulties due to lack of linguistic knowledge from the visual-perceptual task of speech perception. Lip-reading has been investigated for a number of different reasons. Firstly, lip-reading has frequently been investigated when assessing the relative merits of methods of education for the prelinguistically deaf. Different methods place different degrees of emphasis on lip-reading and its training. — Secondly, individual differences in lipreading skill in children from similar educational programmes have been the focus of research. Thirdly, the nature of the linguistic and cognitive processes involved in lip-reading with the prelingually deaf child has been investigated: a relationship between lip-reading and other linguistic abilities including spelling, reading and speech is indicated. — In research, lip-reading is studied under ideal conditions which removes the task from the normal demands of interaction. Under normal language learning circumstances, conditions are rarely optimal. A comprehensive account of the development of lip-reading and its role in language acquisition should include the development of appropriate gaze
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patterns that allow lip-reading to be integrated with interpersonal interaction and tasks that demand visual attention. 6.2.1. Lip-Reading and Educational Methods Some evaluations of different communication methods used in language acquisition introduced confounding socio-cultural and aetiological factors. For example, comparisons of deaf children reared by deaf (signing) parents and those reared by hearing (oral) parents ignored factors that varied systematically with parental hearing status. There appears to be no evidence that any manual form of communication interferes with lip-reading skills or that additional training in lip-reading confers any advantage. However, research which reflects the bilingual nature of language development suggests that the timing of exposure to manual communication may affect the development of lip-reading skills in the longer term (Parasnis 1983). 6.2.2. Predicting Success in Lip-Reading Individual differences in lip-reading have frequently been reported even when the degree of hearing loss and methods of communication are controlled. One variable frequently examined is intelligence, although tests of lipreading and intelligence used have varied between studies. A review of studies by Farwell (1976) stressed variability in the correlations reported for lip-reading and intelligence. Conrad (1979, 192) highlighted some studies omitted from this review which reported significant correlations between lip-reading and intelligence. Some investigators found a positive correlation between intelligence and lip-reading skill which was stronger for better lipreaders but weaker at the lower ranges of ability. Other variables have been investigated and the most reliable finding is that lip-reading measures show a close relationship with other measures of language ability. This is not surprising when lip-reading is the primary means of language reception. However, significant correlations have also been found with finger-spelling and sign usage (Meadow 1968) where the medium of communication is not primarily spoken language. — Conrad (1979, 186) broke new ground by measuring lip-reading relative to the language competence of each individual. Language competence was assessed through the written medium. He found weak significant correlations with intelligence for subjects already grouped
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by severity of hearing loss. — Attempts to explain poor lip-reading in terms of specific learning difficulties have failed. A different approach examined competence in a range of visual-perceptual skills with varying degrees of relevance to lip-reading, including visual memory. This research shed little light on the specific cognitive processes involved in visual speech recognition because it lacked an adequate model of the processes. 6.2.3. Lip Reading and Memory Codes Auditory speech perception entails a coding mechanism for immediate storage of material until completion of higher level processing. Visual speech perception also requires a compatible memory storage system. In auditory perception this has been shown to be based on a phonological code. This code is also implicated in other linguistic skills, such as learning to read (Hanson/Liberman/Shankweiler 1984 ), spelling and speech production (Dodd 1979). Are the hearing-impaired able to develop a phonological code which can be used for working memory in visual speech recognition? Dodd/Hermelin (1977) concluded that the ability to store and use phonological information in an experimental task was not dependent on the auditory modality. However, it is possible that residual hearing was involved in the development of this ability. Conrad (1979, 114 ) showed that in prelingually hearing-impaired school-leavers there were individual differences in the use of a phonological code in an immediate memory task, which varied with hearing loss and intelligence. This suggests two sources of information about the speech signal help to develop a speech-based code although a profound hearing loss did not entirely preclude the use of an internal speech code. Conrad (1979, 193 ff) also demonstrated a relationship between the use of a speech-based code and lip-reading when hearing loss and intelligence were controlled. This relationship broke down at profound levels of hearing impairment. — The development of vibrotactile aids allows the hypothesis that two independent channels of information promote the development of lip-reading skill and a phonological code to be tested. These hearing aids convert acoustic speech signals to a tactile form to supplement lip-reading. Trials with early devices used artificially deafened subjects but there is some evidence that they can enhance success in lip-reading for prelingually hearing-impaired subjects also (De Filippo 1984).
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6.2.4. The Development of Lip-Reading Scientific and educational opinion has been profoundly pessimistic about the ability of severely and profoundly hearing-impaired to acquire oral language through the medium of lip-reading. (Conrad 1979, 203; Brasel/Quigley 1977) Lip-reading appeared to be an inefficient way of communicating information to the hearing-impaired compared with communication that involved combinations of methods or the printed word (Gates 1971). These views lead to the introduction of communication methods that use a variety of visual forms to enhance language learning. However, despite the central role given to lipreading in oral language development, there have been few attempts to study lip-reading developmentally other than recording correlations of skill with chronological age and plotting the rate of progress by age. This implies the nature of the skill is the same throughout the course of development which is unlikely. There is limited evidence that the process changes with development, as is the case with oral language comprehension (Green/Green/Holmes 1980, 1981; De Filippo 1982). A complete developmental account would also include interactional gaze patterns permitting the development of visual speech processing.
7.
Sign Language Acquisition
For many years the sign languages used in deaf communities were stigmatized by the hearing and not accorded the status of a language. This was the case although as many as three-quarters of the deaf adults in the United States were estimated to use American Sign Language in 1969. Linguistic description of sign languages began in 1960 with William Stokoe who worked on Ameslan, American Sign Language. This was followed by the work of Klima/Bellugi (1979, 1 ff). Similar work in Britain on British Sign Language (Brennan 1981) and in France led to similarities between sign languages and between spoken and signed languages being recognized. This work established properties of formal structuring and organizational principles, e. g. constrained systems of features, rules based on underlying forms, recursive grammatical processes. The research also described those characteristics peculiar to sign languages which demonstrated that at all struc-
tural levels sign languages are influenced by the modality. It was found that sign languages had levels analogous to phonology, morphology and syntax but adapted to the visuospatial modality. — Some features of Ameslan acquisition were reported by Schlesinger/ Meadow. This study (Schlesinger/Meadow 1972, 4 5 ff) reported on two children of deaf parents, growing up in homes using Ameslan. This and other studies began to establish that, in spite of the difference in modality, the milestones and the nature of language acquisition were similar to that of hearing children acquiring oral language. Also the nature, rate and language acquired contrasted markedly with comparative data for hearing-impaired children acquiring oral language (Gregory/ Mogford 1981). Schlesinger/Meadow (1972, 87 ff) also stressed that the quality of interaction and experience of language and communication was more relaxed and natural than for deaf children who were learning oral language. One reason for the more advanced and rapid acquisition of sign as a first language in the hearing-impaired when parents are sign language users is that the child’s exposure to language models is not delayed or dependent on diagnosis as with hearingimpaired children in hearing families learning oral language. Such comparisons of language acquisition might suggest that one medium of language acquisition is better than another. Such conclusions cannot be drawn from these studies because they do not provide a controlled evaluation of different communication methods. In addition to differences in age of exposure to language models, the situations are not comparable in many ways. — Sign language acquisition in families where sign language is acquired from competent signing adults is different from instances where a form of signing is learned from hearing parents whose first language is oral and who have no experience of communicating with the hearing-impaired. These parents acquire a second language, in a different modality, at the same time modelling this for their hearingimpaired child. In addition, it is rare for hearing parents to choose to sign exclusively to their child, preferring what Meadow (1980, 23) has termed bi-modal communication, using a combination of signed and spoken English simultaneously, with signs following the pattern of spoken language (see section 1.2.3.). Native signers may be employed to provide language models for hearing-impaired children of hearing parents (Fletcher 1987, 153) but the situation is still not com-
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parable with children who learn sign language from parents who are competent signers. Schlesinger/Meadow (1972, 4 5 ff) also studied the language of two children whose hearing parents were using both signed and spoken English. The children, both diagnosed towards the end of their first year, began bimodal acquisition at different ages, 15 and 37 months (Schlesinger/Meadow 1972, 82 ff). Early acquisition showed similarities with the acquisition of spoken English by hearing children, but later differences in grammatical development were found. These were explained in terms of the perceptual salience of morphemes in the visual and auditory modes. — The nature of the language acquisition task for deaf children learning sign languages has been further elucidated by Bellugi and her associates (Bellugi/van Hoek/Lillo-Martin/ O’Grady 1988). Bellugi argues that the iconic nature of much sign could make the mapping of meaning onto form easier. Longitudinal and cross-sectional studies of American Sign Language acquisition from onset to 10 years of age have found precisely the same order of acquisition for parallel stages at similar ages as hearing children learning spoken languages. They have also found important discontinuities between preverbal gesture and the early linguistic system though superficially signs/gestures may look identical. In these studies there are examples of errors that demonstrate that the child acquiring sign language does not simply imitate the models that he observes. As with hearing children learning spoken language, the mistakes are evidence of the child’s acquisition of a rule based system. These studies seem to indicate that language acquisition can be unimpaired if the deaf child is exposed to a language which is easily perceived. This is the case with sign language even though it uses organizational principles suited to the visual system. — A further aspect of sign language acquisition concerns the reported creation of sign language by children who are unable to profit from the oral models presented by hearing parents. Goldin-Meadow/Feldman (1975) reported that prelingual hearing-impaired children were able to create a sign language to communicate, employing invented signs which they began to combine in ways similar to the first two word combinations in hearing children. However, there have been few other studies that have reported this phenomenon. Indeed, in a similar study Gregory/Mogford (1981) found no evidence of this. The reason
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for this difference has not been satisfactorily explained.
8.
Summary and Conclusions
The character of language development in the prelingually hearing-impaired seems to depend primarily on the form of language which the child acquires and the availability of interaction with competent users of the language. Studies of sign language acquisition in children whose families communicate using sign language show considerable agreement. The pattern, rate and characteristics of the process are similar and parallel to those of hearing children acquiring spoken language. This contrasts strongly with the process of spoken language acquisition in children with hearing parents and accomplishments of prelingually impaired children in learning to read and write, whatever the form of their first language. Even though there are some able individuals who successfully develop oral language, the average pattern of development shows considerable delay in developing linguistic competence. Opinions seem to differ about the developmental, social and educational significance of this delay. There is evidence that the delay and difficulty experienced in understanding and using spoken language affects the learning process itself, altering patterns of interaction between the children and parents, siblings and teachers. When language delay leads to attempts to teach language, this may further affect the character of the language acquired. The difficulties experienced by children with more severe prelingual hearing loss, particularly in lip-reading, and the fact that only a minority of children are born into families who use sign, has encouraged a greater use of simultaneous methods of communication at home and school. Most of these methods, it should be noted, still aim to enable the child to acquire the structure of spoken language. The additional manual forms function to make the structure of spoken language easily accessible through vision. Although there have been studies to evaluate the effect of these approaches on different aspects and stages of language acquisition, a comprehensive review of language acquisition through simultaneous presentation has not been undertaken. There are many versions of simultaneous communication methods and even those methods that go under the same name may vary in
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many subtle ways: in the way they are used; and when and how they are introduced. Preliminary reports describe simultaneous methods in use. They suggest that there is often a gap between what is intended and the language input that occurs. This is sometimes because speakers of oral language have difficulty acquiring more than a simple vocabulary of signs: the grammar of sign language being based on different organizational principles from spoken language. Another problem is coordinating sign and speech. Sign makes use of spatial devices and is more economical in time than speech. Trying to sign and speak simultaneously can result in reduced verbal forms. — Studies of language acquisition in the hearing-impaired have mainly concentrated on children with severe and profound hearing loss. Less attention has been given to those with mild, moderate and unilateral hearing losses. Evidence so far tends to indicate a pattern of language delay which though not severe can still provide educational and social difficulties. — The effect of a hearing deficit acquired during language acquisition is harder to assess. Considerable resources have been invested in studies of the effect of the most common, mild form of childhood hearing impairment that results from middle ear effusion. Improved research methods make the results of studies more reliable but still there is no consensus about the effects. Those delays that have been described are not severe. Differences between children with recurrent episodes and those not effected may persist into later childhood but it is difficult to establish how significant these differences are for individual achievement and why the difficulties persist. If otitis media with effusion has lasting effects on speech discrimination, even after spontaneous recovery or treatment, this is of considerable practical and theoretical concern. There are several possible alternative explanations for the persisting effects of transient hearing loss and these need to be elaborated and then investigated. — The study of language acquisition in the prelingually impaired is not only of practical significance but can also contribute to the understanding of language acquisition in children without impairment. The nature and success of sign language acquisition suggests that any species-specific predisposition to acquire language must be relatively independent of the modality through which it is acquired.
9.
References
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Bruner, J. (1975). From communication to language: A psychological perspective. Cognition, 3, 255—287. Carrel, R. E. (1977). Epidemiology of hearing loss. In S. E. Gerber (Ed.), Audiometry in infancy. 3—17. New York: Grune and Stratton. Chalmers, D., Stewart, I., Silva, P., & Mulvena, A. (1989). Otitis media with effusion in children — The Dunedin Study. Oxford: MacKeith Press with Blackwell Scientific. Cheskin, A. (1982). The use of language by hearing mothers of deaf children. Journal of Communication Disorders, 15, 145—153. Commission of the European Community. (1979). Childhood deafness in the European Community. Contract No. 359—77—9. Ec. 1. UK. Luxembourg: C. E. C. Committee on Medical and Public Health Research. Conrad, R. (1979). The deaf schoolchild: language and cognitive function. London: Harper and Row. Cooper, R. L. & Rosenstein, J. (1966). Language acquisition in deaf children. Volta Rev iew, 68, 58—67. Cornett, O. (1967). Cued speech. American Annals of the Deaf, 112, 3—13. Crystal, D., Fletcher, P., & Garman, M. (1976). The grammatical analysis of language disability: A procedure for assessment and remediation. London: Edward Arnold. Culbertson, J. L. & Gilbert, L. E. (1986). Children with unilateral sensorineural hearing loss: cognitive, academic and social development. Ear and Hearing, 7, 38—42. Curtis, S., Prutting, C. A., & Lowell, E. L. (1979). Pragmatic and semantic development in young children with impaired hearing. Journal of Speech and Hearing Research, 22, 534—552. Dalzell, J. & Owrid, H. L. (1976). Children with conductive deafness: A follow-up study. British Journal of Audiology, 10, 87—90. Davis, J. M. (1977). Reliability of hearing-impaired children’s responses to oral and total presentations of The Test of Auditory Comprehension of Language. Journal of Speech and Hearing Disorders, 42, 520—527. Davis, J. M. (1986). Effects of mild and moderate hearing impairments on language, educational and psychosocial behaviour in children. Journal of Speech and Hearing Disorders, 51, 53—62. De Filippo, C. L. (1982). Memory for articulated sequences and lipreading performance of hearingimpaired observers. Volta Review, 31, 134—146. De Filippo, C. L. (1984 ). Laboratory projects in tactile aids to lipreading. Ear and Hearing, 5, 211—227. DiBartolomeo, J. R. & Gerber, S. E. (1977). Pathology of hearing loss. In S. E. Gerber (Ed.), Au-
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diometry in infancy. 17—44. New York: Grune and Stratton. Dobie, R. A. & Berlin, C. I. (1979). Influence of otitis media on hearing and development. Annals of Otology, Rhinology and Laryngology, 88, (Suppl. 60), 48—53. Dodd, B. (1976). The phonological systems of deaf children. Journal of Speech and Hearing Disorders, 41, 185—198. Dodd, B. (1977). The role of vision in the perception of speech. Perception, 76, 31—40. Dodd, B. (1979). The spelling abilities of profoundly pre-lingually deaf children. In U. Frith (Ed.), Cognitiv e processes in spelling. 423—440. London: Academic Press. Dodd, B. (1980). The interaction of auditory and visual information in speech perception. British Journal of Psychology, 71, 541—549. Dodd, B. (1987). Lip-reading, phonological coding and deafness. In B. Dodd R. Campbell (Eds.), Hearing by eye: The psychology of lip-reading. 177—190. New Jersey: Lawrence Erlbaum. Dodd, B. & Hermelin, B. (1977). Phonological coding by the prelinguistically deaf. Perception and Psychophysics, 21, 413—417. Erber, N. P. (1971). Effects of distance on the visual reception of speech. Journal of Speech and Hearing Research, 14, 848—857. Erber, N. P. (1974 a). Angle, distance and illumination on normal reception of speech. Journal of Speech and Hearing Research, 17, 99—112. Erber, N. P. (1974 b). Visual perception of speech by deaf children. Recent developments and continuing needs. Journal of Speech and Hearing Disorders, 39, 178—185. Farwell, R. M. (1976). Speech reading: a research review. American Annals of the Deaf, 121, 19—30. Fletcher, L. (1987). Language for Ben. A deaf child’s right to sign. London: Souvenir Press. Gates, R. R. (1971). The reception of verbal information by deaf students through a television medium. A comparison of speech reading, manual communication and reading. Proceedings of the Conv ention of the American Instructors of the Deaf. 513—522. Washington: U. S. Government Printing Office. Geers, A. & Moog, J. (1978). Syntactic maturity of spontaneous speech and elicited imitations of hearing-impaired children. Journal of Speech and Hearing Disorders, 43, 380—391. Goldin-Meadow, S. & Feldman, H. (1975). The creation of a communication system: A study of deaf children of hearing parents. Sign Language Studies, 8, 225—236. Green, D. S. (1978). Pure tone air-conduction testing. In J. Katz (Ed.), Handbook of clinical audiology. 98—109. Baltimore: Williams and Wilkins.
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Green, K. W., Green, W. B., & Holmes, D. W. (1980). Speech reading abilities of young deaf children. American Annals of the Deaf, 125, 906—908. Green, K. W., Green, W. B., & Holmes, D. W. (1981). Speech reading skills of young normal and deaf children. American Annals of the Deaf, 126, 505—509. Gregory, S. & Mogford, K. (1981). Early language development in deaf children. In B. Woll, J. Kyle, & M. Deuchar (Eds.), Perspectiv es on British Sign Language and deafness. 218—237. London: Croom Helm. Gregory, S., Mogford, K., & Bishop, J. (1979). Mothers’ speech to young hearing impaired children. Teacher of the Deaf, 3, 42—43. Hanson, V. L., Liberman, I. Y., & Shankweiler, D. (1984 ). Linguistic coding by deaf children in relation to beginning reading success. Journal of Experimental Child Psychology, 37, 378—393. Hoeman, H. W., Andrews, C. E., Florian, V. A., Hoeman, S. A., & Jensema, C. J. (1976). The spelling proficiency of deaf children. American Annals of the Deaf, 121, 489—493. Holm, V. A. & Kunze, L. H. (1969). Effect of chronic otits media on language and speech development. Paediatrics, 43, 833—839. Iran-Nejad, A., Ortony, A., & Rittenhouse, R. (1981). The comprehension of metaphorical uses of English by deaf children. Journal of Speech and Hearing Research, 24, 551—556. Klee, T. M. & Davis-Dansky, E. (1986). A comparison of unilaterally hearing-impaired children and normal-hearing children on a battery of standardised language tests. Ear and Hearing, 7, 27—37. Klein, S. K. & Rapin, I. (1988). Intermittent conductive hearing loss and language development. In D. Bishop & K. Mogford (Eds.), Language dev elopment in exceptional circumstances. 96—109. Edinburgh: Churchill Livingstone. Klima, E. S. & Bellugi, U. (1979). The signs of language. Cambridge, Mass: Harvard University Press. Lawson, L. (1981). The role of sign in the structure of the deaf community. In B. Woll, J. Kyle, & M. Deuchar (Eds.), Perspectiv es on British Sign Language and deafness. 166—177. London: Croom Helm. Lenneberg, E. H., Rebelsky, G. F., & Nichols, I. A. (1965). The vocalisations of infants born to deaf and to hearing parents. Human Dev elopment, 8, 23—37. Markides, A. (1970). The speech of deaf and partially-hearing children with special reference to factors affecting intelligibility. British Journal of Disorders of Communication, 5, 126—140. Meadow, K. P. (1968). Early manual communica-
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tion in relation to the child’s intellectual, social and communicative functioning. American Annals of the Deaf, 113, 29—41. Meadow, K. P. (1980). Deafness and child dev elopment. London: Arnold. Mills, A. E. (1987). The development of phonology in the blind child. In B. Dodd & R. Campbell (Eds.), Hearing by eye: The psychology of lip-reading. 145—161. New Jersey: Lawrence Erlbaum. Mogford, K. (1987). Lip-reading in the prelingually deaf. In B. Dodd & R. Campbell (Eds.), Hearing by eye: The psychology of lip-reading. 191—212. New Jersey: Lawrence Erlbaum. Mogford, K. (1988). Oral language acquisition in the prelinguistically deaf. In D. Bishop & K. Mogford (Eds.), Language dev elopment in exceptional circumstances. 110—113. Edinburgh: Churchill Livingstone. Needleman, H. (1977). Effects of hearing loss from early recurrent otitis media on speech and language development. In B. F. Jaffe (Ed.), Hearing loss in children. 640—649. Baltimore: University Park Press. Nienhuys, T. G., Horsborough, K. M., & Cross, T. G. (1985). A dialogic analysis of interaction between mothers and their deaf or hearing preschoolers. Applied Psycholinguistics, 6, 121—140. Oller, D. K. (1986). Metaphonology and infant vocalisation. In B. Lindblom & R. Zetterstrom (Eds.), Precursors of early speech. 21—36. Basingstoke: Macmillan. Oller, D. K. & Kelly, C. A. (1974 ). Phonological substitution processes of a hard-of-hearing child. Journal of Speech and Hearing Disorders, 39, 65—74. Paradise, J. L. (1981). Otitis media during early life; how hazardous to development? A critical review of the literature. Paediatrics, 68, 869—873. Parasnis, I. (1983). Effects of parental deafness and early exposure to manual communication on cognitive skills and field independence of young deaf adults. Journal of Speech and Hearing Research, 26, 588—594. Presnell, L. (1973). Hearing-impaired children’s comprehension and production in oral language. Journal of Speech and Hearing Research, 16, 12—21. Quigley, S. P. & King, C. M. (1981). An invited article: Syntactic performance of hearing-impaired and normal individuals. Applied Psycholinguistics, 1, 329—356. Quigley, S. P. & Kretschmer, R. E. (1982). The education of deaf children. Issues, theory and practice. London: Arnold. Quigley, S. P., Montanelli, D., & Wilbur, R. (1976). Some aspects of the verb system in the language of deaf students. Journal of Speech and Hearing Research, 19, 536—550.
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Quigley, S. P., Power, D. J., & Steinkamp, M. W. (1977). The language structure of deaf children. Volta Review, 79, 73—84. Roberts, J. E., Sanynl, M. A., Burchinal, M. R., Collier, A. M., Ranney, C. T., & Henderson, F. W. (1986). Otitis media in early childhood and its relationship to later verbal and academic performance. Paediatrics, 78, 428—430. Schlesinger, H. S. & Meadow, K. (1972). Sound and sign. Childhood deafness and mental health. Berkeley: University of California Press. Schirmer, B. R. (1985). An analysis of the language of young hearing-impaired children in terms of syntax, semantics and use. American Annals of the Deaf, 130, 15—19. Skarakis, E. A. & Prutting, C. A. (1977). Early communication: semantic functions and communicative intentions in the communication of the preschool child with impaired hearing. American Annals of the Deaf, 122, 382—391. Smith, N. (1982). Some observations concerning pre-meaningful vocalisations of hearing impaired infants. Journal of Speech and Hearing Disorders, 47, 439—442. Stoel-Gammon, C. & Otomo, K. (1986). Babbling development of hearing-impaired and normally hearing subjects. Journal of Speech and Hearing Disorders, 51, 33—40. Swisher, L. (1976). The language performance of the oral deaf. In H. Whitaker & H. A. Whitaker (Eds.), Studies in neurolinguistics, Vol. II. 59—93.
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London: Academic Press. Tweney, R. D., Hoeman, H. W., & Andrews, C. E. (1975). Semantic organisation in deaf and hearing subjects. Journal of Psycholinguistic Research, 4, 61—73. Ventry, I. M. (1980). Effects of conductive hearing loss. Fact or fiction? Journal of Speech and Hearing Disorders, 45, 143—156. West, J. & Weber, J. A. (1973). A phonological analysis of the spontaneous language of a 4 -year old hard-of-hearing child. Journal of Speech and Hearing Disorders, 38, 25—35. Wilbur, R. (1977). An explanation of deaf children’s difficulty with certain syntactic structures in English. Volta Review, 79, 85—92. Wilcox, J. & Tobin, H. (1974 ). Linguistic performance of hard-of-hearing and normal hearing children. Journal of Speech and Hearing Research, 17, 286—293. Wood, D. & Wood, H. A. (1984 ). An experimental evaluation of the effects of five styles of teacher conversation on the language of hearing-impaired children. Journal of Child Psychology and Psychiatry, 25, 45—62. Wood, D. J., Wood, H. A., Griffiths, A. J., Howarth, S. P., & Howarth, C. I. (1982). The structure of conversations with 6- to 10-year-old deaf children. Journal of Child Psychology and Psychiatry, 23, 295—308.
Kay Mogford-Bevan, Newcastle (U.K.)
66. Language Acquisition and Development with Sensory Impairment: Blind Children 1. 2. 3. 4. 5. 6. 7.
Theoretical and Methodological Issues Phonology Morphology and Syntax Semantics Pragmatics, Input and Interaction Conclusions References
1.
Theoretical and Methodological Issues
1.1. Models of Language Acquisition In those models of language development which have their basis within linguistic theory, in particular those models which assume an innate, specifically linguistic, component, sensory impairment involving lack of vision
should not result in any problems with the acquisition of the formal properties of language (see Chomsky’s claim in his debate with Piaget (Piattelli-Palmarini 1980, 171)). Data from blind children provide therefore a testing ground for such predictions. If language acquisition is viewed as dependent on cognitive development, if only in part, then clearly problems in cognitive development might predict problems in language for blind children. This possibility of prediction is dependent on the assumption of close links between specific areas of cognition and specific areas of language. The cognitive development of blind children certainly appears to be different in some areas (Warren 1977) but it is not clear that these areas are always relevant to language. The data from blind children are of interest in this complex
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issue particularly in relation to aspects of their semantic development. Within a social-interactive framework the way adults interact in communication with blind children and the kind of language that serves as input will directly affect the process of language acquisition. Much recent work on language-disordered populations has been done within this framework, although little direct causal relationship between input and acquisition has been indicated. Research on blind children’s language has been done within a variety of frameworks, although a large number of studies have been observational. Two larger studies (Burlingham 1972; Fraiberg 1977) were within a psycho-analytic perspective. 1.2. Methodological Issues 1.2.1. Definition of Blindness In order to research the relationship between the lack of vision and language acquisition, it is important that the subjects in a particular study form a homogeneous group. This is difficult to control for. Visual handicap varies from no perception of light through to extreme short-sightedness. Blindness is a legal definition which varies between countries. Blindness can also be a functional concept related to a particular task; thus a person may be able to identify features on objects when held close but be functionally blind in terms of orientation at a distance. It is also very difficult to assess visual acuity accurately in very young children. 1.2.2. Age of Onset Comparable to hearing-impaired children, the onset of blindness is important as a variable in a research population. Visual experience during the period of language acquisition should not be underestimated, particularly in relation to the use of nonverbal communicative behaviors. 1.2.3. Frequency of Visual Handicap Figures on the occurrence of blindness in different countries are difficult to come by. In Western industrial societies approximately 2 children in 10,000 are born blind; 18 become blind in the course of later life. This figure is far higher in other societies, where blindness frequently results for example from eye infection. In Western societies blindness as a result of difficult post-natal care in premature ba-
bies (retro-lental fibroplasia) is declining. So too is blindness which is the result of a genetic condition, through the preventive effects of genetic counselling. Apparently increasing is the occurrence of blindness with another handicap. Conservative figures average around 50%; some studies indicate a figure as high as 90% (Jan/ /Scott 1977). Research on the effects of lack of vision need a population in which blindness is the only problem. This population is difficult to find. At the young age at which most language acquisition research needs to take place it is also difficult to be sure of the diagnosis, that is to be sure that blindness is the only handicap. Many studies have taken the form of case studies for these reasons. Through the lack of homogeneity in the populations studied, the comparison and interpretation of results become also problematic.
2.
Phonology
2.1. Babbling Almost all studies which begin in the prelingual period record a normal onset of babbling (e. g. Junefelt 1987; Mills 1987; Warren 1977). Fraiberg (1977) judged the amount of babbling in the ten blind infants she observed to be less than in sighted infants but it was not quantified in this study. Rowland (1984 ) found the frequency of vocalization in the five infants she observed to be within normal ranges but that the vocalizations occurred at different points in the interaction from sighted children. This point will be resumed later (5.1.). In summary, babbling seen as a precursor to the acquisition of speech sounds does not seem to differ greatly from babbling in sighted children. 2.2. Perception of Speech Sounds Few studies have been done in this area and seemingly none with young blind children. Semzova (1961), in an audiometric study of 38 blind children (7—16 years), found no difference. Lucas (1984 ) found better identification of mispronounced words in a story context in children aged between five and seven years, but no detailed phonological analysis was carried out of the material. There is a great deal of work still to be done here, particularly in relation to differences which have been found in speech sound production.
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2.3. Production of Speech Sounds 2.3.1. Early Production A longitudinal study of three young blind children (1—2 years, German-speaking) indicated a clear influence of blindness on the acquisition of speech sound production (Mills 1983; Mills 1987). An analysis was made of the production of consonants categorized according to the visibility of the articulation of the consonant. Thus sounds with highly visible articulation (labials, labio-dentals) were compared with sounds with a less visible articulation (alveolars, velars etc.). The blind children made more errors than the sighted children on the consonants with a highly visible articulation (4 1% vs. 21%). On the production of consonants with a less visible articulation the sighted and blind children did not differ. Thus the sighted children have an advantage in their acquisition of the visible consonants. The pattern of substitution errors made is also slightly different for blind children. Whereas sighted children rarely substitute a sound from a different visual category for a target sound, blind children do this more frequently (34 % such errors vs. 10%). This finding has been substantiated by later work (Dodd 1983; Mulford 1989). 2.3.2. Effect on Early Vocabulary As has been found for sighted children, the pattern of phonological acquisition also affects the vocabulary produced at this age. Since this pattern is different in blind children, it is also reflected in their attempted words: they produce far fewer words containing a highly visible consonant compared to sighted children. The predominance of labials in the early lexicon has been explained by distributional factors and/or physiological factors but clearly the role of visual information must be included here (Vihman/Macken/Miller et al. 1985). It must also be included in a model of phonological acquisition since its absence produces a different pattern of acquisition in blind children. 2.3.3. Adult Phonology Detailed studies of later phonological acquisition are not available. One study of sound production in blind teenagers (Göllecz 1972) indicated differences in lip movements for the articulation of vowels, but minimal differences in acoustic properties. This appears to be due to a compensatory restriction of the
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oral resonance chamber. This constitutes a different endpoint of acquisition for blind children in articulatory terms but not in phonological terms. 2.3.4. Phonological Disorder? The different pattern of acquisition found in younger children does not lead necessarily to a disorder, but means a temporary delay in a specific area of phonology. Some studies do report a higher incidence of articulation problems in older blind children (Elstner 1983; Miner 1963) but it is not clear which particular areas are problematic. Since the populations investigated in these studies are large and multiply-handicapped children are not explicitly excluded, the question arises if blindness is the cause of these problems.
3.
Morphology and Syntax
3.1. Language Onset Several studies report a delay in the onset of language, that is the occurrence of the first word (e. g. Fraiberg 1977; Reynell 1978). Others report a delay in the acquisition of combining two words. These studies are often difficult to interpret since full information on other aspects of development are missing: it is not clear if another handicap is involved. Secondly in the studies cited above, many of the blind children’s language measures fell within the normal range, although the mean for the group indicated a delay. It is clear then that blindness does not mean a necessary general delay in morphology and syntax. Mulford (1989) summarizes results from 14 more recent case studies and finds no major delay in early development. She suggests that the discrepancy between earlier and later studies can possibly be explained by the shift in the cause of blindness in Western industrial societies. As mentioned above, retro-lental fibroplasia (RLF) has declined rapidly over the last twenty years but was a main cause of blindness before then. This condition is caused by the administration of too much oxygen to premature babies. Subsequent research has indicated that too much oxygen can also result in Minimal Brain Damage (MBD), so that earlier populations of blind children may well have included several MBD children. 3.2. Delay in the Verbal Auxiliary There are no indications of major problems in syntax or morphology. However, in a study of three blind children, Landau/Gleitmann
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(1985) recorded a significant delay in the acquisition of the verbal auxiliary in English. This delay in the acquisition of a highly specific aspect of syntax is related to a feature of maternal input. The mothers of blind infants use more imperatives and for longer than mothers of sighted children do on average, and they ask fewer questions. This results in a lower frequency of the verbal auxiliary in English maternal speech. The same relation between input and acquisition of the verbal auxiliary had already been found for sighted children and is one of the few areas in which a clear causal relation can be traced between the form of input and the child’s acquisition of language. The delay in this specific area does not seem to have any major consequences for the further acquisition of English. The question can be asked whether the implications might not be more (or less) severe in languages which use different structures in imperatives and questions. 3.3. Syntax/Pragmatics Interface Most work indicates no problems in older blind children (Maxfield 1936). However, one study with Dutch-speaking children has shown problems in morphology and syntax in both blind and severely visually-impaired children aged between five and ten years (Wegener-Sleeswijk 1986). Two of these children were RLF children with low IQ’s, but of the remaining 17 children 11 made significantly more grammatical errors in a spontaneous speech sample than sighted peers. These children were not significantly different however on measures of complexity of morphology and syntax, that is in use of past tense forms, subordination etc. The errors that they produce frequently involve the omission of constituents and appear to be related to the children’s attempts to produce longer utterances and to apply the complex rules of ellipsis. The problems of these older blind children appear to be more related to the correct pragmatic application of the syntactic rules, rather than to the control of the formal aspects of the syntactic rules themselves, that is the syntax and pragmatics interface (Mills/WegenerSleeswijk 1991). These children also had separate problems in pragmatics which will be discussed below (see 5.6.). 3.4. Summary From the evidence discussed above it seems that blind children do not have serious problems with the acquisition of syntax and mor-
phology. Only a small delay can be seen in the area of the verbal auxiliary in English. Otherwise more serious delays appear to be related to blindness occurring with other disabilities. This suggests that vision is not crucial for acquisition of these formal aspects of language, which would be in accordance with formal theories of language acquisition (see 1.1.).
4.
Semantics
4.1. Early Lexicon Several researchers have examined the acquisition of the early lexicon in blind children (Andersen/Dunlea/Kekelis 198 4 ; Bigelow 1987; Dunlea 1989; Landau/Gleitman 1985). The descriptive findings are similar but their conclusions vary (Mulford 1989). Most studies indicate a normal acquisition of the first 50 words. The spread of the words across different semantic categories is comparable with that of sighted children. A few differences are observed: for example that blind children have more words associated with parent/child routines. They also have more terms for sounds but fewer deictic terms. They also have fewer terms for animals, and more terms related to household items compared with sighted children. Such minor differences are related to the differing experience of the blind children, thus they have more experience of household items and less of animals which sighted children usually gain through book-reading etc. Differences in interpretation occur mainly in relationship to the apparent conceptual development (see 4.2.). 4.2. Semantic and Conceptual Development Blind children do appear to have restricted experience in comparison with’ sighted children. Related to this is the frequent observation that blind children rarely generalize new words to other objects of the same category: for example dog will be used for the one known dog and not for other dogs. This under-generalization, and related lack of over-generalization (otherwise common in this early period of development), has been interpreted as evidence for a delay in the ability of blind children to sort and categorize (Anderson/Dunlea/Kekelis 198 4 ; Dunlea 1984 ). In the spontaneous behavior of the two children studied (up to 3;4 ), no sorting was observed and the children would not
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categorize objects on request. This interpretation has been challenged by work with 22 older children (4 —6 years) in which no lack of ability to categorize was evident as compared with the sighted controls (Dobslav 1991). These blind children were also able to formulate the distinguishing properties of objects. There were only some minor differences in the type of properties named: functional properties were named by blind children but particularly those which were related to the activity of the object itself or those which the child itself carried out. This difference is again related to the type of information a blind child has access to but does not indicate a general cognitive or linguistic deficit. Overextensions, where they do occur in blind children, are on the basis of mainly tactile properties, necessarily not visual properties as in most sighted children. This indicates again that their language development may be different in some respects but that the processes of acquisition do not fundamentally differ. 4.3. Verbalism This term was introduced by Cutsforth (1932) to describe the use of language which does not have a conceptual basis. Since blind children have a sensory deficit, it was assumed that they could not have a conceptual basis for many terms and that their speech was full of verbalisms, indicative of ‘loose thinking’. This label has been disputed by many researchers, although it has been used even recently by Rogow (1986) to describe the speech of both blind children and adults. Landau/Gleitman (1985) showed in their longitudinal study of one child (up to 5) that words with even a high visual content such as the verbs to see and to look are not meaningless for the child but have a gradually developing meaning which approximates the adult form. At the age of three years the child interpreted the two verbs as ‘haptically be aware of’ and ‘haptically explore’ respectively. But by the age of five years she knew that sighted adults could not see an object which was behind a barrier, although they could have felt it. Landau and Gleitman’s general conclusion is that blind children will use the information that they have to build up the meaning of items with a visual component, starting with the information which is most accessible for them, that is in the haptic modality.
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4.4. Terms Related to Space Blind children are still making errors at age six years with spatial deictic terms such as this and here (Mulford 1981). Mulford relates this finding to a delay in the acquisition of the cognitive concept of space, due to the lack of visual information. The use of personal pronouns can also involve deixis and their acquisition may therefore be related to the acquisition of the concept of space (Loveland 1984 ). The use of first and second person pronouns involves a shift of perspective and this shift in perspective appears to be difficult for blind children. They continue to make errors with I and you longer than sighted children. This problem may however also be related to the frequency of pronouns in the input. (Errors in gender in pronouns also take longer to disappear in blind children than in sighted (Mulford 1981)). Blind children have been shown to acquire spatial prepositions in terms of comprehension and production with some delay but with variation in the order of acquisition. Bigelow/ Bryan (1982) showed that blind children can understand the prepositions in, on and under more readily in relationship to themselves than for the relationship between two objects. In understanding spatial relations between objects, blind children acquire prepositions referring to the vertical dimension first as do sighted children (Mills 1988). However they take longer to acquire prepositions referring to the horizontal dimension, particularly the horizontal frontal dimension. Blind children take longer to learn that fronting is relevant to the use of these prepositions, and also to learn to apply that knowledge. 4.5. Summary From the results in the area of semantic acquisition there appear to be some clear differences in the order of acquisition, some of which may be related to a delay in the acquisition of some cognitive concepts. There is little evidence, however, to suggest that blind children have general problems in their conceptual development. Their acquisition of some semantic areas is different but not obviously deficient.
5.
Pragmatics, Input, and Interaction
5.1. Pre-verbal Communication Pre-verbal communication is considered important for the onset and further development of language in the child particularly by those
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researchers who adopt a social-interactive model of language acquisition. A few studies exist on this period of development in blind children and in general offer some support for this model. Gaze and gestures are not available as signals to indicate communicative intentions in general and selection of topic for interaction in particular. Adults interacting with blind children have to learn to pick up other signals which indicate direction of attention and communicative intent. Fraiberg (1977) in a general developmental study of ten blind children observed frequent failure in this area. Als/Tronick/Brazelton (1980) report on successful preverbal interaction and a good development in one blind child; four children studied by Preisler (1990) also show more successful interaction and good communicative development. Studies by Dunlea (1989), Rowland (1983) and Urwin (1983) indicate the problems that appear to arise in this early interaction and relate them to problems in language development. The pre-verbal blind infants were best able to communicate affective states. They also were able to express more general desires such as for the repetition of a play routine by crying, vocalization and some hand movements. All the children did have problems in directing attention to an object. Two of the mothers observed by Rowland clearly failed to repond as frequently to the vocalizations of their children and these children were considerably more delayed in their language development. All three children observed by Rowland (1983, 1984 ), however, showed a different pattern of vocalization compared with sighted children. They produced fewer vocalizations during and after the vocalizations of the adult: they vocalized rather more when alone. Rowland interprets this different pattern as a result of blindness and of the increased importance of the auditory environment, which blind children try to avoid ‘cluttering’ with their own vocalizations. 5.2. Functions of Early Language Several studies have examined the functions for which blind children use their language in the early stages and some of these have related the development to input. Just as for sighted children, requests form a category which emerges early, but in blind children the first requests are those related to self with requests for objects emerging around 20 months (Urwin 1983). Dunlea (1989) found this category
V. Pathologies and Disorders of Language Development
of requests to be dominant around two years. Perez-Pereira/Castro (1990 a), in a study of a blind and sighted twin pair, found that requests decreased similarly in both children (up to the age of 4 years) in favor of questions. However, the blind twin did have in total more functions related to self than the sighted child, e. g. action related to self, reports of internal states. Kekelis/Andersen (1984 ) report more labelling in the early language (up to 22 months) but Perez-Pereira/Castro (1990 a) do not have such a clear finding in the older twins: the sighted child between 2;6 and 3;6 had in fact more labels than the blind child. Kekelis and Andersen relate their finding to a higher incidence of labels in the input speech to the younger children, which they interpret as an impediment to the development of other functions in the language of the child. This would not appear to be a generalizable result however. Kekelis and Andersen also found fewer attributions and descriptions in the language input to the younger children, a surprising finding since it would seem obvious that blind children need more verbal information about the environment in order to organize experience. The children’s language also reflected less use of these functions. The blind twin of Perez-Pereira and Castro also used these functions less than her sighted sister but they do not relate this to input. One can interpret this observation as being a result of greater selforientation rather than necessarily a product of input. Adults talking to young blind children tend to initiate topics more than adults talking to sighted children of the same age (Kekelis/ Andersen 1984 ; Urwin 1983). Kekelis and Andersen also observed that almost half the topics introduced by the adults were related to contexts and referents which the child could not perceive and that the adults have difficulty in establishing what the child is interested in. They interpret this as an impediment to blind children in the development of language oriented to the environment. Both studies found that the topics introduced by the children were mainly self-oriented. As discussed above (3.2.), input from the adult does appear to have an effect on the acquisition of the verbal auxiliary in English. The characteristic of the input was that adults were being more directive and therefore using fewer questions involving the auxiliary. A highly directive interactive style is associated
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with children at an early stage of language development and Kekelis/Andersen (1984 ) interpret this as an indication that input and interaction progress at a lower rate for blind children, thus producing a slower rate of development in the children. This causal effect is not proven, however. 5.3. Imitation It has been noted by many researchers that blind children in the early stages of acquisition produce many more imitations of adults’ utterances than sighted children. Most of these imitations are inappropriate conversationally, whether from sighted or blind children, but the fact that blind children produce more of such utterances and for longer has led to a clinical classification of their speech as ‘echolalic’. Since this is a clinical symptom of autistic children, an association has been made between blind and autistic children by some researchers. Prizant (1984 ) reviews the literature on this and suggests that imitation may occur more often in blind children for various reasons such as acquisition style, better developed rote memory, problems in segmentation due to lack of contextual information. He argues that it is not necessarily to be interpreted as a clinical symptom. Perez-Pereira/Castro (1990 b) present data from the blind twin which confirms a greater use of imitation, but repetition with modification and formulaic speech are also used more. They interpret this as a route into language acquisition, a method of practising structures, much as Speidel (1989) argues for sighted children. 5.4. Verbal Interaction: Older Children It has been reported for some younger blind children that they do not verbalize as much as their sighted peers. Studies of older children (4 to 9 years) indicate however a greater amount of verbalization (Olson 1983; Schwartz 1983). This appears to be related to the function of maintaining interaction in the absence of the availability of visual cues such as eye gaze, smiles and other non-verbal behavior, although social and cultural differences in turn-taking routines may have an influence on the amount of verbalization (see 5.4.). Workman (1986) reports that in children under five years adults could influence the amount of peer-peer interaction, including verbal interaction, when the adult gives the
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blind child information about the social environment, that is who is present, what the activities are, etc. Difficulties in obtaining this information, which is a prerequisite to initiating a conversation, seem to impede younger blind children (see 5.5.). Blind children also are reported to use more questions in their interactions (Erin 1986; Maxfield 1936), which Erin suggests is a reflection of the need to gain access to precisely this information. McGinnis (1981) observed that slightly younger blind children (3 to 5 years) frequently used questions to change topic and did this more often than sighted peers. This too may be a reflection of turn-taking mechanisms (see 5.5.). 5.5. Turntaking Blind people have limited access to the nonverbal cues in regulating turns either as speaker or listener. Early turntaking is supposed to be established in the pre-verbal stage and the lack of eye-contact and smiling in blind infants are a problem for the sighted parents in establishing this proto-conversational organization. Fraiberg (1977) relates this lack of reaction signals to problems in establishing a parent-child bond. In beginning a conversation it is necessary to obtain the attention of the addressee and to direct attention to the topic of discourse if appropriate. This is frequently done non-verbally. Younger blind children use non-visual alternative means such as touching the addressee, pinching, calling the addressee’s name (Mulford 1983) but they are more frequently unsuccessful and can become discouraged in initiating discourse. Facial expression is muted in blind children (and adults), smiling is less frequent as are head nods (Parke/Shalcross/Anderson 1980; Warren 1977)). All these behaviors can function as feedback signals in conversation but since they are used less by blind children (and adults), other feedback signals must be acquired. No detailed research has been done on this so far. It is known from work on blind adults (Junefelt/Mills 1990) that the turntaking patterns are different from sighted adults and are an adaption of the sighted patterns in their own culture. This adaptation varies in effect according to whether the culture can be described as floor-yielding or floor-seizing. Blind children must learn these patterns and adaptations but how this acquisition proceeds is not yet clear.
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5.6. Assessment of Listener In order to make the content and formulation of conversation efficient, it is necessary to assess the information to which the listener has access either directly or indirectly. Children take considerable time in acquiring this ability but blind children seem to take even longer. Their language is more frequently pragmatically deviant because of a failure to take the listener correctly into account (Wegener-Sleeswijk 1986). This is also comparable with autistic children and may be related to a slower development of a theory of mind as has been suggested for that group (cf. art. 78).
6.
Conclusions
In summary it can be said that blind children with no other handicap will develop language without major delay or deficiency. In some aspects they are clearly different. These differences provide evidence for the role of vision in models of language acquisition and indicate the variety of routes of acquisition which such models must account for.
7.
References
Als, J., Tronick, E., & Brazelton, T. (1980). Affective reciprocity and the development of autonomy: the study of a blind infant. Journal of the American Academy of Child Psychiatry, 19, 22—40. Andersen, E. S., Dunlea, A., & Kekelis L. S. (1984 ). Blind children’s language: resolving some differences. Journal of Child Language, 11/3, 645—664. Bigelow, A. (1987). Early words of blind children. Journal of Child Language, 14, 47—58. Bigelow, A. & Bryan, A. (1982). The understanding of spatial prepositions ‘in’, ‘on’ and ‘under’ in blind and sighted pre-school children. Paper to the Canadian Psychological Association Conference, Montreal. Burlingham, D. (1972). Psychoanalytic studies of the sighted and the blind. New York: International Universities Press. Cutsforth, T. D. (1932). The unreality of words to the blind. The Teachers’ Forum, 4, 86—89. Dobslav, G. (1991). Da kann ich nur das Wort sagen. Eine v ergleichende Analyse der Kategorisierungsleistungen und der Inhalte v on Wortbedeutungen über Objekte bei blinden und sehenden Vorschulkindern. Doctoral dissertation, University of Bielefeld, Germany. Dodd, B. (1983). The visual and auditory modalities in phonological acquisition. In A. E. Mills
(Ed.), Language acquisition in the blind child: normal and deficient. 57—61. London: Croom Helm. Dunlea, A. (1984 ). The relationship between concept formation and semantic roles: some evidence from the blind. In L. Feagans, C. Garvey, & R. Golinkoff (Eds.), The origins and growth of communication. 224—243. Norwood: Ablex. Dunlea, A. (1989: Vision and the emergence of meaning in blind and sighted children’s language. Cambridge: C. U. P. Elstner, W. (1983). Abnormalities in the verbal communication of visually-impaired children. In A. E. Mills (Ed.), Language acquisition in the blind child: normal and deficient. 18—41. London: Croom Helm. Erin, J. N. (1986). Frequencies and types of questions in the language of visually-impaired children. Journal of Visual Impairment and Blindness, 80, 670—674. Fraiberg, S. (1977). Insights from the blind. New York: Basic Books. Göllecz, V. (1972). Über die Lippenartikulation der von Geburt an Blinden. In S. Hirschberg, G. Szépe, & E. Vass-Kovoícs (Eds.), Papers in interdisciplinary speech research. 85—91. Budapest: Akadémiai Kiadó. Jan, J. E., Freeman, R. D., & Scott, E. P. (1977). Visual impairment in children and adolescents. New York: Grune & Stratton. Junefelt, K. (1987). Blindness and child-adjusted communication. Doctoral dissertation, University of Stockholm, Sweden. Junefelt, K. & Mills, A. E. (1990). Turntaking in blind and sighted multiparty conversations: Swedish and Dutch compared. Paper to the International Pragmatics Conference, Barcelona, Spain. Kekelis, L. S. & Andersen, E. (1984 ). Family communication styles and language development. Journal of Visual Impairment and Blindness, 78, 54—64. Landau, B. & Gleitman, L. R. (1985). Language and experience: ev idence from the blind child. Harvard: Harvard University Press. Loveland, K. A. (1984 ). Learning about points of view: spatial perspective and the acquisition of ‘I/you’. Journal of Child Language, 11, 535—556. Lucas, S. A. (1984 ). Auditory discrimination and speech production in the blind child. International Journal of Rehabilitation Research, 7/1, 74—76. Maxfield, K. E. (1936). The spoken language of the blind pre-school child. New York: Archives of Psychology, No. 201. McGinnis, A. R. (1981). Functional linguistic strategies of blind children. Journal of Visual Impairment and Blindness, 75, 210—214. Mills, A. E. (1983). Acquisition of speech sounds in the visually-handicapped child. In A. E. Mills (Ed.), Language acquisition in the blind child: normal and deficient. 46—56. London: Croom Helm.
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Mills, A. E. (1987). The acquisition of phonology in the blind child. In B. Dodd & R. Campbell (Eds.), Hearing by eye: experimental studies in the psychology of lipreading. 145—161. Hillsdale, NJ: Erlbaum. Mills, A. E. (1988). Visual handicap. In D. Bishop & K. Mogford (Eds.), Language dev elopment in exceptional circumstances. 150—164. Edinburgh: Churchill Livingstone. Mills, A. E. & Wegener-Sleeswijk, B. (1991). The syntactic-pragmatic interface: some blind children’s problems. Paper to the Groningen workshop on language disorders. Miner, L. E. (1963). A study of the incidence of speech deviations among visually-handicapped children. New Outlook for the blind, 57, 10—14. Mulford, R. C. (1981). Talking without seeing: some problems of semantic dev elopment in blind children. Doctoral dissertation, Stanford University, USA. Mulford, R. C. (1983). Referential development in blind children. In A. E. Mills (Ed.), Language acquisition in the blind child: normal and deficient. 89—107. London: Croom Helm. Mulford, R. C. (1989). First words of the blind child. In M. D. Smith & J. L. Locke (Eds.), The emergent lexicon: the child’s dev elopment of a linguistic v ocabulary. 136—160. New York: Academic Press. Olson, M. R. (1983). A study of the exploratory behaviour of legally blind and sighted preschoolers. Exceptional Children, 49, 130—138. Parke, K. L., Shalcross, R., & Anderson, R. J. (1980). Differences in coverbal behavior between blind and sighted persons during dyadic communication. Journal of Visual Impairment and Blindness, 74, 142—146. Perez-Pereira, M. & Castro, J. (1990 a). A pragmatic analysis of the language of a blind child compared to that of her sighted twin. Paper to International Pragmatics Conference, Barcelona, Spain. Perez-Pereira, M. & Castro, J. (1990 b). Some strategies used by a blind child in the acquisition of language. Paper to the 4 th European Developmental Psychology Conference, Stirling, Great Britain. Piattelli-Palmarini, M. (1980). Language and learning. Cambridge: Harvard University Press. Preisler, G. (1990). Communicative development in young blind children. In G. Conti-Ramsden &
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C. Snow (Eds.), Communicati v e de v elopment. 130—152. Cambridge: CUP. Prizant, B. M. (1984 ). Toward an understanding of language symptology of visually-impaired children. In A. M. Sykanda, J. E. Jan, & S. J. Blockberger (Eds.), Insight in sight. 70—87. Vancouver: CNIB. Reynell, J. (1978). Developmental patterns of visually-handicapped children. Child Care, Health and Development, 4/5, 291—303. Rogow, S. M. (1986). Semantics and the blind child. Semiotica, 62, 297—312. Rowland, C. (1983). Patterns of interaction between three blind infants and their mothers. In A. E. Mills (Ed.), Language acquisition in the blind child: normal and deficient. 114—132. London: Croom Helm. Rowland, C. (1984 ). Pre-verbal communication of blind infants and their mothers. Journal of Visual Impairment and Blindness, 78, 297—302. Schwartz, T. J. (1983). Social cognition in visuallyimpairment and sighted children. Journal of Visual Impairment and Blindness, 77, 377—381. Semzova, M. I. (1961). Besonderheiten der Erkenntnistätigkeit blinder Kinder im jüngeren Schulalter. Die Sonderschule, 6/6, 336—340. Speidel, G. E. (1989). Imitation: a bootstrap for learning to speak. In G. E. Speidel & K. E. Nelson (Eds.), The many faces of imitation in children. 15—39. Berlin: Springer. Urwin, C. (1983). Dialogue and cognitive functioning in the early language of blind children. In A. E. Mills (Ed.), Language acquisition in the blind child: normal and deficient. 142—161. London: Croom Helm. Vihman, M. M., Macken, M. A., Miller, R., Simmons, H., & Miller, J. (1985). From babbling to speech: a reassesment of the continuity issue. Language, 61/1, 397—445. Warren, D. H. (1977). Blindness and early childhood dev elopment. New York: American Foundation for the Blind. Wegener-Sleeswijk, B. (1986). Ik v oel wat geks, wat roods. M. A. thesis, University of Amsterdam, Netherlands. Workman, S. H. (1986). Teachers’ verbalizations and the social interaction of blind preschoolers. Journal of Visual Impairment and Blindness, 80, 532—534.
Anne E. Mills, Amsterdam (Netherlands)
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67. 1. 2. 3. 4. 5.
1.
Language Acquisition and Development in Persons with Mental Retardation Introduction Elements of Language Acquisition Specific Syndromes Summary References
Introduction
The American Association on Mental Retardation defines mental retardation in terms of measured intelligence and adaptive behavior. Mentally retarded persons exhibit significantly subaverage performance on standardized general intelligence tests, two or more standard deviations from the mean, associated with significant deficiencies in the ability to meet “the standards of maturation, learning, personal independence, and/or social responsibilities that are expected for his or her age level and cultural group” (Grossman 1983, 11). Language is related to both aspects of this definition. It is common to think of measured intelligence in terms of a small number of information processing activities such as stimulus encoding, memory storage, memory retrieval, metacognitive activities, and reasoning (see Carroll 1976; Sternberg 1984 ). Persons with mental retardation exhibit deficiencies in virtually all domains of cognitive functioning (see Brooks/Sperber/McCauley 1984 ; Ellis 1979). To the extent that these abilities are necessary for language acquisition, then we would expect the development of language by mentally retarded persons to be delayed. Language is also important to the adaptive functioning of retarded persons. It is an important tool for taking in knowledge, conceptualizing the world, and thinking. It also gives children a useful method for controlling their environment (Jones/Robson 1979). Therefore, language acquisition and development has been one focus of research conducted with mentally retarded persons (see e. g. Rosenberg 1982; Schiefelbusch/ Copeland 1968; Schiefelbusch/Lloyd 1974 ). This review will highlight this research. I will first review studies that examine the relationship between several components of linguistic performance and mental retardation, then focus on language functioning as it relates to several specific syndromes in mental retardation.
2.
Elements of Language Acquisition
2.1. Phonology Articulation problems are common in mentally retarded persons (see Fawcus/Fawcus 1974 ; Ingram 1976). In one study, the incidence of articulation disorders ranged from 65 to 95 percent across etiologies (Schlanger/ Gottsleben 1957), with the highest incidence reported for Down syndrome individuals. Dodd (1976) examined consonant errors in 10 mentally retarded children with Down syndrome, 10 retarded children without Down syndrome, and 10 nonretarded children. Groups were approximately matched on mental age (MA) (36 and 4 8 months) and social background. Mean chronological ages (CAs) were approximately 4 3 months in the nonretarded sample and 128 months in the retarded samples. Subjects took part in a picture naming task and a lexical imitation task. Despite extensive criticism levied against many of Dodd’s procedures (see Rosenberg 1982), some conclusions seem reasonable. In the main articulatory error categories investigated — cluster reduction, production of consonant harmony, and simplification of the phonological system (see Smith 1973) — the Down syndrome subjects made more errors than the other two groups, who did not differ on any of the measures. Also, the Down syndrome subjects’ errors did not conform to expectation based on the performance of the other mentally retarded subjects. However, it did not appear that this difference was a qualitative difference in language performance (cf. Rosenberg 1982). Stoel-Gammon (1980) studied four retarded children with Down syndrome. Mean length of utterances (MLUs) ranged from 1.22 to 2.06 and CAs from 4 6 to 75 months. Approximately three hours of spontaneous speech were recorded for each child. Her analyses of consonant errors led her to conclude the following. First, the majority of errors made by her subjects were not due to an inability to produce the sounds. Her subjects could produce most of the English phonemes. Second, the errors were regular and predictable from adult forms. Third, the errors were similar to those reported in the speech of nonretarded children of similar MLUs.
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To the extent that the findings of these studies generalize to other ability levels and etiologies, it appears that the development of the phonological system of retarded individuals is slower than that of nonretarded individuals. But, there does not appear to be a qualitative difference in phonetic processing. 2.2. Syntax The development of syntax seems to be particularly difficult for persons with mental retardation. Mentally retarded individuals exhibit deficits in the understanding and production of grammatical structures (Bridges/ Smith 1984 ; Kernan 1990), understanding various transformations (Cromer 1975), and mastering morphological structures (Dever 1972). Several examples are described in this section. Bridges/Smith (1984 ) compared the ability of 24 Down syndrome children (mean CA = 11.1 years; verbal comprehension age range 2.5 to 5.2 years) with that of 24 nonretarded children (mean CA = 3.0 years; verbal comprehension age range 2.5 to 5.2 years). Children were required to act out events in eight active and eight passive sentences. Analysis of the relationship between the ability to act out sentences and verbal comprehension age revealed that the Down syndrome and nonretarded children exhibited similar performance curves. However, the performance of the Down syndrome children lagged behind their verbal comprehension age by about one year for active sentences and one-half year for passive sentences. Kernan (1990) compared the comprehension of syntactically ordered sequence in 14 mentally retarded adults with Down syndrome (mean IQ = 56.0) and 14 without Down syndrome (mean IQ = 56.9). Subjects took part in three tasks. On Task 1, subjects manipulated objects in a sequence visually demonstrated by the experimenter. In Task 2, the visual demonstration was paired with a verbal description of the sequence and subjects were asked to verbally indicate what happened first. In Task 3, only the verbal description was provided. The sequences were either naturally or arbitrarily ordered. Both groups of subjects performed best on Task 1 and worst on Task 3. Although delayed, the retarded subjects’ pattern of performance matched that of nonretarded children and adolescents. However, the non-Down syndrome subjects out-performed the Down syndrome subjects on every task and on 36 of
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the 4 0 sentences. So, while they performed in similar fashion, the Down syndrome subjects performed at a level below that of the nonDown syndrome subjects. Abbeduto/Furman/Davies (1989) used the Test for Reception of Grammar (Bishop 1982) to examine the relationship between receptive language and cognitive development in individuals with mental retardation. Sixty school age mentally retarded subjects (IQ range 4 0 to 79) and 60 nonretarded subjects took part, with twenty subjects per group functioning at MA levels of 5, 7, and 9 years. In general, their results indicate that the receptive language of school age retarded children is below expectations based on MA. However, this deficiency did not hold up at every level of MA tested. The retarded subjects who had MAs in the 5 year range were performing at appropriate levels of receptive language, although the authors suggest that this finding may be specific to the test used. The combined results of these studies are consistent with the general literature. Syntax development follows a similar pattern for retarded and nonretarded persons. However, the development of syntax is seriously delayed, even beyond expectations based on cognitive development. In addition, it appears that this delay may be greater for retarded persons with Down syndrome relative to those of other etiologies (e. g. Evans 1977; Kernan 1990). 2.3. Semantic Processing Semantic processing is important for many aspects of linguistic competence. In this section I review studies that investigate three of these areas: (1) the understanding of semantic relations associated with the expression of simple sentences, (2) the acquisition of information about word meanings when novel words are presented in context, and (3) the content and organization of lexical memory. The relative abilities of 12 mentally retarded and 12 nonretarded individuals to understand semantic relationships expressed in various verbal context was studied by Duchan/Erickson (1976). (Twelve language-disordered children also included will not be discussed.) The mentally retarded subjects had CAs of 4 8 to 93 months, IQs of 50 to 80, and a mean MLU of 1.67. The nonretarded subjects had CAs of 18 to 31 months, and a mean MLU of 1.56. The verbal contexts were telegraphic two-word speech (grammatical morphemes absent), expanded speech (gram-
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matical morphemes present), and partially nonsensical speech. The semantic relations included agent-action, action-object, possessive, and locative. There were main effects associated with type of relation and type of utterance, but the mentally retarded and nonretarded subjects did not differ on either dimension. When matched on MLU, retarded and nonretarded children understood the semantic relations expressed in simple sentences in a similar manner. In addition, research has shown that this similarity extends to the analysis of spontaneous speech for subjects matched on MLU (Coggins 1979; Layton/ Sharifi 1979). A recent study examined the ‚fast mapping’ ability of mentally retarded children and MAmatched nonretarded children (Chapman/ Kay-Raining Bird/Schwartz 1990). Fast mapping refers to the ability to acquire information about novel word meanings after limited exposure (usually once or twice) to the word in linguistic and event contexts. Subjects were 4 8 retarded individuals with Down syndrome (mean CA = 12.54 years; mean MA = 4 .58 years) and 4 8 nonretarded children (mean CA = 4 .16 years; mean MA = 4 .71 years). They were approximately equal on vocabulatory comprehension, syntax comprehension, and expressive vocabulary. The subjects with Down syndrome exhibited an expressive language deficiency as evidenced by a fewer number of words, fewer different words, lower percent of complete and intelligible utterances, and a smaller MLU observed in a 12 minute narrative. In the exposure task, children were asked to hide objects that included an object with a novel referent (‚koob’). Various tests of comprehension and production followed. There were no significant differences in the ability of Down syndrome and nonretarded children to: (1) infer that the object and novel referent were connected (i. e., they were willing to hide the object being referred to with the novel word), (2) comprehend the novel referent after one exposure, (3) recall where the novel object was hidden, and (4 ) produce the novel referent correctly when asked. Thus, the Down syndrome subjects exhibit fast mapping skills that were similar to expectations based on MA and exceeded expectations based on expressive language abilities. The nature and organization of semantic memory has been the focus of a number of studies (e. g. Davies/Sperber/McCauley 1981; Merrill 1985; Sperber/Davies/Merrill/Mc-
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Cauley 1982; Sperber/Ragain/McCauley 1976). Sperber et al. (1976; Experiment 1) examined the availability of category information to retarded adolescents (mean IQ = 60; mean CA = 16.3 years; mean MA = 7.25 years) using a semantic priming procedure. In their version of the task, subjects labeled pictures of objects. Pictures were presented in successive pairs in which the objects were either categorically related to each other (e. g. dog-cow) or not related to each other (e. g. table-cow). When a picture is preceded by a picture of a categorically related object, the time to name the second picture of the pair is reduced. This ‚priming effect’ is assumed to reflect knowledge of the categorical relationship expressed in the two pictures (that of ‚animalness’ in the above example). In several studies, the magnitude of semantic priming exhibited by mentally retarded individuals has been found to be similar to that of nonretarded individuals (Davies et al. 1981; Sperber et al. 1976; 1982). The most detailed analysis of semantic priming indicates that the magnitude of the priming effect, and by inference knowledge of category relationships, is more related to MA than to CA (Sperber et al. 1982). But, even though mentally retarded individuals exhibit a knowledge of these category relationships, they often fail to access and use that information when it is prudent to do so (Sperber et al. 1976; Experiment 2), and when they do, they retrieve it less efficiently than do nonretarded persons (Sperber et al. 1982). It has been suggested that this latter result may be due to some general deficit in attentional processing (see Merrill 1985; Sperber/McCauley 1984). The research findings across these three aspects of semantic processing are consistent with those reported for phonetic and syntactic differences of retarded and nonretarded individuals. Semantic development follows the same general pattern, albeit delayed, for mentally retarded and normally developing individuals. 2.4. Communication Skills It is known that mothers of nonretarded children adjust their speech to the level of their children (cf. Snow 1977). Several studies have been conducted to determine whether mothers of mentally retarded children also adjust their level of speech in this fashion (e. g. Cunningham/Reuler/Blackwell/Deck 1981; Peterson/Sherrod 1982; Rondal 1978). One intent of these studies was to determine if lower
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quality verbal interactions between mothers and retarded children may inhibit their children’s language development. However, when subjects are matched on MLU, mothers of retarded and nonretarded children are similar on most syntactic, semantic, and pragmatic features of language (see e. g. Rondal 1978). The few longitudinal investigations that have been conducted also suggest that the adjustments in speech that mothers do make to their retarded children are systematically related to changes in the children’s language and general level of cognitive functioning (e. g. Mauer/Sherrod 1987; McConkey/Martin 1984). In spite of the similarities in the communication styles exhibited by mothers of retarded and nonretarded children, some important differences exist. Mothers of retarded children are more dominant and directive in their communicative style and generally less responsive to the communicative behavior of their children (Cunningham et al. 1981; Mahoney/Robenalt 1986). But, this difference in style may be related to the communicative responsiveness of the retarded children (Jones 1977; Mahoney/Robenalt 1986; Mauer/Sherrod 1987). Mentally retarded children are generally less active communicators, do not initiate communication as frequently, and exhibit poor timing in turn-taking interactions with their mothers than developmentally matched nonretarded children (Fischer 1987; Jones 1977). However, with mentally retarded children who are more active and responsive in their own communication styles, mothers are much more responsive and less dominant and directive (Mahoney 1988; Mahoney/Robenalt 1986). Whether such differences in communication style impact upon the language development of their children is a current topic of investigation (Hoff-Ginsberg 1986; Yoder 1989; Yoder/Kaiser 1989). Researchers have also investigated general communication skills of mentally retarded children and adults. The results of most studies suggest that functional communication skills of mentally retarded persons are at least on par with and may exceed expectations based on measured verbal abilities (e. g. Abbeduto/Rosenberg 1980; Bedrosian/Prutting 1978; Coggins/Stoel-Gammon 1982; Leifer/ Lewis 1984; Price-Williams/Sabsay 1979). Leifer/Lewis (1984 ) compared the conversational response skills of one group of nonretarded subjects (mean CA = 20.8 months; mean MLU = 1.25) with a group of retarded
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subjects matched on CA (mean CA = 20.5 months) but not on linguistic ability (MLU = 0), and with a group of retarded subjects matched on MLU (mean MLU = 1.12) but not on CA (mean CA = 4 .0). Children were taped in free play interactions with mothers. Children’s responses (verbal and nonverbal) were coded as appropriate if the response matched the pragmatic intent of mothers’ questions, inappropriate if they did not, and indeterminate if they were unclear. The CAmatched retarded subjects were seriously deficient in their ability to appropriately respond to mothers’ questions, whereas the MA-matched retarded subjects exhibited greater conversational response skills than the nonretarded subjects. Bedrosian/Prutting (1978) examined the communicative competence of mentally retarded adults in four conversational settings: conversations with a speech-language pathologist, with peers, with parent/guardian, and with a six-year-old nonretarded boy. The subjects were three males and one female (CAs 23—28 years; IQs 29—39). The researchers recorded conversations in each setting over a three month period. They were primarily interested in the conversational relationships of the mentally retarded in terms of the dimensions of dominance-submission and control across the various settings. Only one of the subjects ever assumed the dominant position in the conversations and was only able to do so in conversations with peers and the child. With respect to control, the authors found that the retarded individuals generally used similar types of control to those used by nonretarded adults. However, it was also noted that there were individual differences in the types and frequencies of control used by the retarded adults. Finally, all of the subjects were able to use requests for restatement to signal when a communication breakdown had occurred. Price-Williams/Sabsay (1979) recorded conversational interactions of nine institutionalized Down syndrome men (CA = 29 to 4 9 years; IQ = 17 to 26). Their communicative activities were reported to be very effective. In summarizing 15 hours of recorded conversations between the subjects and each other and the subjects and members of the hospital staff, the authors reported a wide range of communicative skills exhibited by their subject including, for example, greeting exchanges, appropriate turn-taking behaviors, and effective linguistic and nonlinguistic
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strategies for securing the attention of their intended listener. Their subjects were also able to modify conversational styles to prevent and correct failures in communication. These selected studies reveal a general asymmetry between communicative competence and linguistic competence for mentally retarded persons. Communicative competence appears to be greater than expected based on linguistic competence. However, recent data suggests that this advantage may not extend to all aspects of communication. Mundy/Sigman/Kasari/Yirmiya (1988) found that young children with Down syndrome exhibited nonverbal social interaction skills that exceeded their measured MAs, but were deficient relative to MAs in making nonverbal requests for objects or assistance with objects. It may be important to try to evaluate patterns of strengths and weakness in the communicative competence of mentally retarded persons.
3.
Specific Syndromes
Persons with mental retardation are not a homogeneous group. Mental retardation is the result of a variety of etiologies. All of these conditions do not lead to identical patterns of cognitive performance. Therefore, some discussion of how language differences manifest themselves in specific syndromes resulting in mental retardation is important. In this section I consider three syndromes: Down syndrome, fragile-X syndrome, and Williams syndrome. 3.1. Down Syndrome Down syndrome is a chromosomal abnormality resulting from the presence of extra chromosomic material in the body (from chromosome 21). The maximum level of cognitive functioning expected for most is an MA of approximately 4 —5 years. Down syndrome individuals also exhibit physical symptoms that may be associated with defective speech. Abnormalities include a larynx located too high in the neck, an edematous tongue that groves improperly for several speech sounds and is impaired in motility, and undersized mouth cavity, a protruding tongue, and hypotonia of the speech muscles (Benda 194 9; Buddenhagen 1971). They also exhibit a high incidence of auditory problems, the major cause of which is otitis media (Balkany 1980).
Language development, although delayed, is quite similar for Down syndrome and normally developing children. Menn (1985) has reported that phonological development is seriously delayed in individuals with Down syndrome. However, the sequence of development parallels that of normal children. Share (1975) observed a one-year delay in the onset of meaningful one-word utterances, but the number of words that could be understood and used was comparable to MA matched nonretarded children (Mein/O’Connor 1960). When they begin to combine two and three words in an utterance, they understand the same relational meanings as normally developing children matched on MLU (Layton/ Sharifi 1979). A conclusion of many reviews is that there is no compelling evidence of qualitative differences in language development between Down syndrome and normally developing children (Bloom/Lahey 1978; Kiemen 1985; Rosenberg 1982). Despite similarities in the acquisition of language by children with and without Down syndrome, there is a growing belief that the conclusion of language delay without deviance is not entirely correct and may be misleading (see Fowler 1990; Rondal 1988). Fowler (1990) argues for a specific syntactic deficit associated with Down syndrome, and points to a literature that indicates deficits in syntax that far exceed expectations based on general cognitive functioning (e. g. Thompson 1963; Wisniewski/Miezejeski/Hill 1988). Even in the domain of communication there appear to be asynchronies with respect to different aspects of the communication system. Lexical difficulties are less severe than syntactic difficulties (Evans 1977; Hartley 1982) and functional communication skills are often much greater than verbal ability (e. g. Coggins/Carpenter/Owings 1983; Scherer/Owings 1984). Fowler suggests that while general descriptions of language may be similar for retarded persons with and without Down syndrome, the reasons for their language delays may not be. Non-Down syndrome individuals may be limited by general intellectual ability. Down syndrome individuals may be limited by a specific language deficit (cf. Fowler 1990). 3.2. Williams Syndrome Williams syndrome is a rare metabolic disorder associated with moderate to severe mental retardation (Williams/Barrett-Boyes/ Lowe 1961). Features of the syndrome include a narrowing of the aorta, and an unu-
67. Language Acquisition and Developmentin Persons with Mental Retardation
sual facial structure consisting of a stellate or ‚starlike’ pattern in the iris, medial eyebrow flare, an upturned nose, and thick lips with an open mouth posture (Jones/Smith 1975). However, despite impairments in intellectual functioning, delays in attaining motor milestones, and early delays in language development (Thal/Bates/Bellugi 1988), older individuals with Williams syndrome exhibit a surprising facility with linguistic processing (Bellugi/Marks/Bihrle/Sabo 1988) and verbal IQ scores significantly greater than performance IQ scores (Udwin/Yule/Martin 1986). Bellugi et al. (1988) report on three Williams syndrome children. Their CAs were 11, 15, and 16 years, and full scale IQ scores were approximataly 50. They could not perform tasks that would have placed them in Piaget’s stage of concrete operations. They appeared particularly deviant on tests of spatial cognition. Their scores were low on tasks of spatial orientation, spatial arrangement, and drawing. However, they were able to quickly and accurately recognize and discriminate unfamiliar faces. So, even within the visual/spatial domain some aspects of cognition were less deviant than expected. The most striking aspect of the cognitive performance of these children was their facility with language. Bellugi et al. report vocabularies that far exceed MA expectations (ageequivalent scores of 9.0 to 11.7 years) and MLUs ranging from 8.6 to 13.1. Down syndrome individuals of similar MAs exhibited MLUs of 3.0 to 3.5. Bellugi et al. describe the expressive language of older Williams syndrome children as “complex in terms of morphological and syntactic structures including full passives, embedded relative clauses, a range of conditionals and multiple endings” (Bellugi/Marks/Bihrle/Sabo 1988, 183). On tests of grammatical comprehension, the children consistently performed at levels that exceeded MA expectations, and exhibited a high degree of metalinguistic ability in making judgements of grammaticality. Research on individuals with Williams syndrome is relatively new. A longitudinal profile of the acquisition and development of language in these individuals should prove interesting. 3.3. Fragile-X Syndrome Fragile X syndrome is a recently identified chromosome abnormality that primarily affects males. Most males affected with fragile X syndrome exhibit a large head circumfer-
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ence in infancy, long ears, a large lower jaw, and testicular enlargement in postpubertal males (Sutherland/Ashforth 1979; Turner/ Frost 1980). The majority function in the moderately retarded range, although retardation can be severe. Females may be affected, but the degree of their retardation is often less severe. Paul/Cohen/Breg et al. (1984 ) reported on three adolescents with fragile X syndrome. They had CAs of 13.75, 10.5, and 10 years and nonverbal IQs of 4 0, 50, and 70. MAs were 5.5, 5.25, and 7 years. Subjects were given a battery of speech and language evaluations, including an analysis of spontaneous speech. All children exhibited poorer performance on tests of productive syntax than on tests of receptive language, difficulties in articulation when using connected speech despite performing well on single words in tests of articulation, and poor vocal imitation performance. Sudhalter/Cohen/Silverman/Wolf-Schein (1990) compared the linguistic performance of 9 retarded males with Down syndrome (mean CA = 13.9), 12 with fragile X syndrome (mean CA = 15.65), and 12 with autism unrelated to fragile X (mean CA = 11.75). Mean scores on the Vineland Adaptive Behavior scale ranged from 50.75 to 56.33 across groups. Communication domain age equivalent scores ranged from 5.33 to 5.88. Socialization age equivalent scores were 8.34 for the Down syndrome, 6.15 for the fragile X, and 3.80 for the autistic subjects. Subjects were videotaped in a 30 minute session that consisted of 10 minutes of free play, 10 minutes of interaction with a familar adult, and 10 minutes of interaction with an unfamiliar adult. The males affected by fragile X exhibited language that was different from both the Down syndrome and the autistic individuals. The fragile X subjects engaged in more deviant language than the Down syndrome subjects, and the deviant language of the fragile X subjects was distinctly different from the language of the autistic subjects. Wolf-Schein/Sudhalter/Cohen et al. (1987) also reported that subjects with fragile X exhibited more jargon, echolalia, and perseveration in their speech than did subjects with Down syndrome. However, it is not clear from these data whether this is a pattern of deviance that is specific to fragile X syndrome or simply a pattern that distinguishes it from Down syndrome. A comparison with other etiologies will be required before this issue can be resolved.
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4.
Summary
The research discussed here indicates that mentally retarded indviduals exhibit serious deficiencies in the development of language in general, with the most severe difficulties associated with the development of syntax. However, it is clear that many persons with mental retardation exhibit very effective general communication skills. There is currently some debate as to whether or not individuals whose retardation is the result of different etiologies also exhibit diverse patterns of language development. It may be informative to examine specific patterns of language deficits as they relate to specific syndromes that result in mental retardation. But it is important to recognize that searching for language characteristics that are specific to every syndrome that results in mental retardation may not be fruitful given the variability of language skills observed both within and across etiologies (Rondal 1988).
5.
References
Abbeduto, L., Furman, L., & Davies, B. (1989). Relation between the receptive language and mental age of persons with mental retardation. American Journal on Mental Retardation, 93, 535—543. Abbeduto, L. & Rosenberg, S. (1980). The communicative competence of mildly retarded adults. Applied Psycholinguistics, 1, 405—426. Balkany, T. (1980). Otologic aspects of Down’s syndrome. Seminars in Speech, Language, and Hearing, 1, 39—57. Bedrosian, J. L. & Prutting, C. A. (1978). Communicative performance of mentally retarded adults in four conversational settings. Journal of Speech and Hearing Research, 21, 79—95. Bellugi, U., Marks, S., Bihrle, A., & Sabo, H. (1988). Dissociation between language and cognitive functions in Williams syndrome. In D. Bishop & K. Mogford (Eds.), Language dev elopment in exceptional circumstances. 177—189. New York: Churchill Livingstone. Benda, C. E. (194 9). Mongolism and cretinism. New York: Grune and Stratton. Bishop, D. (1982). Test for Reception of Grammar. Department of Psychology, University of Manchester. Bloom, L. & Lahey, M. (1978). Language dev elopment and language disorders. New York: Wiley. Bridges, A. & Smith, J. (1984 ). Syntactic comprehension in Down’s syndrome children. British Journal of Psychology, 75, 187—196. Brooks, P., Sperber, R., & McCauley, C. (Eds.)
(1984 ). Learning and cognition in the mentally retarded. Hillsdale, NJ: Erlbaum. Buddenhagen, R. G. (1971). Establishing v ocal v erbalization in mute mongoloid children. Champaign, III: Research Press. Carroll, J. B. (1976). Psychometric tests as cognitive tasks: A new look at the structure of the intellect. In L. B. Resnick (Ed.), The nature of intelligence. 27—56. Hillsdale, NJ: Erlbaum. Chapman, R. S., Kay-Raining Bird, E., & Schwartz, S. E. (1990). Fast mapping of words in event contexts by children with Down syndrome. Journal of Speech and Hearing Disorders, 55, 761—770. Coggins, T. E. (1979). Relational meaning encoded in the two word utterances of Stage 1 Down syndrome children. Journal of Speech and Hearing Research, 22, 166—178. Coggins, T. E., Chapter, R. L., & Owings, N. O. (1983). Examining early intentional communication in Down’s syndrome and nonretarded children. British Journal of Disorders of Communication, 18, 98—106. Coggins, T. E. & Stoel-Gammon, C. (1982). Clarification strategies used by four Down’s syndrome children for maintaining normal conversational interaction. Education and Training of the Mentally Retarded, 17, 65—67. Cromer, R. F. (1975). Are subnormals linguistic adults. In N. O. O’Connor (Ed.), Language, cognitiv e deficits, and retardation. 169—187. London: Butterworths. Cunningham, C. E., Reuler, E., Blackwell, J., & Deck, J. (1981). Behavioral and linguistic development in the interactions of normal and retarded children and their mothers. Child Dev elopment, 52, 62—70. Davies, D., Sperber, R. D., & McCauley, C. (1981). Intelligence-related differences in semantic processing speed. Journal of Experimental Child Psychology, 31, 387—402. Dever, R. (1972). A comparison of the results of a revised version of Berko’s test of morphology with the free speech of mentally retarded children. Journal of Speech and Hearing Research, 15, 169—178. Dodd, B. (1976). A comparison of the phonological systems of mental age matched normal, severely subnormal and Down’s syndrome children. British Journal of Communication Disorders, 11, 27—42. Duchan, J. F. & Erickson, J. G. (1976). Normal and retarded children’s understanding of speech relations in different verbal contexts. Journal of Speech and Hearing Research, 19, 767—776. Ellis, N. R. (Ed.) (1979). Handbook of mental deficiency, psychological theory and research. Hillsdale, NJ: Erlbaum.
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Evans, D. (1977). The development of language abilities in mongols: A correlational study. Journal of Menal Deficiency Research, 21, 103—117. Fawcus, M. & Fawcus, R. (1974 ). Disorders of communication. In A. M. Clarke & A. D. B. Clarke (Eds.), Mental deficiency: The changing outlook. 3rd Edition. 592—627. London: Methuen. Fischer, M. A. (1987). Mother-child interaction in preverbal children with Down syndrome. Journal of Speech and Hearing Disorders, 52, 179—190. Fowler, A. E. (1990). Language abilities in children with Down syndrome: Evidence for a specific syntactic delay. In D. Cicchetti & M. Beeghly (Eds.), Children with Down syndrome: A dev elopmental perspectiv e. 302—328. New York: Cambridge University Press. Grossman, H. J. (1983). Classification in mental retardation. Washington, DC: American Association on Mental Deficiency. Hartley, X. Y. (1982). Receptive language processing of Down’s syndrome children. Journal of Mental Deficiency Research, 26, 263—269. Hoff-Ginsberg, E. (1986). Function and structure in maternal speech: Their relation to the child’s development of syntax. Dev elopmental Psychology, 22, 155—163. Ingram, D. (1976). Phonological disability in children. New York: Elsevier. Jones, O. H. M. (1977). Mother-child communication with prelinguistic Down’s syndrome and normal infants. In H. R. Schaffer & J. Dunn (Eds.), The first year of life: Psychological and medical implications of early experience. 175—195. New York: Wiley. Jones, A. & Robson, C. (1979). Language training in the severely mentally handicapped. In N. R. Ellis (Ed.), Handbook of mental retardation, psychological theory and research. 367—400. Hillsdale, NJ: Erlbaum. Jones, K. L. & Smith, D. W. (1975). The Williams elfin facies syndrome: A new perspective. Journal of Pediatrics, 86, 718—723. Kernan, K. T. (1990). Comprehension of syntactically indicated sequence by Down’s syndrome and other mentally retarded adults. Journal of Mental Deficiency Research, 34, 169—178. Kiernan, C. (1985). Communication. In A. M. Clarke, A. D. B. Clarke, & J. Berg (Eds.), Mental Deficiency: The changing outlook. 4th Edition. 584—638. London: Methuen. Layton, T. L. & Sharifi, H. (1979). Meaning and structure of Down’s syndrome and nonretarded children’s spontaneous speech. American Journal of Mental Deficiency, 83, 439—445. Leifer, J. & Lewis, M. (1984 ). Acquisition of conversational skills by young Down syndrome and nonretarded children. American Journal of Mental Deficiency, 84, 610—618.
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Mahoney, G. (1988). Maternal communication style with mentally retarded children. American Journal on Mental Retardation, 92, 352—359. Mahoney, G. & Robenalt, K. (1986). A comparison of conversational patterns between mothers and their Down syndrome and normal infants. Journal of the Division of Early Childhood, 10, 172—180. Mauer, H. & Sherrod, K. (1987). Context of directives given to young children with Down syndrome and nonretarded children: Development over two years. American Journal of Mental Deficiency, 91, 579—590. McConkey, R. & Martin, H. (1984 ). A longitudinal study of mothers’ speech to preverbal Down syndrome infants. First Language, 5, 41—55. Mein, R. & O’Connor, N. (1960). A study of oral vocabularies of severely subnormal patients. Journal of Mental Deficiency Research, 4, 130—143. Menn, L. (1985). Phonological development: Learning sounds and sound patterns. In J. BerkoGleason (Ed.), The de v elopment of language. 77—113. Columbus, Ohio: Merrill. Merrill, E. C. (1985). Differences in semantic processing speed of mentally retarded and nonretarded persons: Comparison of short- and longterm memory processing. American Journal of Mental Deficiency, 90, 71—80. Mundy, P., Sigman, M., Kasari, C., & Yirmiya, N. (1988). Nonverbal communication skills in Down syndrome children. Child De v elopment, 59, 235—249. Paul, R., Cohen, D. J., Breg, W. R., Waxton, M., & Herman, S. (1984 ). Fragile X syndrome: Its relationship to speech and hearing disorders. Journal of Speech and Hearing Disorders, 49, 328—332. Peterson, G. & Sherrod, K. (1982). Relationship of maternal language to language development and language delay of children. American Journal of Mental Deficiency, 86, 391—398. Price-Williams, D. & Sabsay, S. (1979). Communicative competence among severely retarded persons. Semiotica, 26, 35—63. Rondal, J. (1978). Maternal speech to normal and Down’s syndrome children matched for mean length of utterance. Monograph of the American Association on Mental Deficiency. Washington, D. C.: American Association on Mental Deficiency. Rondal, J. (1988). Down’s syndrome. In D. Bishop & K. Mogford (Eds.), Language dev elopment in exceptional circumstances. 165—176. New York: Churchill Livingstone. Rosenberg, S. (1982). The language of the mentally retarded: Development, processes and intervention. In S. Rosenberg (Ed.), Handbook of applied psycholinguistics: Major thrusts of research and theory. 329—392. Hillsdale, NJ: Erlbaum. Scherer, N. J. & Owings, N. O. (1984 ). Learning to be contingent: Retarded children’s responses to
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their mothers’ requests. Language and Speech, 27, 255—267. Schiefelbusch, R. & Copeland, R. (Eds.) (1968). Language and mental retardation: Empirical and conceptual considerations. New York: Holt, Rinehart and Winston. Schiefelbusch, R. L. & Lloyd, L. L. (Eds.) (1974 ). Language perspectiv es — Acquisition, retardation, and interv ention. Baltimore, Md: University Park Press. Schlanger, B. B. & Gottsleben, R. H. (1957). Analysis of speech defects among the institutionalized mentally retarded. Journal of Speech and Hearing Disorders, 22, 98—103. Share, J. B. (1975). Developmental progress in Down’s syndrome. In R. Koch & F. F. de la Cruz (Eds.), Down’s syndrome (mongolism): Research, prev ention, and management. 78—86. New York: Bruner/Mazel. Smith, N. V. (1973). The acquisition of phonology. Cambridge: Cambridge University Press. Snow, C. (1977). Mother’s speech research: From input to interaction. In C. E. Snow & C. A. Furguson (Eds.), Talking to children: Language input and acquisition. 1—37. Cambridge: Cambridge University Press. Sperber, R. D., Davies, D., Merrill, E. C., McCauley, C. (1982). Cross-category differences in the processing of subordinate-superordinate relationships. Child Development, 53, 1249—1253. Sperber, R. D. & McCauley, C. (1984 ). Semantic processing efficiency in the mentally retarded. In P. Brooks, R. Sperber, & C. McCauley (Eds.), Learning and cognition in the mentally retarded. 141—163. Hillsdale, NJ: Erlbaum. Sperber, R. D., Ragain, R. D., & McCauley, C. (1976). Reassessment of category knowledge in retarded individuals. American Journal of Mental Deficiency, 81, 227—234. Sternberg, R. J. (1984 ). Toward a triarchical theory of human intelligence. Brain and Behav ioral Sciences, 7, 269—315. Stoel-Gammon, C. (1980). Phonological analysis of four Down’s syndrome children, Applied Psycholinguistics, 1, 31—48. Sudhalter, V., Cohen, I. L., Silverman, W., & WolfSchein, E. G. (1990). Conversational analyses of
V. Pathologies and Disorders of Language Development
males with fragile X, Down syndrome, and autism: Comparison of the emergence of deviant language. American Journal on Mental Retardation, 94, 431—441. Sutherland, G. R. & Ashforth, P. L. (1979). Xlinked mental retardation with macroorchidism and the fragile X site Xq27 or 28. Human Genetics, 48, 117—120. Thal, D., Bates, E., & Bellugi, U. (1988). Language and cognition in two children with Williams syndrome. Journal of Speech and Hearing Research, 32, 489—500. Thompson, M. M. (1963). Psychological characteristics relevant to the education of the pre-school mongoloid child. Mental Retardation, 1, 148—151. Turner, G. & Frost, D. (1980). X-linked mental retardation, macroorchidism, and the Xq27 fragile site. Journal of Pediatrics, 96, 837—841. Udwin, O., Yule, W., & Martin, N. D. T. (1986). Age at diagnosis and abilities in idiopathic hypercalcaemia. Archiv es of Disease in Childhood, 61, 1164—1167. Williams, J. C. P., Barrett-Boyes, B. G., & Lowe, J. B. (1961). Supravalvular aortic stenosis. Circulation, 24, 1311—1318. Wisniewski, K. E., Miezejeski, C. M., & Hill, A. L. (1988). Neurological and psychological status of individuals with Down syndrome. In L. Nadel (Ed.), The psychobiology of Down syndrome. 315—343. Cambridge, MA: MIT Press. Wolf-Schein, E. G., Sudhalter, V., Cohen, I. L., Fisch, G. S., Hanson, D., Pfadt, A. G., Hagerman, R., Jenkins, E. C., & Brown, W. T. (1987). Speech-language and the fragile-X syndrome: Initial findings. Journal of the American Speech and Hearing Association, 29, 35—38. Yoder, P. J. (1989). Maternal question use predicts later language development in specific language disordered children. Journal of Speech and Hearing Disorders, 54, 347—355. Yoder, P. C., & Kaiser, A. P. (1989). Alternative explanations for the relationship between maternal verbal interaction style and child development. Journal of Child Language, 16, 141—161.
Edward C. Merrill, Tuscaloosa, Alabama (USA)
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68. Patterns of Interaction and Communication in Language Development Disorders 1. 2. 3. 4. 5.
1.
Introduction Input: Mothers’ Speech to Language Disordered Children Discourse Features in Language Disordered Children The Concept of Maternal Adjustment Revisited References
Introduction
Many developmental psychologists espouse the meta-theory or ‚philosophy’ that caregiver-child interactions are an important source of the child’s development. That the child does not acquire his/her abilities in a social vacuum is especially true in the case of language development. The child needs a language environment and a caregiver for communicative and interactive exchanges. He/she would not be able to acquire language just by listening to the radio or television (e. g. Sachs/Bard/Johnson 1981). The so-called Motherese research has furnished the very important result that mothers talk in a different way to their languageacquiring children than to older children and adults. They use a special speech style which can be characterized by various features on molecular and molar level. Although many empirical findings take conflicting sides in the question whether certain types of features are conducive to language growth or not, the correlational research to date suggests that at least the following six structures and interactive features of the mothers’ input exert an influence on the child’s rate of language acquisition (Cross 1978, Hoff-Ginsberg 1985, 1986, Nelson/Carskaddon/Bonvillian 1973, Newport/Gleitman/Gleitman 1977, OlsenFulero 1982, Smolak/Weinraub 1983, for summary see Grimm 1990, Hoff-Ginsberg/ Shatz 1982, Menyuk 1988): Frequency of — inverted yes/no questions — wh-questions — partial repetitions of child’s utterances — partial self-repetitions with or without modifications — expansions — conversation-eliciting questions or, more generally speaking, a conversation eliciting maternal interaction style.
The theoretically significant question is how to conceptualize the underlying functional relationships that lead to the empirically established correlations. In the literature these data patterns are mainly interpreted within a ‚maternal influence model’ (Yoder/Kaiser 1989). Specifically it is asked how these structural or interactive features of maternal language can directly or indirectly influence language acquisition. It would certainly be shortsighted to assume very simple effects. There is no direct transfer from the maternal mouth into the child’s mind. It is the child who must make the language input offered to him usable for himself. Since we cannot look into children’s heads, we can only offer theoretically plausible interpretations as to how a facilitation effect may come about (Grimm 1990, Hoff-Ginsberg 1986). Obviously, a specific structural or interactional feature or cluster of features may have many “properties at different levels that make them both communicatively salient and linguistically informative” (Hoff-Ginsberg/Shatz 1982, 9) and thus may help the child directly or indirectly in solving the language learning problem (a) by highlighting and exemplifying structural characteristics and (b) by eliciting conversation and thus increasing the opportunity for language learning. In the following we will mention a few exemplary interpretations to illustrate the reasoning within this research tradition (for a more detailed discussion see e. g. Hoff-Ginsberg/Shatz 1982). The most robust finding is that mothers’ use of auxiliaries in inverted yes/no questions influences the rate at which their children develop the auxiliary system. Since the auxiliaries appear in first position in such sentences (“Have you seen this?”, “Will you pick up the doll?”) they are perceptively salient and are particularly taken note of by children. It is also true for wh-questions (“Where do you want to go?”, “What is this?”) that the elements of verb phrases are made prominent by the transformation of the canonical sentence structure. Partial repetitions of the mother’s own or of the child’s utterances might help in segmentation and in specifying constituent boundaries. For example, when the mother says “Du kannst die Tassen hierher stellen. Die Tassen. Hierher.” [“You can put the cups here. The
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cups. Here.”] she illustrates the particular structural segments of the sequence, thereby facilitating the identification of these segments for the child. The positive influence of expansions could result from the fact that the child can compare two consecutive utterances with each other (Grimm 1985). When the child says “Ich bin des, ich Fuß brocht” [“That’s me, I broken foot”] and the mother responds “Das bist du, als du den Fuß gebrochen hast” [“That’s you when you broke your foot”] then it appears as if the mother were teaching language with intent. She offers the child something like a good verbal form or ‚gestalt’ for the intended content. Thus the child has the opportunity to compare his/her own utterance with this model and can recognize where words have been corrected or added. As Hoff-Ginsberg (1986) has shown, conversation-eliciting speech (in contrast to simple directive speech, see Olsen-Fulero 1982) may also facilitate language acquisition because it encourages the child to produce and practice language. Pure quiz questions such as “What does the cow say?” display no or even a negative empirical relationship to language acquisition. These questions are simple to answer and do not challenge the child’s language production abilities. Real information-demanding questions and reflexive questions, however, are suited to get the child working on language. For example, if the child’s previous utterance was not understood, he/she must try to reformulate it in order to express more clearly what he/she wants to say. Obviously the assumption that some specific structural and/or interactional features might aid language acquisition throughout the course of development is theoretically and empirically unwarranted. In fact, it has been proposed that fine-tuning in the sense of the continual adjustment of child-directed speech to a child-appropriate level is an important candidate for facilitating language acquisition (e. g. Cross 1977). However, the empirical findings are somewhat at odds so that at best there is mixed evidence for the language facilitating influence of fine-tuning (for a review see Snow/Perlmann/Nathan 1987). It is nevertheless important to raise this issue here, since the question whether and in which ways mothers of language disordered children adjust themselves semantically and syntactically to the language level of their children plays an important role in determining the com-
V. Pathologies and Disorders of Language Development
municative environment of these children, as will be shown later in this chapter. The research on language input to language disordered children addresses four main questions: (a) Are the grammatical features and interactional patterns similar to those provided to normally developing children? (b) Are there differences in the directiveness and the initiative behavior between mothers of language disordered children and those of normal language children? Should one interpret these differences in the sense of a child-driven maternal adjustment or rather as an instructional intent? (c) What are the consequences of the language environment provided to disordered children on the language development of these children? (d) What are the consequences of the language input on the cognitive development of the child? Of course we will not be able to give any final answers to these questions; the number of comparative studies is too limited. There is especially a lack of longitudinal and followup studies so that reflections on the consequences of mother’s language input must remain highly speculative. As we will see, with a few exceptions all studies involved English-speaking children. Consequently, the validity of the inferences drawn must be quite limited. During the last few years research with normally developing children which has taken a ‚cultural context’ view has questioned the supposition that there is a best way to speak to children in order to facilitate language development (see for example Shatz/Grimm/Wilcox/NiemeierWind in press). However, research on language disordered children is still determined by the assumption that there must be a generally valid way of ‚teaching’ language. This, however, can only be demonstrated on the basis of intercultural studies. This review focuses on the four main questions already outlined. In particular dyads with specifically language impaired (SLI) or (to use another term) dysphasic children, with autistic children, and with mentally retarded children are included. Whereas at least in previous studies the question was discussed whether the language input to SLI children and to autistic children is deficient and causally responsible for these children’s develop-
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mental disorder, the speech style in the case of mental retardation has always been interpreted as being reactive. Dealing with these three different developmental disorders together only makes sense if we can expect to find similar input structures and interactional patterns. However, this does not exclude the possibility that there may also be communication patterns which are specific to one of the forms of language disorder. The material cited is selective. This is partly to keep this review within bounds but primarily because we wish to report results that are based on a fairly sound methodology. The following restrictions in the coverage should thus be noted. We will neither take into consideration studies with poorly defined or very small samples, nor studies with inadequate statistical data analysis or where it is unclear according to which criteria the material was analyzed. Further, we will not consider comparisons between mothers and fathers or other adults nor will we report on peer interactions. There are simply too few empirical studies in these areas, and those existing are theoretically not very convincing. Thus, for example, it remains completely open to which theoretical conclusions differences in speech style between mothers and fathers can lead.
2.
Input: Mothers’ Speech to Language Disordered Children
2.1. General Interaction Variables The quality of the dialogue between mother and child can be evaluated according to whether they have a ‚common ground’ and whether their communicative exchange displays reciprocity. It is certainly true that the child’s willingness to actively use language for communication depends on the quality of the dialogue. And the engagement in communication again has to do with language acquisition. These relationships have induced researchers of language development disorders to investigate the hypothesis that the quality of communicative exchanges between mothers and their disordered children is poorer than the quality of exchanges with normal children. A very robust result is the finding that mothers of SLI children as well as mothers of mentally retarded children show far more directiveness than mothers of normal chil-
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dren. This result remains valid independent of whether the control children were matched according to language level, mental age, or chronological age. Nearly all studies showed the concurrent result that the mothers of the SLI children use significantly more initiatives and imperatives than mothers of normal children (Bondurant/Romeo/Kretschmer 1983, Conti-Ramsden 1990, Conti-Ramsden/FrielPatti 1983, Grimm 1983, Moseley 1990). On the basis of a rating with the Caldwell Inventory of Home Stimulation Wulbert/Inglis/Kriegsmann/Mills (1975) found additional evidence that the mothers of SLI children displayed less emotional and verbal responsiveness and less involvement than mothers of age-matched normal controls and of Down syndrome children. Since comparatively low Caldwell scores were found through the socioeconomic strata, it appears justified to conclude that language impairment had a stronger influence on the mother-child relationship than socioeconomic factors. That the higher proportion of directive utterances in mothers of SLI children also holds across differing situations has been clearly demonstrated by Bondurant/Romeo/ Kretschmer (1983). They compared the language behavior of 14 mothers with 2;5—5;0year-old SLI children to 14 mothers with agematched normally developing children in a structured and in an unstructured situation. In the unstructured (15-minute) free play situation “each mother and her child were seated on the floor facing each other with (preselected) toys on the floor between them. ... The mother was then instructed to encourage her child to play with the toys.” (Bondurant/Romeo/Kretschmer 1983, 235). In the structured situation mother and child were again seated on the floor facing each other. But only the mother, not the child, “was able to see a constructed model farm built from a commercially produced set. A comparable set was scattered on the floor” (235) and the mother was instructed to help her child build the farm. In both situations the mothers of the SLI children showed significantly less acceptance utterances; in the structured situation they asked significantly less questions and — most interestingly — in the free play situation they provided over twice as many directions and produced numerically more rejection utterances in comparison to the mothers of the normal children. The authors therefore ascertain quite correctly that “the mothers of the language de-
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layed were extremely more directive than the mothers of normal children” (240). It is quite impressive that alone 8 of 13 analyzed studies with mentally retarded children likewise produced evidence that the mothers display pronounced directive behavior (Cardoso-Martins/Mervis 1985, Cunningham/Reuler/Blackwell/Deck 1981, Davis/Stroud/Green 1988, Eheart 1982, Hanzlik/ Stevenson 1986, Mahoney/Fors/Wood 1990, Maurer/Sherrod 1987, Tannock 1988). Cunningham et al. (1981) examined the verbal and behavioral interactions of 18 mothers with their mentally retarded and 18 mothers with their normal children matched for socioeconomic status and for mental age as indicated by the Peabody Picture Vocabulary Test Score. The dyads were observed in 15-minute free play and 15-minute structured task situations. During free play the mothers were instructed to interact with their child as they might do at home; in the structured task they had to have their child tidy up the toys and complete three puzzles. Compared to the controls the mothers of the mentally retarded were much more directive during both settings, i. e., they exerted more control over their children’s play and gave more commands and command-questions (cf. however, Davis/Stroud/Green 1988). On the other hand, their children proved less interactive. Thus the results of Cunningham/Reuler/ Blackwell/Deck (1981) as well as the studies of Eheart (1982) and Tannock (1988) have been interpreted to suggest that the mothers’ directive behavior is dependent on the passivity of their mentally retarded children. In Tannock’s study the mothers of 11 mentally retarded and 11 normal children individually matched for communicative ability, mental age and demographic variables were observed while interacting with their children during 15-minute free play situations. The mothers of the retarded children not only exhibited a higher level of interactional activity than the control mothers; in addition, an inverse relationship between mother’s and child’s interactional activity was observed. The partial correlations controlling for variations in children’s level of communication were highly significant, the partial correlation being rp = —.80 for retarded and rp = —.74 for nonretarded dyads (Tannock 1988, 161). The reason why the frequent initiatives and imperative utterances of the mothers of language disordered children are likewise to be regarded as reactive behavior and not in the
V. Pathologies and Disorders of Language Development
sense of a trait is because the language disordered children behave very passively in dialogue. We will return to this aspect later. At this point it is important to recognize that the high directiveness of mothers of language disordered and of mentally retarded children does not necessarily imply a low sensitivity and responsiveness (see e. g. Crawley/Spiker 1983), as some authors seem to claim. In fact the mothers do display responsiveness in the sense that they react to their children’s language behavior. Thus only very occasionally has empirical evidence been brought (e. g. Cunningham/Reuler/Blackwell/ Deck 1981, Eheart 1982, Wulbert/Inglis/ Kriegsmann/Mills 1975) that these mothers show lower responsiveness than the mothers of normal children. There are, however, far more indications that the way in which the mothers of the developmentally disordered respond to their children’s behavior differs from that of normal children’s mothers. Thus Cross (1981) ascertained that mothers of SLI children produce significantly more non-informative responses than mothers of normal, language age-matched children. In addition, Moseley (1990) found that the mothers of SLI children produced 4 0% nonsustaining utterances whereas the mothers of the MLUmatched normal controls produced only 21%. Further, the mothers of SLI children significantly more often used recasts as ‚meaning illocutions’ (requests, assertives, directives) than as ‚cohesion illocutions’ (responsives, regulatives) in comparison to mothers of MLU-matched control children. The higher frequency of the ‚meaning illocutions’ is interpreted by Conti-Ramsden (1990, 269) as “effort to actively engage the child in dialogue and maintain the interaction, or a consequence of interacting with a passive partner in conversation”. However, this interpretation does not help in understanding why the mothers’ utterances are so often semantically unrelated to their children’s utterances. For example Mahoney/Fors/Wood (1990) found that mothers of mentally retarded children used more ‚mands’ that were not systematically linked to their children’s behavior than control mothers. Very important is also the additional observation that they directed their ‚attention requests’ onto things that were not within their children’s attentional focus. The conclusion that the mothers of retarded children make only restricted attempts to provide a shared focus of attention and to elaborate on a semantic topic
68. Patterns of Interactionand Communication in Language Development Disorders
with their children is also supported by the finding that they introduce more ‚topic switches’ (Tannock 1988) than control mothers and that they more frequently use semantically unrelated utterances (Peterson/Sherrod 1982). An interesting aspect is that in the same study the mothers of the SLI children produced even more semantically unrelated utterances than the mothers of the mentally retarded children. Whereas the findings with regard to mothers of language disordered and mentally retarded children are very similar, the results from studies involving mothers of autistic children take another track. Earlier studies have postulated that deficient parent-childinteractions play a causal role with regard to the language deficits of autistic children, the mothers in particular being blamed for being poorer at communicating meaning and mood, being less responsive to the children’s requests and giving poorer instructions and more ambiguous information than mothers of normal children (Goldfarb/Goldfarb/Scholl 1966, Goldfarb/Yudkovitch/Goldfarb 1973). That the low frequency of language in autistic children may be caused and maintained by a lack of reinforcement for verbalization, a lack of encouragement to speak, and a lack of correction of language has been suggested by Howlin/Cantwell/Marchant et al. (1973). Basing on psychoanalytical theory the social environment on the whole was made responsible for the genesis of autism. It was claimed that the mothers were not warm, supportive, and accepting, but cold, rigid, and rejecting (e. g. Bettelheim 1967; see also art. 78). However, all these assumptions have proved to be untenable. In a study by Rutter/ Bartak/Newman (1971), the behavior of mothers and fathers of 14 intelligent autistic children (“purest kind of autism”) and 11 children suffering from developmental receptive aphasia was evaluated. There were no differences in the ratings for the categories ‚emotional warmth’, ‚empathy’, and ‚enthusiasm’. In accordance with this, comparisons between parents of autistic children and MLU-matched normal children have not furnished any differences with regard to reinforcement of vocalizations, encouragement to speak, or correcting of errors (Wolchik 1983, Wolchik/Harris 1982). Wolchik compared 10 mothers and fathers of autistic children at the age of 29—74 months and with average intelligence (again “purest kind of autism”) with 10 mothers and fathers of MLU-
701
matched control children between the age of 6 and 25 months. Since, as already pointed out, no differences in reinforcement, encouragement, and correction behavior could be found, the conclusion appears justified that deviant parent-child verbal interactions do not play an etiological part in the language disabilities of autistic children (Wolchik 1983, 177). However, this conclusion, although certainly correct, does not necessarily imply that the language environment is optimal for the language development of the autistic child. It could perhaps be the case that the autistic child might need a special and enriched language model. Whereas Wolchik’s study only involved parents of higher functioning autistic children, a recent study by Konstantareas/ Zajdeman/Homatidis/McCabe (1988) compared the maternal speech styles of 10 verbal and higher functioning with 10 nonverbal and lower functioning autistic children as the “two main subgroups of the heterogeneous population of autistic children” (64 9). The higher functioning children (2 f, 8m) were between 28 and 112 months old and had a nonverbal IQ between 68 to 117; their language level lay between 2 and 7 years. The lower functioning children (2 f, 8m) were between 29 and 117 months old; they had no speech and an IQmeasurement could not be made. Of 10 investigated assumptions 7 could be confirmed: (a) the mothers of the lower functioning autistic children control their children’s actions more, reinforce more motoric behavior and use shorter MLUs. (b) The mothers of the higher functioning autistic children answer questions more often and also offer more prompts for spoken language, they expand correct spoken language more often, reinforce more language related behavior, and have longer MLUs. As with the mothers of the mentally retarded and the SLI children, directiveness is interpreted as reaction to difficulties on the part of the child. In summary: In order to evaluate the affective and communicative quality of the mother-child dialogue it was investigated on the molar level whether mothers of developmentally impaired children differ — among other characteristics — in their responsiveness, directiveness and emotional warmth from mothers whose children do not display any developmental disorders. The main result is that the dialogues with the disordered children are more unbalanced in that these mothers direct and maintain the dialogue by means
702
of their initiatives far more than the mothers of normal children. This directive behavior is mainly interpreted as being adaptive in the cases of language impaired, mentally retarded, and autistic children. The mothers are guided to their own behavior style by their children’s passivity. That this reaction can be connected with semantically unrelated utterances and with unmotivated topic changes, i. e. with communication styles which do not fulfill the functions of encouraging language usage in the child, will be treated in more detail later in this chapter. 2.2. Structural Properties of Mother’s Speech It is plausible to assume that children will develop problems in acquiring language when their language input is poor and restricted. On the molecular level the data-providing function (see Hoff-Ginsberg 1986) of mothers’ speech can be studied in at least two respects. On the one hand we can analyze the maternal language input according to its structural features and investigate — among other things — how long and complex the utterances are, whether certain word orders predominate or whether certain word classes such as prepositions are used. On the other hand we can investigate the so-called ‚language teaching strategies’ the mothers use. In order to do this we need to accomplish a formal on-line analysis of dialogue. The aim is to find out whether and how often mothers directly tack on to their children’s utterances by repeating, correcting, or expanding them. It is rather surprising that up to now studies have shown only few or even no differences at all in the structural and strategic characteristics of the mothers of dysphasic, mentally retarded, or autistic children as compared to the mothers of normal children matched according to the level of their cognitive and/or language development. 2.2.1. Grammatical Features Studies for example by O’Kelly-Collard (1978), Rondal (1978), Cunningham/Reuler/ Blackwell/Deck (1981), and Davis/Stroud/ Green (1988), have revealed that the utterances of mothers of mentally retarded children do not differ significantly from utterances of mothers of normal children in terms of MLU, number of propositions per utterance, sentence complexity, and in the number of ungrammatical sentences. The assumption
V. Pathologies and Disorders of Language Development
that the mothers of developmentally disordered children formally adapt to their child’s language ability is also supported for autistic children: Findings reported by Konstantareas/Zajdeman/Homatidis/McCabe (1988) show that the mothers of lower functioning autistic children produced utterances with shorter MLU than mothers of higher functioning autistic children. One of the main hypotheses in searching for the causes of specific language impairment was that the maternal language input is deficient and therefore not suitable to serve as a model for language learning. This hypothesis was self-evident since SLI children do not display any obvious neurological, sensory, or cognitive disorders which could account directly for their language deficits. Interestingly, it was the failure to prove that mothers of dysphasic children offer their children a clearly deficient language model (see Leonard 1987 for a review) which stimulated highly sophisticated studies focusing on causal factors in the SLI children themselves. Even though there is a strong tendency to believe that the language of mothers of dysphasic children does not differ in its structural characteristics from that of mothers of language-matched normal children (see e. g. Cunningham/Siegel/van der Spuy et al. 1985, Grimm 1987, Grimm/Weinert 1990, Lasky/ Klopp 1982, Peterson/Sherrod 1982), contradicting empirical evidence must also be considered in order to modify the over-simplified hypothesis that the mothers of the dysphasic children are completely adapted to their children’s developmental level. For example Cross (1981), who compared the utterances of 10 mothers of SLI children between the ages of 3;10 and 5;1 years with the utterances of 10 mothers of normal language-matched children between the ages of 1;8 and 2;6 years, drew attention to evidence that the mothers of the SLI children produced significantly more unintelligible, disfluent, totally degraded, and run-on sentences; in addition they produced significantly less utterances per turn (but see Peterson/Sherrod 1982). In a comparative study with 10 mothers of SLI children (2;11—5;5 years) and 10 mothers of younger children (1;7—3;1 years) Schodorf/ Edwards (1983) found that the first group of mothers, in addition to more sentence fragments and fewer words also produced sentences with a lower MLU. Accordingly, the authors state that the SLI child is exposed to a different type of linguistic environment; the child received a shorter, simpler input during
68. Patterns of Interactionand Communication in Language Development Disorders
a teaching situation, and overall reduced input, in terms of total utterances spoken by the parents, during free play (Schodorf/Edwards 1983, 79). 2.2.2. Specific Discourse Features In their study Schodorf/Edwards (1983) also made out distinct differences in the so-called ‚language teaching strategies’: the mothers of the SLI children (SLI mothers) responded to their children’s utterances significantly less often with expansions and ready-mades but more often with corrections. Moseley (1990) found supportive data that the SLI mothers also imitate their children’s utterances significantly less often. In clear contradiction to this, however, Cross (1981) discovered significantly more imitations of their children’s utterances in the SLI mothers. However, with respect to expansions, her data again do correspond to those presented by Schodorf/Edwards (1983). In contrast to the findings cited above, Lasky/Klopp (1982) could not find any differences in the language teaching strategies at all. This overall similarity between groups of mothers parallels the results of studies comparing mother-child dyads with languagematched control children to dyads with mentally retarded (Gutman/Rondal 1979, O’Kelly-Collard 1978, Peterson/Sherrod 1982, Rondal 1978) and autistic children (Wolchik 1983, Wolchik/Harris 1982). It is also supported by Grimm (1984 , 1986, 1987) in a study involving German-speaking SLI children. The utterances of the mothers of 8 dysphasic children (ages: 3;9—4 ;8 years) and 8 MLU-matched normally developing children (ages: 2;1—2;11 years) were compared in a longitudinal design. At the first investigation timepoint the mothers of the dysphasic and control children were remarkably similar in their tendency to imitate, to correct, and to transform their children’s preceding utterances or parts thereof. One year later the mothers still did not differ significantly in their imitations and corrections. However, they now did differ significantly in the frequency of transforming their child’s immediate preceding utterance. These transformations consist in systematic variations of the sentence pattern underlying the child’s utterance, for example, in formulating the child’s question as an answer and vice versa (e. g.: Child: “Wo is mein Buch?” [“Where is my book?”] — Mother: “Da ist dein Buch.” [“There is your book”]. Child: “Der kann das
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nicht” [“He can’t do it.”] — Mother: “Kann der das nicht?” [“Can’t he do it?”]). As argued by Grimm (1987, 19), the mothers of the dysphasic children employ this constructive teaching strategy significantly less often than the mothers of the normal children at the timepoint “at which the children have learned to articulate correctly and form simple sentences with correct word order”. This form of reacting to the child’s language progress is difficult to understand given the fact that the mothers of the normal children responded to the language progress of their children significantly more often with these teaching strategies. Could it be that the mothers of the dysphasic children were already satisfied with their children’s progress and that they believed their children were not capable of learning much more? If this were actually the case, their language behavior could be interpreted as an adaptation to a consistently low level of competence. Or do the mothers consider their children to have made such good progress that they no longer need so much support as they used to? This could then probably be interpreted as an overestimation of the child’s independent learning ability. Of course, we do not really know the reasons and can only speculate. The fact remains, however, that in contrast to the mothers of normally developing children the mothers of developmentally disordered children at some point in development seem to make comparatively less effort to demonstrate syntactic rules to their children by using systematic variation of their child’s sentence patterns. It is an open question why this is so and why they do not on the contrary continue to support their children in their laborious language progress by offering them an enriched language input. In any case it might be presumed that the mothers of the dysphasic children were less finely-tuned to their children’s language progress than the mothers of normally developing children. In summary, some investigations clearly indicate that mothers of developmentally disordered children as well as mothers of language-matched or mental age (MA) matched normal children formally adapt their speech to their child’s level of language development; in addition they both use various language teaching strategies. However, there might be differences in the processes and results of calibration (see also Cunningham/Reuler/ Blackwell/Deck 1981 for dyads with retarded children).
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In his review, Leonard (1987) stressed the finding that mothers of SLI children react quite as sensitively to their children’s language abilities as mothers of normal language children. From this he inferred that speech input characteristics cannot be the stuff from which theories of specific language impairment or developmental dysphasia should be made. We feel that the last word has not yet been spoken. The findings of Cross (1981), Cunningham/Reuler/Blackwell/Deck (1981), Grimm (1987), Lasky/Klopp (1982), and Schodorf/Edwards (1983) should stimulate further longitudinal studies over a longer period of time on the reciprocal relationship between the maternal language model and the language progress made by developmentally disordered children.
3.
Discourse Features in Language Disordered Children
3.1. Participating Behavior We have already seen that mothers of disordered children usually show more initiatives than mothers of MA- or language-matched controls. This could be interpreted on the one hand as a ‚dynamic adaptation’ in the sense that the mothers try “to increase the participation of a developmentally immature child” (Tannock 1988, 155) and thus “may facilitate the child’s development of conversational skills”. On the other hand it is also reasonable to suspect that the mothers’ pronounced initiative behavior is not child-driven but is controlled by an instructional intent on the mother’s part to teach her developmentally disordered child something. The mothers so to say take up the reins in order to promote their child’s learning process. We will discuss these two propositions later in detail. The point to be made here is that based on either of these theoretical accounts the prediction can be derived that disordered children are less active in dialogue than normally developing children are. A pronounced passivity is predicted either as a response to maternal control behavior, i. e. the high directive and initiative behavior of their mothers, or as stimulating this maternal behavior. First of all, there is convincing empirical evidence that disordered children produce comparatively less initiatives in dialogue. This has been shown for mentally retarded children (Cunningham/Reuler/Blackwell/Deck 1981, Eheart 1982; but see Mahoney/Fors/
Wood 1990, Tannock 1988 for less clear empirical evidence) compared to younger MAor language-matched controls as well as for SLI children compared to language or agematched controls (Conti-Ramsden 1990, Conti-Ramsden/Friel-Patti 1983, 1984 , Cunningham/Siegel/van der Spuy et al. 1985, Moseley 1990). In addition there are some studies indicating that disordered children may be less responsive in dialogue (Cunningham/Reuler/ Blackwell/Deck 1981, Eheart 1982, Mahoney/ Fors/Wood 1990), but the results are by no means clear cut. For example, Eheart (1982) compared the responsiveness of 8 mentally retarded children (age: 3;3—4 ;9) and 8 younger normally developing children (age: 2;0—2;7) matched for play behavior. Although the mentally retarded children responded to their mother’s initiations significantly more often in terms of absolute frequencies, the differences in the percentages of responding pointed in the opposite direction, since their mothers initiated twice as many interactions as the mothers of the controls did. In the study of Tannock (1988) the retarded children again did not differ in their conditional probability to respond given the mother had taken a turn. And finally, in the study by Cunningham/Reuler/Blackwell/ Deck (1981) the tendency to show lower responsiveness was more pronounced for the retarded children with low compared to high MA. Thus, although developmentally disabled children seem to be less initiative and more passive in dialogue, the empirical evidence suggests that they do not ignore their mother’s questions and initiations, but — like normal children — share their mother’s focus of attention (e. g. Leonard 1986, Moseley 1990 for SLI children; Eheart 1982, Mahoney/Fors/Wood 1990, Tannock 1988 for mentally retarded children). Obviously this cannot hold for autistic children, since a “pervasive lack of responsiveness to other people” (American Psychiatric Association) is one of the diagnostic characteristics of these children. Thus, the 18 autistic children studied by Sigman/Mundy/Sherman/ Ungerer (1986) displayed a much lower frequency of attention sharing behavior with their caregivers than either of two MAmatched control groups of mentally retarded and normally developing children. Interestingly enough, this study also suggests that even autistic children may be responsive to some maternal directions. Actually, the autis-
68. Patterns of Interactionand Communication in Language Development Disorders
tic children under study appropriately responded to positive maternal commands that were predominantly “aimed at behavior regulation rather than social interaction or joint attention” as often as the control groups did (Sigman/Mundy/Sherman/Ungerer 1986, 653). 3.2. Children’s Processing of Their Mother’s Speech The interaction research reviewed is clearly biased towards the analysis of maternal speech. Up to the present almost all studies have neglected to investigate whether disordered children differ from normal children with respect to how often and in which way they openly process their mother’s language input. This is an important question since differences in language processing may allow inferences to be drawn regarding the operation of different acquisition mechanisms. The only existing longitudinal study of SLI children’s processing of maternal speech is that mentioned above by Grimm (1984 , 1986, 1987, 1993). This study is therefore to be reviewed in more detail. Eight dysphasic children (mean age: 4 ;2 years) and 8 younger MLU-matched normal language children (mean age: 2;6 years) were observed in semistructured interaction situations with their mothers, and an analysis was made of the way in which the children openly processed their mother’s speech. All the children’s utterances that were formally related to the directly preceding maternal utterances were registered. In a second step, these formally related children’s utterances were coded according to two main strategies of language processing (see for instance Grimm 1984 , 43—44, Grimm 1987, 16): (1) Elementaristic strategy, in the sense of picking out one single word or phrase from the immediately preceding maternal utterance. E. g. Mother: “Es hat ein Rad verloren” [“It has lost a wheel”]; Child: “Rad” [“Wheel”]. (2) Gestalt-like/holistic strategy comprising two substrategies: (a) The child imitates the whole sentence or picks out more than one phrase. E. g. Mother: “Da können wir ja noch eins bauen” [“Here we can build one again”]; Child imitates with omission: “Da können eins bauen” [“Here can build one”]. Mother: “Wir bauen ein Schloß” [“We are building a castle”];
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Child modifies: “Wir Schloß bauen” [“We castle build”]. (b) The child transforms his/her mother’s preceding sentence. E. g. Mother: “Und das da, das ist die größte” [“And this here, this is the biggest”]; Child: “Und das da? Größte?” [“And this here? Biggest?”]. Mother: “Wo ist der Teufel?” [“Where is the devil?”]; Child: “Da ist der Teufel” [“There is the devil”]. During the one-hour interaction situation on average 14 % of the younger normal language children’s utterances related formally in the defined sense to the maternal utterances. This was true for only 7% of the SLI children’s utterances. This significant quantitative difference is interesting since, as already mentioned above (cf. 2.2.), the mothers of the normal and of the dysphasic children did not differ in how often their utterances were formally related to their child’s immediately preceding utterances; the average for both groups was 24 %. Grimm interpreted these data as evidence that on the one hand almost every fourth utterance the mothers directed towards their children was teachingoriented. On the other hand, the younger normal language children were more learningoriented than the dysphasic children. Or in other words: In the dyads with the dysphasic children one could observe much teaching but little learning. Even more important than this quantitative difference is the qualitative finding that the normal language children significantly more often made use of the gestalt-like strategy of processing than the dysphasic children, who restricted themselves mainly to the elementaristic processing of their mother’s input. One year later this difference still existed. The evidence concerning mentally retarded children is less clear. Although Gutman/Rondal (1979) obtained a significant difference in the number of both ‚modified’ and ‚total echoics’of maternal utterances when comparing 21 Down syndrome and 21 MLUmatched control children, this result is not readily interpretable as showing a deficit in the retarded children’s use of a valuable language learning strategy. This is especially the case since the Down syndrome children were much older (age: 3;2—12;0 compared to 2;0—2;7 for the controls), had higher mental ages (Gutman/Rondal 1979, 4 52) and pro-
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duced more ‚intraverbals’ than the nonretarded control children. In summary we may conclude that the SLI children under study processed incoming language in a different way, at least during the earlier stages of language learning. If it is correct that different acquisition mechanisms underly and are responsible for different processing strategies (e. g. Bates/Bretherton/Snyder 1988) then the most important task is to find out the mechanisms leading to the deficient use of the gestalt-like strategy in SLI children. As one line of research it seems promising to look for memory restrictions. Because of its limited capacity short-term memory may be regarded as the bottleneck of information processing. Therefore, structural and/or procedural deficits in short-term memory may cause problems in the registration, processing and storing of language input, thus leading to a deficient individual data base for language learning. A second, though not necessarily independent hypothesis is that the dysphasic children — who have been shown to be very poor in dealing with rhythm (e. g. Kracke 1975, Lea 1980) — have problems in exploiting the rhythmic-prosodic structure of speech in language processing and in acquiring the underlying rule system (for empirical evidence see Weinert 1991, 1992).
4.
The Concept of Maternal Adjustment Revisited
4.1. Maternal Adjustment Versus Socialization Style In any naturalistic dyadic interaction we have to deal with bidirectional effects. Thus one of the main topics has been whether the more passive language disordered child is created by a directive and initiative mother or whether the mother’s directiveness is just a reactive adaptation to the child’s passivity. Even if, as shown above, the empirical findings seem to speak in favor of the latter effect, this cannot imply that the reactive adaptation to the child’s passivity must always be evaluated positively: the mothers’ reactive directiveness might dampen the children’s initiatives, thereby contributing to a firm establishment of the children’s passivity. This is an important issue for intervention. Particularly in the literature on retarded children the question has been discussed whether the adaptation of mothers to their
child’s passivity is dynamic in the sense that the mothers are finely tuned to their child’s level of participation in dialogue or whether this maternal adaptation is not child-driven but is rather the result of an instructional intent. The mothers are convinced that they must teach their child something and therefore they employ a rather rigid socialization strategy. Above all, two types of empirical results have been interpreted in support of the dynamic adaptation hypothesis: First, the correlational evidence already reviewed (see 2.1.) suggests an inverse relationship between the mother’s and the child’s interactional activity (Tannock 1988; see also Cunningham/Reuler/ Blackwell/Deck 1981, Eheart 1982). This suggests that either one or both interaction partners react to the conversational behavior of the other; obviously, however, correlational data preclude causal interpretations and experimental data are thus urgently needed. A second hint to a dynamic maternal adaptation is given by Tannock’s (1988) results. Although the mothers of the 11 Down syndrome children (age: 1;3—4 ;9) under study exerted significantly greater control in terms of turntaking, topic and response control than the mothers of the younger normal children matched for developmental age and level of communication, there were no group differences in the proportion and in the conditional probabilities of maternal response control. Thus, given the child’s antecedent behavior, the mothers showed comparable responses. However, there is accumulating evidence that the dynamic adaptation hypothesis does not account for all group differences in general interaction variables. First, in the study by Tannock (1988) the differences in maternal topic control remained significant even when proportions and conditional probabilities were computed. Second, basing on their results, Mahoney/Fors/Wood (1990) argue that the differences in the quality and quantity of the children’s interactive behavior were not as pronounced as the child-driven hypothesis presupposes. Third, an ‚instructional intent’ interpretation of maternal behavior is suggested by the fact that the mothers of the mentally retarded children not only produced more but also more demanding ‚action requests’ than the control mothers. In addition, the maternal requests were less directly linked to their children’s current activity (Mahoney/ Fors/Wood 1990). And finally, at least in some studies (Davies/Stroud/Green 1988) dif-
68. Patterns of Interactionand Communication in Language Development Disorders
ferences in interaction style between mothers of mentally retarded and normally developing children were only found in free play situations and disappeared in instruction situations, where the mothers of the control children proved as directive as the mothers of the retarded children. In summary, each of the two hypotheses seems to partly account for the observed group differences in maternal interaction style. The question, however, which effects — positive or negative — the directive and initiative communication behavior of the mothers of developmentally disordered children exerts on the child’s developmental progress needs to be examined by experimental procedures. 4.2. To Which Child Abilities and Features Do Mothers Adjust? What similarities and differences in maternal language input exactly mean is rather unclear. One of the main reasons for this is that, as already mentioned, we only have limited knowledge of which specific abilities the children bring into the dialogue and in which way they react to their mothers. When the mothers of language disordered children adapt to the language production abilities of their children, this might be interpreted as a favorable adjustment if the comprehension abilities of the children are very similar to the production abilities. However, if the children’s comprehension abilities are clearly better than their production abilities, then it is questionable whether a maternal speech style adapted only to the production abilities can support the child’s further language development. Only very few studies deal with this problem. Cunningham/Siegel/van der Spuy et al. (1985) for example inferred from their result that the maternal MLU is greater than the SLI children’s MLU that the mothers show fine-tuning with regard to their children’s comprehension. This data base is, however, rather meager. Additional investigations are urgently needed to explore whether the mothers of children with better comprehension than production abilities differ in the complexity of interactive variables such as expansions and recasts from those mothers whose children have comparable production and comprehension abilities. A second argument is that maternal adjustment to the language level of the language disordered children might then be dysfunctional for cognitive development if the chil-
707
dren’s cognitive abilities are better developed than the language abilities. We find this developmental discrepancy in SLI children since — per definition — these children have an average nonverbal IQ despite their language deficits. There are indications in the literature that the speech style of mothers of dysphasic children is indeed primarily guided by the language level of their children (e. g. Grimm 1983, 1986, Moseley 1990, Peterson/Sherrod 1982, Schodorf/Edwards 1983). As outlined in 2.2.1., SLI mothers were found to produce, for instance, a shorter and simpler input than mothers of normal children. In addition, Grimm (1986, 181) showed that the questions asked by the eight mothers of the dysphasic children she investigated differed significantly from the questions of the eight mothers of the normal MLU-matched children. Thus, questions of the type Say it more exactly were put significantly more often by the SLI mothers. E. g.: Mother: “Was siehst du alles?” [“What can you see there?”]. Child: “Das ist ein Mann” [”That is a man”]. Mother: “Was für ein Mann?” [“What kind of man?”]. In contrast, the mothers of the normal language children significantly more often asked questions of the type Say it by yourself. E. g. Child: “Was ist das?” [“What is that?”]. Mother: “Ja, was kann das denn sein?” [“Well, what could it be?”]. Grimm’s interpretation of these differences was that the SLI mothers question their children in a rigid way whereas the control mothers encourage their children to think about things by themselves. Interestingly, a positive correlation (r = .4 7) was found between questions of the type Say it by yourself and the child’s MLU one year later. On the whole, the dialogues with dysphasic children give the impression of reduced mutuality and connected herewith of reduced semantic meaning or content. In order to prove the assumption that SLI mothers adapt primarily to their children’s reduced speech production ability, thereby neglecting their more advanced language comprehension and cognitive abilities, Grimm (1991) chose the following three groups-design in order to isolate the otherwise inseparably confounded factors of language and cognition: (a) dyads with SLI children, (b) dyads with normal language-matched and therefore much younger children, and (c) dyads with normal age-matched children. Thus, the SLI children
V. Pathologies and Disorders of Language Development
708
share their limited productive speech ability with the younger children, and with the agematched children they share their experience and knowledge of the world. The cognitive quality of the mother’s and children’s utterances was analyzed according to the coding system developed by Blank/Franklin (1980). In this system, four levels of conceptual complexity are differentiated, ranging from simple naming utterances or naming questions up to the verbalization of causal relationships or theoretical conclusions. As hypothesized, the SLI mothers’ utterances were far more similar in their conceptual complexity to the utterances of the mothers of the language-matched younger children than to the utterances of the mothers of the age-matched children. It was even the case that the utterances of the SLI mothers were in part significantly less conceptually complex than the utterances of the mothers of the younger children. And most interestingly of all, even the SLI children produced higher level initiatives more often than their mothers. Without going into more detail here, it could be clearly demonstrated that the dysphasic children are primarily offered initiatives with low 1-level quality, which are even below the standard of what is considered appropriate for cognitively less advanced younger children. In contrast, the mothers of the younger children exceeded the level shown by their children, in that they produced distinctly fewer level 1 initiatives and distinctly more initiatives at the next, conceptually more complex level. This development-promoting aspect in the sense of fine-tuning was completely lacking in the SLI mothers. Since the additional analyses of answering behavior also showed very clearly that the SLI mothers produced significantly more answers at the conceptually simplest level in comparison to all other mothers, even though the previous initiatives of the SLIchildren and the younger children were very similar, Grimm concluded that the SLI mothers’ information is adapted primarily to the perceived limited language production ability and not to the children’s age-appropriate knowledge of the world. Her interpretation is that from the deficient language performance in the easily perceptible production area the mothers infer an overall immaturity and therefore apply an unspecific ‚toddler teaching strategy’. Or put otherwise: The reductive adaptation to the children’s language production level has as a negative side-effect a non-adaptive restriction of the cognitive quality of the verbal utterances pro-
duced. That the ‚toddler teaching strategy’ is not restricted to developmental dysphasia but is also adopted by mothers of deaf children was demonstrated by Nienhuys/Horsborough/ Cross (1985) who also used the Blank/Franklin scheme for analyzing the conceptual complexity of the utterances of mothers of twoand five-year-old deaf and hearing children. In addition, the results presented by Matey/ Kretschmer (1985) show that mothers of normally intelligent hearing-impaired children do not differ in their communication style from mothers of mentally retarded Down syndrome children. These accumulated findings certainly need to be taken into account in intervention. The mothers should be informed that they may not confound their children’s speech production with their mental ability. They should refrain from using a generalized language instruction style and recognize that conceptually more complex topics can well be expressed in simple words.
5.
References
Bates, E., Bretherton, J., & Snyder, L. (1988). From first words to grammar. Indiv idual differences and dissociable mechanisms. Cambridge: Cambridge University Press. Bettelheim, B. (1967). The empty fortress: Infantile autism and the birth of the self. New York: Free Press. Blank, M. & Franklin, E. (1980). Dialogue with preschoolers: A cognitively-based system of assessment. Applied Psycholinguistics, 1, 127—150. Bondurant, J. L., Romeo, D. J., & Kretschmer, R. (1983). Language behaviors of mothers of children with normal and delayed language. Language, Speech and Hearing Serv ices in Schools, 14, 233—242. Cardoso-Martins, C. & Mervis, C. B. (1985). Maternal speech to prelinguistic children with Down syndrome. American Journal of Mental Deficiency, 89, 451—458. Conti-Ramsden, G. C. (1990). Maternal recasts and other contingent replies to language-impaired children. Journal of Speech and Hearing Disorders, 55, 262—274. Conti-Ramsden, G. C. & Friel-Patti, S. C. (1983). Mothers’ discourse adjustments to language-impaired and non-language-impaired children. Journal of Speech and Hearing Disorders, 48, 360—367. Conti-Ramsden, G. C. & Friel-Patti, S. C. (1984 ). Mother-child dialogues: A comparison of normal
68. Patterns of Interactionand Communication in Language Development Disorders
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Grimm, H. (1986). Ontogenese der Sprache als Fortsetzung nicht-sprachlichen Handelns. In H. G. Bosshardt (Ed.), Perspektiv en auf Sprache. Interdisziplinäre Beiträge zum Gedenken an Hans Hörmann. 166—184. Berlin: de Gruyter. Grimm, H. (1987). Developmental dysphasia: New theoretical perspectives and empirical results. The German Journal of Psychology, 11, 8—22. Grimm, H. (1990). Über den Einfluß der Umweltsprache auf die kindliche Sprachentwicklung. In K. Neumann & M. Charlton (Eds.), Spracherwerb und Mediengebrauch. 99—110. Tübingen: Narr. Grimm, H. (1991). Entwicklungskritische Dialogmerkmale in Mutter-Kind-Dyaden mit dysphasisch sprachgestörten und sprachunauffälligen Kindern. Paper presented at the 10th Meeting of Developmental Psychology, Cologne, Germany, 25.— 27. 9. 1991. Grimm, H. (1993). Syntax and morphological difficulties in children with specific language impairment (developmental dysphasia): Implications for diagnosis and intervention. In H. Grimm & H. Skowronek (Eds.), Language acquisition problems and reading disorders: Aspects of diagnosis and intervention. 25—63. New York: de Gruyter. Grimm, H. & Weinert, S. (1990). Is the syntax development of dysphasic children deviant and why? New findings to an old question. Journal of Speech and Hearing Research, 33, 220—228. Gutman, A. J. & Rondal, J. A. (1979). Verbal operants in mothers’ speech to nonretarded and Down’s syndrome children matched for linguistic level. American Journal of Mental Deficiency, 83, 446—452. Hanzlik, J. R. & Stevenson, M. B. (1986). Interaction of mothers with their infants who are mentally retarded, retarded with cerebral palsy, or nonretarded. American Journal of Mental Deficiency, 90, 513—520. Hoff-Ginsberg, E. (1985). Some contributions of mothers’ speech to their children’s syntactic growth. Journal of Child Language, 12, 367—385. Hoff-Ginsberg, E. (1986). Function and structure in maternal speech: Their relation to the child’s development of syntax. Dev elopmental Psychology, 22, 155—163. Hoff-Ginsberg, E. & Shatz, M. (1982). Linguistic input and the child’s acquisition of language. Psychological Bulletin, 92, 3—26. Howlin, P., Cantwell, D., Marchant, R., Berger, M., & Rutter, M. (1973). Analyzing mothers’ speech to young autistic children: A methodological study. Journal of Abnormal Child Psychology, 1, 317—339. Konstantareas, M. M., Zajdeman, H., Homatidis, S., & McCabe, A. (1988). Maternal speech to verbal and higher functioning versus nonverbal and lower functioning autistic children. Journal of Autism and Developmental Disorders, 18, 647—655.
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Kracke, I. (1975). Perception of rhythmic sequences by receptive aphasic and deaf children. British Journal of Disorders of Communication, 10, 43—51. Lasky, E. Z. & Klopp, K. (1982). Parent-child interactions in normal and language-disordered children. Journal of Speech and Hearing Disorders, 47, 7—18. Lea, J. (1980). The association between rhythmic ability and language ability. In F. M. Jones (Ed.), Language disability in children. 217—230. Lancaster: MTP Press. Leonard, L. B. (1986). Conversational replies of children with specific language impairment. Journal of Speech and Hearing Research, 29, 114—119. Leonard, L. B. (1987). Is specific language impairment a useful construct? In S. Rosenberg (Ed.), Adv ances in applied psycholinguistics (1): Disorders of first-language dev elopment. 1—39. Cambridge: Cambridge University Press. Mahoney, G., Fors, S., & Wood, S. (1990). Maternal directive behavior revisited. American Journal on Mental Retardation, 94, 398—406. Matey, C. & Kretschmer, R. (1985). A comparison of mothers’ speech to Down’s syndrome, hearingimpaired, and normal-hearing children. Volta Review, 87, 205—213. Maurer, H. & Sherrod, K. B. (1987). Context of directives given to young Down syndrome and nonretarded children: Development of two years. American Journal of Mental Deficiency, 91, 579—590. Menyuk, P. (1988). Language dev elopment. Knowledge and use. Boston: Scott, Foresman & Comp. Moseley, M. J. (1990). Mother-child interaction with preschool language-delayed children: structuring conversations. Journal of Communicativ e Disorders, 23, 187—203. Nelson, K. E., Carskaddon, G., & Bonvillian, J. D. (1973). Syntax acquisition: impact of experimental variation in adult verbal interaction with the child. Child Development, 44, 497—504. Newport, E. L., Gleitman, H., & Gleitman, L. R. (1977). “Mother, I’d rather do it myself”: some effects and non-effects of maternal speech style. In C. Snow & C. A. Ferguson (Eds.), Talking to children: Language input and acquisition. 109—150. Cambridge: Cambridge University Press. Nienhuys, T. G., Horsborough, K. M., & Cross, T. G. (1985). A dialogic analysis of interaction between mothers and their deaf or hearing preschoolers. Applied Psycholinguistics, 6, 121—140. O’Kelly-Collard, M. (1978). Maternal linguistic environment of Down’s syndrome children. The Australian Journal of Mental Retardation, 5, 121—126. Olsen-Fulero, L. (1982). Style and stability in mother conversational behavior. Journal of Child Language, 9, 543—564. Peterson, G. A. & Sherrod, K. B. (1982). Relation-
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ship of maternal language to language development and language delay in children. American Journal of Mental Deficiency, 86, 391—398. Rondal, J. A. (1978). Maternal speech to normal and Down’s syndrome children matched for mean length of utterance. In C. E. Meyers (Ed.), Quality of life in sev erely and profoundly mentally retarded people: Research foundations for impro v ement. 193—265. Washington D. C.: American Association of Mental Deficiency. Rutter, M., Bartak, L., & Newman, S. (1971). Autism — a central disorder of cognition and language? In M. Rutter (Ed.), Infantile autism: Concepts, characteristics and treatment. 148—171. Edinburgh: Churchill. Sachs, J., Bard, B., & Johnson, M. L. (1981). Language learning with restricted input: Case studies of two hearing children of deaf parents. Applied Psycholinguistics, 2, 33—54. Schodorf, J. K. & Edwards, H. T. (1983). Comparative analysis of parent-child interactions with language-disordered and linguistically normal children. Journal of Communication Disorders, 16, 71—83. Shatz, M., Grimm, H., Wilcox, S., & NiemeierWind, K. (in press). Culture-specific speech styles in Germany and the United States: Mothers’ modal verbal expressions and two-year-olds’ modal development. Child Development. Sigman, M., Mundy, P., Sherman, T., & Ungerer J. (1986). Social interactions of autistic, mentally retarded and normal children and their caregivers. Journal of Child Psychiatry and Psychology, 27, 647—656. Smolak, L. & Weinraub, M. (1983). Maternal speech: strategy or response? Journal of Child Language, 10, 369—380. Snow, C. E., Perlman, R., & Nathan, D. (1987). Why routines are different: toward a multiple-factors model of the relation between input and language acquisition. In K. E. Nelson & A. van Kleeck (Eds.), Children’s language, Vol. 6. 65—97. Hillsdale, N. J.: Lawrence Erlbaum Associates. Tannock, R. (1988). Mothers’ directiveness in their interactions with their children with and without Down syndrome. American Journal of Mental Retardation, 93, 154—165. Weinert, S. (1991). Spracherwerb und implizites Lernen. Studien zum Erwerb sprachanaloger Regeln bei Erwachsenen, sprachunauffälligen und dysphasischsprachgestörten Kindern. Bern: Huber. Weinert, S. (1992). Deficits in acquiring language structure: The importance of using prosodic cues. Applied Cognitive Psychology (Special Edition). Wolchik, S. A. (1983). Language patterns of young autistic and normal children. Journal of Autism and Developmental Disorders, 13, 167—180. Wolchik, S. A. & Harris, S. L. (1982). Language environments of autistic and normal children
69. Disorders of Written Language Development:Definitions and Overview
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Yoder, P. J. & Kaiser, A. P. (1989). Alternative explanations for the relationship between maternal verbal interaction style and child language development. Journal of Child Language, 16, 141—160.
Hannelore Grimm, Bielefeld (Germany)Sabine Weinert, Bielefeld (Germany)
69. Disorders of Written Language Development: Definitions and Overview 1. 2. 3. 4.
Learning to Read: The Alphabetic Principle and Stage Models of Reading Development Reading Disorders: Definitions, Methods and Some History Reading Disorders: Alternative Conceptions References
This article will focus mainly on developmental disorders of reading and will deal only occasionally with spelling.
1.
Learning to Read: The Alphabetic Principle and Stage Models of Reading Development
The process of learning to read is dependent on the writing system. The alphabetic writing system used in so many literate languages involves correspondence of letters (graphemes) and speech sound units (phonemes). This ‚alphabetic principle’ defines a ‚productive writing system’ (Perfetti 1985) because from a small, definite number of graphic signs an indefinite number of words may be constructed. Such economy in writing production seems to be paralleled by a similar advantage in learning alphabetic systems. In contrast to the Chinese system, for instance, the alphabetic system does not require an enormous number of specific paired-associates of sign and meaning to be stored in memory. Instead, when the learner has acquired the relatively few grapheme-phoneme-correspondences and has also learned about the context dependency of the various sound representations of a single letter he can apply this knowledge directly, grapheme by grapheme, or, in the case of grapheme clusters, by analogy (cf. Goswami 1986, 1988) to reading or ‚decoding’ any word or non-word. This task might be
easier in languages like Finnish or Polish, with very transparent and regular relations between spelling and pronunciation. ‚True’ alphabetic writing, i. e. writing arbitrary signs that represent words and not objects or concepts, pays for economy by loss of ‚ideographic’ or pictorial concreteness. To acquire the alphabetic principle, the learner must first focus on the formal aspect of speech, i. e. speech sounds and phonology, and understand the abstract nature of the ‚phoneme’ (Valtin 1984 ). Such abstraction occurs because the phoneme does not represent one fixed sound but instead refers to a set of slightly different pronunciations of, say, ‚p’ depending on the patterns of the surrounding vowels and consonants in a word. To add to the difficulties, neither in listening nor in speaking can the flow of speech be separated into phonemes as natural or physical units (cf. Liberman/Cooper/Shankweiler/StuddertKennedy 1967). Second, the reader needs to exert cognitive control over his eye movements. Before starting to read, no saccadic eye movements in a specified direction are required. A further major problem is the focussing of attention on the relevant parts of words or texts in order to draw information. Third, the human species is not only endowed by nature to learn and use oral language for communication but is also socialized smoothly into it. Considered on a world scale, with billions of illiterates, this does not apply to written language (Kamhi/ Catts 1989). Thus it seems plausible that learning to read (and to spell) takes a lot of conscious resources and effort and may easily be doomed to failure whenever the subtle balance of interacting biological, cognitive, psychosocial and environmental factors is disturbed by slight but cumulative deprivations in one or more of these areas.
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Up to now, development in reading has been described by means of catalogues of skills to be acquired or by developmental stages. Learning to read requires a set of prerequisite skills (e. g. Gibson/Levin 1976) which cannot be separated easily from the actual skills of decoding. The question as to which prerequisites are necessary and/or sufficient and in what order they develop is yet to be answered (Morais/Alegria/Content 1987). Many researchers in reading development (e. g. Clay 1970, Ehri 1979, Perfetti 1985, Rozin/Gleitman 1977) have listed the following language processes: — phonemic analysis — segmenting and discriminating sounds — associating sound and phonetic codes and retrieving them from memory — blending of sounds — becoming aware that words are units in speech, even if not marked either auditorily or semantically — developing phonological awareness. The latter skill is regarded as the most important and the most difficult to acquire. Without developing an understanding or at least having access to the phonological organization of language as prerequisite for discovering the alphabetic principle, even decoding of two-phonemic units will prove extremely difficult (Valtin 1984). As visual processes are listed (e. g. Gibson 1971, Venezky 1976): — recognizing letters (discriminating distinctive features) — recognizing clusters of letters — recognizing the serial order of letters from left to right — cognitive control of eye movements. Finally, to guarantee steady improvement of reading, the isolated skills have to be coordinated and integrated by proficiency processes (cf. Perfetti 1985, Samuels 1976): — integrating graphic and linguistic information — combining and coordinating linguistic and visual processes. In stage theories of reading development it is assumed that all children pass through an ordered sequence in learning word recognition. Authors of stage theories (Frith 1985, Høien/Lundberg 1988, Marsh/Friedman/ Welsh 1981, Mason 1980, Seymour/MacGregor 1984 ) have proposed from 3 to 4
V. Pathologies and Disorders of Language Development
stages, differently labeled. The frequently cited, original model by Frith (1985) may be sketched as follows: In their first unguided attempts at reading children will use the same perception and memory skills for decoding printed material as for other visual objects and events. A linkage of spoken and printed words, defined by minimal cues, is established by a process of paired-associate learning. This is the stage of ‚logographic’ reading. Of course, this strategy of pre-alphabetic reading will break down when the ‚sight vocabulary’ exceeds fifty to eighty printed words in a very short time. Because of inaccuracies and increasing difficulties in recognizing unfamiliar words, it is necessary to use the strategy of sequential decoding or the ‚alphabetic’ stage, using knowledge of letter-sound relations. This stage has been recognized by many authors (e. g. Weigl 1976) as the most important ‚qualitative jump’. In spontaneous writing children give many examples of ‚phonetic’ spelling, which is orthographically incorrect but is based on inventive letter-sound correspondences. The third, ‚orthographic’ stage or hierarchical decoding is reached when the learner masters the deviation from ‚normal sound’ and uses conditional spelling rules, e. g. those governing the stretching of vowels. — To represent the specific interplay of reading and spelling in stimulating development Frith (1985, 1986) differentiated the three stages of her original model into two substages each, so that either reading or writing functions “as the pacemaker of the strategy” (Frith 1985, 310) characteristic of the stage in question — logographic, alphabetic or orthographic. For German-speaking countries it was slightly modified by Günther (1986) to the effect of further subdivisions in each stage. More detail to stage-specific variation dependent on individual development and method of instruction came from Ellis/Cataldo (1990), Scheerer-Neumann (1989) and Seymour/Elder (1986). The general model was questioned on theoretical grounds by Eichler (1986) and on theoretical as well as empirical grounds by Stuart/Coltheart (1988) and Wimmer/Hartl/Moser (1990). Especially for German-speaking children the existence of a logographic stage is questionable. — Compared to models of the reading process stage theories do not describe the component processes in detail. Instead the focus is on qualitative changes in reading strategies, i. e. on how children approach the word recognition task. The evidence cited in support of
69. Disorders of Written Language Development:Definitions and Overview
stage concepts demonstrates in general that phonological processing and integration of component processes (proficiency) improve in the course of reading development. Errors in reading and spelling allow ex post conclusions with regard to the developmental stage of word processing. As is the problem with all outcome measures reading errors and other reading results do not address the details of reading processes. Particularly on higher levels of reading skills (sequential or hierarchical decoding) the interpretation of mere outcomes is questionable. Since the eye-voicespan is considerable, supposed reading errors could prove to be errors of recall. To some degree, stage theories also appear to be influenced by the specific type of reading instruction and by the regularity of sound-spelling relations in a language. — More recent models of written language acquisition, based on a connectionist framework, postulate a set of functionally different modules and routes of transmission. Models of this type are proposed by Seidenberg/ McClelland (1989) and Van Orden/Pennington/Stone (1990).
2.
Reading Disorders: Definitions, Methods and Some History
As a rule, current definitions of reading disorders do not refer to existing definitions of reading. Rather they refer to deviation from or discrepancy to a norm such as general achievement or intelligence. This type of definition goes back to a medical model of reading disorders. In reviewing the history of ideas and concepts in research of reading disorders up to the present, three general routes can be detected: — from the idea of a unitary syndrome via the search for a few categorical subtypes to the description of reading disorders in a multi-dimensional space; — from exclusionary definitions to a more comprehensive and positive delimitation of reading disorders; — from a medical model of reading disorders searching for organismic causes and associated symptoms to a psychological and educational model focusing on reading difficulties per se and on processes of learning and instruction. — Despite gradual convergence and restriction to phonological processing skills as the key variable in first reading disorders, re-
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search in this field for the last two decades is still burdened by an enormous diversity of methods, definitions and concepts. This diversity makes evaluation of empirical findings extremely difficult since many unaccounted interactions of designs, sampling, measurement and concepts produce a barely manageable host of results (Stanovich 1988b, 1989, 1990a, b). 2.1. Defining by Discrepancy from Potential: Dyslexia Fortunately, in societies where formal schooling is obligatory, most children master the complex skill of reading to a functional degree. Against this background, cases of children with otherwise normal achievement but ‚unexpected’ failure in learning to read were highly salient and attracted early attention in the medical profession. The notion that there are children with specific reading difficulties of supposedly constitutional origin (‚congenital word blindness’) is credited to Morgan (1896) at the turn of the century and was made popular by the writings of Hinshelwood (1917), besides others (cf. Ellis 1985, Warnke 1990). Hinshelwood also seems to have been the first to link reading difficulties to disorders of the left brain hemisphere. This idea was taken up and expanded by Orton (1937) who is thought to be responsible for the theory that specific reading difficulties (dyslexia) go back to deviations in the distribution of visual information processing between the two cerebral hemispheres. Orton was the first to speak of developmental alexia (i. e. absolute inability to read) so that dyslexia came to stand for the wider range of ‚incomplete alexias’ (Harris/Hodges 1981). He is also known for adding letter reversals and word confusions to the diagnosis of ‚dyslexia’. So it gradually became quite common to think of dyslexia as a unitary syndrome with associated neurological and behavioral manifestations. In German-speaking countries the equivalent term, with a similar history, is ‚legasthenia’ (Ranschburg 1916). Amongst the many and various definitions of dyslexia or legasthenia, that formulated by the World Federation of Neurology from 1968 is perhaps the most widely quoted: “(Dyslexia is) a disorder manifested by difficulty in learning to read despite conventional instruction, adequate intelligence and sociocultural opportunity. It is dependent upon fundamental cognitive disabilities which are
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frequently of constitutional origin” (Critchley 1970, 11). The host of definitions may be classified (Marx 1985) as follows: (1) Etiological definitions, e. g. “Reading weakness or legasthenia I call ... that inferiority of mental equipment in consequence of which children of school age can’t acquire verbal reading during the first grades, despite normal sensory abilities” (Ranschburg 1916, 111). (2) Descriptive definitions, like the one by the World Federation of Neurology quoted above or the one by Linder, which has become a classic in German-speaking countries: “Unter Legasthenie verstehen wir eine spezielle und aus dem Rahmen der übrigen Leistungen fallende Schwäche im Erlernen des Lesens (und indirekt auch des selbständigen orthographischen Schreibens) bei sonst intakter (oder im Verhältnis zur Lesefähigkeit) relativ guter Intelligenz.” [“Legasthenia is conceived of as a specific weakness in learning to read (and indirectly also in learning to spell correctly), in the context of generally better school achievement and of intact or relatively good intelligence, compared to reading skill”] (Linder 1951, 100). (3) Operational definitions, e. g. “Als Legastheniker gelten Kinder mit mindestens durchschnittlicher Begabung (IQ ≥ 90), deren Leistungen im Lesen und Rechtschreiben jeweils einem Prozentrang von ≤ 15 (T ≤ 4 0) entsprechen.” [“Children are ranked as legasthenics when they score at or below percentile 15 (T ≤ 4 0) in reading and spelling, and when their intelligence is at least average (IQ ≥ 90)”] (Niemeyer 1974 , 28). Or: “A dyslexic is a child who is normal or above at least in non-verbal IQ, two years behind in reading achievement, and with a reading disability that is not explainable primarily by social, economic, motivation or emotional factors” (Perfetti 1985, 180). As is evident from these examples, most authors start out in their definitions from deviations from norms but not from a common base in concepts and methods. They agree that the term dyslexia (or legasthenia) should be reserved for the subgroup of ‚unexpected’ reading disabled and not applied to poor reading in general. 2.2. Problems with Definition by Exclusion Definitions may be more or less comprehensive or explicit, but most if not all are exclusionary in character. Thus, some poor readers
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are excluded from the group of dyslexics by factors that might contribute to reading disorders in general: low intelligence, poor schooling, sensory deficits, brain damage etc. In addition, the definition of dyslexia by exclusion raises some other serious problems (Kamhi/Catts 1989). First, the definitions depend solely on the discrepancy between reading achievement and general achievement, or intelligence, or chronological age or grade level. However, measurements of reading achievement and intelligence overlap to some degree. By different reading measures different children are assigned accordingly to the group of the disabled (Rudel 1985, Schlee 1976). Second, the exclusion of children with IQs below 90 from the group of dyslexics implies that these children display other disorders. This view is contradicted by those authors who point out that there is continuity of dyslexic disorder across all ranges of intelligence (Ellis 1985, Thomson 1984 ) and that performance profiles of dyslexics cannot be distinguished reliably from those of poor readers (Taylor/Satz/Friel 1979). Third, since environmental causes are excluded, the search for deprivations in educational experience tends to be neglected (Vellutino 1979). Last and most regrettably, definition by exclusion has often facilitated neglect of the low-intelligent poor reader (Schlee 1976). In conclusion, according to Rutter (1978, 12), this type of definition looks like “a counsel of despair”: “A negative definition of this kind not only fails to aid conceptual clarity but also it implies that dyslexia cannot be diagnosed in a child from a poor or unconventional background. In short it suggests that if all the known causes of reading disability can be ruled out, the unknown (in the form of dyslexia) should be invoked”. 2.3. Methods and Paradigms in Search for Causes and Consequences In the search for causes of reading disorders five designs to cope with different methodological problems can be distinguished: — (1) Extreme-groups design: Up to the seventies, the host of comparisons done with this design finally demonstrated that performance or achievement differences between the comparison groups will occur on the condition that the skills measured are directly or indirectly linked to literacy skills. Unequivocal evidence with regard to causal direction cannot be expected from this design (Valtin 1975, 1978/79) since reading difficulties might be
69. Disorders of Written Language Development:Definitions and Overview
cause as well as effect of the observed deficits in the dependent variables measured; both lower performance might also be the effect of a third, unknown determinant. The value of research in this design lies mainly in confirming supposed correlations on which base more incisive hypotheses for research on causal relations may be generated. — (2) Reading-level match design: In this design, which was introduced by Guthrie (1973) into research on reading difficulties, an older group of reading disordered children is matched on reading level with a younger group of ‚normal’ readers. Reading level is measured by reading age. Whether reading age is measured by word recognition and decoding or by tests of reading comprehension, or by both makes an important difference. When equating reading level, performance differences in correlated variables cannot be reduced to differences in reading achievement. On the other hand, as in the extremegroups comparison, the observed differences in cognitive and other characteristics should not be interpreted as causes of reading disorder — as is sometimes erroneously done (Bradley/Bryant 1978, Treiman/Hirsh-Pasek 1985). Recently, different authors (Goswami/ Bryant 1989, Jackson/Butterfield 1989, Stanovich/Nathan/Zolman 1988, Vellutino/Scanlon 1989) have critically dealt with scope and limits of this design. — (3) Garden-variety control design: In this design, two groups of reading disabled children are compared — ‚dyslexic’ children with at least average intelligence but low reading achievement, and generally backward children of the same reading level but also low in intelligence. Differences (e. g. Jorm/Share/ Maclean/Matthews 1986) or similarities (e. g. Taylor/Satz/Friel 1979) in associated variables between these groups are seen as evidence for or against the formation of subgroups in the reading disordered population. — (4 ) Longitudinal design: Supposed prerequisite skills and abilities (e. g. phonological awareness) are measured before school entrance to predict criterial literacy achievement at successive stages (e. g. Skowronek/Marx 1989). If first measures are really taken before formal reading instruction starts, confounding of predictor and criterion achievement is avoided. Close examination of times of predictor measurements and considering the extent to which reading is already offered in kindergarten (in the Anglo-American educational system) raises doubts whether in some
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studies (e. g. Butler/Marsh/Sheppard/Sheppard 1985, Lundberg/Olofsson/Wall 1980, Share/Jorm/Maclean/Matthews 198 4 , Vellutino/Scanlon 1987) confounding really has been avoided (Marx 1989). — (5) Intervention-design: Inadequately developed prerequisite or predictor skills relevant to acquisition of literacy are trained for a fixed period of time up to a predetermined level of competence. Ideally, the deficits should be not only diagnosed but also remedied before entering school. If post-training comparisons with control children matched in prerequisite skills show that trained children perform better in reading and spelling, the positive causal influence of these skills on literacy achievement is demonstrated. The well-controlled study by Lundberg/Frost/Petersen (1988) clearly shows that the trained skills (phonological awareness) are necessary but not sufficient for the acquisition of literacy. Training in school or in close cooperation with schools (e. g. Bradley/Bryant 1985, Mannhaupt 1990) incurs the risk that specific effects of intervention in relevant skills cannot be separated clearly since intervention interacts in unknown ways with ongoing reading instruction. Again, confounding of predictor and criterion measurements seems possible (cf. Ehri 1989). 2.4. Approaches in Subtyping of Reading Disorders As is the case in learning disabilities in general and as already mentioned above the field of reading disorders is plagued by heterogeneity. Evidence shows that poor readers differ from normals in a broad range of dimensions — cognitive, attentional, perceptual-motor, social-emotional, basic skills and strategies — and the individual patterns of deficits may vary enormously (Kavale/Nye 1986, Miles 1983, Stanovich 1986a, Zielinski 1980). To reduce complexity and make this diversity more intelligible — for reasons of theory development, of better diagnosis and more specific treatment — researchers and clinicians made early efforts at classification of distinct patterns of disorders. Indeed, it seems still a major concern to professionals to identify more homogeneous subgroups and bring order to an otherwise amorphous field (Adelman/Taylor 1985). — To this end, a comprehensive and standardized description of relevant phenomena is required. However, there are doubts whether this requirements is fulfilled to an
716
acceptable degree (Kavale/Forness 1987). How reading order is defined, whether by exclusion or by inclusion, will also exert a major influence on the results of subtyping. Including all poor readers will probably lead to many and not clearly separable groups whereas selective sampling of ‚dyslexics’ only, according to strict psychometric criteria will render homogeneous groupings differing along few causal lines. There are two approaches to subgrouping: classification by clinical inference, i. e. by applying various theoretical distinctions and organizing data patterns intuitively, and the more recent approach of classification by multivariate descriptive statistics such as Qfactor analysis and cluster analysis. In the following each approach will be characterized by a few representative studies. Detailed critical reviews treating both conceptual and methodological issues are given by Fletcher/ Satz (1985), Kamhi/Catts (1989), Kavale/Forness (1987), Malatesha/Dougan (1982) and Satz/Morris (1981). — (1) Clinical inference: The most obvious distinction, grounded in very basic though largely unexamined assumptions about categorical differences in cognitive and neuropsychological characteristics, is between dyslexics and ‚garden-variety’ poor readers (Gough/Tunmer 1986). Rutter/Yule (1975), for instance, addressed this distinction and found that ‚generally backward readers’ could indeed be distinguished from ‚specific reading retarded’ (or dyslexics for our purposes). The authors based the distinction on two lines of evidence: First, they got a ‚hump’ at the lower end of the reading achievement residuals distribution, i. e. significantly more under achievers than could be predicted from normal distribution. Second, they found the two groups to differ on various neurological and behavioral characteristics, whereas deficiencies in oral and written language performance were equally prevalent in both groups. These and other differential results appeared very cogent so that the old distinction seemed confirmed. Since then, various authors have questioned its validity (Rodgers 1983, Share/ McGee/McKenzie et al. 1987, Taylor/Satz/ Friel 1979, Van der Wissel/Zegers 1985) because of flaws in method or because the findings could not be replicated in well-controlled samples. To quote one of the concluding statements, the comparisons on a wide array of measures showed “that the dyslexic subgroup could not be distinguished from the
V. Pathologies and Disorders of Language Development
nondyslexic poor readers along any of several dimensions, including the initial severity and progression of reading disturbance, frequency of reversal errors, familial reading and spelling competencies, math skills, neuro-behavioral performance, or personality functioning.” (Satz/Morris 1981, 113). — Another influential and frequently cited study of the clinical type is that of Boder (1973). Her classification of developmental dyslexia is based on direct quantitative and qualitative measures of reading and spelling. Boder found three subtypes of dyslexic children: the dysphonetic (comprising 67%) with deficiencies in analyzing and blending sounds, the dyseidetic (10%) with rather intact phonological skills but impaired storing of visual patterns of letter strings, and a mixed, practically alexic group (23%). Lacking statistical verification and replication, the merit of this study lies primarily in a rich clinical description and heuristic quality. Error types used by Boder may also occur in younger normal children beginning to read so that their specific diagnostic value for dyslexics is seriously doubted. Perfetti (1985) has also noted that the difference between the dysphonetic and the dyseidetic might rest only upon spelling ability. — Summarizing their critical comments on clinical-inference studies reviewed, Satz/Morris (1981, 120) state that “subject selection, sample size, tests and observer rules are quite different.” Also, the terms used for description are highly abstract and carry surplus meaning that may mask finer distinctions or even be misleading. Furthermore, most studies did not include independent comparison groups of normal and non-dyslexic poor readers in order to control for the uniqueness of achievement profiles in dyslexic subtypes. — (2) Statistical classification: Quantitative analysis of multivariate data sets entered the study of subtypes in reading disability about ten years ago. Among the first authors to use this method were Petrauskas/Rourke (1979). Factor analysis (Q-technique) applied to a broad range of neuro-psychological measures from a (preselected) group of dyslexic readers and a small group of normal readers resulted in three reliable subgroups which classified just 50% of the subjects. It should be noted that two (of 27) normal readers were classified into subtype 3, together with 11 dyslexic readers. The authors’ main conclusion was that language deficiencies were dominant in variables associated with specific reading retar-
69. Disorders of Written Language Development:Definitions and Overview
dation, whereas other deficiencies, e. g. of a visuo-perceptual kind, were involved to a much lesser degree. — Supplementing the often-used cross-sectional design in a more recent study (Morris/ Blashfield/Satz 1986), which is part of the Florida Longitudinal Project, longitudinal data from normal and reading disabled children were analyzed. This study combined factor analysis with cluster analysis. Clustering resulted in three groups of poor readers: Type A children showed deficient verbal skills throughout the seven-year-interval whereas early deficits in perceptual-motor skills disappeared. Type B children, from average family background, started with average performance at kindergarten age but showed increasing weaknesses in the verbal-conceptual dimension at school age. Type C children rated below average on all measures. This group is rarely found in other classification studies which most often focus on the dyslexic and therefore miss the less intelligent (IQ below 90) and educationally deprived characteristic of Type C. — The two studies mentioned above exemplify only few of the problems inherent in quantitative classification. To sum up the major caveats from various sources (cf. particularly Kavale/Forness 1987, Satz/Morris 1981) one has to keep in mind that — the Q-factor technique is controversial, especially the use of correlations as a measure of similarity between subjects, and on data in which the assumption of linearity is dubious; — clustering methods are of more heuristic value since they are not well-tested statistically; — by clustering methods any data set (“garbage in, clusters out”) can be organized; thus the data set must first be tested for real clustering tendencies; — what subtypes and labels emerge from clustering depends on what samples of subjects and tests have been used; e. g. standardized tests of reading/spelling achievements may probe a much too restricted range of relevant skills; — only part of the sample may be grouped into clusters, and clusters may overlap so that reading retarded are grouped with normal subjects; — external validation of subtypes is often neglected. Aside from these criticisms and even though the many studies diverging in theo-
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retical assumptions and methods do not combine to consistent patterns, subtyping research in the clinical-inferential mode as well as in quantitative classification has added to our knowledge of reading/spelling disorders. Generally, it confirmed hypotheses about components of literacy skills, clarified the context of associated abilities and language development and stressed the need for more comprehensive and formalized description of the field.
3.
Reading Disorders: Alternative Conceptions
For about two decades the ‚medical model’ of dyslexia as a unitary, neuro-psychological ‚syndrome’ has been challenged by an alternative, ‚educational-psychological’ approach (Scheerer-Neumann 1979, Snowling 1987). It is argued that children with difficulties in reading acquisition should be identified directly on the basis of (deficient) learning processes and not on the basis of indirect signs or remote symptoms. Today, many signs formerly held as highly diagnostic of ‚dyslexia’ are no longer valid: they have been uncovered as normal developmental features, the most prominent examples being reversal and sequencing errors (e. g. b/d, was/saw) which have, among other things, turned out as an instance of base-rate fallacy (Stanovich 1986a). In many years of clinical work with dyslexic children Miles (1983) developed a ‚dyslexia test’ examining diverse performances which are commonly thought to be characteristic of dyslexia like right-left discrimination, repeating polysyllabic words etc. His results speak for an enormous heterogeneity: no single symptom occurred in all of over 200 cases whereas some children failed in only one or two of the items. Generally, disorders of basic visual processes, of intersensory integration and of serial order recall have been discredited as causes of reading disorder by a host of evidence from well-controlled studies and from evaluations of visually oriented remedial instruction (Kavale/Mattson 1983, Vellutino 1979). The more experiments succeeded in isolating perceptual factors, the less poor and good readers differed in these factors (Stanovich 1986a). Yet this general conclusion does not preclude that a minor group of poor readers may be characterized by some sort of visual deficit — although this is probably
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more specific to the task of reading than to ‚basic visual processes’. It might be rooted in insufficient encoding, storing and/or accessing of visual-orthographic memory patterns (Stanovich 1988b). 3.1. The Role of Phonological Processing Under the converging influence of developmental psychology, psycholinguistics and models of information processing in cognitive psychology, the search for causal factors in developmental disorders of written language has focussed on skills of auditory analysis of speech sounds and of processing phonological information. These skills are directly involved in cracking the alphabetic code (Gough/Hillinger 1980, LaBerge/Samuels 1974 ). There is ample evidence now that deficits in processing of speech sound information in its various aspects characterize the majority of poor readers — from implicit sensitivity to sound structure of speech to explicit segmenting of phonemes (Ellis/Cataldo 1990, Valtin 1984 ), and from phonological encoding to retrieving phonological memory codes (Wagner/Torgesen 1987). Which specific causal relations exist between reading achievement and phonological processing skills (cf. Ehri 1989, Morais/Alegria/Content 1987) is still controversial. It is discussed whether these skills are prerequisite to or a consequence of reading instruction or whether — most probably — the relation is a reciprocal one, phonological processing and reading interacting by mutual stepwise support (cf. Wagner/Torgesen 1987). Nevertheless, summarizing the evidence these conclusions seem warranted: — Children who already in preschool appear sensitive for units of speech below the syllable and/or for rhyming and alliteration have a reliable prognosis for not becoming reading disabled (Bryant/Bradley/Maclean/Crossland 1989, Ellis/Large 1987, 1988, Maclean/ Bryant/Bradley 1987, Tunmer/Nesdale 1985). — Children with language disorders in preschool age are predicted as reading disordered if language disorders persist up to school entrance (Bishop/Adams 1990). On the other hand, language disorders do not prevent children from developing phonological skills, even though with some lag, to about the same level reached by children without language problems (Bishop/Edmundson 1987a, b). — Children who in preschool age undergo an extended training in phonological skills show, as a group, better achievement in reading than
V. Pathologies and Disorders of Language Development
an untrained comparison group (Lundberg/ Frost/Petersen 1988). — Children who in first grade undergo a phonological skill training combined with acquiring the letters of the alphabet as a rule show better achievement in reading/spelling than children who were trained separately or who were offered only one of these training modes (Bradley 1988, Bradley/Bryant 1985, Wise/Olson/Anstett et al. 1989). — Children who achieve in reading/writing below their age or — depending on definition of sample — general intellectual ability frequently show difficulties in segmenting speech (Frith/Snowling 1983, Liberman/Shankweiler 1979). — To adult illiterates, it is very difficult to master tasks of phonological awareness, if they succed at all (Mann 1986, Morais/Cary/ Alegria/Bertelson 1979). — Children who have learned a non-alphabetic writing system or who have not been explicitly taught how to segment speech sounds, are able to learn alphabetic reading (Read/Zhang/Nie/Ding 1986, Seymour/Elder 1986). — At least for decoding processes only rudimentary intellectual abilities are required (Cossu/Marshall 1990). Focussing on the role of phonological processing reinforces a wider view of language development in general. As pointed out above, there is growing evidence that poor readers have more pervasive language problems. Relevant reviews (e. g. Catts 1989b) demonstrate that in many cases reading disorder reflects a language problem persisting from early years to adulthood. Late utterance of first words and morphologic or syntactic deficiencies may precede difficulties in learning to read and to spell, and problems in learning from print are to follow (Johnson/ Blalock 1987). Returning to the problems of defining developmental dyslexia (or legasthenia), the way is now paved for a more satisfying inclusionary definition that resorts to this wider context of complex language development: “Dyslexia is a developmental language disorder that involves a specific deficit(s) in the processing of phonological information. The disorder is generally present at birth and persists into adulthood. A prominent characteristic of the disorder is a specific reading disability. Preceding, accompanying, and following this reading disability, the disorder manifests itself in various difficulties in phonological coding,
69. Disorders of Written Language Development:Definitions and Overview
including problems in encoding, retrieving, and using phonological codes in memory. In addition, difficulties may be observed in speech production and in the metalinguistic awareness of speech sound segments” (Catts 1989a, 58). 3.2. Dimensional Continuity of Reading Disorders: the Phonological-Core Variable-Difference Model Search for homogeneous subtypes is not the only way to deal with well-known heterogeneity of reading disorders. Discussing general principles of classification Morris/Satz (1984 ) distinguish three models. The first is hierarchical, as known from classifications into families, genera and species in biology, placing subjects into distinct, non-overlapping, systematically related subsets. The field of reading disorders might be apt, as we have seen, for the second, categorical mode of subtyping. However, when the search for ‚homogeneous’ subtypes provides unclear results a third mode of classification may recommend itself: the dimensional model that orders subjects along axes in a multi-dimensional space. Categorical classification assumes heterogeneity with clustering. In contrast, the dimensional models admits heterogeneity without clustering — which might be the more realistic frame for ordering reading problems. It seems a well-founded opinion of many authors (e. g. Ellis 1985, Olson/Kliegl/ Davidson/Foltz 1985, Seidenberg/Bruck/Fornarolo/Backman 1985, Share/McGee/McKenzie et al. 1987) that we are not dealing with discrete entities of dyslexia like ‚expected’ or ‚garden-variety’ poor reading but with graded continuity. As Andrew Ellis (1985) remarked, the proper analogy for dyslexia might not be a disease like measles, but instead a condition like obesity, with people forming a continuum from the extreme lean to the overly fat. What dimensions are proper candidates for spreading the above mentioned multidimensional space? Defining dyslexia with reference to (at least) normal intelligence or causally attributing it to deficits of intersensory integration or visual perception or any other general mono-cause means relying on what Fodor (1983) calls ‚horizontal’ abilities, i. e. global abilities independent of the material (e. g. alphabetic script) on which they are to operate. This impresses as somewhat paradoxical since from the beginnings of theorizing about reading disorders the assumption
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of specificity was clearly implied (Hall/ Humphreys 1982). Consequently, Stanovich (1988a) judges any view invoking global processes, also of the more recent type such as general linguistic awareness or generalized metacognitive functioning (Torgesen 1977), to be “on the wrong track”. Instead, one should look for in Fodor’s sense ‚vertical’ and domain-specific processing mechanisms that are closely tied to the reading task and lead to fast automatic functioning on the basic level of word recognition (Gough/Tunmer 1986, Perfetti 1985, Vellutino 1979). Adults reading texts within their ability level show fairly autonomous word recognition, without support from context (Seidenberg/Bruck/Fornarolo/ Backman 1985, Stanovich/West 1983). This line of argument meets with much of the above cited evidence concerning the linkage of phonological processing to proficiency in reading/spelling. In sum, phonological processing has been demonstrated as uniquely contributing to variance in reading skill after intelligence and other cognitive measures have been partialled out (Bradley/Bryant 1985, Lundberg/Olofsson/Wall 1980, Tunmer/Nesdale 1985). So it appears as sufficiently independent of other more global cognitive abilities to qualify for the postulated modular, domain-specific key ability. In the model of ‚phonological-core variable-difference’ proposed by Stanovich (1988b) to account for ‚heterogeneity without clustering’, phonological processing stands for the core of deficient performance in reading disorders common to both dyslexics and ‚garden-variety’ poor readers whereas ‚variabledifferences’ is to take care of the contrasts between the two groups. These contrasts originate from the dyslexic readers’ general cognitive abilities being average or even superior. Compared to generally backward readers, their better ‚horizontal’ abilities enable dyslexics to compensate for inferior word recognition by richer vocabulary, memory and world knowledge when reading comprehension is the criterion of achievement. On the basis of findings from experiments of context use by dyslexic children Snowling (1987, 137) comes to similar conclusions: “Hence, in the face of phonological difficulties, the reading development of dyslexic children may be fostered by the use of stored lexical and semantic information as well as by use of more general knowledge resources”. On the other hand, the garden-variety poor readers with phonological deficits — which might not be as severe
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as those of dyslexics — and inferior general cognitive abilities would show a broad-based developmental lag in reading achievement; Stanovich (1988b) provides evidence for this lag from longitudinal comparisons. — Admittedly, this model neglects a group of dyslexics which, though relatively small, is marked by different authors: so-called morphemic dyslexics (Seymour/MacGregor 1984 ) with difficulties in using the direct, visualorthographic route of accessing the lexicon. However, the model would predict all other processing characteristics in reading performance of the visual-orthographic group similar to the phonological-deficit group. Another complication not covered by the model is the existence of ‚Matthew-effects’ (Stanovich 1986b), i. e. progressive falling back in reading achievement and, as a consequence, in more global cognitive performance of the reading disordered compared to normal achievers. The above ideas fit well with the dimensional model inaugurated by Ellis. Passing through his “complete and unbroken gradation of intermediate dyslexics” (Ellis 1985, 192), linking the ‚pure’ psychometrically defined dyslexic to the ‚pure’ generally backward reader, “we will move from a processing deficit localized in the phonological core to the global deficits of the developmentally lagging garden-variety poor reader” (Stanovich 1988b, 602).
4.
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Helmut Skowronek/Harald Marx, Bielefeld (Germany)
70. Developmental Dyslexia and Language Disorders 1. 2. 3. 4. 5. 6. 7. 8.
1.
Introduction Spoken Language Deficits in Dyslexic Children Written Language Deficits in Dyslexic Children Individual Differences Amongst Dyslexic Children Higher-Level Language Difficulties in Dyslexic Children? Treatment Implications Conclusions and Future Directions References
Introduction
Impairments in language skills are common in dyslexic children. Parental reports show that they often learn to talk later than normal and, in interviews, they may show evidence of less complex language than normal children of the same age; it is also common for dyslexic children to show higher performance, than verbal, IQ scores. Language, however, is a complex system that can break down in different ways. Linguists stress the different levels of analysis necessary for adequately describing language processing. In particular, we need to distinguish between semantic processes concerned with meaning; syntactic processes concerned with grammar; phonological processes concerned with the sound structure of language; and pragmatics concerned with language use. These different levels of language clearly interact during processing. In
dyslexic children, there is considerable evidence for the primary deficit being in phonological processing.
2.
Spoken Language Deficits in Dyslexic Children
2.1. Phonological Awareness Phonological awareness refers to the ability to reflect explicitly on the sound structure of spoken words. Most research on phonological awareness has been concerned with its predictive relationship to reading in unselected samples of children. There is considerable evidence showing that phonological awareness tasks are among the best predictors of reading skill and, typically, these relationships can be shown to account for significant amounts of variance in reading skill, even after the effects of intelligence have been partialled out (see Goswami/Bryant 1990, 4 and Wagner/Torgesen 1987 for recent reviews). The strongest evidence for a link between phonological awareness and learning to read has been produced by Bradley and Bryant. In their first study, they compared a large group of dyslexic children with normal children of the same reading age and IQ on a sound categorization task (Bradley/Bryant 1978). Dyslexic children were much worse on this auditory task than normal children who were some 3½years younger, but read at the
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same level. This established that dyslexic children have difficulty in categorizing words on the basis of their sound and that this difficulty is not simply a consequence of their poor reading skills. Bradley/Bryant (1983) set out to test whether difficulties with sound categorization were a cause of reading difficulties. This was a longitudinal study. At the beginning, the sound categorization ability of over 4 00 4 and 5-year-old children was assessed before they started to learn to read. Over three years later, their reading and spelling ability and verbal intelligence were assessed. Performance on the sound categorization task was predictive of later reading scores, even when measures of intelligence and memory were taken into account. To try to check that this correlation between early sound categorization skills and reading reflected a causal influence, Bradley and Bryant included a training study. Sixtyfive children who initially were poor at sound categorization were split into four groups. One group was trained in sound categorization, and a second in addition to this was taught letter-sound correspondences. There were also two control groups: one group was taught to group words according to semantic categories and the other received no training. After training, spread over two years, the group that had been taught sound categorization and letter sound correspondences was some 8 to 10 months ahead of the untaught control group in reading scores. The group that had only been taught to categorize sounds was about 4 months ahead of the control group in reading, but this difference was not statistically significant. These results fail to clinch the argument for the causal role of sound categorization in learning to read. To prove this would require evidence that the group taught only to categorize words on the basis of their sound was significally ahead of the group taught to categorize on the basis of meaning. There was a tendency for this to happen, but not to a statistically reliable degree. Nonetheless, the association between phonological awareness and reading ability is highly robust, having been obtained in a number of studies. Lundberg/Olofsson/Wall (1981) gave a large group of Swedish children a battery of measures of phonological awareness. They found that these tests were predictive of reading scores 1 ½years later. A similar result to this has also been obtained by Stanovich/Cunningham/Cramer (1984 ), who
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found that a battery of measures of phonological awareness administered before starting to learn to read, predicted success in reading a year later. The different tests of phonological awareness were highly intercorrelated, suggesting that they were measuring some common underlying skill. More recently, attention has been drawn to the fact that different types of phonological awareness may develop at different rates and bear different relationships to the process of learning to read. This argument has been developed most fully by Goswami/Bryant (1990, 97). Their argument depends upon recognizing that there are different levels of analysis for spoken words and awareness of these develops at different rates. They stress the importance of the syllable, and two sub-syllabic units; namely, the onset and the rime. Within each syllable of English, the rime comprises the vowel and succeeding consonants, if any; the onset refers to the consonant or cluster which precedes the vowel. So, for example, the monosyllabic word string consists of an onset, /str/, and a rime, /ing/. One task that taps young children’s sensitivity to rimes is rhyme detection; for example, asking children to pick the odd (nonrhyming) word out from a group of four spoken words (Bradley/Bryant 1978). As we have seen, this task can be performed quite adequately by four- and five-year-olds, before they have learned to read, and is highly predictive of their later success in reading and spelling. The ability to segment words by phonemes appears later, possibly as a consequence of learning to read. It is a very difficult task for young children and shows serious impairment in dyslexic children. Goswami/ Bryant (1990, 97) argue, following a review of a very large number of studies, that it is awareness of onset and rime that is crucial to learning to read, whereas awareness of smaller speech segments (phonemes) arises at least partly as a consequence of learning to read. 2.2 Verbal Repetition Deficits Clinical reports often comment upon the tendency for dyslexic children to mispronounce words or produce Spoonerisms; for example, saying parcark for car park. Snowling (1981) asked dyslexic children to repeat a series of words of 2, 3 and 4 syllables and also a series of analogous nonwords derived from the words by changing one or two phonemes to others that were made either in the same place in the mouth or in the same manner. She
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compared their performance with that of a group of younger normal readers, who were matched with the dyslexics in terms of reading ability. Interestingly, while the dyslexics were as good as the control group when repeating the words, they made significantly more errors when repeating the nonwords. This difficulty was interpreted in terms of problems with the segmentation operations required for compiling new motor articulation programs that were needed for the repetition of nonwords. Snowling / Goulandris / Bowlby / Howell (1986) extended these findings to confirm that dyslexic children have specific difficulty with nonword repetition. In this experiment, subjects were required to repeat high-frequency words, such as dog and trick, low-frequency words, such as glades and chef, and nonwords made up by changing the first phoneme of the high-frequency words, such as tog and drick. All of the stimuli were of one-syllable, and they were presented either in a clear background, or with noise masking that was designed to reduce the signal to noise ratio. The dyslexic children were 10-year-olds, reading on average at the 8-year level. The first clear finding of the study was that although noise masking increased the error rate in the repetition task, it did so to the same extent for dyslexics as for normal readers. Therefore, it could be concluded that the dyslexics did not have any differential difficulty with the auditory perception of the word and nonword stimuli they had to repeat. However, there were interesting group differences with respect to the repetition of different stimulus types. None of the children had any difficulty in repeating high-frequency words but, interestingly, the dyslexics could repeat low-frequency words only as well as younger reading-age matched controls. In repeating nonwords, however, dyslexic children made even more errors than younger children reading at the same level. This was a striking finding that confirmed earlier reports of nonword repetition deficits in dyslexic children. The problems could not be attributed to perceptual difficulties because the dyslexics were affected no more by noise masking than the control group, and it could not be attributed to peripheral articulation difficulties, because in that case their pronunciation of all words should have been affected. The conclusion that they had specific difficulties with the segmentation processes required in order to assemble a new motor program, therefore, seemed the most likely explanation.
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It could be argued that a direct consequence of this difficulty in processing nonwords for pronunciation would be a delay in the acquisition of new lexical entries in the spoken language system. Initially, all unfamiliar words are ‘nonwords’ to a young child until, through learning, lexical entries are created for them. Dyslexics’ difficulty in repeating low-frequency items, relative to agematched controls fits in with this hypothesis, suggesting that they might be slower to expand their spoken vocabulary of words than expected, given their I. Q. Also consonant with this view is the finding of naming difficulties in dyslexics. 2.3. Auditory Perceptual Problems The language deficits with which we have been concerned arguably could be related to difficulties first in establishing, and later in accessing, adequate phonological representations. A number of studies have suggested that these problems may themselves be perceptual in origin. That is, developmental difficulties with speech perception could interfere with phonological processing. Brandt/ Rosen (1980) investigated the perception of stop consonants (e. g. d) by dyslexic and normal readers. They found that the dyslexics performed like children at an earlier developmental stage, a finding similar to that of Godfrey/Syrdal-Lasky/Millay/Knox (1981), who found that dyslexics were inconsistent in their phonetic classification of auditory cues in both discrimination and identification tasks. More recently, Reed (1989) carried out several experiments that pointed to the existence of a perceptual deficit in some dyslexic children. In Reed’s study, dyslexics had more difficulty in determining the order in which two stop consonants or two brief tones were presented than normal readers of the same age (7 to 10 years). In contrast, temporal order judgments that involved steady state vowels caused no difficulty. Similarly, the dyslexic children had more difficulty with a word identification task in which an auditorily presented word had to be matched with one of two pictures, differing by a single phoneme; e. g., goal paired with a pictorial representation of GOAL and BOWL. They were also less consistent in their phonemic categorization of stimuli, as evidenced by poorer identification of syllables in synthetic speech that were near a phoneme category boundary, as well as by poorer discrimination of syllable pairs that crossed the category boundary.
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Taken together, these findings seemed to suggest that the dyslexic children had difficulty with the perception of brief auditory cues, a difficulty that could plausibly account for their impaired performance on a range of phonological processing tasks. So far, the evidence we have reviewed paints a fairly clear picture as to the language deficits that are characteristic of dyslexic children. Foremost among these are difficulties with the processing of speech sounds, which, undoubtedly, would interfere with the child’s developing awareness of the phonological structure of words and also with the establishment of adequate phonological representations of spoken words. These deficits may also be directly implicated in reading failure.
3.
Written Language Deficits in Dyslexic Children
There is ample evidence that children make use of a sight vocabulary when reading, and they also can resort to the use of phonological strategies when presented with unfamiliar words. Furthermore, it seems clear that awareness of the phonological structures of words will be central to the development of decoding competence since this relies upon knowledge of correspondences between letters and letter sequences and sounds. It can be predicted, therefore, that dyslexics will have more difficulty with the acquisition of phonological reading strategies than normally developing children. 3.1. Phonological Deficits in Reading 3.1.1. Evidence from Single Word-Reading Tasks Words in English orthography vary in the directness of mapping sound onto spelling. Experimental studies often contrast regular words with irregular (or exception) words. The logic here is that irregular words should be read less well by children and adults according to the extent to which they utilize rules about spelling patterns in order to decode them. If dyslexics are poor at using such rules, they might be expected to show little difference in their ability to read regular and irregular words, as compared to normal children reading at the same level. Frith/Snowling (1983) found that dyslexic children were not susceptible to a regularity effect in their reading. While normal readers read a greater number of regular than matched irregular words,
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dyslexic children did not. Along similar lines, Szeszulski/Manis (1987) asked dyslexic readers to read regular and irregular words and nonwords comparing their performance with that of normal readers who were reading at the same grade level. Among children reading at the second-grade level, there were some interesting group differences; there was a larger regularity effect for normal readers, although the effect was apparent in both groups, and the dyslexics made fewer rulebased pronunciations of nonwords than the control group. These results from group comparisons suggest that dyslexics are less skilled in the use of decoding strategies. 3.1.2. Evidence from Nonword Reading One advantage of focusing on nonword reading in comparisons of dyslexic and normal readers is that nonwords are unfamiliar items. Reading them, therefore, taps into the processes that are used in learning to read which, by implication, are deficient in dyslexic readers. Snowling (1981) asked subjects to read monosyllabic and disyllabic nonwords of varying complexity. Overall, the dyslexics were slower and more error prone than reading-age matched controls when reading the nonwords aloud and they found the longer and more complex nonwords particularly difficult. Since this early study, many others have examined nonword reading skill in dyslexics. There is not space here to review these numerous studies (for a full review see Snowling/ Rack 1991). Suffice it to say that although a number of studies have challenged the view, there is considerable empirical support for the position that dyslexic children have specific difficulties with the acquisition of phonological reading strategies as indicated by specific difficulties in reading nonwords. This is particularly true when a stringent criterion of normal IQ is applied in the selection of dyslexic readers and when they are compared with normal readers matched for reading comprehension (Aaron 1989). This does not rule out the possibility, however, that some dyslexics may develop their use of graphemephoneme correspondence rules, following an initial setback and use them in a number of reading tasks; for example, in lexical decision.
4.
Individual Differences Amongst Dyslexic Children
Dyslexic children have difficulties with many tasks that require explicit phonological pro-
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cessing. Studies of their reading have suggested that their problems are mainly with the development and use of phonological strategies. It is tempting to argue that these weaknesses in the use of phonological reading strategies are caused by their weak underlying phonological skills. However, a major problem for this argument is that the findings are based entirely on group studies. By their very nature, group studies average across subjects and, therefore, overlook individual differences. These individual differences are of potential importance in theorizing about the specific impact of cognitive deficits on the acquisition of reading skills. While good evidence in favor of distinct subtypes is certainly lacking (Seymour 1986, 250; Treiman/Hirsh-Pasek 1985), most systematic studies of individual differences among dyslexics have revealed important variations in their reading and spelling skills. Researchers utilizing a cognitive-neuropsychological approach have provided unequivocal evidence that individual dyslexic children, studied at one point in time, can vary qualitatively with respect to their patterns of reading (and spelling) performance. First, developmental dyslexics who have a specific problem with phonological reading strategies, as revealed by their superior word reading ability compared to their nonword reading skill, have been likened to neurological patients with acquired phonological dyslexia following brain damage (Campbell/Butterworth 1985; Seymour/MacGregor 1984 ; Temple/Marshall 1983). In contrast, dyslexics who have relatively less difficulty with phonological reading strategies but have problems with direct lexical strategies, as evidenced by problems with the reading of irregular words, have been labelled developmental surface dyslexics (Coltheart/Masterson/Byng et al. 1983) or developmental morphemic dyslexics (Seymour 1986). The findings of cognitive-neuropsychological studies have enhanced our understanding of the different ways in which reading can break down following brain damage and, to some extent, as the consequence of developmental difficulties, but attempts to link these impairments with underlying processing deficits have been limited. Campbell/Butterworth (1985) speculated that the problems encountered by their subject, R. E., a developmental phonological dyslexic, stemmed
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from this individual’s inability to carry out phonemic parsing because of her extremely limited short-term memory capacity. However, since R. E. was already an adult by the time that she was studied, much of their argument remains conjecture, as does that of Funnell/Davidson (1989), who have recently described a similar case. Moreover, even within one so-called ‘subtype’, there is variation: Snowling/Stackhouse/Rack (1986) described seven developmental phonological dyslexics all of whom read nonwords significantly less well than expected, given their word recognition levels. Closer examination of the phonological skills of the individuals case by case suggested that the precise locus of their deficit affected the nature of the ‘dyslexia’ that they exhibited. Among dyslexics of lower reading age, this could be seen very clearly by an examination of their spelling errors. Perhaps most importantly, it might be deduced that phonological skills are a good predictor of future prognosis. In order to explore this possibility, longitudinal studies are needed for the purpose of mapping the cognitive profiles of individual dyslexic children and conducting ongoing follow-up of these children for an extended period of time to discern their eventual outcome in terms of reading and spelling processes. To this end, one of the children originally studied by Snowling/Stackhouse/Rack (1986), J. M., has been followed for now some six years. When first assessed, J. M. had problems primarily with output phonology (segmentation, memory, and repetition difficulties), and these difficulties persist to date, although he is now 14 years old (Hulme/ Snowling 1991). Interestingly, J. M. still cannot read nonwords effectively, and his spelling is markedly dysphonetic, despite several years of remediation that included phonics training (Snowling/Hulme 1989). One aspect of J. M.’s performance that may be of importance is that his visual skills are excellent. We have, therefore, speculated that he has learned to read by relying on his visual strengths. Potentially, then, individual case studies provide powerful tools for exploring the relationships between cognitive deficits and reading failure. The case of J. M. provides excellent confirmation for the picture emerging from group studies: there is a highly specific association between phonological deficits in the processing of both spoken and printed words.
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5.
Higher-Level Language Difficulties in Dyslexic Children?
A possible objection to the argument we have put forward, both with respect to single case and group studies, is that we have focused solely upon the processing of single words in spoken language and in reading tasks. Our argument has been that most dyslexic children’s primary deficit is with the phonological aspects of language. However, a number of recent studies have suggested difficulties with syntactic processing. Bowey (1986), for example, showed that there was a strong correlation between a measure of syntactic awareness and decoding skill, and that good readers performed at a higher level on tasks designed to tap the ability to judge grammatical wellformedness than poor readers. A problem with these studies, and others of similar ilk, is that it is possible that certain syntactic structures (for example, relative clauses) are only encountered with any degree of frequency in written language. It follows that poor readers will have had less exposure to such structures than good readers and so will have difficulty in dealing with them. In the absence of data from reading-age matched controls, it is not possible to judge the validity of these findings. Similarly, there have been a number of reports concerning the language comprehension abilities of dyslexic readers (Byrne 1981; Stein/Cairns/Zurif 198 4 ). Together, these studies have contributed to the formulation of the “structural lag hypothesis,” which asserts that dyslexics are delayed in their acquisition of certain syntactic structures (Shankweiler/Crain 1986). However, recent work has suggested that, rather than lacking knowledge of certain syntactic structures that emerge late in language acquisition, poor readers are subject to processing limitations that cause comprehension failure in particular contexts. In this regard, Macaruso/BarShalom/Crain/Shankweiler (1989) presented groups of good and poor seven-year-old readers with spoken sentences containing temporal terms; for example, Before you push the car, push the horse and After you pick up the truck, pick up the horse. The children were asked to move toys in line with the instructions in the test sentences. One experiment explored their performance when processing load was varied. One manipulation of processing load was brought about by adding pronominal modifers to half
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of the test sentences; for example, Push the second smallest horse before you push the car. A second manipulation was of context, so that subjects were first asked to choose one of the toys and then this item was included in the subordinate clause, thereby making the context helpful. Poor readers were found to make more errors with the interpretation of the complex noun phrases than with the simple versions, and also to have fewer problems in the context conditions. Overall, the results went against the structural lag hypothesis and suggested, instead, that poor readers are subject to processing limitations. It can be argued that these processing limitations arise because of their phonological deficits and, more specifically, their memory coding problems. Turning to written language processing, there is virtually no evidence that dyslexic children have difficulties with syntactic or comprehension processes which cannot be explained by the basic difficulty that they have with decoding skills (Perfetti/Goldman/Hogaboam 1979; Stanovich 1986). In fact, Stanovich (1980) argued that poor readers are likely to use context more during reading than good readers, to compensate for their slow decoding speed. In line with this position, Frith/Snowling (1983) found that dyslexic readers were as good as reading-age matched controls at selecting the missing words in a written text, using a modified cloze procedure. In short, we would argue that experiments exploring language processing beyond the single word level have failed to find deficits in dyslexia which cannot be explained in terms of relatively low-level phonological difficulties such as word-finding and short-term memory problems. These data underscore the specificity of the problem facing dyslexic readers, a problem that resides in the processing of speech-based material and one that has an impact on the development of phonological coding capacities for both written and spoken language.
6.
Treatment Implications
Despite the enormous number of published studies on developmental dyslexia, there has been scarcely any research directed at the question of how best to treat these difficulties. A number of studies carried out in dyslexia clinics in U. K., using variants of multi-sensory teaching techniques have reported gains in reading performance but these studies have
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lacked appropriate experimental controls, limiting their validity (Andrews/Shaw 1986; Hornsby/Miles 1980). In Canada, Lovett/ Ransby/Barron (1988) compared the effectiveness of three teaching regimes, one providing training in word recognition and decoding skills, one in both oral and written skills and one in ‘classroom survival skills’, an alternative treatment control. There was a posttraining advantage for readers defined as accuracy disabled and rate disabled, for those who received the training in word recognition and decoding. Once again, however, it is difficult to evaluate the specific aspects of treatment which led to gains, given the realistic but, therefore, uncontrolled teaching regimes. The predominant approach to teaching dyslexic children recognizes their difficulty with sounds. The most popular teaching schemes embody highly structured phonic teaching with explicit emphasis on learning to relate spelling patterns to sound (Hornsby 1985). There is, however, a dearth of empirical evidence to substantiate claims for the effectiveness of these approaches. Moreover, there is reason to suppose that these methods, which involve teaching children to decode words phoneme by phoneme, will place a burden on skills of phonemic awareness, short-term memory, and sound blending, all of which tend to be deficient in dyslexic children. It may be the case that some dyslexic children fail to respond to these programmes for reasons related to the extent and severity of their (phonological) impairment, and learn to read using an alternative whole-word approach. Certainly, J. M., whom we discussed earlier, has been taught by these methods, yet he has evidently learned to read slowly and without developing phonological reading strategies (Snowling/Hulme 1989). A possible reason for the failure of phonic methods to help J. M. and some other dyslexics is that the traditional phonic approach to teaching these children is based on a very crude theoretical position: dyslexic children are deficient in phonic skills and they need to be taught them explicitly. In fact these techniques may simply place excessive demands upon many dyslexic children’s ability to deal with speech sounds. The work described earlier concerned with phonological awareness and the distinction between the sub-syllabic units, onset and rime, is relevant here. The predictive relationship between the ability to detect rhymes and learning to read most likely arises because children use their
V. Pathologies and Disorders of Language Development
knowledge of the shared sound similarities between words to categorize the written versions of these words. Hence, knowing that TRAIN, BRAIN and MAIN rhyme may allow a child to read brain and main by analogy with train (Goswami 1988) and to spell them alike. This work leads naturally, therefore, to a tentative suggestion for a method for teaching dyslexic children to read and spell. Since we know that sensitivity to rhyme normally develops prior to sensitivity to phonemic units, teaching methods should capitalize on the relative ease of segmenting words into onset and rime units. Analysis of words into onset and rime units should increase sensitivity to mappings between groups of letters and sound segments (e. g. /ight/ is pronounced /ite/), and thereby facilitate the learning of spelling patterns to sound relationships. In essence, teaching through onset-rime divisions may represent a fruitful new approach because it will encourage the development of analytic reading strategies without overburdening the dyslexic’s weak phonological skills. There is some preliminary evidence from experimental studies to support this approach to teaching. Bradley/Bryant (1983) found that training children to categorize words according to their sounds (onsets and rimes) in combination with training in representing the sounds of words with letters led to significant improvements in these children’s reading and spelling skills. More recently, Wise/Olson/ Treiman (1990) have looked directly at teaching normal children to read words divided into onset and rime units, using a computer. The word to be learnt was presented on a monitor screen and groups of letters within the word could be separately highlighted. At the same time a text-to-speech system would produce the sound of the part of the word which was highlighted. Sometimes the division of the word coincided with the onset/ rime division, sometimes it did not. They found that words taught by separating them into onset and rime were learned better than those that were not. However, this was far from a realistic teaching study. The children were only seen once, and we do not know whether such learning would be durable or show generalization. Nevertheless, this study provides an excellent starting point for more realistic teaching studies. It seems possible that methods based on the onset rime distinction may prove particularly useful for dyslexic children.
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7.
Conclusions and Future Directions
There can be little doubt, to our minds, that research in this field has made massive strides forward in recent years. The research reviewed here indicates with some precision the range of phonological deficits that affect many dyslexic children. Furthermore, there are good grounds for believing that these phonological deficits play a role in causing these children’s reading difficulties. What then should research in the near future be trying to achieve? There are three issues which, to us, stand out as being important and worthy of more scrutiny. The first is to continue to forge explicit links between underlying phonological deficits and problems in learning to read and to spell. There is by now no doubt that many dyslexic children experience difficulties with a wide variety of phonological skills such as phonological awareness and nonword repetition. A major issue is to relate these deficits more explicitly to the patterns of reading and spelling difficulties in these children. The second issue follows directly from the first and concerns the problem of individual differences. The charge that experimental psychologists too often ignore individual differences amongst their subjects is far from novel. In the field of dyslexia it is potentially very important, however. It is a truism that dyslexic children, like normal children, differ. We badly need more precise information about these differences and the origin (in terms of underlying cognitive processes) of different patterns of reading and spelling problems. Such knowledge is of great theoretical interest in terms of understanding the cognitive processes involved in learned to read. In practical terms such knowledge undoubtedly will have an important bearing upon the development of teaching techniques. This brings us to our final issue which concerns remediation. We have spent relatively little time in this chapter talking about remediation. This, we would argue, is an unfortunate reflection upon our current state of knowledge. The balance of research in this area has been very much to focus on the difficulties that characterize dyslexic children rather than how these difficulties can be treated. To some extent this is defensible, before trying to tackle a problem it is undoubtedly useful to have an accurate description of its nature. Having read this far, we hope people will agree with our view that we now know a considerable amount about the nature of dyslexia; the time is now ripe to turn to studies
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which directly confront treatment. We have made some fairly specific suggestions about the implications of current knowledge about the cognitive deficits in dyslexic children for teaching. It is to be hoped that in the near future these important practical issues are given more attention in research studies. Studies of treatment and its effectiveness in the long term are very powerful ways of assessing the adequacy of our current theories about the underlying causes of dyslexia. Authors’ note: This chapter was written while the first author was in receipt of MRC Grant No. G 8801538 N and while the second author was in receipt of a Nuffield Foundation Social Science Research Fellowship.
8.
References
Aaron, P. G. (1989). Qualitative and quantitative differences among dyslexic, normal and non dyslexic poor readers. Reading & Writing, 1, 291—309. Andrews, N. & Shaw, J. (1986). The efficacy of teaching dyslexics. Child: care health and dev elopment, 12, 53—62. Bowey, J. A. (1986). Syntactic awareness in relation to reading skill and ongoing reading comprehension. Journal of Experimental Child Psychology 41, 282—299. Bradley, L. & Bryant, P. E. (1978). Difficulties in auditory organisation as a possible cause of reading backwardness. Nature, 271, 746—747. Bradley, L. & Bryant, P. E. (1983). Categorising sounds and learning to read: a causal connexion. Nature, 301, 419—421. Brandt, J. & Rosen, J. (1980). Auditory-phonemic perception in dyslexia: categorised identification and discrimination of stop consonants. Brain & Language, 9, 324—327. Byrne, B. (1981). Deficient syntactic control in poor readers: is a weak phonetic memory code responsible? Applied Psycholinguistics, 2, 201—212. Campbell, R. & Butterworth, B. (1985). Phonological dyslexia and dysgraphia in a highly literate subject; a developmental case with associated deficits of phonemic awareness and processing. Quarterly Journal of Experimental Psychology, 37 A, 435—475. Coltheart, M., Masterson, J., Byng, S., Prior, M., & Riddoch, J. (1983). Surface dyslexia. Quarterly Journal of Experimental Psychology, 35 A, 469—496. Frith, U. & Snowling, M. (1983). Reading for meaning and reading for sound in autistic and dyslexic children. British Journal of Dev elopment Psychology, 1, 329—342.
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Funnell, E. & Davidson, M. (1989). Lexical capture: a developmental disorder of reading and spelling. Quarterly Journal of Experimental Psychology, 41 A, 471—487. Godfrey, J., Syrdal-Lasky, A., Millay, K., & Knox, C. (1981). Performance of dyslexic children on a speech perception test. Journal of Experimental Child Psychology, 32, 401—424. Goswami, U. (1988). Orthographic analogies and reading development. Quarterly Journal of Experimental Psychology, 40A, 329—268. Goswami, U. & Bryant, P. (1990). Phonological skills and learning to read. London: Erlbaum. Hornsby, B. (1985). A structured phonetic-linguistic method for teaching dyslexics. In M. Snowling, M. (Ed.), Children’s written language difficulties. 119—133. Windsor: NFER-Nelson. Hornsby, B. & Miles, T. (1980). The effects of a dyslexia centered teaching programme. British Journal of Educational Psychology, 50, 236—242. Hulme, C. & Snowling, M. (1991). Deficits in output phonology cause developmental phonological dyslexia. Mind and Language, 6, 130—134. Lovett, M., Ransby, M., & Barron, R. (1988). Treatment, subtype and word type in dyslexic children’s response to remediation. Brain & Language, 34, 328—349. Lundberg, I., Olofsson, A., & Wall, S. (1981). Reading and spelling skills in the first school years predicted from phonemic awareness skills in kindergarten. Scandinav ian Journal of Psychology, 21, 159—173. Macaruso, P., Bar-Shalom, E., Crain, S., & Shankweiler, D. (1989). Comprehension of temporal terms by good and poor readers. Language and Speech, 32, 45—67. Perfetti, C., Goldman, S., & Hogaboam, T. (1979). Reading skill and the identification of words in discourse context. Memory and Cognition, 7, 273—282. Reed, M. (1989). Speech perception and the discrimination of brief auditory cues in reading disabled children. Journal of Experimental Child Psychology, 48, 270—292. Seymour, P. H. K. (1986). Cognitiv e analysis of Dyslexia. London: Routledge and Kegan Paul. Seymour, P. H. K. & MacGregor, C. (1984 ). Developmental dyslexia: a cognitive experimental analysis of phonological, morphemic and visual impairments. Cogniti v e Neuropsychology, 1, 43—82. Shankweiler, D. & Crain, S. (1986). Language mechanisms and reading disorder: a modular approach. Cognition, 24, 139—164. Snowling, M. (1981). Phonemic deficits in developmental dyslexia. Psychological Research, 43, 219—234.
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Snowling, M. & Hulme, C. (1989). A longitudinal case study of developmental phonological dyslexia. Cognitive Neuropsychology, 6, 379—401. Snowling, M., Goulandris, N., Bowlby, M., & Howell, P. (1986). Segmentation and speech perception in relation to reading skill. Journal of Experimental Child Psychology, 41, 489—507. Snowling, M. J. & Rack, J. P. (1991). Dyslexia: deficits in grapheme-phoneme correspondence? In J. Stein (Ed.), Vision and Visual Dyslexia. 189— 195. London: MacMillan. Snowling, M. J., Stackhouse, J., & Rack, J. P. (1986). Phonological dyslexia and dysgraphia: a developmental analysis. Cogniti v e Neuropsychology, 3, 309—339. Stanovich, K. E. (1980). Toward an interactivecompensatory model of individual differences in the development of reading fluency. Reading Research Quarterly, 16, 32—71. Stanovich, K. E. (1986). Cognitive processes and the reading problems of learning-disabled children: Evaluating the assumption of specificity. In J. Torgeson & B. Wong (Eds.), Psychological and educational perspectiv es on learning disabilities. 58—84. New York: Academic Press. Stanovich, K. E., Cunningham, A. E., & Cramer, B. B. (1984 ). Assessing phonological skills in kindergarten children: Issues of task comparability. Journal of Experimental Child Psychology, 38, 175—190. Stein, C., Cairns, H., & Zurif, E. (1984 ). Sentence comprehension limitations related to syntactic deficits in reading-disabled children. Applied Psycholinguistics, 5, 305—322. Szeszulski, P. & Manis, F. (1987). A comparison of word recognition processes in dyslexic and normal readers at two different reading age levels. Journal of Experimental Child Psychology, 44, 364—376. Temple, C. & Marshall, J. (1983). A case study of developmental phonological dyslexia. British Journal of Psychology, 74, 517—533. Treiman, R. & Hirsh-Pasek, K. (1985). Are there qualitative differences in reading behavior between dyslexics and normal readers? Memory and Cognition, 13, 357—364. Wagner, R. & Torgeson, J. (1987). The nature of phonological processing and its causal role in the acquisition of reading skill. Psychological Bulletin, 101, 192—212. Wise, B., Olson, R., & Treiman, R. (1990). Subsyllabic units as aids in beginning readers word learning: Onset-rime versus post-vowel segmentation. Journal of Experimental Child Psychology, 49, 1—19.
Margaret Snowling, Newcastle upon Tyne (United Kingdom)/ Charles Hulme, York (United Kingdom)
71. Developmental Dyslexia and Cognitive Processes
71. 1. 2. 3. 4. 5.
1.
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Developmental Dyslexia and Cognitive Processes Methodological Issues: Trying to Establish Causes Visual Problems Verbal Memory Problems Conclusions and Future Directions References
Methodological Issues: Trying to Establish Causes
In the present chapter we will consider some of the many studies concerned with cognitive deficits in dyslexic children. One important aim will be to evaluate the likelihood that the deficits described are causes of these children’s reading difficulties. It may be comparatively straightforward to measure the extent of dyslexic children’s reading problems and describe some associated difficulties. It is much more difficult, however, to try to show the underlying causes of their reading problems. Most of the evidence we have about dyslexia comes from studies which compare dyslexic with normal readers of the same age. Studies of this sort reveal a number of differences between normal and dyslexic children in, for example, language and memory tasks. These studies provide important clues as to the possible causes of the reading problem, but they are in themselves logically incapable of demonstrating causes. Effectively, what they show is a correlation between performance on a given task and reading ability. Logically there are three possible explanations for correlations of this sort. It may be, as commonly suggested, that a task that is performed badly by dyslexic children taps a cause of their reading difficulty. Alternatively, the causal connection could be of the opposite form; their poor performance on a task could be a consequence of not having learned to read. A third possibility is that some deficits may be irrelevant to the reading difficulty. If dyslexic children show neurological immaturity, it seems likely that their performance on many psychological tasks will deviate from that of normal children; but many of these deviations may be quite irrelevant to the cause of their reading problems. There are three ways of reducing the ambiguities of such correlational findings. First, one may add a further control group matched for reading achievement and IQ but whose
reading is appropriate for their age, i. e. a younger control group (e. g. Bradley/Bryant 1978). If the dyslexic children are inferior on a given measure in comparison to such a group, this difference cannot be attributed to their lack of reading experience or ability. The probability of it being related to the cause of the reading problem is therefore increased. The logic behind this type of comparison is in fact exactly the same as in longitudinal studies. In these studies measurements of certain abilities are made in children before they have started to learn to read. Their progress in reading is then followed and related to these early measurements. If these measures are predictive of later reading failure at least one can be sure that this does not depend upon the effects of such failure. The results of longitudinal studies, or those in which subjects are matched for reading age, still have a major problem of interpretation because any deficits found which relate to dyslexia may be irrelevant to its cause. Interpretations here will be guided by the logical relationship between the task and the process of learning to read. A causal interpretation in such a case can be strengthened by forging explicit links between the observed deficit and the dyslexics’ difficulties. For example, if it could be shown that some dyslexic children have poor visual memories, the causal status of this finding might be supported by showing that their spelling errors tended to be visually dissimilar to the correct form of the word, but similar phonetically (c. f. Boder 1973). The third and most direct (and also the most difficult) way out of this correlational problem is to perform training studies aimed at correcting the inferred deficit and observe the effects of this on reading. Although difficult to conduct, studies of this type probably provide the most direct route for demonstrating the causes of dyslexia. A problem for studies of this type, however, is that some deficits that we find in dyslexic children, which seem likely candidates as causes of their reading problem, may not be amenable to improvement by training. It will be clear from all this, that the problems facing us in trying to establish the causes of dyslexia are formidable. Once we accept the idea that different causes may operate in different cases (see below) and that there may be multiple causes that interact in complex
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ways, the task becomes even more daunting. We will try, nevertheless, in what follows to assess the likelihood that various findings do tap a cause of the reading problem.
2.
Visual Problems
If dyslexic children had some generalized weakness in perceiving and remembering visual patterns, such as words, this would provide a good explanation for difficulties in learning to read. There has been a large amount of research addressed to testing this idea. Most of this research provides a clear answer: for most dyslexic children problems of visual perception and memory are not the cause of their problems. Much of this research has been reviewed in detail before (see, for example, Hulme 1981, 33; Jorm 1983); it will be sufficient here to summarize some of the more prominent findings of the older studies in this area. Vellutino and his colleagues have demonstrated normal visual memory abilities in dyslexic children in several studies. Vellutino/ Pruzek/Steger/Meshoulham (1973) showed Hebrew words to normal and dyslexic children and asked them to draw them from memory. Both groups did this equally well though children who were learning to read Hebrew, not surprisingly, did better than either group. This experiment looked at shortterm memory. In a further study, long-term memory for Hebrew letters was assessed by recognition either immediately, or after 24 hour or six-month delays. Once again there were no differences between normal and dyslexic children (Vellutino/Steger/DeSetto/Phillips 1975). Dyslexic children have also been found to perform normally on visual pairedassociate tasks (Goyen/Lyle 1971; Vellutino/ Steger/Pruzek 1973). The tasks in these studies are demonstrably similar in their visual requirements to learning to read, and yet dyslexic children perform normally on them. Taken together therefore they argue persuasively against the idea that dyslexic children typically have visual problems that cause their reading problems. More recently there have been attempts to revive the idea of a visual deficit as a cause of dyslexia using different tasks. We will consider three such attempts in some detail now. 2.1. Eye Movements Skilled reading involves the control of complex sequences of eye movements. Eye move-
ments were one of the first aspects of reading to attract interest in the studies of experimental psychologists. It was soon noticed that people who read poorly showed abnormal eye movements (Tinker 1958). As Tinker pointed out, however, the peculiar eye movements of poor readers were a consequence and not a cause of their poor reading. Recently this old idea about the cause of reading difficulties has resurfaced. Pavlidis (1981) reported that a group of dyslexic children showed erratic eye movements when asked to track a series of sequentially illuminated lights. He argued that these disordered eye movements might be a direct cause of the reading problem, or alternatively both the reading and eye movement problems might reflect some underlying ‘general sequencing disability’. It is now clear that this alleged problem with the control of eye movements is not a reliable correlate of dyslexia. Three separate studies have failed to replicate Pavlidis’s findings. Brown/Haegerstrom/Portnoy/Adams et al. (1983) and Stanley/Smith/Howell (1983) found absolutely no difference in the eye movements of normal and dyslexic children when tracking sequences of lights. Most convincingly Olson/Kliegl/Davidson (1983) set out to conduct an exact replication of Pavlidis’s study, and as in the other two attempted replications, found no difference between dyslexic and control children’s eye movements. It seems an inescapable conclusion that, contrary to the original claims of Pavlidis, dyslexic children do not have difficulty with such tasks. There may be very rare cases of individuals with neurological damage who show grossly abnormal eye movements which interfere with their ability to read (e. g. Pirozzolo/Rayner 1978). There is no evidence, however, that a significant number of dyslexic children suffer from some basic deficit in the control of eye movements that prevents them from learning to read. 2.2. Eye Dominance The old idea that dyslexia might relate to the lateralization of visual function was advanced by Dunlop/Dunlop/Fenelon (1973) using a test to determine the ‘dominant’ or ‘reference’ eye. In this test the child looks down two tubes so that each eye has a view of one of two similar slides. In both slides there is a picture of a house with a central front door and the subject is asked to fixate the centre of this door. In one slide there is a small tree to the left of the front door and in the other
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there is a larger tree to the door’s right. To begin with the tubes converge and the subject has the impression of a fused image of a single house with a tree on either side of the door. When the tubes are made to diverge, before fusion breaks down, most subjects apparently get a strong impression that one of the trees moves towards the door. The eye whose image remains static is said to be the ‘dominant’ or ‘reference’ eye. The neurological basis of this effect is little understood. Dunlop/Dunlop/Fenelon (1973) reported that crossed reference i. e. a reference eye on the opposite side to the preferred hand, was associated with dyslexia. They proposed a causal theory on the basis of these findings suggesting that the failure to develop an appropriate reference eye leads to perceptual problems which interfere with learning to read. Just why crossed reference should be so crucial in this respect is not clear. This idea was pursued by Stein/Fowler (1982). They studied a large group of dyslexic children and a matched group of normal children who were classified as showing ‘fixed’ or ‘unfixed’ dominance. Contrary to Dunlop/ Dunlop/Fenelon many of the dyslexic children showed unfixed dominance whilst crossed dominance was less common in the dyslexic children than the normals. Stein/ Fowler (1985) then reported an intervention study designed, by occluding one eye, to produce fixed ocular dominance in dyslexic children. They claimed that occluding one eye had beneficial effects both on ocular dominance and reading progress, and concluded a causal factor (at least for some children) had been identified. Unfortunately there are a number of problems with this study which make such conclusions far from secure. These problems include the fact that allocation to treatment and control groups was not random, and that the characteristics of the children in the different groups in terms of their ages, reading ages and IQs are not given. In a detailed critique of this study Bishop (1989) conducted a reanalysis of the data and found no evidence for the importance of ocular dominance as a cause of dyslexia. One final problem concerning this research is the failure of other studies to confirm the association between ocular dominance and reading problems. Both Bishop/Jancey/Steel (1979) and Newman/Karle/Wadsworth et al. (1985) in large unselected groups of children did not find any evidence of an association
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between reading problems and the Dunlop test of ocular dominance. 2.3. Brief Visual Displays Many studies show that dyslexic children have difficulty in dealing with rapid visual displays. An early example of this is in the work of Lyle/Goyen (1975). They looked at the recognition of abstract shapes presented in a tachistoscope to normal and dyslexic children. Dyslexic children were less accurate in recognizing the forms but only at very brief exposures. There was no difference between the groups at longer exposure durations, and both groups were similarly affected by making the discriminations required more difficult. More recently the idea of an association between deficits on tasks involving rapid visual displays and dyslexia has been pursued further by Lovegrove/Martin/Slaghuis (1986) who argued that a low-level visual deficit in a large proportion of dyslexic children may be a cause of their reading problems. They summarize a large body of carefully conducted studies of visual processing in dyslexic children and provide three major types of evidence concerning their visual abilities. (1) The function relating visible persistence to spatial frequency differs in dyslexic compared to control children. (2) On measures of pattern contrast sensitivity there are small but consistent differences between dyslexics and controls. Dyslexics are less sensitive than controls to low spatial frequency gratings but are equally, or more sensitive to high spatial frequencies. (3) With flickering gratings, dyslexics are less sensitive at all flicker rates but particularly so at high rates. These results are taken as evidence that retarded readers have a deficit in the visual transient subsystem (Kulikowski/Tolhurst 1973). In a fourth series of experiments, designed to measure the sustained subsystem, no differences between retarded readers and normal children were found. The idea of a deficit in the transient system of retarded readers appears to offer a useful link between a varied set of findings. The idea that such a deficit is responsible for these children’s reading difficulties seems highly implausible, however. Hulme (1988) argued that the visual requirements of the tasks used to assess the functioning of the transient system in these experiments are remote from the conditions experienced by children learning to read, and that the hypothesis predicts that dyslexic children should have
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most difficulty when reading prose rather than when reading isolated words. In fact the opposite pattern seems to characterize the majority of dyslexic children. Hulme argued that the deficit demonstrated in these experiments is most likely an irrelevant correlate of these children’s reading difficulties, possibly related to their neurological immaturity. 2.4. Individual Differences Amongst Dyslexic Children and the Role of Visual Problems It seems an inescapable conclusion that visual perceptual and memory problems are not a cause of the reading difficulties of most dyslexic children. A persistent idea, however, is that there may be a minority of dyslexic children whose reading difficulties do stem from visual difficulties (Hulme/Snowling 1988). Recently evidence for this view has come from a case study of a development dyslexic, J. A. S., studied when an adult by Goulandris/Snowling (1991). J. A. S. had good phonic decoding skills but in her reading she confused homophones (e. g. pair-pare; pair-pear) which require the use of visual information to discriminate their meaning when presented in isolation. Her spelling was highly error prone but extremely phonetic, suggesting a poor memory for the visual appearance of words. In line with this hypothesis J. A. S. had severe visual memory deficits, these deficits we believe are a plausible cause of her reading failure. We badly need more studies of cases such as J. A. S. whose reading and spelling difficulties seem related to visual deficits. The best evidence we have so far indicates that such cases are probably quite rare.
3.
Verbal Memory Problems
This is one area that has been investigated a great deal in dyslexic children. Learning to read draws heavily upon verbal memory and it is clear that problems in this area are likely causes of reading problems. 3.1. Short-term memory A common measure of short-term memory is digit span: the number of digits a child can repeat in correct serial order immediately after hearing them. As is usual in short-term memory tasks, here the person has to remember a small amount of information for a relatively short time and the order of recall is important. There is ample evidence that dys-
lexic children typically do poorly on digitspan tests and other measures of short-term memory (Jorm 1983, Siegel/Linder 1984 ). Moreover, the claim has often been made that their memory problems are attributable to difficulties with the use of phonological codes (Shankweiler/Liberman/Mark et al. 1979). This claim was based on findings that they did not exhibit the classic phonemic confusability effect in short-term memory (memory for lists of rhyming items being shorter than memory for lists of nonrhyming items.). The validity of this claim was first questioned by Hall/Wilson/Humphreys et al. (1983) who showed that, provided the level of task difficulty was equated for good and poor readers, they were equally susceptible to phonemic confusability effects in memory. A series of studies by Johnston and colleagues provide corroborative evidence (Holligan/ Johnston 1988; Johnston 1982, Johnston/ Rugg/Scott 1987). For example, Johnston/ Rugg/Scott (1987) compared groups of poor readers (of average or below average intelligence) with age-matched and Reading Agematched controls on memory span tests, having first adjusted task-difficulty for each child by pre-testing performance on memory for lists of dissimilar items. Performance of the four groups at two age levels (eight and eleven years) was then assessed when recalling strings of phonemically similar letters (e. g. b, c, d, g, p). All groups here showed a phonemic similarity effect. It can be concluded that dyslexic children are, on average, subject to impairments of verbal short-term memory though it does not seem to be the case that they use different coding processes. Thus, dyslexic and normal readers show evidence of speech-based coding of information, as assessed by the occurrence of the phonemic similarity effect (see Hulme/Tordoff 1989, for discussion of the mechanisms responsible for this effect and its development). An important question is how short-term memory problems in dyslexics might hinder learning to read. Short-term memory is often held to serve as a working memory system when reading (Baddeley/Hitch 1974 ), the idea being that this system is used to keep track of the order of words in phrases and sentences (e. g. Kleiman 1975). Impairments of shortterm memory might, therefore, be expected to lead to problems in the comprehension of prose, particularly when word order is crucial to the meaning. However, there is no evidence that dyslexic children have any particular dif-
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ficulties with reading prose, over and above those attributable to their difficulties in identifying words. It is less obvious how short-term memory problems could create difficulties in learning to identify individual words which is where, we would argue, the dyslexic’s problems lie (cf. Aaron 1989). One possibility, however, is that these problems lead to difficulties with phonic blending. When decoding a word that is not known the child must produce a set of possible pronunciations for the letters in the word. These separate sounds must then be blended to produce a possible pronunciation for the word as a whole. Beginning readers can often be heard to go through this process overtly. Torgeson/Wagner/Balthazar et al. (1989) showed that beginning readers find blending tasks easier if the individual sound segments are presented at a fast rate, thereby reducing memory load. Thus, it is indeed possible that short-term memory problems could make the blending procedure difficult for dyslexic children. Torgeson/Rashotte/Greenstein et al. (1988) tested this possibility. They compared a group of dyslexic children selected for low digit-span scores with normal readers, and a group of dyslexic children with normal digit spans, on a sound blending test from the Illinois Test of Psycholinguistic Abilities. In this test a series of words and nonwords is spoken to the child, one at a time, in segmented form (e. g. b-a-g) and the child is asked to say the word (bag). The dyslexic children with low spans were very much worse on this task than the normal readers, or the dyslexic children with normal spans, who did not differ. It seems likely that some dyslexic children’s short-term memory problems contribute to the difficulties they have with phonics. An alternative explanation for the shortterm memory problems of dyslexic children is that they are a consequence, and not a cause, of their reading problems. Perhaps learning to read brings improvements in short-term memory. One approach to this is to compare dyslexic children with normals of the same reading age. When this is done the groups do not differ on short-term memory tasks but it is always possible that this is because of the age-advantage which then accrues to the dyslexics. A better approach is to conduct longitudinal studies, where memory is assessed before children start to learn to read. The evidence from this sort of study on the whole suggests that memory difficulties precede
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reading difficulties. Jorm/Share/MacLean/ Mathews (1984 ) gave a large group of 5-yearolds a sentence memory task on entry to school. They tested all the children again on the memory test when they were almost 7, and also gave them an IQ and a reading test. Memory scores at first testing correlated with later reading scores when the effects of age and IQ were partialled out. This indicates that good memory scores before learning to read are predictive of later success in reading and is consistent with the possibility of a causal influence of memory ability on reading ability. It is worth noting that the memory test used here, involving sentences, differs from conventional short-term memory tasks which involve meaningless strings of items. However, Mann/Liberman (1984 ) assessed memory for unrelated strings of words in kindergarten children before they started reading and found that this did correlate with reading scores one year later. In conclusion, it seems quite possible that the short-term memory problems commonly found in dyslexic children do contribute to their difficulties in learning to read. The most obvious way in which this might come about is because of difficulties with phonic blending. In addition short-term memory problems may lead to difficulties in holding partially decoded words in mind whilst they are compared with the pronunciations of words retrieved from long-term memory. The idea that short-term memory problems are causally related to reading problems is far from firmly established however. It is clear that there is an association between short-term memory problems and reading problems. The slight inconsistencies in the evidence on this probably reflect the fact, very nicely demonstrated by Torgeson/Rashotte/Greenstein et al. (1988), that these problems are not characteristic of all dyslexic children. The time would now seem ripe for studies designed to show that this association reflects a causal link between memory problems and reading problems. The natural way to do this would be to conduct training studies which attempt to improve the short-term memory abilities of dyslexic children. If such training was effective and led to improvements in reading this would be good evidence for a causal connection. 3.2. Long-term Memory Even if short-term memory problems were of no consequence as causes of reading difficulties, it might still be the case that problems
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with more durable forms of memory were important. Rather surprisingly, studies of long-term memory in dyslexic children are less common than those of short-term memory. One long-term memory task that has been studied a good deal is paired-associate learning. Here the child has to make an arbitrary association between a stimulus and a response. The most relevant task to learning to read is visual-verbal paired-associate learning. Here the child has to learn a name to go with some visual stimulus (often an abstract shape). The evidence from paired-associate tasks is very clear: when these tasks involve a verbal component, dyslexic children almost invariably perform more poorly than normal children of the same age (Hulme 1981, 42). It is plausible that difficulties of this sort could lead to problems in learning to read. In the early stages of learning to read, children may develop a considerable sight vocabulary by simply learning arbitrary associations between certain patterns of letters and their spoken counterparts. A child who has difficulty with paired-associate learning will have difficulty at this most elementary stage in learning to read. The other major way of learning to read is by phonics. Here the child learns rules relating the letters used to spell words to their constituent sounds. A necessary step for this to happen is that the child learns the sounds of the letters. This again is an example of paired-associate learning and many dyslexic children have profound difficulty in mastering the names and sounds of letters. Another way of exploring the long-term memory system of normal and dyslexic readers is by the use of recognition memory or cued recall tasks. Here the evidence is relatively consistent in pointing to the tendency for normal readers to make use of phonological memory codes, and for this tendency to be reduced in dyslexics (Byrne/Shea 1979; Mark/Shankweiler/Liberman/Fowler 1977). However, Olson/Davidson/Kliegl/ Davies (1984 ) found this phonetic confusability effect decreased with age for normal readers but increased for dyslexics. This shows the dyslexics were delayed in the acquisition of these codes but they were by no means completely deficient. These findings, together with analyses of error data in this experiment are compatible with the hypothesis that the absence of phonological coding strategies at a specific developmental stage, might induce the use of compensatory (visual)
V. Pathologies and Disorders of Language Development
memory strategies. In line with this ‘compensation’ hypothesis, Rack (1985) found differences between 12- to 13-year old dyslexics and younger Reading Age-matched controls, suggesting that dyslexics used orthographic codes in cued recall whereas normal readers used phonological codes. In the first part of this experiment, subjects carried out a rhyme judgement task on pairs of words and, in the second part, they were shown one item from each pair and they had to recall the item which had appeared with it previously. Dyslexic and normal readers performed as well as each other in the rhyme judgements and their overall levels of recall were the same (note that the normal children were younger). However, while normal readers recalled a greater number of the rhyming stimuli, regardless of orthographic similarity, the dyslexics recalled more of the orthographically similar items, irrespective of rhyming similarity. These results suggested that the dyslexics were relying less upon the use of phonological memory codes than their younger Reading Agematched controls. A similar result was reported by Holligan/Johnston (1988) comparing eight-year-old poor readers with age- and Reading Age-matched controls. In a recognition memory task, following written rhyme judgements, the poor readers tended to choose orthographically similar pairs whereas the normal controls chose phonologically similar pairs. Thus, it is quite plausible that dyslexic readers have difficulty with the use of phonological codes in long-term memory. These difficulties could create significant problems during reading which requires the ongoing retrieval of phonological information in response to the visual input of printed words. 3.2.1. Naming Deficits Another task that requires the retrieval of phonological information from long-term memory is naming. Word finding difficulties are often reported in dyslexic children and experimental studies using rapid automatized naming tasks (RAN) usually report deficiencies in dyslexics. The classic study of this was by Denckla/Rudel (1976) who gave normal children and dyslexic children random lists of objects, colours, letters and numbers to name as fast as possible. The dyslexic children were very much slower here and, although appropriate analysis is not reported, it looks as
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though the older dyslexic children were actually slower than younger normal children of the same reading age. The dyslexic children’s difficulty here is probably not simply a consequence of their poor reading skill. Extending these findings, Katz (1986) used the Boston Naming Test, to compare the performance of dyslexic eight-year-old readers with average and good readers of the same age. The Boston test requires the naming of pictured objects presented without contextual cues. The dyslexic children were less able to label the objects and had particular difficulty with low-frequency names and polysyllabic words. In fact, naming performance correlated with reading skill even when the children’s receptive understanding of the names was controlled. In an extension of this study, Rubin/Zimerman/Katz (1989) found that poor readers did not differ from good readers in their ability to select the initial phonemes or rhymes of object names they had not produced spontaneously and they were equally able to use initial phoneme prompts to retrieve the names. Overall these findings from studies of naming deficits are consistent with the view that dyslexic children experience relatively specific problems in retrieving phonological information from long-term memory. One difficulty with these studies is that they did not include a Reading Age comparison group. In the absence of this control group, the possibility that the naming problems are a consequence of the reading difficulty cannot be ruled out. To address this question, Snowling/van Wagtendonk/Stafford (1988) asked dyslexic children to name objects either following picture presentation or following a spoken definition, and they compared their performance with that of children of the same age as well as with children of a similar level of reading ability. All subjects found it more difficult to name the items following spoken definition but the group differences in performance were similar on both tasks. Essentially, dyslexics made more naming errors than children of the same age and a similar number to children of the same reading level. To confirm this finding, a second experiment carefully matched dyslexic children with normal readers of the same age and who scored at the same level on the British Abilities Scales test of Word Definitions, a vocabulary test. The two groups were then presented with a receptive vocabulary test in which one of four pictures had to be selected
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to match a spoken word, and subsequently with a naming task. The results were clear cut; dyslexics did as well as controls on the receptive vocabulary test but made more errors on the naming task. In summary, dyslexic children have naming difficulties which are unexpected given their age and I. Q., and are out of line with their receptive vocabulary. This suggests that they have difficulty in retrieving the phonological representations of words that they know. However, since they do not seem to be any worse at this than younger children of the same reading age, this might be a consequence of their reading difficulty. Logically however, such a possibility does not seem particularly appealing. There seems no compelling theoretical reason to expect reading to produce such changes in retrieval from long-term memory. An alternative view is that these naming deficits are one manifestation of an underlying weakness in information processing systems dealing with phonological information which are causally related to these children’s reading difficulties.
4.
Conclusions and Future Directions
In the present chapter we have focussed on some of the prominent cognitive deficits associated with developmental dyslexia. In discussing these deficits we have paid particular attention to the difficulties inherent in trying to demonstrate the causes of these children’s difficulties in learning to read. The evidence concerning visual perceptual and visual memory difficulties shows that these are not areas of difficulty for most dyslexic children. Some of the best documented difficulties of this type, such as those in tasks that tap the functioning of the visual transient sub-system, seem highly implausible as causes of the reading problems in dyslexia. Nevertheless, we argued that it is important not to lose sight of the fact that different children may experience difficulties in learning to read for different reasons. It appears that there may be a minority of children whose reading difficulties stem from an underlying deficit in visual processing. We understand relatively little about the nature of the visual deficits in these cases however and we badly need further studies of this issue. In contrast to the picture that emerges from studies of visual perceptual tasks, evidence from memory tasks indicates that dyslexic children commonly experience difficul-
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ties with verbal, but not with visual, memory tasks. These difficulties occur with both shortand long-term verbal memory tasks and may plausibly be related to their reading difficulties; though definite evidence for such a causal relationship is lacking. These deficits on verbal memory tasks, may relate to the difficulties with other language tasks, particularly those involving phonological information, that we discussed in the last chapter (cf. art. 70). An important task for future studies is to clarify the relationship between these different verbal difficulties in dyslexic children and relate them more explicitly to the patterns of reading and spelling difficulties they experience. Such studies ideally might lead to suitable training studies to evaluate the feasibility of ameliorating these deficits. If such studies were successful they would provide powerful evidence bearing on the causes of these children’s difficulties, and also have the important practical benefit of leading directly to better forms of treatment. Authors’ Note: This chapter was written while the first author was in receipt of a Nuffield Foundation Social Science Research Fellowship and while the second author was in receipt of MRC Grant No. G 8801538 N.
5.
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Kleiman, G. M. (1975). Speech recoding in reading. Journal of Verbal Learning and Verbal Behav iour, 14, 323—339. Kulikowski, J. J. & Tolhurst, D. J. (1973). Psychophysical evidence for sustained and transient detectors in human vision. Journal of Psychology, 232, 149—162. Lovegrove, W., Martin, F., & Slaghuis, W. (1986). A theoretical and experimental case for a visual deficit in specific reading disability. Cognitiv e Neuropsychology, 2, 225—267. Lyle, J. G. & Goyen, J. G. (1975). Effect of speed of exposure and difficulty of discrimination on visual recognition of retarded readers. Journal of Abnormal Psychology, 84, 673—676. Mann, V. & Liberman, I. Y. (1984 ). Phonological awareness and verbal short-term memory: Can they presage early reading success? Journal of Learning Disabilities, 17, 592—599. Mark, L. S., Shankweiler, D., Liberman, I., & Fowler, C. (1977). Phonetic recoding in the beginning reader. Memory and Cognition, 5, 623—629. Newman, S. P., Karle, H., Wadsworth, J. F., Archer, R., Hockly, R., & Rogers, P. (1985). Ocular dominance, reading and spelling: a reassessment of a measure associated with specific reading difficulties. Journal of Research in Reading, 8, 127—138. Olson, R. K., Kliegl, R., & Davidson, B. J. (1983). Dyslexic and normal readers’ eye movements. Journal of Experimental Psychology: Human Perception and Performance, 9, 816—825. Olson, R. K., Davidson, B. J., Kliegl, R., & Davies, S. E. (1984 ). Development of phonetic memory in normal and disabled readers. Journal of Experimental Child Psychology, 37, 187—206. Pavlidis, G. Th. (1981). Do eye movements hold the key to dyslexia? Neuropsychologia, 19, 57—64. Pirozzolo, F. J. & Rayner, K. (1978). The neural control of eye movements in acquired and developmental reading disorders. In H. Avakian-Whitaker & H. A. Whitaker (Eds.), Adv ances in neurolinguistics and psycholinguistics. New York: Academic Press. Rack, J. (1985). Orthographic and phonetic coding in normal and dyslexic readers. British Journal of Psychology, 76, 325—340. Rubin, H., Zimerman, S., & Katz, R. (1989). Phonological knowledge and naming ability in children with reading disability. Reading & Writing, 1, 393—404. Shankweiler, D., Liberman, I., Mark, L., Fowler, C., & Fischer, F. (1979). The speech code and learn-
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ing to read. Journal of Experimental Psychology: Human Learning and Memory, 5, 531—545. Siegel, L. & Linder, B. (1984 ). Short-term memory processes in children with reading and arithmetic disabilities. Dev elopmental Psychology, 20, 200— 207. Snowling, M., van Wagtendonk, B., & Stafford, C. (1988). Object naming deficits in developmental dyslexia. Journal of Research in Reading, 11, 67— 85. Stanley, G., Smith, G. A. & Howell, E. A. (1983). Eye movements and sequential tracking in dyslexic and control children. British Journal of Psychology, 74, 181—187. Stein, J. F. & Fowler, S. (1982). Diagnosis of dyslexia by means of a new indicator of eye dominance. British Journal of Ophthalmology, 66, 332—336. Stein, J. F. & Fowler, S. (1985). Effect of monocular occlusion on visuo motor perception and reading in dyslexic children. Lancet, July 13, 69—73. Tinker, M. (1958). Recent studies of eye movements in reading. Psychological Bulletin, 55, 215—231. Torgeson, J., Rashotte, C., Greenstein, J., Houck, G., & Portes, P. (1988). Academic difficulties of learning disabled children who perform poorly on memory span tasks. In H. L. Swanson (Ed.), Memory and learning disabilities: Adv ances in learning and behav ioral disabilities. Greenwich, Conn: JAI Press. Torgeson, J. K., Wagner, R. K., Balthazar, M., Davis, C., Morgan, S., Simmons, K., Stage, S., & Zirps, F. (1989). Developmental and individual differences in performance on phonological synthesis tasks. Journal of Experimental Child Psychology, 47, 491—505. Vellutino, F. R., Pruzek, R. M., Steger, J. A., & Meshoulham, U. (1973). Immediate visual recall in poor and normal readers as a function of orthographic-linguistic familiarity. Cortex, 9, 368—384. Vellutino, F. R., Steger, J. A., DeSetto, L., & Phillips, F. (1975). Immediate and delayed recognition of visual stimuli in poor and normal readers. Journal of Experimental Child Psychology, 19, 223— 232. Vellutino, F. R., Steger, J. A., & Pruzek, J. M. (1973). Inter- versus intra-sensory deficit in pairedassociate learning in poor and normal readers. Canadian Journal of Behavioral Science, 5, 111—123.
Charles Hulme, York (United Kingdom)/ Margaret Snowling, Newcastle upon Tyne (United Kingdom)
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72. Single and Multiple Component Developmental Dyslexias 1. 2. 3. 4. 5.
1.
History and Background Surface Dyslexia Phonological Dyslexia Deep Dyslexia References
History and Background
It is nearly a century since the term “congenital word-blindness” was introduced (Morgan, 1896) to refer to cases of reading disability which occur developmentally as a selective impairment and without recognisable etiology. The name was taken from the term “word-blindness” which had been coined in 1877 by Kussmaul to refer to acquired disorders of reading resulting from brain damage. Kussmaul noticed that “a complete textblindness may exist, although the powers of sight, the intellect and the powers of speech are intact.” From the first suggestion of congenital word-blindness as a clinical entity, similarities were conjectured between it and acquired word-blindness which resulted from neurological injury or disease. In both conditions word without letter-blindness was discovered (Dejerine 1892; Kerr 1897) and Fisher (1910) speculated that a congenital aplasia of the angular gyrus, a structure known to be damaged in many cases of acquired word-blindness, might underly problems in learning to read. Hinshelwood (1917) was particularly concerned with the similarities between the two groups of disorders. He made the connection explicit and stated the following: “The complex processes involved in vision proceed smoothly and harmoniously during health in the region of the unconscious cerebration, but when disease disturbs the delicate mechanism of the brain, there are revealed to us glimpses of its intimate working, a knowledge of which we would not acquire otherwise. It is for this reason that we have studied at such length the symptoms of acquired word-blindness, the knowledge of which will enable us to interpret and explain the phenomena of the congenital form. An adequate knowledge of former condition is an essential preliminary to the proper understanding of the latter. It is the absence of this necessary and fundamental knowledge which has given rise to much of the ambiguity and vagueness
which characterise many recent accounts of this condition.” Despite Hinshelwood’s recommendations, most subsequent researchers were not concerned with such comparisons between congenital and acquired word-blindness. Systematic investigations of the developmental reading disorders in the light of acquired disorders of reading did not re-surface until the 1970’s. During the 20th Century many different terms have been applied to refer to the condition which Morgan (1896) and Hinshelwood (1900; 1917) called “Congenital WordBlindness”. Among these were Strephosymbolia (Orton 1928), Specific Dyslexia (Hallgren 1950), Constitutional Dyslexia (Skysgaard 194 2), Developmental Alexia (Orton 1937), Analfabetia Partialis and Congenital Dyslexia (Hinshelwood 1917). Currently, the term dev elopmental dyslexia is widespread in use among neuropsychologists and neurologists, though educational psychologists, teachers and others often prefer the term Specific Reading Retardation or Specific Reading Disability. The term Developmental Dyslexia will be employed here and is used to refer to children in whom there is a significant discrepancy between the reading level which would be expected on the basis of their general intelligence and other skills and the reading level which they attained. These reading disorders exist despite the absence of any conspicious reason why education has not progressed normally. The term Developmental Dyslexia is not generally used to encompass those children who are learning disabled in a more general way and have difficulty in the acquisition of many different skills and abilities. However, there is no reason why the types of analysis which will be discussed below cannot also be applied to other children independent of their level of intellectual development. Previous chapters in this volume have documented the cognitive neuropsychological analyses which have been prevalent throughout the 1980s and early 1990s. One of the justifications for the case study methodology employed in these investigations is the heterogeneity of patients. Investigations in which patient performance was averaged across the group would mask the individual performance profile of each subject. The objective is
72. Single and Multiple Component Developmental Dyslexias
not to categorise neurological patients into boxes but to utilise a method of analysis of the patient’s performance which is interpretable in relation to a single model of the cognitive process of interest. One objective is to gain a better understanding of the nature of the patient’s difficulty with a view to subsequent remediation. Another objective is to use the dissociations in the patient’s performance to expand the model of normal cognitive systems. Up until the advent of cognitive neuropsychology, it was popular to investigate reading disorders in children using a group study methodology. However, such group studies assumed a degree of homogeneity which now appears unwarranted. There is a limitation to the amount of information which may be obtained with group studies if the group involved is not homogeneous with respect to the factor under investigation. Since the early 1960s a number of researchers have pointed out that developmental dyslexics do not all display similar patterns of disability. The multiple-syndrome nature of developmental dyslexia has increasingly been stressed. Some of the early attempts to categorise the developmental dyslexias into subgroups describe symptom complexes or constellations of features which were believed to co-occur in particular dyslexic populations. Some of the features involved in these constellations did not relate to the reading process itself. However, with increasing investigation of these disorders it has been difficult to substantiate these different syndrome groups. While certain symptoms will sometimes occur together, in other children there is fractionation and they occur apart. The cognitive neuropsychology methodology has therefore been applied to the developmental dyslexias in a similar way to its application to the acquired dyslexias. Detailed psycho-linguistic analyses have been carried out on individual cases of developmental dyslexia in order to see whether the patterns of reading performance may be interpreted in relation to a single model of reading development. The patterns of performance described have been compared with the patterns of performance which have emerged from comparable analysis with the acquired dyslexias. For certain syndromes directly analogous conditions have been described, but for others a pure developmental analogue has
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been more elusive. In 1980 Shallice/Warrington divided the acquired dyslexias into those that they refer to as single-component dyslexias and those which they refer to as multiple-component dyslexias. The single-component dyslexias including phonological dyslexia could be interpreted in relation to a model of normal reading by postulating a single abnormality in the system. The syndrome of deep dyslexia was perceived as being more complex with the necessity of multiple impairments to the underlying system and was referred to as a multiple component dyslexia. The extent to which the developmental dyslexias may be considered as single or multiple-component developmental dyslexias will now be discussed.
2.
Surface Dyslexia
The term surface dyslexia was introduced by Marshall/Newcombe (1973). They describe the case of a 4 5 year old man, J. C., who had sustained at the age of 20, a severe penetrating missile wound to the left temporo-parietal region. J. C. had only very mild residual aphasic symptoms but had a persistent reading disorder. He was particularly sensitive to the regularity of spelling of the words he was trying to read. Words with regular spelling to sound patterns were read more easily than those with irregular spelling to sound patterns. This means that captain is an easy word to read and yacht is a difficult word to read for a surface dyslexic. The pattern of errors was of a characteristic nature. Mis-readings suggested the application of a rule-based system for working out pronunciations. Marshall/Newcombe (1973) described these errors as “partial failures of grapheme-phoneme conversion”. The phonetic value of some letters are affected by the letters which surround them. J. C. had difficulty using this context of a letter within a word to achieve its pronunciation. Thus, errors were made on ambiguous letters. Voiced consonants were sometimes produced in unvoiced form e. g. disease “deceased”. Silent letters were assigned phonetic values e. g. island “izland”. The “rule of e” was rarely applied e. g. bike ‚bik”. Vowel digraphs which represent one sound were generally read as only one of the component letters. In addition consonant clusters provoked difficulty and there were stress errors. J. C. also had greater difficulty
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in reading long words than in reading short words. Word imageability and frequency did not affect reading performance and there was no particular difficulty in pronouncing aloud unfamiliar non-words or unfamiliar regular words. Nor was there any particular difficulty in reading aloud short grammatical functional word such as in, on and but. So, J. C. like all surface dyslexics found it easier to read regular than irregular words and made regularisation errors. In 1981 Coltheart predicted that this pattern of reading performance would lead to particular difficulty with homophonic stimulae. He predicted that even when these words were read aloud correctly there would be confusion as to their meaning. Thus, if asked to read the words blue and blew a surface dyslexic would read them aloud correctly but would not know which item was being read when they were being asked what the word meant. This homophone confusion has been found to be a consistent characteristic of surface dyslexia. The suggestion that this pattern of reading performance might also be found within the developmental dyslexias was first discussed by Holmes (1973). In her doctoral thesis, she described cases of children with developmental reading disorder whose pattern of reading performacne appeared to mimic that of acquired surface dyslexia. This hypothesis received substantiation by Coltheart/Masterson/Byng et al. (1983) who described in detail a case of dev elopmental surface dyslexia which was compared to a case of acquired surface dyslexia. C. D. an 18 year old girl of average intelligence but with a reading age of 10 years, displayed a significant regularity effect on reading aloud. Her errors showed the application of a rule-based system e. g., bear → “beer”; subtle → “subtill’. She also displayed homophone confusion. For example, she defined pane as something which hurts. Thus, in many features the case description of Coltheart/Masterson/Byng et al. (1983) directly parallels the earlier case descriptions of acquired surface dyslexia. The cases of acquired surface dyslexia have received several theoretical interpretations. Dual route models of reading suggest that reading may be accomplished by a p h o n o l o g i c a l r e a d i n g r o u t e which parses a word, assigns a phonological representation to each of the parsed segments and then blends these together to produce the pronunciation. Alternatively, a s e m a n t i c or l ex i c a l r e a d i n g r o u t e allows a word to trigger a
V. Pathologies and Disorders of Language Development
representation in the input-logogen system, a word-store postulated by Morton (1969) to include entries which have variable thresholds. The output of the logogen system activates a semantic representation. This semantic representation contains the meaning associated with the word. This meaning-based code then activates an output logogen which stores the words ultimate pronunciation. The semantic reading route is dependent upon the meaning of the word but does not attend to the structural pronunciation of the word. In triple-route models a third route, the d i r e c t r e a d i n g r o u t e, passes directly from input to output logogens bypassing the semantic system. Acquired surface dyslexia can be explained in relation to a dual or triple route model in terms of the impairment of both the semantic and direct reading route but the relative preservation of the phonological reading route, leading to an over-emphasis on phonological reading. This means that regular words are read accurately and there is no difficulty with non-words or function words, but words with irregular letter to sound patterns produced difficulty leading, to both regularity effect and regularisation errors. Since meaning is only assigned subsequent to the activation of pronunciation from the rule based system there is homophone confusion. A comparable theoretical interpretation can be postulated for developmental surface dyslexia. In this case it is argued that the d eve l o p m e n t of the direct reading route and of the semantic reading route are impaired in some way. Nevertheless, the phonological reading route has developed effectively and the child is able to read aloud many regular words. The error pattern is dominated by regularisation errors and there is particular difficulty with irregular words. Homophones are confused because meaning is assigned after pronunciation has been attained. One of the difficulties with the original case description described by Coltheart/Masterson/Byng et al. (1983) is that their surface dyslexic C. D. also had difficulty with phonological route reading. The phonological reading route in this case has not developed well. This laid the case open to subsequent criticism. However, it would be a mistake to conclude that surface dyslexia is always associated with impaired development of the phonological reading route, in addition to the defective development of the other reading systems. Other surface dyslexics have been
72. Single and Multiple Component Developmental Dyslexias
described who show much better development of the phonological reading route. In these cases the dissociation between the development of the routes is clearer and crisper. A clear example of this sort has been described by Temple (1984 a). Temple describes a case of surface dyslexia in a child with epilepsy. This child, N. G., was able to read regular words whether familiar or unfamiliar with perfect accuracy. Irregular words frequently provoked regularisation errors. All of N. G.’s reading performance could be accounted for by the strict application of a rule based system. His phonological route performed excellently. Control children of a similar reading age to N. G. were compared to him on their reading performance with regular and irregular words. Although all the children showed small trends in favour of regularity effects, none showed the degree of regularisation effect that N. G. displayed. His performance lay outside the control range. N. G. was also significantly poorer than the control children at reading irregular words. Finally N. G. displayed homophone confusion. Eleven out of 22 words read correctly were defined as their respective homophones. Whilst N. G. is a pure case of developmental surface dyslexia and in many ways he resembles the acquired case described by Bub/ Cancelliere/Kertesz (1985), several other cases of developmental surface dyslexia have also been described in which there is a clear dissociation between the development of their phonologically based reading skills and their impaired development of other reading skills. There are several other theoretical explanations which may be produced to account for the patterns of reading disorder in surface dyslexia. Shallice and Warrington have produced a theoretical explanation for acquired surface dyslexia which varies a little from the traditional two and three route models (Shallice/Warrington 1980; Shallice/Warrington/ McCarthy 1983). They assume that within the phonological reading route the stored orthographic to sound correspondences are not restricted to graphemes. They suggest that there are correspondences for various sizes of orthographic unit. These include graphemes, consonant clusters, subsyllabic units, syllables and morphemes. They postulate a ‚visual word form’ system which can detect letter groups of different sizes and then send information about them to corresponding units in the phonological system. Shallice and Warrington assume that as a result of neurological
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pathology, when the route is impaired larger units are affected more severely than the smaller units. Increasing impairment leads to increased reliance on smaller and smaller units. In surface dyslexia therefore reliance is on orthographic units which are too small to cope effectively with the notorious irregularity of English orthography. Shallice and Warrington’s model also differs from that of Marshall and Newcombe in that they abandon the direct route and incorporate it into their expanded phonological route. In Shallice and Warrington’s terms the developmental surface dyslexic is using small orthographic units as a basis for processing in the phonological route and has failed to develop the ability to process larger segments. Analogy theorists have argued that there is no need for multiple routes to reading aloud, and that all words are read by a single route. Unfamiliar words are read by analogy with previously known words. Although analogy theory has had some success in accounting for developmental surface dyslexia it cannot account successfully for some of the other forms of dyslexia which will be discussed below. Some of the ideas of analogy theory have resurfaced in modified form within the parallel distributed processing models which have been a contemporary interest. These models and systems can successfully mimic aspects of learning to read and the performance pattern of surface dyslexia but again the other dyslexic disorders are problematic. Temple (1985a) has discussed some variation within the pattern of performance of developmental surface dyslexics and has suggested that both they and acquired surface dyslexics could be interpreted more fully if her expanded model is utilised which includes a broader version of the phonological reading route. If the dual route model of reading is postulated then developmental surface dyslexia may be interpreted as a single component developmental dyslexia in which there is impaired development of the lexical-semantic reading route but relatively normal development of the phonological reading route. If a triple route model of reading development is invoked then there must be impaired development of both the lexical-semantic reading route and also of the direct reading route but with relative preservation of the phonological reading route. In this sense the deficit is no longer single component since two different reading routes are postulated to be impaired.
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Nevertheless a unified description can be expressed of developmental surface dyslexia by saying that phonological reading skills have developed normally but non-phonological processes have not become properly established. It is generally assumed that reading has been introduced into our civilisation after the end of the evolutionary processes which produced homo-sapiens and his apparently superior cortical development. In this case the reading mechanisms which are being discussed must be parasitic upon mechanisms which previously evolved within the brain to carry out some alternative process. If there is selective impairment in the development of some non-phonological processes, a question arises as to the underlying cognitive basis of these deficits. What is the system whose impairment has led to difficulty with these nonphonological processes? What was it used for before man developed reading within his cognitive repertoire. Marshall (1984 ; 1987) gets around this type of discussion by suggesting that reading may have entered our cognitive repertoire far earlier than we have previously realised. He suggests that we have been biased by the preserved written records but that we have no evidence that reading was not in existence prior to this time. He suggests that the reading system is ‚preformed’ in structure and that experience and education fills out the system’s content. Other, such as Ellis (1985; 1987) have suggested that the system which normally builds up the reading skills required for lexical-semantic reading processes are dependent upon systems which are adapted for analysing visually similar complex patterns. He suggests that the processes involved in face recognition could be relevant in this regard. He postulates that cases of surface dyslexia may be associated with difficulty with some forms of face recognition. However, there is little evidence to substantiate this idea. Preliminary investigations do not indicate a high degree of correlation between face recognition skills and word recognition skills. Indeed, the evidence suggests that these processes are dependent upon different systems within the brain and may be fractionated as a result of neurological insult and developmentally. It remains possible that some other form of selective visual memory for complex configurational items is impaired in children with surface dyslexia but there is, as yet, no substantiation of this view.
V. Pathologies and Disorders of Language Development
Marcel (1980) pointed out that the reading patterns of normal children often resemble those of surface dyslexia. Current models of reading development are often in a postPiagetian stage style. In these models, processes involved in the acquisition of phonological reading skills precede those involved in the processes of lexical-semantic reading. Thus, for example, in Frith’s (1985) model of reading development there are three reading stages. The first stage concerns logographic reading. In this stage words are recognised as complete entities. This form of reading functions on a variation of an abstracted template matching. The words are not decomposed into their constituent sounds nor into their constituent orthographic components. The child identifies the whole word and selects as a vocal response a word within his or her vocabulary. This preliminary reading system is able to learn to recognise the first few words in a child’s reading vocabulary. Subsequently the child progresses to an alphabetic stage of reading development. Within the alphabetic stage the child learns to master the associations between letters and sounds so that they are able to ‚sound out’ words to attain their pronunciations. It is at this stage that their pattern of performance resembles that of some developmental surface dyslexics and acquired surface dyslexics. However, for the normal child according to Frith (1985) reading development continues into the orthographic stage. Within the orthographic stage major sub-components of words are identified rapidly. Orthographic reading is normal adult reading. Words are not systematically sounded out prior to recognition. Morphemic units are easily and rapidly recognised and blended together. In relation to Frith’s model (1985) of normal reading development, surface dyslexia may be interpreted as arrestment at the alphabetic stage. Follow-up studies of surface dyslexics indicate that they do not go on to develop an orthographic reading process (Temple 1987) rather their alphabetic system continues to expand but they are increasingly handicapped as time passes since in English the proportion of irregular words which have to be acquired increases with the increase in complexity of the language as the child goes through the educational process. Developmental surface dyslexia therefore makes greater impact in the later educational years. The reaction time studies of Seymour (1986) indicate that surface dyslexics whom
72. Single and Multiple Component Developmental Dyslexias
he refers to as morphemic dyslexics have response times which lie outside those of normal children. Thus, although the overall pattern of surface dyslexics resemble the pattern of some normal children they are distinguishable from them. The case descriptions of surface dyslexia have been rather sparse in number, although the syndrome has now been described in relation to a variety of different European languages. It would appear that developmental surface dyslexia is less common than developmental phonological dyslexia.
3.
Phonological Dyslexia
The term ‚phonological alexia’ was first used by Beauvois/Derouesné (1979), to describe a French patient with an acquired reading disorder. Subsequently, phonological alexia or acquired phonological dyslexia has been described in many other languages. The dominant characteristic of acquired phonological dyslexia is that the patients have difficulty with reading non-words or unfamiliar words. Misreading of non-words results either from failed attempts to decode analytically or attempts to produce a word which resembles the non-word. So, for example, the French patient described by Beauvois and Derouesné presented with the word v ina said “c’est presque vinaigre”. In comparison word reading is good. Individual words are read aloud with high levels of accuracy. Misreadings consist of morphological errors, in which the base of the word is read correctly but an affix is dropped, added or substituted; visual errors in which the response shares 50% of the letters of the stimulus; and omissions. There can also be function word substitutions, where one short grammatical word is substituted for another. There is much variation in the characteristics of the reported cases of acquired phonological dyslexia but the salient feature is that non-word reading is impaired in relation to word reading. Some acquired phonological dyslexics are reported to be more successful at reading non-words that are homophonic with real words than pronouncable but non-homophonic non-words. Thus, floo is easier than ploo (Beauvois/Derouesné 1979; Patterson 1982). The validity of this claim has been questioned: in reported cases, visual similarity to real words has often been a confounding factor (Martin 1982; Patterson 1982). Acquired phonological dyslexia
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has been given the opposite theoretical interpretation to that of acquired surface dyslexia. It is suggested that the phonological reading route has become selectively impaired as a result of neurological injury whereas lexical and semantic reading routes and direct reading routes are intact. Shallice/Warrington (1980) consider that whereas surface dyslexia is a multiple component dyslexic syndrome, requiring more than one functional lesion for explanation, phonological dyslexics have a highly selective deficit involving grapheme phoneme translations. Phonological dyslexia is therefore a single component dyslexic syndrome. The first description of dev elopmental phonological dyslexia was provided by Temple/ Marshall (1983). They described the case, H. M., of a 17 year old girl. Speech appeared early with no apparent abnormality and milestones were reported to be normal. There was no clear-cut history of specific reading difficulty although there was comment that the mother’s brother did not learn to read well. There was no history of serious family illness and H. M. had no known neurological abnormality. H. M. came to the attention of the education authorities prior to her formal examinations at school when attempts were made to obtain extended time limits for her. H. M. was found to be of good intelligence with a verbal I. Q. of 114 and a performance I. Q. of 115. She had a single word reading age of 10 years 11 months on the Schonell test and a reading age for accuracy of 9 years 7 months on the Neale test. H. M. was significantly poorer at reading aloud non-words than at reading words. Errors consisted of either neologisms such as fex → “feg”; klower → “kanowla” or were lexicalisations in which the non-word was read as a word with some visual similarity to the stimulus. Examples of lexicalisations are as follows: chait → “chit”: inlect → “inlet”: fince → “finish”. Reading of whole words proceeded with relatively good accuracy. Errors in whole word reading were of a specific nature. A number were morphological errors in which the base of the word was read correctly but an affix was dropped, added or substituted. Examples of these errors were beautiful → “beauty”; removal → “remove”; weigh → “weight”. In total for H. M., 16% of all errors were morphological paralexias. She made only a small number of neologistic responses. Her other errors were either visual paralexias or visuo-semantic paralexias e. g. thinness → “thickness”; arrange-
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ment → “agreement”; politics → “policies”; liquor → “liqueur”. Whilst H. M. did not have difficulty with function word reading when the function words were presented in isolation, she did have significant difficulty in dealing with function words and the grammatical endings of words in text reading. She was presented with the following passage: “Among animals the fox has no rival for cunning. Suspicious of man, who is its only natural enemy, it will, when pursued, perform extraordinary feats, even alighting on the backs of sheep to divert its scent trail.” She read it as follows: “Amongst animals the fox has no rivals for cunning. Surprisingly, of man, who is its only natural enemy at will, with pursued performance extraordinary feat, even alighting on the backs of sheep to divert its scent trial.” This pattern of reading is paragrammatic (Kleist 1934 ). H. M. did not display any significant level of homophone confusion nor did she make regularisation errors or display any form of regularity effect. Her pattern of reading performance is explicable in relation to a model of normal reading by saying that she has had difficulty in developing the phonological reading route. Many further cases of phonological dyslexia in children have been described (e. g. Temple 1984 b; c; Snowling/Stackhouse/Rack 1986; Campbell/Butterworth 1985; Seymour 1986). There have also been descriptions in a variety of European languages. This pattern of reading impairment in children appears to be relatively pervasive amongst the developmental dyslexias. Long term follow up by Temple (1990) of a developmental phonological dyslexic A. H., indicates that the pattern of reading performance persists in character over time. Six years after initial investigation A. H. continued to show a pattern of phonological dyslexia. The overall qualitative characteristics of his reading had not altered or resolved with time. His overall level of performance had however improved and he had developed strategies to deal with a number of his difficulties. In the long term there is some evidence that phonological dyslexia is less handicapping than surface dyslexia since it is possible to build up a very large repertoire of words which can be instantly recognised. Difficulties only emerge if reading aloud is required particularly of long unfamiliar items and difficult names. For a surface dyslexic the problem is more extreme because of the degree of irreg-
V. Pathologies and Disorders of Language Development
ularity in the language. Surface dyslexia in languages such as Spanish and Italian in which the orthographic script is regular in relation to its spelling sound pattern is much less problematic and may only appear on occasional dialect words. In the traditional group studies of developmental dyslexia, it is observed that children with developmental dyslexia on average have greater difficulty than normal on sound related tasks and phonological processing tasks. Pennington/Van Orden/Smith et al. (1990) narrow this difficulty to phonemic awareness rather than phonemic perception, (retrieval of phonology), or articulatory speed. However, not every dyslexic child has difficulty with phonological tasks. Temple (1987) has argued that whilst phonological dyslexics have difficulty with phonological tasks surface dyslexics are unimpaired. Phonological dyslexia is associated with difficulty on rhyming tasks and sound segmentation tasks even when these are presented in purely oral format. It is therefore possible that underlying the poor development of the phonological reading route there is a fundamental deficit in the sound based aspects of language processing. Evidence of a direct association however, is not yet substantiated and both of these deficits may merely be correlational symptoms of some other underlying impairment. A study of callosal agenesis (Temple/ Jeeves/Vilarroya 1989) has indicated that these children have impairment on phonological processing tasks. They have difficulty with sound segmentation tasks and they have difficulty with rhyming tasks. If such impairments are causal in developmental dyslexia one would also expect these children to display developmental dyslexia. However, the investigation by Temple/Jeeves/Vilarroya (1990) indicates that the previously studied children with callosal agenesis do not have developmental dyslexia in the sense that their word recognition skills are at a normal level for age. Given that the definition of developmental dyslexia requires that a child is not attaining the level expected for age and intelligence these children do not conform to such a description. However, a detailed investigation of the pattern of their reading performance indicated that their reading style was not normal. Whereas their reading of whole words and irregular words was accurate, their reading of non-words was impaired. Thus, whilst their overall word-recognition levels were good the pattern of their reading per-
72. Single and Multiple Component Developmental Dyslexias
formance indicated an impairment in the development of the phonological reading route. There was no impairment in their ability to develop the lexical-semantic reading route and their level of competence with this reading system was sufficiently great that they did not display overt dyslexic symptoms on formal word recognition reading tests. This pattern of performance would be consistent with the notion that underlying phonological difficulties could be causal in creating difficulty with the development of the phonological reading route but cannot in and of themselves be causal in producing an overall pattern of developmental dyslexia. Phonological dyslexia is not easily explicable in relation to models of normal reading development. Frith’s model of reading development (1985), as described earlier, refers to three different stages of reading development: logographic, alphabetic and orthographic. Whereas surface dyslexia could be described as arrestment of reading development at the alphabetic stage, phonological dyslexia cannot be explained in relation to arrestment at a particular stage. The phonological dyslexics appears to have acquired orthographic reading skills without going through the alphabetic stage. The only alternative explanation is to suggest that they have a significantly expanded logographic reading system which is able to incorporate thousands of words. No such logographic reading system has ever been described in normal children. If phonological dyslexics have attained an orthographic reading stage without going through an alphabetic reading stage then Frith’s model for reading development does not refer to a series of stages which are invariant in order. In traditional models the series of stages in developmental schemes are invariant in order and each must be passed through before one can progress to the subsequent stage. The existence of phonological dyslexia may suggest that there are alternative models to reading acquisition and that not all children proceed through the same detailed set of stages. The question then arises whether phonological dyslexia reflects a peculiar variant which is never manifest in the normal population or whether amongst the children who develop reading normally there are also children who proceed to an orthographic stage without fully mastering the alphabetic stage or proceed to master the alphabetic stage later in time. If this were true then it
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would indicate individual differences in the acquisition of reading. These differences might emerge in later reading styles and Baron/Strawson (1976) have pointed out that adult reading styles vary. They describe both Phonecian and Chinese readers. The Phonecian readers show enhanced abilities in phonological reading whereas the Chinese readers show enhanced abilities in non-phonological reading. Such variations in the development of reading and reading styles could easily be accommodated by suggesting that the multiple routes in a reading model may develop relatively independently of each other. The patterns of performance in data gathered from the developmental dyslexics is consistent with the notion that these systems can be fractionated in this way and may develop in relative isolation. Such patterns of performance cannot be accounted for in relation to any single stage model of reading development. Morton (1989) has attempted to break down one way in which an information processing model of reading incorporating multiple reading routes could be developed. However, he incorporates into his model a fixed order in the acquisition of components so that the model ties in with the single multiple stage reading acquisition system. This may be unnecessarily restrictive. Phonological dyslexia is a common form of developmental dyslexia in which there is severe difficulty in the development of the phonological reading route. The early case description by Coltheart/Masterson/Byng et al. (1983) of surface dyslexia also had a mild impairment of the phonological reading route but it was above argued that this case was unrepresentative of surface dyslexia as a whole and that in other cases of developmental surface dyslexia the phonological reading route is intact. However, some argue that phonological reading deficits are always present in developmental dyslexia but in surface dyslexia their presence is rather mild and can be overlooked whereas in phonological dyslexia their effect is more profound. Such theorists could argue that developmental dyslexics may be placed along a scale in relation to their degree of phonological impairment. For the opposing view in which surface dyslexics have a phonological reading route which is normal and appropriate to their age and intelligence, there is a qualitative as well as a quantitative distinction between phonological and surface dyslexia.
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4.
Deep Dyslexia
The first of the acquired dyslexias to be described using a cognitive neuropsychological framework was deep dyslexia which was described in 1966 by Marshall/Newcombe. They described a patient G. R. who made a characteristic type of error which has subsequently been named a semantic error. When presented with single words out of context to read aloud, G. R. would substitute words which were related in meaning though not in visual appearance or in pronunciation. Thus for example when presented with the word parrot, he read it as “canary”. These semantic errors attracted a great deal of interest and investigation. Although the next case of deep dyslexia was not described until the early 1970’s there have now been many descriptions in a range of languages. The syndrome has been difficult to interpret in any simple way in relation to contemporary reading models. The patients have no phonological reading skills at all and are completely unable to read any non-words or pronounce aloud any individual letters. They have complete impairment of the phonological reading route. However, there is further disruption of the semantic-lexical reading route since semantic errors are prevalent and they also make morphological errors. Moreover, their overall level of reading performance is much poorer than in phonological dyslexia, with greatest ease of reading for high frequency and concrete words with well elaborated meaning. More unusual words or more abstract words are difficult to read. Deep dyslexia according to the classification of Shallice/Warrington (1980) is certainly a multiple component dyslexic disorder and in relation to contemporary reading models as many as four or five deficits have been required to be postulated to account for the full range of features. Coltheart (1980) proposed that the reading performance in deep dyslexia could be accounted for by suggesting that it reflected reading emanating from the right hemisphere of the brain. He noted the similarity between many of the characteristics of deep dyslexic reading and the characteristic of reading described in the isolated right hemisphere of the commissurotomy patients. The commissurotomy patients provided evidence that the right hemisphere of the brain does not have phonological reading skills and when required to read aloud concrete words has a tendency to substitute words with similar meanings
though no obvious relationship in phonological pattern or visual appearance (Zaidel 1981). This pattern of reading performance has also been described in the isolated right hemisphere of left hemispherectomy patients. There has been much subsequent debate and argument about this theoretical interpretation, since others argue that the pattern of reading performance in deep dyslexia emanates from an impaired left hemisphere and does not result from right hemisphere reading. However, recent imaging studies support the Coltheart hypothesis (Coltheart/Weekes/ Savage et al. 1991). Dev elopmental deep dyslexia has been an elusive disorder. If the reading disorder which represent the developmental dyslexias are interpretable in relation to a comparable reading model to that used to explain the acquired dyslexias, then in principle developmental deep dyslexia should exist. One possible explanation for its rare appearance is that the numerous deficits required to produce deep dyslexia in the neurological patient seldom co-occur in the developing child or if they do they may be sufficiently severe to prohibit the development of reading at all. There have been a small number of descriptions of children who do produce some semantic errors in reading aloud and some of whose characteristics resemble those of deep dyslexia. Such descriptions have been provided by Johnston (1983) and Siegel (1985). Temple (1988) showed that her subject K. S., a nine year old boy, made semantic errors at a level significantly above that that would be expected on the basis of chance. He also had severe difficulty with phonological processing. However, all the case descriptions to date have either related to children of rather limited intellectual ability, or children of very limited overall reading ability. Even the case K. S. described by Temple (1988) referred to a child where there was a question relating to the degree of his hearing ability. A partial hearing ability could be sufficient to significantly impair the development of the phonological reading route. In K. S. this was combined with an impairment of visual memory. In combination the deficits may have produced something which resembled deep dyslexia. Amongst normal children learning to read, Seymour/Elder (1986) have described occasional semantic errors. Their study addressed a group of Scottish children whose reading instruction did not include explicit phonological instruction. In the early logographic
72. Single and Multiple Component Developmental Dyslexias
phase of reading development some of these children made occasional semantic errors. In relation to the models of reading development postulated by Frith and others it could be argued that developmental deep dyslexia, when it does occur, reflects arrestment at the logographic stage of reading development. However, Temple (1988) compared the incidence of errors of the semantic component in her subject K. S. with the errors of a semantic component described by Seymour/ Elder (1986) in their studies of normal reading development in Scottish children. The incidence of these errors types for K. S. was significantly above those for the control children. It therefore, appears that the reading pattern described for K. S. is not a simple arrestment of the logographic stage of development. Wimmer/Hummer (1990) argue a logographic strategy for normal or poor readers is very limited and does not arise naturally when the writing system is phonologically transparent as in German and grapheme-phoneme correspondences are part of the instruction. So if developmental deep dyslexia is ever described in German it may be more significantly different from the normal pattern than is evident in English.
5.
References
Baron, J. & Strawson, C. (1976). Use of orthographic and word-specific knowledge in reading words aloud. Journal of Experimental Psychology: Human Perception and Performance, 2, 386—393. Beauvois, M. F. & Derouesné, J. (1979). Phonological alexia: Three dissociations. Journal of Neurology, Neurosurgery and Psychiatry, 42, 1114— 1124. Bub, D. N., Cancelliere, A., & Kertesz, A. (1985). Whole-word and analytic translation of spelling to sound in a non-semantic reader. In K. E. Patterson, J. C. Marshall & M. Coltheart (Eds.). Surface Dyslexia. 15—34. Hillsdale, N. J.: Erlbaum. Campbell, E. & Butterworth, B. (1985). Phonological dyslexia and dysgraphia and a highly literate subject: A developmental case with associated deficits of phonemic processing. Quarterly Journal of Experimental Psychology, 37 A, 435—477. Caramazza, A., Miceli, G., & Villa, G. (1986). The role of the (output) phonological buffer in reading, writing and repetition. Cognitiv e Neuropsychology, 3, 37—76. Coltheart, M. (1980). Deep dyslexia: A right hemisphere hypothesis. In M. Coltheart, K. E. Patterson, & J. C. Marshall (Eds.). Deep Dyslexia. 326—380. London: Routledge and Kegan Paul.
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Coltheart, M., Masterson, J., Byng, S., Prior, M., & Riddoch, J. (1983). Surface dyslexia. Quarterly Journal of Experimental Psychology, 35 A, 469— 495. Coltheart, M., Weekes, B., Savage, K., Simpson, L., Zurinsky, Y., & Gordon, E. (1991). Deep dyslexia and right hemisphere reading — a regional cerebral blood flow study. Paper presented at the meeting Deep Dyslexia. Birbeck College, October. Dejerine, J. (1892). Contribution a l’etude anatomopathologique et clinique des differentes varieties de decite verbale. Compte Rendues des Seances de la Society de Biologie, 4, 61—90. Derouesné, J. & Beauvois, M. F. (1979). Phonological processes in reading: data from alexia. Journal of Neurology, Neurosurgery and Psychiatry, 42, 1125—1132. Ellis, A. W. (1985). The cognitive neuropsychology of developmental (and acquired) dyslexia: A critical survey. Cognitive Neuropsychology, 2, 169—206. Ellis, A. W. (1987). On problems in developing culturally transmitted cognitive modules. Mind and Language, 2, 242—251. Fisher, J. H. (1910). A case of congenital word blindness (inability to learn to read). Transactions of the Ophthalmological Society, 30, 216—225. Frith, U. (1985). Beneath the surface of developmental dyslexia. In K. E. Patterson, J. C. Marshall, & M. Coltheart (Eds.). Surface Dyslexia. 301—330. Hillsdale, New Jersey: Erlbaum. Hallgren, B. (1950). Specific Dyslexia (“congenital word blindness”): a clinical and genetic study. Acta Psychiatrica et Neurologica Scandinav ica Supplement, 65. Hinshelwood, J. (1900). Congenital word-blindness. Lancet, 1, 1506—1508. Hinshelwood, J. (1917). Congenital Word Blindness. Glasgow: H. K. Lewis. Holmes, J. (1973). Dyslexia: A neurolinguistic study of traumatic and developmental disorders of reading. Unpublished PhD thesis, University of Edinburgh. Johnston, R. S. (1983). Developmental deep dyslexia? Cortex, 19, 133—140. Kerr, J. (1897). School Hygiene, its mental, moral and physical aspects. Journal of the Royal Statistical Society, 10, 613—680. Kleist, K. (1934). Gehirnpathologie. Leipzig: Barth. Kussmaul, A. (1877). Disturbances of Speech. Ziemssen’s Cyclopaedia, 14. Marcel, T. (1980). Surface dyslexia and beginning reading: a revised hypothesis of the pronunciation of print and its impairments. In M. Coltheart, K. E. Patterson, & J. C. Marshall (Eds.) Deep Dyslexia. 227—258. London: Routledge & Kegan Paul. Marshall, J. C. (1984 ). Toward a rational taxomy of the developmental dyslexias. In R. N. Malatesha
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and H. A. Whitaker (Eds.). Dyslexia: A Global Issue. 45—58. The Hague: Nijhoff. Marshall, J. C. (1987). The cultural and biological context of written languages: Their acquisition, deployment, and breakdown. In J. R. Beech and A. M. Colley (Eds.) Cognitiv e Approaches to Reading. 15—30. Chichester: John Wiley. Marshall, J. C. & Newcombe, F. (1966). Syntactic and semantic errors in paralexia. Neuropsychologia, 4, 169—176. Marshall, J. C. & Newcombe, F. (1973). Patterns of paralexia: A psycholinguistic approach. Journal of Psycholinguistic Research, 2, 175—199. Martin, R. C. (1982). The pseudohomophone effect: the role of visual similarity in non-word decisions. Quarterly Journal of Experimental Psychology, 34 A, 395—409. Morgan, W. P. (1896). A case of congenital wordblindness. British Medical Journal, 2, 1378. Morton, J. (1969). Interaction of information in word recognition. Psychological Re v iew, 76, 165—178. Morton, J. (1979). Word recognition. In J. Morton and J. C. Marshall (Eds.) Psycholinguistic Series, 2, 107—155. Cambridge, Mass: MIT Press. Morton, J. (1989). An information-processing account of reading acquisition. In A. Galaburda (Ed.), From Reading to Neurons. 43—66. Cambridge, MA: MIT Press. Newcombe, F. & Marshall, J. C. (1980). Transcoding and lexical stabilization in deep dyslexia. In M. Coltheart, K. E. Patterson, & J. C. Marshall (Eds.). Deep Dyslexia. 176—188. London: Routledge & Kegan Paul. Newcombe, F. & Marshall, J. C. (1981). On psycholinguistic classification of the acquired dyslexias. Bulletin of the Orton Society, 31, 29—44. Newcombe, F. & Marshall, J. C. (1985). Reading and writing by letter sounds. In K. E. Patterson, J. C. Marshall, & M. Coltheart (Eds.). Surface Dyslexia. 35—51. Hillsdale, N. J.: Erlbaum. Orton, S. T. (1928). Specific reading disability strephosymbolia. Journal of the American Medical Association, 90, 1095—1099. Orton, S. T. (1937). Reading, Writing and Speech Problems in Children. New York: Norton. Patterson, K. E. (1982). The relation between reading and phonological coding: Further neuropsychological observations. In A. Ellis (Ed.). Normality and Pathology in Cognitiv e Functions. 77—111. London: Academic Press. Pennington, B. F., Van Orden, G. C., Smith, S. D., Green, P. A., & Haith, M. M. (1990). Phonological processing skills and deficits in adult dyslexics. Child Development, 61, 1753—1778. Seymour, P. H. K. (1986). Cognitiv e Analysis of Dyslexia. London: Routledge & Kegan Paul.
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Seymour, P. & Elder, L. (1986). Beginning reading without phonology. Cognitiv e Neuropsychology, 3, 1—36. Seymour, P. & MacGregor, C. J. (1984 ). Development dyslexia: A cognitive analysis of phonological, morphemic and visual impairments. Cognitive Neuropsychology, 1, 43—82. Shallice, T. & Warrington, E. K. (1980). Single and multiple component central dyslexic syndromes. In M. Coltheart, K. S. Patterson, & J. C. Marshall (Eds.). Deep Dyslexia. 119—145. London: Routledge & Kegan Paul. Shallice, T., Warrington, E. K., & McCarthy, R. (1983). Reading without semantics. Quarterly Journal of Experimental Psychology, 35 A, 111—138. Siegel, R. (1985). Deep dyslexia in childhood? Brain and Language, 216, 16—17. Skydsgaard, H. B. (194 2). Den konstitutionelle dyslexi. Kobenhavn. Snowling, M., Stackhouse, J., & Rack, J. (1986). Phonological dyslexia and dysgraphia: A developmental analysis. Cogniti v e Neuropsychology, 3, 309—339. Temple, C. M. (1984 a). Surface dyslexia in a child with epilepsy. Neuropsychologia, 22, 569—576. Temple, C. M. (1984 b). New approaches to the developmental dyslexias. In Rose, C. (Ed.). Progress in Aphasiology. 223—232. London: Plenum Press. Temple, C. M. (1984 c). Developmental analogues to acquired phonological dyslexia. In R. N. Malatesha & H. A. Whitaker (Eds.). Dyslexia: A Global Issue. 143—158. The Hague: Nijhoff. Temple, C. M. (1985a). Surface dyslexia: Variation within a syndrome. In K. Patterson, J. C. Marshall, & M. Coltheart (Eds.). Surface Dyslexia. 269—288. Hillsdale, N. J.: Erlbaum. Temple, C. M. (1985b). Reading with partial phonology. Journal of Psycholinguistic Research, 14, 523—541. Temple, C. M. (1987). The nature of normality, the deviance of dyslexia and the recognition of rhyme. Cognition, 27, 103—108. Temple, C. M. (1988). Red is read but eye is blue: A case study of developmental dyslexia and followup report. Brain and Language, 34, 13—37. Temple, C. M. (1990). Foop is still Floop: A six year follow-up of phonological dyslexia and dysgraphia. Reading and Writing: An Interdisciplinary Journal, 2, 209—221. Temple, C. M., Jeeves, M. A., & Villaroya, O. (1989). Ten, pen, men: Rhyming skills in two children with callosal agenesis. Brain and Language, 37, 548—564. Temple, C. M., Jeeves, M. A., & Villaroya, O. (1990). Reading in callosal agenesis. Brain and Language, 39, 235—253.
73. Treatment of Developmental Reading and Spelling Disorders
Temple, C. M. & Marshall, J. C. (1983). A case study of developmental phonological dyslexia. British Journal of Psychology, 74, 517—533. Wimmer, H. & Hummer, P. (1990). How Germanspeaking first readers read and spell: Doubts on the importance of the logographic stage. Applied Psycholinguistics, 11, 349—368.
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Zaidel, E. (1981). Reading by the disconnected right hemisphere aphasiological perspective. In Y. Zotterman (Ed.). Wenner-Gren Symposium on Dyslexia. 67—91. London: Plenum Press.
Christine M. Temple, Essex (United Kingdom)
73. Treatment of Developmental Reading and Spelling Disorders 1. 2. 3. 4. 5. 6.
1.
The Scope of Remedial Approaches Methodological Issues in Evaluating Intervention Psychological and Educational Approaches Medical and Neurological Approaches Future Research References
The Scope of Remedial Approaches
The scope of remedial approaches to reading and spelling disability is very impressive. It ranges from medication to psychotherapy and from motor training to direct instruction of reading and spelling. This heterogeneity is partially due to the fact that the different scientific disciplines contributing to the analysis of reading disability (education, psychology, linguistics, medicine) are also involved in conceptualizing intervention. Furthermore, some remedial methods have been developed in an applied context and their theoretical foundations are rather coarse. Table 73.1 gives a survey of different therapeutic approaches. Whereas all aim to improve the disabled child’s reading and spelling, there is a distinction in terms of the level at which therapy is directed: Intervention is either directed at the child’s cognitive abilities, the reading and spelling processes themselves, the emotional behavior, the sensory organs or the brain. The present chapter will give a survey of all treatments, concentrating, however, on the different branches of the ‚Direct Instruction’ approach. The theoretical background of each approach and method will be elaborated as it is presented. Although remedial teaching is required to be adaptive to the child’s particular problems, so far no treatment has been found to be differentially effective for specifically reading disabled children as compared to generally backward readers. Consequently, studies us-
Psychological and educational intervention — Training of perceptual and cognitive abilities (‚Prescriptive teaching’) — Training reading and spelling (‚Direct instruction’) — Promoting the alphabetic strategy (training phoneme analysis and synthesis) — Improving orthographic skills — Structural approaches — Lexical approaches — Behavior modification — Training memory stategies — The language experience approach — Psychotherapy Medical and neurological approaches — Ophtalmological intervention — Pharmacotherapy — Methods related to laterality Table 73.1: Survey of different therapeutic approaches in intervention with reading and spelling disabled children ing samples from either population will not be reported separately. Further, there is no other classificatory scheme for disabled readers and spellers from which appropriate treatment programs could be convincingly deduced.
2.
Methodological Issues in Evaluating Intervention
Considering the high quality research on the analysis of reading disabled children’s cognitive abilites and processes (Hulme/Snowling cf. art. 71, Snowling/Hulme cf. art. 70 for review), one would expect to find comparable efforts also in the realm of intervention. However, this is not the case. Only few interven-
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tion studies reach the methodological standards required for empirical research. There are several reasons for this. On the one hand, there is the urgent need to help reading and spelling disabled children; on the other hand, methodological difficulties in evaluative studies are almost unsurmountable: — Consensus exists that reading disabled children need to be taught in an adaptive, individual manner. Yet in empirical designs all children should be preferably treated by the same method. — Consensus again exists that reading and spelling disabled children need to be treated for an extended period of time in order to show substantial improvement; however, it is very difficult to control longterm treatment. — In all intervention studies, control groups present immense problems: For ethical reasons it is not possible to treat control children with any type of placebo over a longer period of time or simply leave them untreated. Yet, if no control group is involved it is difficult to estimate the size of regression, the Hawthorne effect and ‚normal’ development and learning. — There are also many variables which are difficult to control, although they basically c a n be controlled or at least documented. These include on the child’s side the particular type of the reading and spelling problem and other cognitive variables, motivation, and social background, and on the therapist’s side enthusiasm, optimism, and a positive relationship to the child. Particularly the latter variables are rarely controlled. The present chapter will focus mainly on intervention studies which were basically welldesigned, although they could not circumvent all the methodological shortcomings mentioned above. However, for the benefit of completeness, some remedial approaches will be presented, even when no appropriate data are available.
3.
Psychological and Educational Approaches
The majority of therapeutic approaches for reading and writing disabled children are rooted in the psychological and educational domain. While many educational programs developed in the sixties and early seventies intended to strengthen underlying psycholog-
ical abilities (cf. 3.1.) there is now a tendency to directly train reading and spelling skills (cf. 3.2.1.). Within the skill oriented approach, different theoretical systems like behaviorism and cognitive psychology have influenced the development of training programs. 3.1. The Training of Perceptual and Cognitive Abilities (‚Prescriptive Teaching’) The training of perceptual and cognitive abilities, which is known as ‚Prescriptive Teaching’, is still part of everyday remedial teaching (Lewis 1983). The basic idea is the following: Reading disabled children usually show deficits in a number of perceptual and cognitive abilities (as compared to high achievers) and these should be compensated as a prerequisite for reading and spelling. Training programs have been developed in the area of visual perception (e. g. Frostig/Horne 1964 ), of auditory perception, in the motor or visualmotor domain (e. g. Delacato 1963, Kephart 1960) and in various linguistic areas. None of the areas is directly related to the partial processes of reading and spelling. The materials used in these programs (e. g. Frostig/ Horne 1964 ) are often nonverbal and are thus motivating for children who have failed in reading and spelling tasks. However, the approach has not been found to be effective. At best progress is observed in the ability trained; yet there is no transfer to reading and spelling. This is particularly true for the visual domain which is often favored by teachers. Larsen/Hammill (1975) and Arter/Jenkins (1979) in reviewing a large number of studies found that the majority of methodologically acceptable studies do not support the effectiveness of ‚Prescriptive Teaching’. The training of ‚basic’ cognitive abilities also does not necessarily increase the effect of subsequent direct teaching. Edler/Ostrau/ Schulze (1978) trained third grade disabled spellers to use more efficient problem solving strategies in visual tasks. Appropriate strategies were modeled and taught by a method of verbal self-control (see Meichenbaum/ Goodman 1969). After 12 training sessions the trained children showed better performance in most of the tasks used in training; however, there was no transfer to spelling (not even a Hawthorne effect). The children then participated in a spelling program; they profited from this training, but no more than a
73. Treatment of Developmental Reading and Spelling Disorders
previously untrained control group. Training in visual attention had not improved the children’s cognitive prerequisites for direct spelling instruction. Several reasons why the ‚prescriptive teaching’ approach has failed can be given. Concepts such as ‚visual perception’ or ‚auditory perception’ do not seem to be valid entities in the sense that they can be trained as such and manifest themselves in a variety of different tasks. It is known from the information processing literature that the processes involved in visual tasks depend on the stimulus material and the specific task requirements (Neisser 1967). Hence transfer of training between nonverbal and verbal stimuli can hardly be expected. The child who confuses 〈d〉 and 〈b〉 has to learn with which visual stimulus to associate the phoneme /d/; training visual discrimination with pictorial stimuli is irrelevant to the problem. The conclusion that training needs to be specific to reading and writing is supported by studies from the auditory domain. Whereas a general auditory discrimination training does not affect reading (see Sabatino 1973 for review), improving phoneme analysis skills in kindergarten leads to better reading scores in first grade (e. g. Lundberg/Frost/ Peterson 1988). Programs training phonological skills will be discussed in more detail in a subsequent section (3.2.2.) as a branch of the ‚Direct Instruction’ approach. 3.2. Direct Instruction There is no doubt that direct instruction is the most effective approach to improve literacy in reading and spelling disabled children (Branwhite 1983, Lewis 1983). ‚Direct Instruction’ refers to programs which basically implement reading and writing instruction, starting if necessary at a first grade level. Although there are differences in detail, common elements are found in almost all remedial approaches using direct teaching: Consensus exists that, whatever the method, teaching should be adaptive, i. e. be tailored to the child’s present knowledge and progress (Hornsby/Miles 1980, Thomson 1988). Many studies show improvement in reading disabled children’s reading and writing with different types of direct instruction (Scheerer-Neumann 1979). Indeed, it appears somewhat difficult for a treated group not to display at least a short-term effect as compared to a control group. The reason for this is rather obvious: Reading disabled children usually
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experience a ‚teaching deficit’ because the instruction offered to them at school outstrips their actual needs. So any type of adaptive help is almost predestined to have some positive effect. However, if a program is really effective, it should not just show statistically significant improvement as compared to a control group, but also substantial effects with regard to the child’s chronological age. Yet substantial effects can only be found in long-term studies and these present the methodological problems pointed out above. However, in spite of methodological shortcomings, good evidence can be found in largescale and long-term studies indicating that within comprehensive and intensive programs direct instruction really can boost childrens’ achievements in reading and spelling (Balow/ Fuchs/Kasbohm 1978, Hornsby/Miles 1980, Thomson 1988). The severely reading and spelling retarded children in Thomson’s (1988) study increased their reading and spelling ability by almost four years within a treatment period of two and a half years. Previous pessimism (e. g. Silberberg/Silberberg 1969) is not justified. 3.2.1. Direct Instruction within a Developmental Perspective The theoretical foundations of the different methods within direct instruction approach are quite heterogeneous. While some programs are based on recent experimental evidence on poor readers’ deficiencies in the phonological and structural components of reading (e. g. Bradley/Bryant 1983, Scheerer-Neumann 1981), others are rooted in more general therapeutic theories (e. g. the behavior modification approach) and still others are rather eclectic in origin (e. g. Thomson 1988). It is surprising that the literature on efficient spelling instruction for poor spellers (e. g. Hulme 1981) does not seem to be integrated in more general issues of memory development. At times, different theoretical assumptions lead to similar methods: Orton (1937) believed dyslexics’ problems to be mainly visual (he coined the term ‚strephosymbolia’), but this assumption was not confirmed empirically. His coworkers Gillingham/Stillman (1969) developed a training program based mainly on phonics. Their idea was to teach children according to their strengths and not according to their weaknesses. Today similar methods are uses under the presumption that reading and spelling disabled children have problems in the phonological domain.
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Whereas the theoretical backgrounds of different therapeutic programs are heterogeneous, their goals seem to fit well into a model of reading and spelling development which has recently been published by Frith (1985) (see also Marsh/Friedman/Welch/Desberg 1981). Frith proposes that children’s predominant reading and spelling strategies change during the acquisition of literacy; the stages she postulates are the logographic, the alphabetic and finally the orthographic stage. The logographic strategy in reading refers to the instant recognition of familiar words; there is no process of phonological assembly. Logographic writing is writing by rote. The alphabetical strategy is basically a phonological strategy. In reading it translates graphemes into phonemes in a systematic, sequential way. Alphabetic spelling implies the segmentation of words into their constituent phonemes and the translation of phonemes into graphemes. The orthographic strategy is again more ‚direct’, since it uses abstract orthographic patterns for word recognition and spelling. While reading and spelling disabled children seem to be quite proficient in logographic processing (Rozin/Gleitman 1977), they primarily have problems with the alphabetic strategy: There is abundant literature demonstrating poor readers’ and spellers’ deficits in phonological skills like phoneme analysis and phoneme synthesis which are basic components of alphabetic processing (see Kamhi/Catts 1989, Snowling/Hulme cf. art. 70, and Wagner/Torgeson 1987 for review). However, difficulties often persist up to the orthographic stage (Seymour/McGregor 1984 ). Although the question is still open whether orthographic problems are mainly due to a delayed alphabetic stage or rather are an issue in themselves, it is obvious that they need to be treated. There seem to be less problems with reading comprehension once basic decoding skills are acquired. Therefore only training programs are reported which are directed at promoting either the alphabetic or the orthographic strategy. 3.2.2. Promoting the Alphabetic Stategy Taking a look at the actual methods used in direct remedial instruction, it is apparent that exercises directed at alphabetic processing are most often preferred in the initial stages of teaching. Indeed, phoneme-grapheme-correspondences, phoneme analysis and phoneme blending are at the core of effective remedial
V. Pathologies and Disorders of Language Development
programs (Gillingham/Stillman 1969, Hornsby/Miles 1980, Kossow 1972). However, the programs and in particular the evaluative studies differ with respect to the actual methods used to promote alphabetic processing. a) Comprehensive ‚Phonics’ Approaches The phonics approach usually includes the teaching of letter and sound correspondences, phoneme analysis tasks, phoneme blending tasks, and a thorough control of reading material which increases slowly in difficulty on several dimensions. One of these dimensions is consonant-vowel-structure, another the number of syllables per word. Some programs which start with phonics include two additional features: The programs developed by Kossow (1972) and by Dummer/Hackethal (1984 ) teach the child to become conscious of the movements of his/her speech organs when pronouncing sounds (see also Skjelfjord 1976). Although there are no data on the effectiveness of this particular feature of the programs, it fits very well with observations on the actual processes involved in children’s phonemic analysis: Children tend to analyze their own articulation (Schreuder/van Bon 1989, Skelfjord 1976). An additional feature of the programs developed by Kossow (1972) and Dummer/ Hackethal (1984 ) is the introduction of hand signs corresponding to single phonemes. This method is believed to be particularly helpful for children with severe reading problems. Again, we do not have any good data on the effectiveness of this method, but many remedial teachers like to use it. It is not quite clear, though, why hand signs should be effective. Some of Kossow’s signs are related to the visual form of the letter and some to articulatory movements (e. g. /e/, /i/ refer to the opening of the mouth when pronouncing the vowels) so the sign could serve as an additional memory code. It is also possible that the child might be helped by the clear sequential order of signing which models the spoken word much better than the parallel visual input of the written word. Williams (1979) tested a comprehensive phonics program (The ABD of reading = Analysis, Blending, Decoding) with generally learning disabled children in a field study. The children (7—10 years of age) were trained daily for a period of two years. The author reports that in comparison to an untrained control group the trained children made outstanding progress on phonemic tasks as well as in reading and spelling. A similarly im-
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pressive effect was found in a field study by Wallach/Wallach (1979). First grade low-income children were given daily additional training in phoneme analysis, letter-sound correspondences, decoding of simple regular words, and in reading regular classroom reading material. The differences in reading and writing achievement between the trained children and an untrained control group were not only statistically significant, but also “sufficiently large in their magnitude to be important in practical terms” (Wallach/Wallach 1979, 212). Working with older children (M = 11 years) Lovett/Ransby/Barron (1988) studied the effect of training word recognition and decoding skills as compared to a more general language program which included comprehension of oral language, reading, and written composition. Although both groups scored higher on a word recognition task and in a reading test than a control group after 4 0 treatment sessions, it was the ‚decoding’ group which gained most. In long-term studies with school-children a variety of phonological tasks is used and these are complemented rather early by a word training; it is thus difficult to isolate the effects of the different phonological tasks. b) Training Phoneme Analysis and Synthesis Several studies have looked at the effects of a phoneme analysis and/or blending training in a more controlled setting (Ball/Blachman 1988,1991, Bradly/Bryant 1983, Content/Morais/Alegria/Bertelson 1982, Fox/Routh 1984 , Hohn/Ehri 1983, Kerstholt/van Bon/Schreuder 1991, Lie 1991, Mannhaupt 1990, Rosner 1971, Tornéus 1984 , Treiman/Baron 1983, Vellutino/Scanlon 1984 ). Unfortunately, most of these used unselected preschoolers as subjects; hence the results may not be directly transferable to reading disabled children. Still, some issues are probably of general relevance. The main result of the cited studies is the finding that, while phonemic analysis does not seem to develop spontaneously in preschool children (in contrast e. g. to sensitivity to rhymes), it can be trained quite successfully (e. g. Ball/Blachman 1991, Bradley/Bryant 1983, Lundberg/Frost/Peterson 1988). Effects are visible even after a very short training period (e. g. Content/Kolinsky/Morais/Bertelson 1986). Secondly, the training of phonemic analysis and blending in kindergarten has been shown to directly improve reading
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and spelling skills (Ball/Blachman 1991, Fox/ Routh 1984 ) or to accelerate the acquisition of reading and writing in the early school years (Bradley/Bryant 1983, Lundberg/Frost/ Peterson 1988). In a long-term setting training is also effective for children with low scores on pretest. In Bradley/Bryant’s (1983) study the children trained on phoneme categorization tasks during preschool and first grade attained better scores in reading and writing as compared to an untrained control group even several years after training ended. Tornéus (1984 ) showed that training in phoneme segmentation and blending in first grade had a particularly strong effect on children with low pretest scores in phonological tasks. Lie (1991), who also trained first graders, found that children of lower intelligence profited most from phonological training in posttest reading and spelling. What method of teaching phonological skills is most effective and shows optimal transfer for later reading and writing? In her review of training studies, Lewkowicz (1980) concluded that the most effective phonological tasks are those which are most closely related to reading and spelling, i. e. sequential phonemic analysis (as compared e. g. to a positional analysis of single phonemes) and blending. This conclusion has been confirmed empirically by Lie (1991), who studied the influence of a ‚positional phoneme analysis’ training (which sound do you hear in the beginning of a word? in the middle? at the end?) compared to a complete ‚sequential analysis’ training during kindergarten on later reading and writing. Whereas there was no differential effect on reading ability at the end of first grade, the children trained in complete sequential analysis reached better scores in spelling. However, the differential effect was reduced by the end of second grade. Another important issue is the question whether phonemic analysis should be complemented by some kind of visual structure or even by letters. Lewkowicz/Low (1979) found a positive effect of visual squares representing the number of phonemes early in training (see also Elkonin 1973). Hohn/Ehri (1983) showed that phoneme analysis can be promoted even more by introducing the corresponding letters. The authors argue that letters provide the children with a mental symbol system for representing the phonemes. The superiority of a letter condition in phoneme analysis tasks has not been supported
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unequivocally in studies using reading disabled children. Confirmative evidence comes from Bradley/Bryant (1983) who introduced plastic letters in their second year of training for one group of children. On the other hand, Mannhaupt (1990), who trained phonemic segmentation in low achievers in the second half of first grade, did not obtain differential effects between a letter and a blank tile condition. Working with older reading disabled children (7—10 years of age) Kerstholt/van Bon/Schreuder (1991) could not confirm the advantage of a training condition with letters and/or squares as visual support. Thus it seems that the introduction of letters within a phoneme training program is mainly effective for preschoolers who might not be aware of the structure of an alphabetic writing system prior to training. This interpretation can be supported by data from Cunningham (1990), who found better transfer from a phoneme segmentation training to reading when the children (1st grade) were explicitly introduced to the value and utility of phoneme awareness for the activity of reading. Older reading disabled children who have already learned the basics of the correspondence between the spoken and the written language apparently do not profit as much from letters as support for phonemic analysis. In future research, efforts definitely need to be directed at training phonological skills in reading disabled children; mere extrapolation from preschool studies is certainly not justified. What is also needed is an analysis of the microstructure of phoneme segmentation. First attempts have found onset and rime (e. g. c-at) as possible functional units (Schreuder/van Bon 1989, Wise/Olsen/Treiman 1990). Schreuder/van Bon (1989) also looked at the influence of word structure on phonemic analysis and found that different parts of a word influence each other so that a strictly serial model for phoneme segmentation cannot be adequate. In conclusion of this section it should be mentioned that although phoneme analysis and blending certainly are important partial processes of reading and spelling, they need not necessarily be trained in isolation. Ehri (1987) and Morais/Alegria/Content (1987) argue that phonological skills are acquired while learning to read and to spell. Particularly in ‚creative spelling’ (Read 1986) children are constantly required to analyze words into their constituent phonemes (cf. 4.).
V. Pathologies and Disorders of Language Development
3.2.3. Improving Orthographic Skills While segmentation and blending single phonemes seem to be necessary skills for attaining literacy in an alphabetic script like English, they are not sufficient for advanced reading and writing. The competent reader and speller has to deal with many words which do not conform to simple phoneme-grapheme correspondences; these words either display higher order phonographic, graphotactic, or morphemic structure or are orthographically irregular. There are basically two different educational approaches to teach children how to cope with regular but complex and irregular words: The ‚structural’ approach introduces the child to higher order regularities of the written language; the ‚lexical’ or ‚wordspecific’ approach teaches strategies for directly learning the orthographic code of regular and/or irregular words. In long-term programs these approaches are usually combined. a) Structural Approaches Although not all programs using a structural approach are theory oriented, basic research has provided overwhelming evidence that orthographic structure is used in mature reading and writing (Gibson/Shurcliff/Yonas 1970, Glushko 1979, Seidenberg 1987, Taft 1979, 1987 and others). The higher order regularities can be phonographic, graphotactic or morphemic in origin. Although more evidence is emerging constantly (see Coltheart 1987 for review), the exact nature of the utilization and — particularly — the acquisition of orthographic structure is still open for further research. Gibson/Shurcliff/Yonas (1970) believe that invariant spelling patterns are being learnt; Goswami (1986) suggests that children may use analogies to extract rules. Connectionist models of reading acquisition (Seidenberg/McClelland 1989) may be opening new research avenues. There is evidence that reading and writing disabled children do not make as much use of orthographic structure as better readers and spellers (Guthrie/Seifert 1977, Manis/ Morrison 1985, Morrison/Manis 1982, Scheerer-Neumann 1981). While Guthrie/Seifert (1977) regard this deficit as a consequence of delayed reading acquisition rather than as a basic cause of reading retardation, Manis/ Morrison (1985) feel that reading disabled children have general difficulties in learning complex and inconsistent rules.
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In any case, the utilization of orthographic structure is basically teachable. Graphophonic regularities in reading can be taught by rules like “‚i’ before ‚e’”. Insight into the morphemic structure of words allows children to take avantage of building blocks like the 〈ed〉-ending of the past tense in English or the suffix 〈ig〉 in German (Siemens 1985). The syllable structure of long words in particular can also be used to facilitate decoding. Scheerer-Neumann (Scheerer-Neumann 1981, Scheerer-Neumann/Ahola/König/Reckermann 1978) trained reading disabled third graders how to segment written words into syllables using the vocalic center group as reference. The children were quite proficient at phoneme blending, but had problems in decoding long words. After only 12 training sessions there was a considerable decrease in oral reading errors particularly for words with three or more syllables. Syllables are very helpful as segments because they are the units of spoken language and as such are easily accessible to the children (Liberman/Shankweiler/Liberman et al. 1977). Within syllables onset and rime might be useful structural segments. Wise/Olson/Treiman (1990) trained first graders to read a set of four letter words: The scores on post-test were better for those words which had been presented during training in onset-rime segmentation than those in a post-vowel segmentation condition. However, using Dutch third graders as subjects, van Bosch (1991) failed to replicate this facilitatory effect. Whether the discrepancy is due to differences in subjects’ age or to structural differences between written English and Dutch is questionable. It is conceivable that in English the rime more often has a decisive effect on the preceding vowel than in Dutch. The structural approach is frequently used in remedial spelling. The programs developed by Hornsby/Miles (1980) and Thomson (1988) make intensive use of orthographic regularities. In Germany this approach has been proposed by Kossow (1972) and Scheerer-Neumann (1988). Scheerer-Neumann taught spelling rules to poor fifth-grade spellers of average intelligence who were basically proficient in the alphabetic strategy. The rules selected included capitalization of nouns and morphemic constancy, i. e. graphemic constancy of morphemes even in words with a deviant pronunciation. The pupils learned the orthographic rules and how
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to apply them; additionally some of the relevant words were also taught lexically by the ’look-cover-write-check’ method. The posttest included a subset of the trained words as well as untrained words in order to investigate a possible transfer effect. After 30—35 training sessions distributed over 4 months errors related to the trained orthographic regularities decreased by 4 5% with trained words and by 38% with transfer words. This result shows both a very good transfer effect, suggesting that orthographic regularities really had been learnt and could be applied, as well as an effect of word-specific training. On the other hand there was almost no transfer effect to words whose structural difficulties had not been trained. Thus, although there was evidence for transfer to new words when they had the same structure as the trained words, there was almost no transfer to new orthographic structures. b) Lexical (Word-Specific) Approaches Lexical or word-specific approaches in remedial reading and spelling instruction rely solely on the direct teaching of the orthographic properties of words. The basic idea is that children systematically build up a reading or spelling vocabulary with single words as units. Word training procedures have been developed within diverse theoretical traditions: For behavior modification approaches single words are manageable units of reading and writing behavior. Cognitive models of reading and spelling assume that phonological and orthographical processes are complemented by direct access of the stored orthographic representations of words (the ‚orthographic lexicon’, Coltheart 1989), and/or their constituent morphemes. Finally, single word training is also an issue in human memory research (e. g. Hulme 1981). — Behavior Modification Within the behavior modification approach learning to read is considered as operant discrimination learning. Consequently, the correct reading or writing of a word is positively reinforced (Machemer 1972) or, alternatively, errors are punished in a response-cost system (Reuter 1977). Since no assumptions are made about the nature of the cognitive processes involved in reading and writing, the children receive no hints as to the linguistic or psychological structure of the words trained. Instead great care is given to the number and spacing of the trials: The words to be learned are repeated several times during a training period according to a scheme which is derived
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from learning theory; distributed practice with shorter intervals for newly introduced words has been shown to be more effective than massed practice (see Kerr/Lambert 1982, for review). This technique can easily be implemented and has been shown to be very effective even with parents as trainers (Machemer 1972). Some programs also control the rehearsal behavior during each trial: Murphy/ Hern/Williams/McLaughlin (1990) observed that the copy-cover-write-check procedure combined with systematic repetitions lead to better results in spelling than more traditional training methods. Lenz/Singh/Hewett (1991) suggest that it is the component of directed rehearsal which makes “overcorrection” a powerful procedure in academic remediation. Some training studies conducted within the cognitive reading research tradition have also used repeated presentations of words to improve word recognition. It seems rather easy to increase a child’s reading accuracy and speed in word recognition by systematically practising a set of words. That it is in fact word-specific knowledge which is acquired by this type of procedure is demonstrated by the absence of a transfer effect to untrained words (Fiedorowicz 1986, Reitsma/Dongelmans 1988). — Training Memory Stategies Whereas behavior modification methods mainly control the number and spacing of trials and rehearsals, memory strategies can also be modified more directly. The vast literature on memory development has convincingly shown that younger children do not use as effective memory strategies as older children (e. g. Ornstein/Naus 1978; for a review see Hagen/Jongeward/Kail 1975, Ornstein 1978). Reading disabled and generally learning disabled children resemble chronologically younger children (Bauer 1979, Bauer/Newman 1991, Dallago/Moely 1980). When learning the spelling of new words spelling disabled children often display an impulsive, non-strategic behavior; they do not take enough time and commit more errors than their peers (Kossow 1972). There is also a vast literature showing that the use of more efficient memory strategies can be trained (Hagen/Hargrave/Ross 1973; for review, see Bauer 1987, Hagen/Jongeward/Kail 1975). The task therefore is to determine which strategies are most effective to retain the orthographic code of words. There are some shortterm experimental studies on this question
V. Pathologies and Disorders of Language Development
which are also relevant for comprehensive remedial programs. The main issue refers to the modality of the code used: This is the classic question whether learning is most efficient using the visual, the auditory or the kinesthetic modality, or a combination of any two or three. Gillingham/Stillmann (1956) proposed a strategy they called ‚simultaneous oral spelling’; while copying (later in training writing by rote) a word the child names each letter. Since this procedure involves a visual, an auditory, and a motor component it is often referred to as ‚multisensory teaching’. The importance of the motor component has also been stressed by Fernald (194 3) and by Montessori (1913). Hulme (1981) tested the efficiency of different spelling codes experimentally and some other studies have followed. In a very convincing study Hulme/ Bradley (1984 ) found that retarded spellers (M = 11 years) profited most from simultaneous oral spelling compared to a condition without letter naming and a condition which used letter cards instead of writing. Performance under the ‚simultaneous oral spelling’ condition improved even 4 weeks after training. The results were dissimilar for normal readers who were chronologically younger (M = 6 years, 8 months) but of the same spelling age: They did not show any differential effects under the various conditions. In a study using an intraindividual design Bradley (1981) found that merely pronouncing the word while writing was not as helpful as simultaneous spelling. That simply pronouncing the word is not as efficient as simultaneous spelling is not surprising, since the spoken word does not contain the complete orthographic information. Taken together, these results show that multiple coding improves the memory performance of retarded readers. This is in agreement with basic memory research. Paivio (1971) has demonstrated that items which can be coded both visually and verbally are better retained in memory. The question then remains, why the additional auditory code does not improve spelling in normal readers. Although Hulme/Bradley (1984 ) do not report relevant data it is probable that normal spellers use some type of verbal code spontaneously. For languages with more regular phoneme-grapheme correspondences like German, this verbal code seems to be the ‚overpronunciation’ of the word with respect to its spelling rather than the letter names (Scheerer-Neumann 1986a). When ‚multisen-
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sory’ training is regarded as an instance of multiple code learning, it should also be helpful to include structural properties of the word as an additional code (e. g. the morphemic structure of a word like “child/ish”). Most importantly, Hulme/Bradley’s (1984 ) data fit the picture of inefficient memory strategies in poor spellers, which can be improved by training. This conclusion is supported by research showing that in spelling instruction particularly poor spellers need a memorization set in order for successful learning to come about. Bosman/de Groot (1991) found that copying a stimulus word while it was still in view was totally ineffective for poor spellers (grade 1), while it had a small effect in good spellers. The low level performance of poor spellers probably has to do with their inability to spontaneously generate additional codes while copying. The finding that a memorization set is necessary for appreciable retention to come about conforms with the idea of the child as an active learner whose task it is to select and code information. This is very different from the conception of the orthographic lexicon as a store of ‚photographic word-pictures’ which has been prominent among teachers for many years (Scheerer-Neumann 1986b). There are some additional data which demonstrate active processes in spelling acquisition: Kauffman/Hallahan/Haas et al. (1978) and Hasselbring (1982) found greater improvement in spelling when the children were shown their errors together with correct spellings instead of the correct spellings alone. This finding demonstrates that children do not just store correct spellings but rather pay attention to the letters they missed before. Word training programs can be implemented very well by a microcomputer. A computer program has the advantage of being easily adapted to a child’s basic level and daily performance, a feature which is essential for spelling disabled children. Adaptive spelling programs for disabled spellers have been reported among others by Hasselbring (1982) and Breuninger/Betz (1989). 3.3 The Language Experience Approach The ‚Language experience approach’ or ‚whole language approach’ stresses the child’s own language as a bridge from oral to written language (e. g. Hildreth 1965). The child’s attention is focussed on the functional aspects rather than on the structural properties of
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written language. Instead of basal readers, children’s literature is used as reading material as early as possible. Children are encouraged to communicate by writing even at a stage where they cannot be expected to avoid spelling errors. Errors are not only tolerated but considered as signs of certain developmental stages (Read 1986). Stahl/Miller (1989) have recently completed a meta-analysis of a large number of studies comparing the effectiveness of the language experience approach with a basal reader approach. They found that, overall, the approaches were similar in their effectiveness, although there were also differential results. The language experience approach was more effective in teaching children concepts about print and reading at the kindergarten level. Unfortunately, the authors did not look specifically at slow learners; yet data are reported on disadvantaged children and a large overlap between the learning disabled and the disadvantaged population can be assumed. The disadvantaged children also profited from the language experience approach at the kindergarten level; however, at the first grade level the basal reader approach proved more effective. The authors conclude that — in Downing’s (1979) terms — the language experience approach is more efficient in the ‚cognitive phase’, when children become aware of print and reading, but that the basal reader approach is more helpful during the ‚mastering phase’. The advantage of the basal reader approach on the skill acquisition phase complies with a presupposition underlying most remedial approaches particularly within the direct instruction tradition: Most of them explicitly demand a step-by-step procedure where nothing is left to chance and no transfer is expected from the child (Dummer/Hackethal 1984 , Hornsby/Miles 1980, Thomson 1988). On the other hand, the language experience approach does rely upon learning which is not explicitly taught. In practice, both approaches can be combined to a certain extent. It is possible to use the highly motivating elements from the language experience approach, have children read and write on their own very early and still introduce elements of the written language in a rather systematic form. In a study which included kindergarten and first grade Sawyer (1988) found best results for children who were poor phoneme segmenters when a combination of a phonics and a language experience ap-
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proach was used. Spontaneous, creative writing, one important element of the language experience approach, implies extensive practice in phoneme analysis since the children often want to write words whose spelling they are not familiar with. They have to construct these words out of known elements, usually phoneme-grapheme correspondences. Although words constructed by children in creative spelling are frequently not yet correct orthographically, early spelling errors do not seem to have a negative effect on later orthographic skills: Clarke (1988) found that creative writing even leads to better spelling achievements at the end of first grade than more traditional teaching methods. Creative writing can be facilitated by a text processor (e. g. Levin/Boruta/Vasconcellos 1983) which can also be used for checking the spelling. Computers offer new possibilities to help reading disabled children; the scope has not yet been fully explored. 3.4. Psychotherapy Psychotherapy has been suggested by Axline (194 7) and others as a treatment of reading disability. There may indeed be cases where reading disability should be viewed as neurotic behavior and treated accordingly. However, in the majority of cases, emotional and behavioral problems in reading disabled children are secondary to their failure at school. Constant problems in important school subjects affect most children’s self concept severely. Most school systems are not flexible enough to allow children to progress at their own pace. Thus for some children psychotherapy is needed as a precondition for more direct instruction. Child guidance institutions usually offer integrated remedial programs including counseling, help in emotional problems and remedial instruction (e. g. Betz/ Breuninger 1987). Unfortunately, there are no appropriate data to document the influence of each line. It would be of particular interest to find out whether successful remedial instruction has in itself a positive effect on the child’s emotions and behavior.
4.
Medical and Neurological Approaches
4.1. Ophthalmological Intervention Although reading disability is defined as a
condition without sensory dysfunction, some subtle visual perceptual problems may occur in reading disabled children. Binocular instability has been suggested as one possible disorder; unstable fixation degrades the visual stimulus and might thus interfere with reading (Stein/Fowler 1982). The argument that many good readers also show the same condition (Newman/Karle/Wadsworth et al. 1985) does not necessarily disprove the point, since unstable fixation might be compensated by superior linguistic skills. Occlusion of one eye has been proposed as a remedy for children with ocular instability. A positive effect has been claimed by Stein/Fowler (1985); however, the data are not entirely conclusive. Another alleged remedy in the visual domain is the use of a tinted overlay or tinted lenses. Reports of improved reading with this method are mainly anecdotal. However, there are two recent case studies which show a tremendous qualitative improvement in the children’s reproduction of visual patterns with tinted overlays (Hannell/Gole/Dibden et al. 1991): Whereas the reproductions appear to be fairly normal under the condition of tinted overlays, the contours appear to be ‚fuzzy’ under normal viewing conditions. One of the children introspectively reported a ‚furriness’ in the perception of normal black and white print. The mechanism why tinted lenses should be helpful for some children is not yet clear; it is, however, known that tinted lenses slow the transmission of impulses along the primary visual pathway. Eye-movements are another topic in the field of poor reader’s visual perception. Extensive research in eye-movements has basically shown that deviant behavior in this domain is a by-product rather than a cause of reading disability (Pirozzolo 1983). Pavlidis’ (1981) contradicting results have not been replicated (e. g. Olson/Kliegl/Davidson 1983). However, this chapter is not yet closed. Bassou/Pugh/Granie/Morucci (1991) have recently reported on divergent eye-movements during reading in some children, i. e. their eyes moved in different directions while reading. However, the authors are very cautious in interpreting their results. It is also open for questions what remedies could be developed if divergent eye-movements really would turn out to be a major stumbling block for reading disabled children. In any case, it seems that only a minority of reading disabled children are afflicted with visual-perceptual problems. Individual diagnoses are certainly indicated.
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4.2. Pharmacotherapy In the past decades the drug Ritalin had the reputation of improving reading disabled children’s achievements. However, Gittelman/Klein/Feingold (1983) have shown convincingly that reading disabled children receiving both Ritalin and specific reading instruction perform no better on reading measures than a control group receiving specific reading instruction and a placebo. More recent studies investigated the effects of the drug Piracetam which is supposed to be a ‚nootropic’ drug, influencing specifically the ‚higher’ functions of the brain, particularly those which normally reside in the left cerebral hemisphere. It has also been hypothesized that it influences transcallosal transfer, but apparently there is no sound evidence for this assumption (Wilsher 1986). Some experimental studies show that Piracetam improves verbal short-term memory in normal adults (i. e. college students) (e. g. Dimond/Brouwers 1976). Thus it is not very surprising that in several well designed double blind studies the drug has also been shown to improve reading in reading disabled children (e. g. Conners/ Reader 1987). However, although significant improvement on some reading measures was found in the experimental groups as compared to placebo control groups, the extent of the effects seems to be rather small and thus of questionable practical relevance. It is also not clear which cognitive processes are affected by the drug. It could be that children just performed better on a posttest; alternatively the effect could be attributable to more efficient learning at school. These questions might be answered by appropriate experimental designs. 4.3. Methods Related to Laterality Delacato (1963) has been the main proponent of the idea that motor training — like throwing a ball — can promote a consistent lateral dominance and thereby improve reading and spelling in disabled children. This approach turned out to be a blind alley: Although the relationship between laterality in the sense of the functional differentiation of the two hemispheres and reading disability is still under discussion, there has been no sound evidence that motor training has any influence on reading and spelling (Arter/Jenkins 1979). However, there has been a recent attempt to influence directly the two hemispheres’ involvement in the reading task. Bakker/van
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Leeuwen/Spyer (1987) claim that they can accelerate slow readers’ performance by flashing words to the left hemisphere and improve inaccurate but fast reading by flashing words to the right hemisphere. While the basic idea that the hemispheres contribute differentially to literacy is well taken, Bakker’s et al. (1987) empirical evidence is not entirely conclusive due to the lack of convincing control groups.
5.
Future Research
This chapter has reviewed a wide scope of remedial approaches. Empirical evaluation of the different methods has not been sufficient so far. Even in studies with adequate research designs the dependent variables are mostly too coarse; simple pre- and posttests using scores from reading or spelling tests as criterion give a clue as to the general efficiency of a program but do not convey any insight into the processes which were actually altered by the training. However, this insight is needed if programs are to be implemented successfully under conditions which do not exactly reproduce every single variable of the original research study. As a first step in understanding the actual learning processes, the children’s reading and spelling problems should be analyzed in detail before training. Secondly, the programs should specify exactly what skill or partial process they intend to improve and hence predict which differential effects are expected. Differential prediction is not only important for the evaluation of a program but can also serve as support — or rejection — of the underlying theory.
6.
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74. Hyperlexia and Precocious Reading 1. 2. 3. 4. 5.
1.
Definitions and Issues Mechanisms Underlying Hyperlexic Reading Parallels with Normal Precocious Reading Conclusions References
Definitions and Issues
Since the introduction of the term ‚hyperlexia’ to the psychological literature over two decades ago, the consensus definition of this condition has been: precocious and uninstructed reading recognition ability, emerging in the preschool years and appearing in the context of delayed or disordered cognitive and language functioning (e. g., Welsh/Pennington/ Rogers 1987). Ironically, the original term coined by Silberberg/Silberberg (1967) did not include the criterion of cognitive or behavioral disorder, although more than half of their original subject sample did manifest some condition suggesting cerebral dysfunction (Silberberg/Silberberg 1967). The authors proposed that exceptional word decoding skills may be an example of a physiological variant (Hallgren 1950) that distributes normally across the population and varies independently from other normal variants, such as intelligence. However, the majority of studies on hyperlexia have not adequately tested the Silberbergs’ proposal by examining this isolated precocity in a range of both typical and atypical populations of children. The vast majority of research and clinical case reports exploring the phenomenon of hyperlexia have involved children whose reading proficiency is concomitant with some form of behavioral pathology. This approach dove-tailed with an early and influential literature on savant and ‚splinter’ skills in the severely retarded (Bergman/Escalona 194 8; Eisenberg/Kanner 1956; Kanner 194 3; Mahler/Elkisch 1953; Parker 1919; Philipps 1930). There is, after all, a strong motivation to understand the remarkable achievement of a mentally-retarded, noncommunicative, autistic child who exhibits an ‚island of ability’ with regarded to word decoding skills. The phenomenon in which reading recognition far outstrips comprehension and general intelligence is obviously more salient in the context of cognitive impairment, and thus, the burgeoning research literature became dominated with studies of children with a variety of
diagnoses, such as autism or ‚autistic features’, hyperactivity, language and speech disorders or childhood schizophrenia (Aram/ Rose/Horwitz 1984 ; Cobrinick 1974 ; 1982; Elliot/Needleman 1976; Fontenelle/Alarcon 1982; Frith/Snowling 1983; Goldberg/Rothermel 198 4 ; Graziani/Brodsky/Mason/Zager 1983; Healy/Aram/Horwitz/Kessler 1982; Huttenlocher/Huttenlocher 1973; Mehegan/ Dreifuss 1972; Richman/Kitchell 1981; Siegel 198 4 ; Silberberg/Silberberg, 1967; 1971; Snowling/Frith 1986; Welsh/Pennington/ Rogers 1987; Whitehouse/Harris 1984). Irrespective of the substantial overlap between autism and hyperlexia (Whitehouse/ Harris 1984 ), precocious reading is clearly not a pathognomonic sign of autism (Cobrinick 1982), nor is the behavior restricted to this diagnosis. Snowling/Frith (1986) recently concluded that hyperlexia was not a syndrome-specific phenomenon after finding that both autistic and nonautistic mentally retarded children exhibited a similar decoding precocity and comprehension deficit. Whereas all of the studies cited above, excepting one (Richman/Kitchell 1981), included at least some low-IQ children in their samples, it is also the case that the range of IQ scores represented in many subject samples is quite broad. For example, in the Whitehouse/Harris (1984 ) sample of 20 autistic children who exhibited precocious reading, the IQ scores ranged from 20 to 14 4 ! The wide range of psychological disorders and IQ levels represented in the hyperlexia literature may support a plasticity view of the condition (Bender 1966), in which accelerated word recognition skill is dissociated from the other cognitive and language impairments resulting from various forms of brain dysfunction. Thus, we have a situation in which most of the research regarding hyperlexia involves behaviorally and/or intellectually impaired children. However, the phenomenon is observed in a variety of clinical syndromes and across a broad band of intellectual function. There has been much theoretical debate as to the connection between hyperlexia and developmental dyslexia (e. g., DeHirsch 1971; McClure/Hynd 1983), as well as evidence suggesting similarities in the reading processes utilized by hyperlexic readers and individuals with the acquired syndrome of surface dyslexia (Aram/Rose/Horwitz 1984 ; Welsh/Pen-
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nington/Rogers 1987). However, there has been a general lack of integration of the respective literatures involving hyperlexia and normal precocious reading. This chapter will explore possible parallels between the reading behaviors exhibited by ‚classic’ hyperlexics and by developmentally normal precocious readers. By building a bridge between the two separate literatures, one can begin to address whether the word decoding facility observed in hyperlexic children is also exhibited by behaviorally normal children, suggesting that this precocity is n o t a symptom of pathology. Documenting the existence of accelerated word decoding skills in a wide range of children will have implications for the normal physiological variant position of Silberberg/ Silberberg (1971).
2.
Mechanisms Underlying Hyperlexic Reading
The recent empirical literature examining hyperlexia can be characterized as falling into two ‚camps’ with regard to the mechanisms hypothesized to underlie the condition. One position emphasizes the cognitive impairments characterizing hyperlexia, such as the absence of an internal organizing framework to guide text comprehension. A second position suggests that hyperlexia represents accelerated cognitive skills in the areas of visual and/or auditory memory or phonological processing. Neither framework alone has generated a complete description of the full range of cognitive strengths and weaknesses characteristic of hyperlexic. The comprehension deficit has been attributed to deficiencies in the ability to structure, categorize and associate the semantic and syntactic information necessary for meaningful processing (Fontenelle/Alarcon 1982; Healy/Aram/Horwitz/Kessler 1982; Huttenlocher/Huttenlocher 1973; Richman/Kitchell 1981; Snowling/Frith 1986). For example, Healy/Aram/Horwitz/Kessler (1982) interpreted the data as reflecting a lack of interaction between the ‚bottom-up’ perceptual decoding skills and ‚top-down’ conceptual processing to give text meaning. Similarly, Snowling/Frith (1986) found that retarded hyperlexic children exhibited comprehension deficits that reflected ineffective use of sentence context and generally poor metacognitive skill. Overall, the studies focusing on cognitive weaknesses view hyperlexia as a
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d e f i c i t 1condition rather than as a precocity and, with few exceptions (e. g., Healy/Aram/ Horwitz/Kessler 1982) in-depth investigations of ‚bottom-up’ decoding skills have been lacking. Research examining the strengths of the hyperlexic reader originally evaluated the proposal that superior single-word reading resulted from advanced memory abilities for unrelated auditory and visual stimuli (Cain 1969; Goodman 1972) that have been observed in some hyperlexic children. In this research, word recognition was generally interpreted as rote memory for the visual gestalt or total configuration of the word (Cobrinick 1974 ; 1982; DeHirsch 1971; Elliot/Needleman 1976; Fontenelle/Alarcon 1982), rather than the result of decoding individual graphemic units. However, this exclusive visual memory interpretation has been compromised by recent evidence demonstrating that reading is guided to a large extent by grapheme-phoneme correspondence (GPC) rules. Evidence of GPC rule use derives from studies demonstrating adequate, and even advanced, nonword reading in hyperlexic children (Frith/Snowling 1983; Goldberg/Rothermel 198 4 ; Healy/ Aram/Horwitz/Kessler 1982; Siegel 1984 ; Welsh/Pennington/Rogers 1987). Moreover, hyperlexic children often are more accurate reading ‚regular’ words that correspond to GPC rules than ‚irregular’ words that violate these rules (Aram/Rose/Horwitz 1984 ; Welsh/ Pennington/Rogers 1987), suggesting a greater reliance on phonological decoding of words than on direct access to the lexicon (Welsh/Pennington/Rogers 1987). An empirical question requiring further examination is the degree to which superior visual and auditory memory abilities contribute to the d eve l o p m e n t of an effective GPC rule system in these children. Clarification regarding the areas of reading-related strength and weakness in hyperlexic children can be achieved by using general intelligence as a baseline for expected reading achievement. Given this approach, it appears that reading recognition, as defined by single word reading, is a relative strength as compared to general intelligence. This exceptional word decoding performance appears to be facilitated by precious and advanced phonological processing according to GPC rules. In contrast, single-word reading comprehension is generally commensurate with IQ and, therefore, is n o t a specific deficit
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per se. When reading comprehension of hyperlexic children has been found to be a specific area of weakness, comprehension has been evaluated with connected discourse requiring the effective use of an intact knowledge base, metacognitive control processes and other topdown strategies (e. g., Snowling/ Frith 1986). It is certainly possible that reading comprehension of single words is limited by the child’s general intellectual level; whereas, the additional demands of integrating prose stresses the fragile system and limits comprehension skills to an even greater degree. It must be noted that there is still a lack of agreement as to the reading profile that best defines the phenomenon of hyperlexia. Both McClure/Hynd (1983) and Snowling/ Frith (1986) have suggested that ‚true’ hyperlexia’ be reserved for those children exhibiting advanced word decoding and impaired comprehension in relation to IQ. Irrespective of the currently unresolved nosological issues, a consistent theme emerging from the study of hyperlexia is the apparent functional dissociation between the phonological and semantic processing systems underlying reading (Snowling/Frith 1986; Welsh/Pennington/ Rogers 1987). The independence of cognitive mechanisms underlying reading is consistent with current models of reading (Perfetti 1985) and this theoretical proposal has been supported by the descriptions of reading behavior in acquired brain lesion cases (Patterson/ Marshall/Coltheart 1986).
3.
Parallels with Normal Precocious Reading
For years there have been anecdotal reports by parents and educators of early reading observed in normal children (Torrey 1973), as well as curriculum-based studies of preschool readers in the education literature (Durkin 1970). In an unselected group of four-yearolds attending a university-operated preschool, Mason (1980) found that the largest percentages of children read words through the use of nonlinguistic context or through visual recognition of very frequent words. By far, the smallest category of children employed what Mason called letter-sound analysis in which multisyllabic words were read through accurate phonological decoding. Interestingly, it is just this skill that appears to be accelerated in hyperlexic readers in spite
of concomitant behavioral and/or intellectual impairments. To date, the most systematic program of research on normal children who read precociously has been conducted by Jackson and her colleagues (Jackson/Biemiller 1985; Jackson/Donaldson/Cleland 1988; Mills/Jackson 1989). This research has evaluated the specific reading-related skills and more general cognitive patterns exhibited by a group of kindergarten children identified by their teachers as advanced readers. Essentially, teachers were asked to nominate children that they thought were reading at or above the thirdgrade level. It is important to note that the term ‚reading’ referred to reading c o m p r eh e n s i o n, as well as reading recognition. Thus, there is a subjective difference between most research on hyperlexia and these studies of precocious reading; the former usually defines advanced reading in terms of word recognition alone, while the latter focuses on reading w i t h comprehension. Nonetheless, the findings of this set of studies provide interesting points of comparison with the data base on hyperlexic reading, and together the two research domains have important implications for theories of normal reading acquisition and development. Jackson (Jackson/Biemiller 1985; Jackson/Donaldson/Cleland 1988) found that efficiency in lower-order skills, such as letter identification speed and phonological decoding, were facilitative of early reading, but not necessarily a prerequisite. In fact, the authors concluded that no single lower-order skill was responsible for reading precocity, and instead, overall verbal ability, a superior knowledge base, and metacognitive strategies may contribute to reading success. Many of their findings converged on the notion that the strengths of these precocious readers were top-down executive abilities that effectively utilized the bottom-up perceptual information in the text. In a follow-up study of these children at 10 to 12 years, Mills/Jackson (1989) found that it was general verbal ability that was as good a predictor of current reading comprehension as early reading-related skills. Although as a group the precocious readers were advanced in both lower-level perceptual skills and higher-level conceptual strategies, withingroup analyses found these reading processes to be uncorrelated. How do these findings regarding normal precocious reading compare and contrast with the characterization of hyperlexic read-
74. Hyperlexia and Precocious Reading
ers in the clinical literature? One important similarity is that both literature provide empirical support for the independence of different systems underlying reading. Specifically, phonological skills and semantic skills appear to function relatively independently of each other in both developmentally normal readers and clinically diagnosed hyperlexics. In addition, both samples of readers exhibit a dissociation of GPC decoding ability from overall intelligence and/or verbal ability (Jackson/Butterfield 1986). Therefore, both literatures support the notion first advanced by Silberberg/Silberberg (1967): word decoding may represent a normal physiological variant that distributes independently of other normal variants such as IQ. Given that a superiority in word decoding has been found in such diverse clinical populations as the mentally retarded, autistic, language disabled, as well as in behaviorally normal children, this precocity is clearly not a pathognomonic marker of any one clinical condition, nor does it appear to be symptomatic of general neurological dysfunction. A key difference between the literatures that limits direct comparison lies in the definition of precocious reading. Normal early readers were advanced in b o t h reading comprehension and word decoding, and these precocities were in relation to a ge and not to intelligence. The sample of children studied by Jackson and colleagues had an average IQ of 128 and, thus, comprehension and decoding skills at the third grade level did not represent a striking deviation from intelligence. For example, the estimates of mental age for verbal intelligence and for reading comprehension were nearly equivalent in this kindergarten group. In contrast, hyperlexic readers have frequently been found to exhibit decoding skills that far exceed their general or verbal IQ levels. However, like precocious readers, their reading comprehension scores are generally commensurate with intelligence. A second point of divergence between the two reading groups involves the degree to which top-down processes deriving from an intact knowledge base and metacognitive strategies aid the development of advanced reading skills. In the case of precocious readers, it appears that a ‚good balance’ between top-down integrative processes and bottomup perceptual processes is most responsible for their advanced reading levels (Jackson/ Biemiller 1985). In fact, it may general verbal ability that contributes most to continued
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success in reading in the later school years (Mills/Jackson 1989). This stands in striking contrast to the typical characterization of the hyperlexic child in which bottom-up and topdown reading skills may fail to interact at all to give text meaning (Healy/Aram/Horwitz/ Kessler 1982). Clearly, the strong suit for hyperlexic readers is word decoding according to GPC rules, and n o t strategic use of text context and knowledge base, as has been found for normal precocious readers. However, recall that the criterion for advanced reading is often different for these two groups of advanced readers. Given that superior reading recognition w i t h comprehension is typical of the normal precocious reader, it is not surprising that top-down processes would play a more prominent role.
4.
Conclusions
Thus, two themes have emerged from this review of the hyperlexia and precocious reading literatures. First, it appears that underlying reading mechanisms can function relatively independently from one another and from general intelligence, and that word decoding in particular may be a modular skill that represents a physiological variant (Silberberg/Silberberg 1967). Second, as traditionally studied, hyperlexic children with concomitant clinical conditions and developmentally normal precocious readers differ with regard to the relative contributions to superior reading of bottom-up perceptual processes and top-down semantic processes. This chapter will close with a brief description of one study conducted in our laboratory that provides an interesting bridge between the hyperlexia and precocious reading literatures. Pennington/Johnson/Welsh (1987) conducted a case study of a child with superior intelligence and no signs of autism or neurological dysfunction who, nevertheless, exhibited precocious, uninstructed reading prior to age 3. The child’s reading strengths and weakness in relation to IQ were examined with many of the same measures used by Welsh/Pennington/Rogers (1987) to study autistic hyperlexic readers, facilitating a direct comparison of performance profiles. Like the precocious readers studied by Jackson and others, this subject had above-average intellectual endowment and reading comprehension commensurate with this ability level. However, unlike the precocious readers, this child did n o t exhibit a particular strength in
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conceptual, integrative, or metacognitive skills. Instead, this subject demonstrated an outstanding ability to decode words according to GPC rules that far exceeded general intelligence, similar to the autistic hyperlexic readers studied by Welsh/Pennington/Rogers (1987). Thus, again there is evidence for a dissociation between word decoding mechanisms and general ability in a behaviorally normal child. This precocity far outstripped other above-average intellectual and readingrelated skills, but was not in itself a sign of behavioral pathology, neurological dysfunction, or language disorder as some have suggested (e. g., DeHirsch 1971; McClure/Hynd 1983; Richman/Kitchell 1981; Snowling/Frith 1986). In conclusion, the continued exploration of hyperlexic reading in a variety of clinical and nonclinical samples should provide important insights regarding the typical and atypical course of reading acquisition and development. A promising avenue for future research would be the application of similar criteria and methodologies for the study of advanced reading in both clinical and nonclinical samples of precocious readers. At present, there is a lack of convergence and integration between the research programs exploring hyperlexia and normal precocious reading, although the apparent parallels in the underlying processes and mechanisms would seem to warrant such a collaboration in the future.
5.
References
Aram, D. M., Rose, D. F., & Horwitz, S. J. (1984 ). Developmental reading without meaning. In R. M. Malatesha & H. A. Whitaker (Eds.), Dyslexia: A global issue. 517—531. Nato ASI Series. Bender, L. (1966). The concept of plasticity in childhood schizophrenia. In P. H. Hoch & J. Zubin (Eds.), Psychopathology of schizophrenia. 354—365. New York: Grune & Stratton. Bergman, P. & Escalona, S. (194 8). Unusual sensitivities in very young children. Psychoanalytic study of the child. New York: International University Press, V. 3 and 4. Cain, A. C. (1969). Special “isolated” abilities in severely psychotic young children. Psychiatry, 32, 137—149. Cobrinick, L. (1974 ). Unusual reading ability in severely disturbed children: Clinical observations and a retrospective inquiry. Journal of Autism and Childhood Schizophrenia, 4, 163—175. Cobrinick, L. (1982). The performance of hyper-
lexic children on an “incomplete words” task. Neuropsychologia, 20, 569—577. DeHirsch, K. (1971). Are hyperlexics dyslexics? The Journal of Special Education, 5, 243—245. Durkin, D. (1970). A language arts program of pre-first grade children: two-year achievement report. Reading Research Quarterly, 4, 543—565. Eisenberg, L. & Kanner, L. (1956). Early infantile autism, 194 3—1955. American Journal of Orthopsychiatry, 26, 556—566. Elliot, D. E. & Needleman, R. M. (1976). The syndrome of hyperlexia. Brain and Language, 3, 339—349. Fontenelle, S. & Alarcon, M. (1982). Hyperlexia: Precocious word recognition in developmentally delayed children. Perceptual and Motor Skills, 55, 247—252. Frith, U. & Snowling, M. (1983). Reading for meaning and reading for sound in autistic and dyslexic children. British Journal of Dev elopmental Psychology, 1, 329—342. Goldberg, T. E. & Rothermel, R. D. (1984 ). Hyperlexic children reading. Brain, 107, 759—785. Goodman, J. (1972). A case of an “autistic savant”: Mental function in the psychotic child with markedly disrepant abilities. Journal of Child Psychology, Psychiatry, 13, 267—273. Graziani, L. J., Brodsky, K., Mason, J. C., & Zager, R. P. (1983). Variability in IQ scores and prognosis of children with hyperlexia. American Academy of Child Psychiatry, 22, 441—443. Hallgren, B. (1950). Specific dyslexia: A clinical and genetic study. Acta Psychiatrica et Neurologica, Supplement 65. Healy, J. M., Aram, D. M., Horwitz, S. J., & Kessler, J. W. (1982). A study of hyperlexia. Brain and Language, 17, 1—23. Huttenlocher, P. R. & Huttenlocher, J. (1973). A study of children with hyperlexia. Neurology, 23, 1107—1116. Jackson, N. E. & Biemiller, A. J. (1985). Letter, word, and text reading times of precocious and average readers. Child Development, 56, 196—206. Jackson, N. E. & Butterfield, E. C. (1986). A conception of giftedness designed to promote research. In R. J. Sternberg & J. E. Davidson (Eds.), Conceptions of giftedness. 151—181. New York: Cambridge University Press. Jackson, N. E., Donaldsen, G. W., & Cleland, L. N. (1988). The structure of precocious reading ability. Journal of Educational Psychology, 80, 234—243. Kanner, L. (194 3). Autistic disturbances of affective contact. Nervous Child, 21, 217—250. Mahler, M. S. & Elkisch, P. (1953). Some observations on disturbances of the ego in a case of infantile psychosis. Psychoanalytic study of the
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child. New York: International University Press, V. 8. Mason, J. M. (1980). When do children begin to read: An exploration of four year old children’s letter and word reading competencies. Reading Research Quarterly, 2, 203—227. McClure, P. H. & Hynd, G. W. (1983). Is hyperlexia a severe reading disorder or a symptom of psychiatric disturbance? Nosological considerations. Clinical Neuropsychology, 5, 145—149. Mehegan, C. C. & Dreifuss, F. E. (1972). Exceptional reading ability in brain damaged children. Neurology, 22, 1105—1111. Mills, J. R. & Jackson, N. E. (April, 1989). Predictiv e significance of early giftedness: The case of precocious reading. Paper presented at the biennal meeting of the Society for Research in Child Development, Kansas City, MO. Parker, S. W. (1919). Pseudo-talent for words. Psychology Clinics, 11, 1—7. Patterson, K. E., Marshall, J., & Coltheart, M. (Eds.) (1986). Surface dyslexia. Hillsdale, NJ: Erlbaum. Pennington, B. F., Johnson, C., & Welsh, M. C. (1987). Unexpected reading precocity in a normal preschooler: Implications for hyperlexia. Brain and Language, 30, 165—180. Perfetti, C. A. (1985). Reading ability. New York: Oxford University Press.
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Philipps, A. (1930). Talented imbeciles. Psychology Clinics, 18, 246—265. Richman, L. C. & Kitchell, M. M. (1981). Hyperlexia as a variant of developmental language disorder. Brain and Language, 12, 203—212. Siegel, L. (1984 ). A longitudinal study of a hyperlexic child: Hyperlexia as a language disorder. Neuropsychologia, 22, 577—585. Silberberg, N. E. & Silberberg, M. C. (1967). Hyperlexia: Specific word recognition skills in young children. Exceptional Children, 34, 41—42. Silberberg, N. E. & Silberberg, M. C. (1971). Hyperlexia: The other end of the continuum. Journal of Special Education, 5, 233—267. Snowling, M. & Frith, U. 81986). Comprehension in “hyperlexic” readers. Journal of Experimental Child Psychology, 42, 392—415. Torrey, J. (1973). Learning to read without a teacher. In F. Smith (Ed.), Psycholinguistics and reading. 14 7—157. New York: Holt, Rinehart, & Winston. Welsh, M. C., Pennington, B. F., & Rogers, S. (1987). Word recognition and comprehension skills in hyperlexic children. Brain and Language, 32, 76—96. Whitehouse, D. & Harris, J. C. (1984 ). Hyperlexia in infantile autism. Journal of Autism and Dev elopmental Disorders, 14, 281—289.
Marilyn C. Welsh, Greeley, Colorado (USA)
75. Aspects of Metalinguistic Abilities in Specific Language Impairment (Developmental Dysphasia) and Dyslexia 1. 2. 3. 4. 5.
6.
7. 8. 9.
Metalinguistic Abilities: Theoretical Framework Populations Exhibiting Deficits in Metalinguistic Awareness Relation Between Developmental Language Disorders and Reading Disabilities Experimental Studies of Metalinguistic Skills Evidenced by SLI Children Experimental Investigations of the Relation Between Metalinguistic Skills and Reading Development/Disabilities Claims Regarding the Role of Metalinguistics in Language Disorders and Reading Disabilities Clinical Implications: Assessment and Remediation Directions for Future Research References
1.
Metalinguistic Abilities: Theoretical Framework
Theoretical discussions of the nature and development of metalinguistic abilities abound in the literature (Bialystok 1986; Bialystok/ Ryan 1985 a, b, c; Cazden 1972, 1975; Clark 1978; Hakes 1980, 1982; Karmiloff-Smith 1986; Mattingly 1972; Menyuk 1985, 1991; Tunmer/Bowey 198 4 ; Tunmer/Herriman 1984 ; van Kleek 1982, 1984 a, b; Vygotsky 1962). The relation between metalanguage and metacognition has been debated (cf. Bialystok/Ryan 1985 c; van Kleeck 1982, 1984 a), and various cognitive frameworks underlying metalinguistic skills have been proposed (Bia-
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lystok/Ryan 1985 a,c; Karmiloff-Smith 1986; van Kleeck 1982). Theorists have recognized varying levels of meta-abilities from intuitive to conscious knowledge. However, definitions of metalinguistic abilities have generally focused on the endpoint involving conscious awareness of language units and rules. For example, van Kleeck (1982, 237) defines metalinguistic skill as “the ability to reflect consciously upon the nature and properties of language.” The distinction between linguistic and metalinguistic abilities has been depicted in a number of ways in the literature. It has been suggested that metalinguistic tasks require that language be treated as ‚opaque’, in contrast to typical listening and speaking situations in which language is ‚transparent’ (Cazden 1972, 1975). Similarly, metalinguistic awareness has been characterized as entailing the ability to treat language as an object of thought (Ehri 1975; Tunmer/Bowey 1984 ), and a contrast has been made between primary linguistic activities involved in speaking and listening and secondary linguistic activities involved in conscious language knowledge (Mattingly 1972). It is typically assumed that metalinguistic awareness requires some degree of primary linguistic competence for the child to reflect on (van Kleeck 1982), and that metalinguistic activities are more difficult in that they demand higher degrees of cognitive control (Bialystok/Ryan 1985 a,c; Hakes 1982). There is considerable disagreement regarding the hypothesized role of metalinguistic skills in language acquisition. Clark (1978) has espoused the view that the motivating force for language development is children’s realization of the inadequacy of their own version of language, which prompts a move to the next stage of development. This claim is based on a variety of types of evidence for language awareness in young children, including spontaneous self-repairs, corrections of utterances of other speakers, and language play. Likewise, Menyuk (1991) has advanced the notion that children achieve awareness of linguistic categories and relations as language is acquired and that these meta-abilities may be the catalyst for developmental change. Specifically, she contends that awareness evolves as children compare what is known about language to the linguistic input they receive. As these comparisons are made, children may observe discrepancies which lead them to make modifications in the representations of their linguistic knowledge. Within
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this framework, Menyuk has proposed a three-stage progression in the development of metalinguistic skills ranging from intuitive use of linguistic knowledge to conscious language knowledge to automatic processing of this knowledge. In contrast to the views of Clark (1978) and Menyuk (1991), Karmiloff-Smith (1986) has argued that metalinguistic awareness has little or no role to play in language acquisition macrodevelopmentally. Other researchers have adopted the stance that explicit metalinguistic judgments serve a minimal function in first language acquisition, but have pointed to the importance of these abilities in the development of literacy skills (Hakes 1982; Kamhi/Catts 1989 a; Kamhi/ Koenig 1985). These conflicting viewpoints likely stem, at least in part, from differing definitions of metalinguistic abilities (cf. Bialystok/Ryan 1985 c) and different ideas about what constitutes evidence of language awareness. Since the 1970’s theorists have emphasized the linguistic bases of reading (Mattingly 1972; Perfetti 1985; Stanovich 1986; Vellutino 1977, 1979). This has led to an increasing interest in the role of metalinguistic skills in the development of literacy (Bialystok/Ryan 1985 a,c; Hakes 1982; Tunmer/Bowey 1984 ; Tunmer/Herriman 1984 ). Varying views have been expressed concerning the relationship between metalinguistic awareness and reading. Some researchers have stressed the notion that certain metalinguistic skills are a prerequisite for learning to read (Mattingly 1972, 1984 ). Others have suggested that conscious awareness of language is an outgrowth of reading experience and instruction (Vygotsky 1962). More recent evidence has prompted a number of researchers to hypothesize a bidirectional interaction between metalinguistic and reading abilities (Catts 1989; Downing 1984 ; Ehri 1979). Tunmer/Bowey (1984 ) contend that the following four categories of metalinguistic abilities are implicated in beginning to skilled reading: word awareness (recognizing that sentences are composed of and can be divided into individual words), phonological awareness (knowledge that words consist of sounds), grammatical awareness (an understanding that sentences follow certain syntactic and semantic rules), and pragmatic awareness (knowledge of rules governing connected discourse). Tunmer and Bowey hypothesize that word and phonological awareness are related to reading performance during the early stages of reading when
75. Aspects of Metalinguistic Abilities in Specific Language Impairment (Developmental Dysphasia) and Dyslexia
the focus is on decoding. Grammatical and pragmatic awareness are thought to play a greater role at later stages of skilled reading as children develop text comprehension skills.
2.
Populations Exhibiting Deficits in Metalinguistic Awareness
Deficits in metalinguistic abilities have been documented in two groups of children who are the focus of this chapter. The first group consists of children who have been identified in the literature as having specific language impairment (SLI) (cf. Lahey 1988). These children display substantial problems in oral language functioning that cannot be attributed to emotional disturbance, deficits in hearing, oral motor function, or general intelligence (Johnston 1988; Tallal 1988). Historically, the term ‚developmental dysphasia’ has also been used to refer to these children (Lahey 1988). The second population of children who exhibit difficulties in language awareness are children who have marked reading impairment in the absence of intellectual, sensory, emotional, or environmental deficiencies (Harris/Hodges 1981; Perfetti 1985). These children are alternately referred to in the literature as dyslexic or reading disabled (RD) (Kamhi/Catts 1989 b). These terms will be used interchangeably throughout this chapter. Research has demonstrated the heterogeneous nature of reading disabilities and the existence of various distinct subgroups of dyslexic children (see review by Kamhi/Catts 1989 b). The concern here is with the large proportion of RD children who clearly exhibit language-related difficulties (Perfetti 1985; Vellutino 1977); though it can be argued that language problems are implicated at some level in all reading disabilities (cf. Kamhi 1989).
3.
Relation Between Developmental Language Disorders and Reading Disabilities
There is evidence that a substantial number of children with early histories of oral language deficits experience academic difficulties when they enter school and that these children are particularly at risk for reading and written language problems (Aram/Ekelman/Nation 1984 ; Aram/Nation 1980; Hall/Tomblin 1978; Stark/Bernstein/Condino et al. 1984 ). The issue of a language-learning disorder ‚connec-
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tion’ and the possibility of changes in the symptoms of language disability over time have been discussed by Maxwell/Wallach (198 4 ), among others. Nevertheless, as Kamhi/Catts/Mauer et al. (1988) have pointed out, researchers have identified a group of school-age SLI children who are apparently distinct from the more general population of learning disabled and RD children (Johnston/Ellis Weismer 1983; Liles 1987; Savich 1984 ). Although dyslexic children have been found to perform within normal range on standardized language tests (Hessler/Kitchen 1980), many children with reading disabilities exhibit subtle linguistic deficits that are not revealed by these measures of oral language functioning. A comprehensive review of this research is provided by Roth/Spekman (1989). Compared to normally developing children, studies have demonstrated that RD children evidence various deficiencies in language abilities including word finding problems (Denckla/Rudel 1976; German 1982), syntactic and morphological deficits (Stein/Cairns/Zurif 1984 ; Vogel 1977), deficits in figurative language skills (Lee/ Kamhi 1990) and in narrative discourse (Feagans/Short 1984 ). Yet, direct comparisons of oral language abilities in SLI and RD children indicate that the children with reading problems outperform the SLI children (Lee/Kamhi 1990; Masterson/Kamhi 1985). Various researchers have speculated about the link between oral language deficits and reading impairment (Donahue 1986; Kamhi 1989; Kamhi/Catts 1986; Kamhi/Catts/ Mauer et al. 1988). Donahue (1986) has proposed that within the reading disabled population at least three subgroups of language disorders exist. The first subgroup consists of children with more severe language problems who are identified during the preschool period as language impaired. The second group of students are those who are not identified as having problems before entering school. These children may have phonological processing deficits that interfere with decoding skills in beginning reading; or they may have subtle higher-order linguistic deficits that impact upon text comprehension and ‚reading to learn’ at about the fourth grade (Chall 1983). The third subgroup suggested by Donahue are children who fail to develop adequate reading abilities for a variety of reasons such as problems in motivation or attention. Although these children began school with age-appropriate language abilities, their read-
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ing difficulties result in less experience with the more complex, literate vocabulary and syntactic structures that characterize written language (cf. Nippold 1988) and lead to a complex interplay between limitations in oral language proficiency and restricted reading abilities. Clearly, the relation between oral language disorders and reading problems is not straightforward, but we can conclude that children who exhibit problems in one of these areas are at risk in the other area as well.
4.
Experimental Studies of Metalinguistic Skills Evidenced by SLI Children
Recently there has been increasing interest in the development of language awareness in SLI children. Anecdotal reports of metalinguistic deficiency in SLI children were provided by Wiig/Semel (1976). The majority of experimental investigations since that time have involved studies focusing on grammatical judgment tasks (Buday/Newhoff/Perry 1983; Fujiki/Brinton/Dunton 1987; Kamhi/ Koenig 1985; Liles/Shulman 1981; Liles/Shulman/Bartlett 1977; Perry/Newhoff/Buday 1983) or tasks tapping lexical or phonological awareness (Kamhi/Catts 1986; Kamhi/Koenig 1985; Kamhi/Lee/Nelson 1985). In addition, there have been a few investigations of communicative awareness exhibited by children with language disorders (Lee/Kamhi/Nelson 1983; Meline/Brackin 1987). To date, the only longitudinal study of SLI children’s metalinguistic abilities is one conducted by Liebergott/Menyuk/Chesnick/Korngold (1988, as cited by Menyuk 1991). Liles/Schulman/Bartlett (1977) examined metalinguistic skills in 5 to 8-year-old normally developing and SLI children who were matched for age and receptive vocabulary level. They compared the groups’ proficiency in judging and correcting sentences containing errors of syntactic agreement, lexical restriction, and word-order in an attempt to determine what factors children apply to their definition of grammaticality. Normal language controls identified significantly more agrammatical sentences involving syntactic agreement and word-order violations than the SLI subjects. SLI subjects not only recognized fewer errors than the controls, they also displayed a disparity between their identification accuracy level and correction level in that they recognized errors they could not correct. This was particularly
the case for the syntactic errors. In a followup study, Liles/Shulman (1981) compared the performance of SLI and normal language children (5;4 —6;7) on a grammatical judgment task and a comprehension task to assess whether the ability to make grammatical judgments about a form is related to comprehension of the form. Although both groups performed similarly on the comprehension task, the SLI children scored significantly worse on the judgment task than the normal language subjects. Several other studies have also demonstrated deficits in SLI children’s grammatical awareness. Fujiki/Brinton/Dunton (1987) compared SLI and normally developing first, second, and third graders’ performance on a judgment and correction task involving three types of errors: syntactic omission, word order, and syntactic number agreement. They found a significant difference between the normal language and SLI first and second grade groups on this task. Studies by Newhoff and colleagues (Buday/Newhoff/Perry 1983; Perry/Newhoff/Buday 1983) have indicated that older SLI children (9 to 14 -year-olds) evidence greater difficulty than language agematched controls in identifying and explaining why sentences were ‚wrong’ that contained errors on -s morphemes (plural, possessive, third-person singular, contractible auxiliary is) and tense-marking morphemes (past -ed, progressive -ing, past irregular). Kamhi/Koenig (1985) examined metalinguistic abilities in SLI and normal language controls (4 to 7 years of age) who were matched on receptive language level and mental age. SLI subjects scored significantly lower than controls on sentences containing syntactic errors; however, the two groups were comparable in terms of identification and correction of semantic and phonological errors. Like the Liles/Shulman (1981) study, these results do not support the notion that comprehension deficits can account for the language impaired children’s limitations in grammatical awareness given that subjects in both groups were matched on receptive language skills. Further, the SLI children’s scores on the language measures were not correlated with their performance on the syntactic judgment task. It is likely that the nature of the phonologically anomalous sentences (e. g. John has two tig [big] cars) in the Kamhi/ Koenig study contributed to the lack of differences between groups. Other studies have
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found correction of phonological errors to be at least as difficult as correction of syntactic errors (Smith/Tager-Flusberg 1981). Kamhi/ Koenig note that children may have been attending primarily to semantic and syntactic features of the sentence rather than focusing on phonological judgments. Similar findings have been reported by Kamhi/Catts (1986). They found that SLI children scored significantly poorer than normal language controls on a morpheme judgment task, but the groups displayed comparable performance on tasks tapping lexical and phonological awareness. Task variables again appeared to impact on these demonstrated findings. The control subjects demonstrated a ceiling effect on the word division tasks, whereas the phoneme segmentation task was too difficult for all subjects. Using a syllable segmentation task to assess phonological awareness, Kamhi/Catts/Mauer et al. (1988) also failed to find a significant difference between the performance of SLI and normal language controls. On the other hand, evidence that SLI children’s metalinguistic deficits extend beyond problems in making grammatical judgments has been provided by an investigation by Kamhi/Lee/Nelson (1985). The performance of SLI children (3 to 6 years of age) was compared to a group of mental age-matched (MA) controls and a language age-matched (LA) group. Subjects were presented sentence and word division tasks based on tasks used by Fox/Routh (1975) with normal 3 and 4 year-olds. These tasks included dividing sentences into words, dividing bisyllabic words into syllables, and dividing monosyllabic words into sounds. A second experimental procedure involved a series of questions designed to tap word awareness (e. g. Say a short word. What makes that a short word?). Responses were assigned developmental stage scores based on Papandropoulou/Sinclair’s (1974 ) findings with normally developing children. The results indicated that SLI children performed significantly worse than both control groups in dividing sentences and words. Less than half of the SLI subjects could divide any of the sentences or bisyllabic words into smaller units, compared to all of the MA group and over 70% of the LA group. Dividing monosyllabic words into their component sound units was especially difficult for the SLI children. Only 2 SLI subjects (15%) could perform the task in contrast to 80% of the MA group and over half of the LA group. Significant differences were found in
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the distribution of stage scores for the word awareness task, with the MA group’s performance being superior to the SLI and LA groups. Kamhi/Lee/Nelson (1985) contend that these findings suggest that SLI children do not just have difficulty in accessing extant language knowledge, but are also restricted in their ability to acquire knowledge about linguistic elements that compose sentences and words such that they are at risk for reading problems. Investigations of SLI children’s communicative awareness have also revealed deficits. Lee/Kamhi/Nelson (1983) presented ten unintelligible sentences to children in a 30-minute play session. SLI children rarely made requests for clarification whereas the normal language children asked for clarification in the majority of instances. Lee et al. have suggested that SLI are less sensitive to their own communicative needs than normally developing children; therefore, language impaired children assume it is their fault when they fail to understand. These findings concur with the results of studies by Meline and colleagues (Meline 1986; Meline/Meline 1983) regarding the reticence of SLI children when confronted with a communicative obstacle. Meline/Brackin (1987) further investigated SLI children’s awareness of inadequate messages employing a paradigm used by Robinson/Robinson (1977) with normally developing 5 and 6-year-olds. Stories were presented which included a speaker and listener. In the story, the speaker makes a vague request and his intention is not understood. Subjects were asked to determine whose fault it was that the speaker did not get what he wanted. SLI and younger controls matched on receptive language abilities were predominately listener-blamers in contrast to age-matched controls who were speaker-blamers. Meline and Brackin discuss their findings in terms of Bialystok/Ryan’s (1985 a, c) model of cognitive requisites underlying metalinguistic abilities. They consider various explanations for the poor performance by the SLI children, including a lack of specialized knowledge, inexperience with analytical problem solving, lack of cognitive control, and insensitivity to their own communicative needs. Similarly, learning disabled children have been characterized as exhibiting ‚passivity’ in conversational situations. They have also been found to be less likely to request clarification of inadequate messages than controls, though they detected comprehension problems as
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well as the normal language subjects so the problem was not one of lack of awareness (Donahue/Pearl/Bryan 1980). Liebergott et al. (1988, as cited by Menyuk 1991) have conducted a longitudinal investigation of metalinguistic development over a three-year period in three groups of children (N = 135): SLI children; ‚iffy’ children who had displayed early language delays, but had outgrown the difficulties to a large extent; and very-low-birth-weight premature children. At the start of the study, children ranged in age from 4 ;6 to 5;6. On a battery of standard language measures, the SLI group scored lowest, the iffy group’s performance fell in the middle, and the premature children obtained the highest scores. Performance on the language measures was compared to scores on a battery of metalinguistic tasks which were designed to tap awareness of categories and relations at various levels of language including phonological, lexical, ‚semantactic’, and discourse. Menyuk reports that the three groups differed from each other on the metalinguistic battery in the same way they did on the battery of standard language measures. A cluster analysis indicated that some of the children in the other two groups scored as poorly as the SLI children on the metalinguistic tasks. The SLI group was reconstituted to include these low-performing iffy and premature subjects. Significant differences were found between this lowest achieving group and the other subjects at each of the three time periods tested. Different developmental patterns were observed across the groups. In contrast to the other children, those in the lowest performing group (which primarily consisted of SLI children) did not demonstrate steady improvement in metalinguistic abilities. With the exception of the area of discourse (a story recall task), this group’s abilities on the metalinguistic battery improved slowly and plateaued at the midpoint of the study. It should be noted that the tasks in this study designated as requiring metalinguistic processing included measures such as comprehension of complex sentences and story recall that many researchers would consider to tap primary linguistic abilities rather than metalinguistic awareness (though the tasks are just listed, not described). Therefore, these findings reflect a somewhat different view of metalinguistics than that adopted in the studies described previously. In summary, there is increasing evidence that children with specific language impair-
ment exhibit deficits in metalinguistic abilities relative to normal language children matched on chronological age, mental age, or receptive language level. Results from experimental studies have consistently demonstrated that SLI subjects perform significantly more poorly than controls on tasks measuring grammatical awareness. A limited number of investigations of SLI children’s communicative awareness have also pointed to deficiencies in that area. Mixed results have been reported regarding SLI children’s lexical and phonological awareness, which may underlie beginning reading skills. There is also evidence that SLI children display different patterns of metalinguistic development than normally developing children, though more investigations are needed that clearly distinguish acquisition of primary language abilities from language awareness.
5.
Experimental Investigations of the Relation Between Metalinguistic Skills and Reading Development/Disabilities
The aspect of metalinguistic abilities that has received the greatest attention in terms of its relation to reading is phonological awareness. Research employing a variety of experimental paradigms, across different languages and varying ages of subjects, has consistently found a strong positive relation between children’s phonological awareness and their reading abilities (Blachman 1984 ; Blachman/ James 1985; 1986 as cited by James 1988; Cossu/Shankweiler/Liberman et al. 1988; Fox/Routh 1975; Liberman/Shankweiler/ Fischer/Carter 197 4 ; Lundberg/Olofsson/ Wall 1980; Mann/Liberman 1984 ; Rosner/Simon 1971; Share/Jorm/Maclean/Matthews 198 4 ; Stanovich/Cunningham/Cramer 198 4 ; Zifcak 1981). There appears to be a reciprocal relation between phonological awareness and reading skills such that awareness of phonological aspects of the language may be both a precursor of reading development and a result of reading experience (Ehri 1979, Perfetti/Beck/Bell/Hughes 1987; Stanovich 1986). Studies examining children’s metalinguistic abilities prior to the initiation of formal reading instruction, have demonstrated that early sound awareness is a good predictor of later literacy (Bradley/Bryant 1983; Lundberg/Olofsson/Wall 1980; Maclean/ Bryant/Bradley 1987; Mann/Liberman 1984 ;
75. Aspects of Metalinguistic Abilities in Specific Language Impairment (Developmental Dysphasia) and Dyslexia
Stanovich et al. 1984 ). Maclean et al. (1987) conducted a 15-month longitudinal study of preschoolers’ performance on rhyming and alliteration tasks. They found that 3-year-olds exhibited rudimentary phonological awareness skills and that performance on these phonological tasks predicted the ability to read words at 4 years of age. Most studies have compared kindergartners’ awareness of phonemes, rhyme, and syllable structure to their reading skills in first grade. However, the impact of informal literacy instruction has not been controlled. In an attempt to take this factor into account, Bradley/Bryant (1983) included as subjects only 4 to 5-year-olds who evidenced no reading abilities on a standardized reading test. Their findings indicated that awareness of rhyme and alliteration was significantly correlated to reading skills three years later. On the other hand, some phonological awareness skills are apparently not requisite for reading but emerge with reading instruction (Ehri 1989; Perfetti/Beck/Bell/ Hughes 1987). For example, the findings of Perfetti et al. indicated that children’s phoneme deletion skills develop only after some reading experience. Further insight into the impact of reading instruction on phonological awareness has been gained from cross-cultural investigations and studies of illiterate adults (Morais/Bertelson/Cary/Alegria 1986; Read/Ruyter 1985; Read/Zhang/Nie/Ding 1986). Results of these studies have indicated that more advanced phonological analysis skills involving explicit awareness of phonemic segments seem to be dependent upon instruction in an alphabetic orthography. For more comprehensive discussions of the relationship between phonological awareness and reading abilities refer to Bailet (1991), Blachman (1984 ), Catts (1989), and Wagner/Torgesen (1987). A limited number of investigations have examined children’s word awareness and grammatical awareness in relation to reading skills. Studies have shown that it is difficult for young children to separate words from their referents (Ianco-Worral 1972) and to segment utterances into words (Ehri 1975). Notable improvement in word awareness is observed once children begin to learn to read (Francis 1973; Papandropoulou/Sinclair 1974 ). Furthermore, awareness of aurally presented word boundaries has been found to be a significant predictor of reading achievement in beginning first graders (Evans/Taylor/ Blum 1979; McNinch 1974 ). With respect to
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grammatical awareness, research has demonstrated that the ability of elementary school-aged children, adolescents, and adults to identify and revise agrammatical sentences is significantly correlated with reading performance (Blachman/James 1985, 1986 as cited by James 1988; Flood/Menyuk 1983; Forrest-Pressley 1983; Menyuk/Flood 1981). Blachman/James (1985; 1986 as cited by James 1988) conducted a longitudinal study of metalinguistic and reading abilities in first, second, and third grades. Subjects were presented a set of oral language tasks and a battery of reading achievement measures. The metalinguistic tasks included a grammatical judgment and correction task involving word order and morphological errors, a word referent task, a riddle task that involved lexical or structural ambiguity, and a phoneme segmentation task. The results indicated that grammatical awareness and phonological awareness were significantly correlated to reading achievement in beginning readers (grades 1 and 2) and were significant predictors of reading performance. Word awareness was not strongly related to reading achievement. The ability to explain ambiguity in riddles, which reflects both grammatical and word awareness, was most strongly correlated to more skilled reading that involved text comprehension. Blachman and James contend that these findings are consistent with Tunmer/Bowey’s (1984 ) hypotheses about the role of various aspects of metalinguistic skills in reading development. Metalinguistic investigations of children with deficient reading skills have primarily focused on phonological awareness. Poor readers have been shown to have more difficulty than good readers in detecting rhymes, segmenting speech into phonemic and syllabic units, and deleting, substituting and manipulating phonemes (Bradley/Bryant 1978; Bryant/Bradley 1981; Fox/Routh 1975, 1980; Katz 1986; Lenchner/Gerber/Routh 1990; Liberman/Shankweiler/Fischer/Carter 4 197 ; Morais/Cluytens/Alegria 1984 ; Snyder/Downey 1991). An investigation by Bradley/ Bryant (1978) examined rhyming and alliterative skills in dyslexic children and controls matched on reading level who were 3 ½years younger than the dyslexic subjects. Subjects were instructed to select the odd item that did not belong with the others in a series of spoken words. Dyslexic subjects scored significantly lower on this task than the younger normal readers. Fox/Routh (1980) employed
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a task in which they asked first grade children to say just a little bit of spoken syllables. Subjects consisted of children identified as having average, mildly depressed or severely depressed reading skills. Those with severely depressed reading abilities were unable to divide syllables into phonemes in contrast to the two other groups who performed quite well on the task. The ability of third grade RD children to identify the number of syllables in words was examined by Katz (1986). The task involved asking subjects to decide whether or not the names of pictured objects had the same number of syllables (object names were usually one or three syllable in length). Even when the RD subjects demonstrated that they knew the names of the objects, they performed worse than the normal readers in making length judgments. Snyder/ Downey (1991) investigated phonological awareness in normally achieving and RD students (ages 8—14 years) using a pig latin task designed to assess the ability to manipulate phonological elements. The normally achieving subjects performed significantly better than the RD subjects on this task even when differences between the groups’ short-term auditory memory skills were statistically removed. Lenchner et al. (1990) compared the performance of third and fourth graders identified as poor vs. good readers on six different measures of phonological awareness that evaluated the ability to segment, blend, and manipulate phonemes. Results indicated that for the poor readers, scores on the phoneme deletion and substitution tasks were significantly correlated with decoding and word attack skills. The deletion task was deemed to be the most valid of the tasks used, in that it correlated most highly with the other phonological awareness tasks and with the decoding measures. A few investigations have compared metalinguistic abilities exhibited by dyslexic children to that of children with other types of deficits. In a large-scale study of first grade children, Felton/Wood (1989) found that children with impaired reading skills performed significantly more poorly than children with attention deficit disorder on phonological awareness tasks, as well as on confrontation and rapid automatized naming tasks. Two studies by Kamhi and his colleagues (Kamhi/ Catts 1986; Kamhi/Catts/Mauer et al. 1988) have compared phonological processing abilities and metalinguistic skills of RD and SLI children. In the Kamhi/Catts (1986) study,
V. Pathologies and Disorders of Language Development
three groups of children (6 to 9 years of age) served as subjects: RD children with no history of speech-language impairment, SLI children, and normally developing controls. The three groups were matched for mental age on a nonverbal measure of intelligence. Six tasks were administered that assessed phonological, lexical, and morphological awareness. Phonological processing abilities were additionally assessed via word and sentence repetition tasks. The metalinguistic measures consisted of sentence division, bisyllabic and monosyllabic word division, elision (phoneme deletion), phoneme segmentation, and a morpheme judgment and correction task. The elision task (used by Rosner/Simon 1971) required the child to determine what would be left if a particular sound (first or last) were deleted from a word, e. g. (t)all. The segmentation task involved a tapping procedure used by Liberman/Shankweiler/Fischer/ Carter (1974 ) in which children indicated the number of phonemes in spoken syllables. The findings rather surprisingly revealed that the performance of RD and SLI children was equivalent on measures of phonological lexical, and morphological awareness. The SLI children scored significantly lower than the RD subjects only on measures of word and sentence repetition (i. e. production tasks). Both the RD and SLI subjects performed significantly worse than normal language controls on the morpheme judgment task. The performance of the RD subjects was significantly poorer than that of the controls on the sentence division task and the elision task. Regression analyses indicated that elision task scores were the best predictor of reading performance, accounting for roughly 50% of the variance for each of three reading measures. Performance on the word repetition task, on the other hand, was the best predictor of language abilities. Further investigation of phonological processing abilities of RD and SLI children by Kamhi/Catts/Mauer et al. (1988) revealed similar findings. That is, dyslexic children performed significantly better than SLI subjects only on a multisyllabic word repetition task. The scores of the two experimental groups were not significantly different on a syllable segmentation task, though the dyslexic subjects’ performance was significantly worse than that of the normally developing controls. These investigations support the findings from studies reviewed previously which indicate that RD and SLI children display deficits in various aspects of me-
75. Aspects of Metalinguistic Abilities in Specific Language Impairment (Developmental Dysphasia) and Dyslexia
talinguistic abilities compared to children who are developing oral and written language skills normally. They do not, however, provide any evidence that children with reading impairment can be distinguished from those with oral language disorders on the basis of language awareness skills. Based on the existing literature, we can conclude that metalinguistic abilities play an important role in reading and reading disabilities. Numerous studies have demonstrated a strong relationship between phonological awareness and reading performance. Grammatical awareness and word awareness have also been shown to be linked to literacy skills. The bulk of the evidence might seem to suggest that dyslexic children are primarily deficient in phonological awareness skills in contrast to SLI children who are mainly lacking in grammatical awareness abilities; however, the little information that is available concerning direct comparisons of these two groups performing the same tasks does not support this interpretation.
6.
Claims Regarding the Role of Metalinguistics in Language Disorders and Reading Disabilities
Factors that have motivated the investigation of metalinguistic abilities in SLI children include the following: 1) a desire to characterize the interaction between the development of language performance and linguistic awareness (Liles/Shulman/Bartlett 1977); 2) consideration of the metalinguistic demands of language assessment and remediation procedures (Kamhi/Koenig 1985; van Kleeck 1984 b); 3) concern that metalinguistic deficits may place SLI children at risk for reading problems (James 1988; Kamhi/Lee/Nelson 1985); and 4 ) a search for underlying causes of developmental language impairment (Menyuk 1991). The strongest claim regarding the role of metalinguistic deficits in oral language disorders has been made by Menyuk (1991). Based on findings of metalinguistic studies of normally developing and SLI children, she puts forth the argument (which she concedes is highly speculative) that “these children are delayed in language because of metalinguizing difficulties” (Menyuk 1991, 319). Menyuk postulates that SLI children intuitively acquire knowledge of language but have problems achieving conscious awareness of that
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knowledge. She proposes that such awareness is needed to firmly establish linguistic representations and to retrieve them automatically. Deficits in SLI children’s meta-abilities are therefore thought to disrupt the development and automatic retrieval of linguistic representations, delaying the development of language skills. Menyuk contends that alternate explanations of language delay that appeal to reduced processing rates or memorial problems might be subsumed by a metalinguistic deficit explanation which incorporates the construct of automaticity limitations. Although there has been some interest in the impact of other aspects of metalinguistic abilities on reading skills (James 1988), the vast majority of claims focus on the extensive literature dealing with the role of phonological awareness in beginning reading. A number of researchers have proposed that reading disability is linked to deficits in phonological awareness (see reviews by Stanovich 1986; Wagner 1986, 1988; Wagner/Torgesen 1987). Stanovich (1986, 393) has suggested that, “If there is a specific cause of reading disability at all, it resides in the area of phonological awareness. Slow development in this area delays early codebreaking progress and initiates the cascade of interacting achievement failures and motivational problems.” Other researchers have attributed reading disability to inadequate bootstrapping of phonological awareness on orthographic awareness (Foorman/Liberman 1989). A dissenting viewpoint is represented by investigators who claim that phonological awareness is a product rather than a prerequisite of learning to read (Ehri 1989; Morais/ Bertelson/Cary/Alegria 1986). Ehri (1989) adopts the position that the type of phonological deficits demonstrated by dyslexic children are primarily due to inadequate reading and spelling instruction. It is certainly the case that there is evidence that SLI and RD children display significantly poorer performance on metalinguistic tasks than normally developing children and that reading proficiency has been shown to be correlated with aspects of linguistic awareness. However, the exact nature of the relationship between metalinguistic deficits and impairments in oral language or reading skills is unresolved. Relatively little information pertaining to SLI children is available at this point and claims regarding the role of metalinguistic deficits in oral language disorders are speculative at best. Researchers have attempted to gain insight into the causal con-
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nection between phonological awareness and reading abilities through training studies (reviewed in 7.) or advanced statistical techniques such as path analysis (Torneus 1984 ; Wagner 1988). Yet, a number of questions remain as to how these findings should be interpreted. Although facility in metalinguistic awareness appears to be linked to language and reading disorders, it would be imprudent to ignore the evidence concerning various other potential factors underlying specific language impairment (cf. Johnston 1988; Tallal 1988) and reading disabilities (cf. Kamhi 1989; Perfetti 1985; Stanovich 1986).
7.
Clinical Implications: Assessment and Remediation
In light of the relationship between metalinguistic abilities and reading proficiency and the fact that SLI children demonstrate deficits in language awareness, it has been suggested that these skills should be assessed in all children suspected of having language or reading disabilities (James 1988, 1989). James (1989) recommends that language evaluations should incorporate measures designed to tap phonological, word, grammatical, and pragmatic awareness by means of tasks such as: segmentation of words and sentences, separation of words from their referents, judgment of grammatical acceptability of sentences, detection of ambiguity, and judgment of message adequacy and appropriateness of communicative interactions. A description of tasks that might be used for this type of informal assessment of metalinguistic awareness has been provided by James (1988). A grammatical judgment screening test for elementary school-aged children has recently been developed by Fujiki/Brinton/Dunton (1987). Based on screening test scores on this measure, approximately 82% of SLI and normal language subjects were correctly categorized. This percentage would have been considerably higher if the scores for the third graders had not been included. Blachman (1989) has argued that despite the role that phonological awareness, in particular, seems to play in beginning reading, traditional reading readiness tests and reading assessment batteries do not place an emphasis on this ability. She notes that kindergartners’ performance on measures of phonological awareness have been shown to predict reading proficiency in first grade as well as or better
than reading readiness tests or intelligence measures (Stanovich/Cunningham/Cramer 1984 ). Blachman suggests that measures of phonological awareness such as word segmentation, sound categorization of words, or sound deletion tasks should be included in assessments of beginning readers. The impact of metalinguistic training on reading development has been investigated in terms of phonological awareness skills. Studies with beginning readers and prereaders have demonstrated that training in phonological awareness has a positive effect on reading achievement, particularly when links are established between the sound segments of the word and the letters which represent those segments (Bradley/Bryant 1983, 1985; Fox/ Routh 1984 ; Lundberg 1987; Treiman/Baron 1983). For an indepth review of this research refer to Blachman (1989). There is also evidence that reading instruction which incorporated a focus on phonological awareness was beneficial for learning disabled children (Williams 1979, 1980). Vellutino/Scanlon (1987) have demonstrated the effectiveness of phonemic segmentation training in improving word recognition in normal and poor readers in the second and sixth grade. It should be noted, however, that not all researchers endorse the view that metalinguistic training is an important aspect of reading instruction programs (Singer 1984 ). Relatively little consideration has been given to the influence of metalinguistic training on children’s oral language abilities; though some investigators have suggested that clinical objectives targeting metalinguistic skills might profitably be included in remediation programs for SLI children (Kamhi/Lee/Nelson 1985; van Kleeck 1984 b). Training efforts to this point have focused more on abilities that are generally subsumed under the rubric of metacognitive skills rather than metalinguistic awareness per se. In one of the few investigations in this area, Dollaghan/Kaston (1986) reported success in improving awareness of message adequacy in SLI children. A study by Olsen/Wong/Marx (1983) indicated that training cognitive control strategies had a positive influence on pragmatic awareness and language use by learning disabled children, but the trained skills failed to generalize. Westby (1989) has described means of assessing and facilitating comprehension monitoring skills for children with language and reading problems.
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8.
Directions for Future Research
Compared to the research examining the role of metalinguistic abilities in reading and reading disorders, there has been relatively little empirical investigation of the relationship between metalinguistic skills and oral language deficits. Future research efforts might profitably be focused in a number of directions. Additional longitudinal investigations of SLI children (extending into the school-age years) would be useful to chart the course of development in metalinguistic awareness. By comparing the development of specific linguistic relations and categories with awareness of those particular aspects of language and observing plateaus and growth spurts in both of these areas, insights might be gained about the nature of the interaction between linguistic and metalinguistic skills. There is also a need for studies that further investigate phonological and word awareness in SLI children to determine the extent which deficits in these abilities might predict difficulties in beginning reading skills for certain children with oral language deficiencies. The role of grammatical and pragmatic awareness deficits in later stages of reading deserves greater consideration. Similarly, investigation of the link between these aspects of metalinguistic awareness and other cognitive and metacognitive processes involved in comprehending both spoken and written discourse would be informative. For example, studies might assess the extent to which poor language awareness interacts with SLI and RD children’s deficits in constructive cognitive processes (i. e. semantic integration and inference construction) involved in the comprehension and retention of connected discourse (Ellis Weismer 1985; Klein-Konigsberg 1984 ). There is also a need for training studies that explore the impact of instruction aimed at improving various aspects of metalinguistic awareness (in addition to phonological awareness) on language and reading skills in SLI and RD children. Finally, additional investigations involving direct comparisons of children with developmental language disorders and those with reading disabilities may lead to an enhanced conceptualization of the complex nature of the relationship between linguistic abilities and metalinguistic skills.
9.
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Susan Ellis Weismer, Madison, Wisconsin (USA)
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76. Communicative Behavior with Neurotic Developmental Disorders: Elective Mutism 1. 2. 3. 4.
Introduction Traumatic mutism Elective mutism References
1.
Introduction
There are two forms of psychological mutism — traumatic and elective; both are dramatic and both are rare. The main theme of this paper is an account of elective mutism. The rarity of mutism may be the reason for the lack of a substantial literature on the subject of elective mutism. Following the original classic article by Tramer (1934 ), over the next half century there were only about half a dozen major contributions to the literature on this subject, culminating in the article by Kolvin/Fundudis (1981). And in the recent years there has been only one further research report of a controlled study with more than 20 electively mute children (Wilkins 1985).
2.
Traumatic Mutism
This has an acute onset following a psychological or physical shock or injury. Some consider it to be an hysterical phenomenon as it is not associated with any disorder of the structures subserving speech functioning (lips, tongue, palate or vocal cords) and, furthermore, the patient is able to cough normally. The literature suggests that it is common, but a wide clinical survey has attested to its considerable rarity (Kolvin/Fundudis 1981).
3.
Elective Mutism
This is the term coined by Tramer (1934 ) to describe a fascinating group of children, whose talking is confined to familiar situations, usually the home, and to a small group of intimates. It needs to be distinguished from the inordinate shyness that occurs relatively frequently in reception classes in school (Brown/Loyd 1975; Wright 1968), by its severity and persistence. The literature suggests that the earliest manifestations are in the pre-school years, with the parents being unaware of significant abnormality because there has been a period
of relatively normal speech development (Elson/Pearson/Jones et al. 1965; Reed 1963; Salfield 1950). Kolvin/Fundudis (1981) report that commonly an inordinate degree of shyness was present from the early years of life in the majority of cases and only in a small percentage were there indications that it had emerged for the first time at a later stage in development. 3.1. Epidemiology From their epidemiological study, Fundudis/ Kolvin/Garside (1979, 15) report a rate of 0.4 per thousand children in a total city cohort of 3,300 seven-year-olds. To put this in perspective, this is less common than broadly defined autism by a factor of two. Subsequently, the same team (Kolvin/Fundudis 1981) identified 24 electively mute children, over a period of six years, gathered from a wide survey of clinical departments of speech pathology and child psychiatry serving a large population in the North East of England. However, other workers have reported on larger samples of clinically or epidemiologically identified elective mute children. For instance, Brown/Lloyd (1975) report a prevalence of 7.2 per thousand of children who do not speak at school at the age of 5. Thus, some eight weeks after starting school, 4 2 out of 6072 children were not speaking, but after 12 months the rate had fallen to 0.33—0.66 per thousand. Thus, their rate of ‚persistent elective mutism’ is closely comparable to that reported in the Kolvin and Fundudis epidemiological survey. Brown and Lloyd’s survey is complicated by ethnic factors and they used a rather broad definition of elective mutism. Nevertheless, it confirmed that persistent elective mutism is rare. Hayden (1980) reports on the results of a clinical study of 68 cases of elective mutism, based on a five-centre study in the U. S. A. However, the diagnostic criteria employed are questionable: they are rather broad and the duration of mutism was often very brief; there was inadequate specification of the settings in which the child refuses to speak, and there was diverse co-morbidity. 3.2. Diagnosis and Differential Diagnosis A number of important themes merit consideration. First, previously there was both a tendency to emphasize the importance of mo-
76. Communicative Behavior with Neurotic Developmental Disorders:Elective Mutism
tivation in the diagnosis of elective mutism and acceptance of the notion that the presence of abnormalities of speech and language precluded such a diagnosis. However, such earlier views were based on anecdotal material or small case studies without controls. As indicated above, studies of more representative series of cases indicate that such previous accounts were often misleading. Second, in a pilot observational study of pre-school children, Kolvin/Nolan (1979) observed that unusual shyness occurred frequently, especially in girls, but this tended to be transient. The behavior consisted of a tendency to speak in a soft voice or an unwillingness to speak to their mothers or to play in the presence of strangers, combined with a tendency to cling and hide behind their mother’s skirts. This reluctance to talk proved to be a transient phenomenon which is likely to reflect normal separation anxiety compounded by transient adaptation reactions to the usual stresses and unfamiliarity of the new school situations. Thus with familiarity, this anxiety diminishes and the child may begin to talk (Cantwell/Baker 1985). The latter authors suggest that many of the children in the Brown/Lloyd (1975) sample may have demonstrated this behavior. Hence, it is not unexpected that confusion may arise with those excessively shy infant school children who do not speak when first attending school. However, shyness is not specific to elective mutism (Wilkins 1985). Hence Kolvin/Fundudis (1981) go on to suggest that a distinction needs to be made between such transient states of inordinate shyness and those behaviors which are pathological, in both severity and persistence. They therefore apply more rigorous criteria when defining elective mutism as persistent, severe and pathological shyness beyond the home situation, which is usually associated with abnormalities of temperament and of relationships of the child with his/her mother. If the mutism had been evident at the start of school life, then it had to show no signs of abating in the following year. If the mutism appeared to have a later onset, there had to be no evidence of diminution, again over a period of at least a year. Third, there is little diagnostic difficulty with the early-onset (Kolvin/Ounsted/Humphrey et al. 1971) and the late-onset psychoses of childhood (Kolvin/Berney 1990; Kolvin et al. 1971), about which there is now considerable agreement.
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Fourth, another crucial issue concerns the distinction between elective mutism and Asperger’s syndrome (Asperger 194 4 ). Although both groups of children have initial problems of social adjustment, which mainly declare themselves outside the home, there are many important differences. In both there is evidence of a lifelong personality deviation rather than an illness with a definite onset (Kolvin/Fundudis 1981; Wolff/Barlow 1979). Whereas the children with Asperger’s syndrome are often described by their mothers as solitary, remote and strange, in the case of electively mute children the parents are often not aware of anything unusual until the children first attend school (Kolvin/Fundudis 1981). The children with Asperger’s syndrome are described as showing obstinacy and aggressive outbursts, especially when attempts are made to persuade them to conform. However, the obstinacy of elective mutism is more usually combined with degrees of withdrawal or retreat. Next, while obsessionality is almost universal in Asperger’s syndrome, it occurs only occasionally in elective mutism. By definition, none of the elective mutes speak outside the home or at school, whereas in the case of Asperger’s syndrome only a few refuse to speak at school. Finally, whereas electively mute children use gestures and other forms of non-verbal communication, children with Asperger’s syndrome tend not to communicate well by such means. A further issue is the classification of children who speak rather little. We endorse, first, the view that those children who speak very little in all circumstances should not be assigned the diagnosis of elective mutism (Blake/Moss 1967), and second, the view that those children who display ‚reluctant speech’, i. e. they will not speak spontaneously but will answer questions which have been asked, should also be excluded from the specific diagnosis (Williamson/Sewell/Sanders/Haney 1977). 3.3 Developmental and Biological Factors In most major studies of elective mutism there is a consistent pattern of an excess of girls to boys, which is unusual for childhood disorders (Kolvin/Fundudis 1981; Wilkins 1985; Wright 1968). In the investigation by Kolvin and Fundudis, the control group was drawn from a general population sample, whereas in Wilkins’ research the elective mute sample was compared with a matched sample of clinic children who had been diagnosed as
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having an emotional disorder. In both studies there was an excess of birth complications but this was significant only in the former study. However, Kolvin/Fundudis (1981) report evidence of slow or uneven development compared with the controls and this included delay in onset of speech, excessive developmental mispronunciation with associated problems of speech and bowel and bladder function, and also EEG immaturity. The casenote study by Wilkins provides an account of one in three of the electively mute children having delayed speech, whereas none of the children with emotional disorders had such problems. Although he does not report any other developmental anomalies, it should be remembered that in a case-note study there has not necessarily been a specific focus on particular deficits, and therefore a lack of listing does not necessarily imply absence of deficit. To recapitulate, Wright (1968) found that about one in five of his study children had an underlying speech or language delay or problem; Kolvin/Fundudis (1981) report as many as 50 percent and Wilkins (1985) reports 33 percent. Kolvin/Fundudis (1981) report that electively mute children are born significantly early in the sibship but Wilkins (1985) did not replicate this finding. However, electively mute children in both studies come from families of similar size as those of the controls. 3.4. Personality and Temperament In addition to inordinate shyness and social and communication problems, a diversity of other personality and temperamental anomalies have been described in these children (Kolvin/Fundudis 1981). Evidence of an insidious development of shyness has been reported in over 80% of cases and even in those where it appeared acute, it may well be that the essential abnormality became dramatically obvious only when the child entered the school setting (Kolvin/Fundudis 1981; Wright 1968). In addition, a wide variety of complex personality patterns often occur, such as oppositional behavior and poor malleability both at school and at home. The commonest personality pattern was of sulkiness combined with aggressiveness, with a child presenting as sulky to strangers and aggressive within the home. Many of these children are described as having powerful personalities, with ‚wills of steel’. About a quarter showed a combination of
V. Pathologies and Disorders of Language Development
shyness in social situations with submissiveness at home. Another quarter seemed to be rather sensitive children. In addition, there was an important trend for such children to be more withdrawn in relation to peers than to adults. In addition to the above personality patterns, there were a varied group of patterns of problem behaviors in over two-thirds of the children. These included excessive and unusual motor activity. Wilkins (1985) was not able to study personality and behavior systematically, and therefore merely listed those features which occurred more frequently in the elective mutes than in children with emotional disorders. His analysis appears to play down shyness and emphasize anxiety and depression as symptoms in the elective mute group, but he does report manipulative behavior. However, it must again be stressed that a retrospective case-note study from a psychiatric clinic may not be sufficiently focused on features under scrutiny and inevitably there may be distortions in the data. 3.5 Cognitive Aspects Again, literature review reveals few studies quoting psychometric findings with even modest-sized samples of electively mute children (Kolvin/Fundudis 1981; Wright 1968). The evidence available shows that although electively mute children as a group cover most ranges of intellectual ability as measured on non-verbal IQ, there is a distinct shift to the left. Thus, while the majority fall within the normal range of intelligence, a substantial concentration of elective mutes is found within the dull — normal and lower categories of non-verbal intelligence (Kolvin/Fundudis 1981; Wright 1968). The reason for the poorer performance on nonverbal IQ remains obscure. Nevertheless, there are a number of other features among elective mute children which may have important associations with their poorer performance: first, as indicated above, electively mute children display a wide variety of complex temperamental, personality and behavioral patterns (Kolvin/Fundudis 1981) which may vary according to the circumstances in which the child is assessed; further, underpinning these various patterns of temperamental expression is a ‚will of iron’ and a determination to get his/her own way. In general terms, when electively mute children do speak — which they do within the confines of their own homes — their vocab-
76. Communicative Behavior with Neurotic Developmental Disorders:Elective Mutism
ulary, verbal conceptualisation of ideas and grammatical structure of sentences are usually normal. 3.6. Assessment Enlisting co-operation of the electively mute child for the purpose of psychological/psychiatric assessment usually constitutes a challenge, the bases of which are the complex emotional and attitudinal expressions which accompany the refusal to talk. Thus, co-operation is best facilitated by the clinician adopting a style of communication which avoids expectation of the child to talk. In contrast, pressure by the clinican is likely to intensify the child’s resistance, which is compounded by the excessive reserve/shyness and/or passive hostility which accompanies the child’s refusal to talk. For younger children, drawing and play materials as a medium for preliminary interaction is often helpful. Subsequently, standardized non-verbal measures are the main source of assessment, particularly among the older children. The use of play materials and other purposeful tasks or activities can prove a helpful and meaningful way of not only engaging the child but also of obtaining a productive cognitive assessment. In those children with more highly resistant attitudes, the assessment may have to be carried out over a number of sessions with the tasks and measures being administered in a piecemeal fashion. Skill, flexibility and patience are the guiding principles for achieving a useful and valid psychological/psychiatric assessment. They are also important for understanding the child’s cognitive potential, personality, strengths and vulnerabilities and for establishing the basis of an individually tailored, multimodal, therapeutic programme. 3.7. Family and Social Factors There is a tendency to assume that more of the families of electively mute children come from the lower end of the social class spectrum, but the evidence is that the families of these children are represented at all levels of socio-economic strata (Brown/Lloyd 1975; Kolvin/Fundudis 1981; Wright 1968). Of greater importance is the nature of the psychological dynamics within these families. The literature abounds with examples of parents with unusual personalities and psychiatric problems which are often offered as explanations for the elective mutism of their
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children (Elson/Pearson/Jones/Schumacher 1965; Parker/Olsen/Throckmorton 1960; Wergeland 1979). The confidence placed in these findings must be limited by the lack of controls and small sample size of the studies upon which the theories are based. Some of the factors which have been viewed as causative include the following: maternal rejection and paternal disinterest (Elson et al. 1965), maternal anxiety, fearfulness and overprotectiveness (Parker et al. 1960; Wergeland 1979), the influence of ‚family secrets’ and the child’s fear of parental retaliation (Pustrom/Speers 1964 ), abusive behavior by alcoholic fathers (Adams/Glasner 1954 ), and the effects of a symbiotic relationship between parent and child (Browne/Wilson/Leybourne 1963). However, most of these notions derive from older publications. Evidence from a controlled and larger study of 24 cases (Kolvin/Fundudis 1981) does not suggest the presence of a common set of family dynamics, but rather the origins appear multifactorial. In that study, one-third of the parents of electively mute children were found to have personalities that were characterized by serious or marked reserve and shyness. Taking into account all of the personality problems of the parents, irrespective of type, in two in five of the families one or other of the parents had a personality which could best be described as odd or unusual. As to psychiatric problems, severe neurotic disorder was found in one of the parents in about one-sixth of the families and depression in one of the parents, again in one-sixth, with a combination of these two disorders occurring in a number of the families. When serious psychiatric disturbance or major personality problems were considered in combination with serious marital disharmony it was found that six of ten of the families were affected. Thus, however, the disturbance in families is defined, the available evidence points to an excess of psychological morbidity in families of elective mute children compared with families of normal control children (Kolvin/Fundudis 1981). For instance, these authors noted that 20% of mothers and 16% of fathers of elective mute children had received specialist psychiatric help, compared with only 8% of mothers and 3% of fathers of normal control children. In a study of 24 families, Wright (1968) reported a 75% rate of parental psychological disturbance. This higher rate was probably due to the inclusion of the use of a much broader definition of disturbance, for instance
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including the trait of parental shyness as one of the criteria. Further, as shyness in parents of electively mute children appears to be fairly common (Brown/Lloyd 1975; Kolvin/Fundudis 1981; Wright 1968), it raises the interesting possibility of a familial or even a genetic link between shyness of the parents and elective mutism of the child. The latter possibility is enhanced by the finding of a number of affected siblings (Wright 1968) or twins (Halpern/Hammond/Cohen 1971; Mora/ DeVault/Schopler 1962) in different series of electively mute children. On the other hand, the influence of learning/modelling cannot be discounted. 3.8. The Aetiology of Elective Mutism As evident above, numerous workers have postulated a diversity of psychogenic bases for elective mutism; others imply that it is a learnt pattern of behavior, and yet others implicate temperamental or personality factors which have a familial basis. Another suggestion is that it may be a secondary psychological reaction to some biologically based symptoms; for instance, some children may avoid speaking because they are teased when they mis-pronounce words (Rutter 1977); other work suggests an important maturational component. This diversity of aetiological factors suggests that the origins are multiple and the condition heterogeneous. 3.9. Intervention and Outcome Elective mutism has been, and continues to be, a challenge to psychodynamically and behaviorally oriented psychotherapists. The reported success rates of the different methods of intervention have been variable; however, it is difficult to draw any conclusions from such studies because of the differences in diagnostic criteria used, the severity of the mutism and the criteria of improvement. For example, Wright (1968) reported that at followup of 19 of 24 cases, 79% had achieved ‚excellent’ or ‚good’ adjustment, whereas Kolvin/ Fundudis (1981) report an adjustment rate of 4 6%. Further, the confidence in success rates reported in other studies is limited by small samples and poor specification of improvement criteria (e. g. Elson/Pearson/Jones/Schumacher 1965; Kupietz/Schwartz 1982; Pustrom/Speers 1964 ). For example Elson et al. (1965) noted that m o st of the children “tended to have made a fairly good adjustment” following their discharge from hospi-
V. Pathologies and Disorders of Language Development
tal, but that there was a “tendency to be somewhat reserved” (Elson et al. 1965, 185). The problem of defining treatment success or improvement has been further highlighted by Pustrom/Speers (1964 ) who report that, in three cases, after intervention some improvement was achieved in terms of readiness to talk to others, but they resisted talking to the therapist. The authors concluded that “failure to speak to his therapist represents a lastditch stand against giving up his omnipotent control over others” (Pustrom/Speers 1964 , 296). Such statements emphasize the intractability of elective mutism to psychotherapy, in that although degrees of improvement are usually reported, the s p o n t a n e i t y of interpersonal communication of the electively mute child is seldom fully shifted. The emphasis of earlier treatment approaches on intrapsychic dynamics (e. g. motives, drives, personality traits) of the electively mute child and/or the parents (e. g. Browne/Wilson/Legbourne 1963; Chetnik 1973; Elson et al. 1965); have tended to give way to the more recently developed behavioral strategies (e. g. Kupietz/Schwartz 1982; Nolan/Pence 1970; Norman/Broman 1970). Such a shift is not surprising because the resistance of elective mutism to treatment has continued to pose a challenge to therapists of all persuasions. However, some reviewers conclude that behavioral therapies have been found to have greater effectiveness than the psychodynamic therapies (Kratochwill/ Brody/Piersel 1979). In keeping with the more pragmatic stance of the behaviorists it has been argued that intervention should be directed not only at ‚mutism’ but more broadly at ‚social skills’ (Kratochwill/Brody/Piersel 1979). Consistent with the above is the proposal of a multidimensional management approach (Friedman/Karagan 1973) consisting of the following: a) avoidance of strategies that are likely to put pressure on the child to talk; b) inclusion of the child in small peer group activities; c) use of reading, story-telling and other verbal activities which do not make the child feel especially uncomfortable (e. g. within the family context); d) encouragement by parents for relatives and peers to visit within the electively mute child’s home to create a natural social context of conversation but without putting pressure on the child to talk; e) encouragement within the classroom situation for the electively mute child to engage in non-verbal, non-threatening interpersonal relationship through the use of such activities as puzzles and workbook
76. Communicative Behavior with Neurotic Developmental Disorders:Elective Mutism
exercises; f) a gradual process of encouragement involving the electively mute child in a one-to-one situation where appropriate stimuli (e. g. pictures which require to be identified and labelled, e. g. what is this?) are used as a means of creating a spontaneous form of verbal communication on the part of the electively mute child, and then including one or two other children in the activity; g) the electively mute child and any others in whose presence the child is prepared to talk are encouraged to engage in activities outside the home. This broadbased behavioral approach seems attractive but it merits more careful evaluation.
4.
References
Adams, H. M. & Glasner, P. J. (1954 ). Emotional involvement in some forms of mutism. Journal of Speech and Hearing Disorders, 19, 59—69. Asperger, S. (194 4 ). Die autistischen Psychopathen im Kindesalter. Archiv für Psychiatrie und Nerv enkrankheiten, 1, 76—137. Blake, P. & Moss, T. (1967). The development of socialization skills in an electively mute child. Behavioral Research and Therapy, 5, 349—356. Brown, J. B. & Lloyd, H. (1975). A controlled study of children not speaking at school. Journal of the Association of Workers of Maladjusted Children, 3, 49—63. Browne, E., Wilson, V., & Leybourne, P. C. (1963). Diagnosis and treatment of elective mutism in children. Journal of the American Academy of Child Psychiatry, 2, 605—617. Cantwell, D. P. & Baker, L. (1985). Speech and language: Development and disorders. In M. Rutter & L. Hersov (Eds.), Child and adolescent psychiatry: Modern approaches. 526—544. London: Blackwell Publications. Chetnik, M. (1973). The intensive treatment of an elective mute. Journal of the American Academy of Child Psychiatry, 12, 482—498. Elson, A., Pearson, C., Jones, C. D. & Schumacher, E. (1965). Follow-up study of childhood elective mutism. Archiv es of General Psychiatry, 13, 182—187. Friedman, R. & Karagan, N. (1973). Characteristics and management of elective mutism in children. Psychology in the Schools, 10, 249—252. Fundudis, T., Kolvin, I., & Garside, R. (1979). Speech retarded and deaf children: Their psychological development. London: Academic Press. Halpern, W. I., Hammond, J., & Cohen, R. A. (1971). A therapeutic approach to speech phobia: Elective mutism re-examined. Journal of the American Academy of Child Psychiatry, 10, 94—107.
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Hayden, T. L. (1980). Classification of elective mutism. Journal of the American Academy of Child Psychiatry, 19, 118—133. Kolvin, I. & Berney, T. (1990). Childhood schizophrenia. In B. J. Tonge, G. D. Burrows, & J. S. Werry (Eds.), Handbook of studies on child psychiatry. Amsterdam: Elsevier. Kolvin, I. & Fundudis, T. (1981). Elective mute children; psychological development and background factors. Journal of Child Psychology and Psychiatry, 22, 219—232. Kolvin, I. & Nolan, J. (1979). Personal observation. Kolvin, I., Ounsted, C., Humphrey, M., & McNay, A. (1971). The phenomenology of childhood psychoses. British Journal of Psychiatry, 118, 385—395. Kratochwill, T. R., Brody, G. H., & Piersel, W. C. (1979). Elective mutism in children. In G. B. Lahey & A. E. Kazdin (Eds.), Adv ances in clinical child psychology. 193—239. New York: Plenum Press. Kupietz, S. S. & Schwartz, I. L. (1982). Elective mutism: Evaluation and behavioural treatment of three cases. New York State Journal of Medicine, 82, 1073—1076. Mora, G., DeVault, S., & Schopler, E. (1962). Dynamics and psychotherapy of identical twins with elective mutism. Journal of Child Psychology and Psychiatry, 3, 41—52. Nolan, J. & Pence, C. (1970). Operant conditioning principles in the treatment of an electively mute child. Journal of Consulting and Clinical Psychology, 35, 265—268. Norman, A. & Broman, H. J. (1970). Volume feedback and generalization techniques in shaping speech of an electively mute boy: A case study. Perceptual and Motor Skills, 31, 463—470. Parker, E. B., Olsen, J. F., & Throckmorton, M. (1960). Social casework with elementary schoolchildren who do not talk in school. Social Work, 5, 64—70. Pustrom, E. & Speers, R. W. (1964 ). Elective mutism in children. Journal of the American Academy of Child Psychiatry, 3, 287—297. Reed, G. F. (1963). Elective mutism in children: a re-appraisal. Journal of Child Psychology and Psychiatry, 4, 99—107. Rutter, M. (1977). Delayed speech. In M. Rutter & L. Hersov (Eds.), Child psychiatry: Modern approaches. 698—716. Oxford: Blackwell Scientific Publications. Salfield, D. M. (1950). Observations of elective mutism in children. Journal of Mental Science, 96, 1024—1032. Tramer, M. (1934 ). Electiver Mutismus bei Kindern. Zeitschrift für Kinderpsychiatrie, 1, 30—35. Wergeland, H. (1979). Elective mutism. Acta Psychiatrica Scandinavica, 59, 218—223.
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Wilkins, R. (1985). A comparison of elective mutism and emotional disorders in children. British Journal of Psychiatry, 146, 198—203. Williamson, D. A., Sewell, W., Sanders, S., & Haney, J. (1977). The treatment of reluctant speech using contingency management procedures. Journal of Behav ior Therapy and Experimental Psychiatry, 8, 155—156. Wolff, S. & Barlow, A. (1979). Schizoid personality
77. 1. 2. 3. 4. 5. 6. 7.
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in childhood. Journal of Child Psychology and Psychiatry, 20, 29—46. Wright, H. L. (1968). A clinical study of children who refuse to talk. Journal of the American Academy of Child Psychiatry, 7, 603—617.
Israel Kolvin, London (United Kingdom)Trian Fundudis, Newcastle upon Tyne (United Kingdom)
Language and Communicative Behavior in Childhood Psychosis Definition Symptomatology Speech and Language Behavior in Schizophrenic Children Differential Diagnosis Relationship between Language Disorders and Communicative Behavior Conclusions References
Definition
From the beginning, the definition of what is called ‚schizophrenia’ has always been a great problem which could not even be satisfactorily solved by the setting up of various classification systems. Meanwhile one can find countless publications dealing with the definitional and nosological problems of this term. This has resulted in considerable heterogeneity of opinion with regard to the terminological meaning and nosological differentiation of ‚schizophrenia’. The same is true for childhood schizophrenia, and, as Stutte (1975) ascertained, no other term in the history of child psychiatry up to the present has undergone such changes in meaning as that of the childhood psychoses. Even today, especially in the Anglo-American literature, the term ‚childhood schizophrenia’ stands for a collection of heterogeneous syndromes, which again are referred to by various labels such as ‚childhood psychosis’, ‚infantile autism’, ‚atypical child’. ‚symbiotic psychosis’, ‚dementia praecocissima’, ‚dementia infantilis’, ‚schizophrenic syndrome of childhood’, ‚pseudo-psychopathic schizophrenia’, and ‚latent schizophrenia’. Accordingly, under these terms a broad range of psychomotoric and/or neurologically im-
paired or retarded children are subsumed. Of course, one or two children classified under these syndromes might indeed be inflicted by a real schizophrenic psychosis and also as adults display the typical schizophrenic condition, but these remain exceptions. The younger the child suffering from a psychotic-like condition, the greater the probability that this is due to an organic brain disturbance. This is the reason why, at diagnosis, neurological symptoms are relatively frequent (psychomotoric and speech retardation, spasticity, epileptic seizures, ataxia, disturbances in motor coordination, sensory disturbances). Even though the etiology is varied, clinicians nevertheless diagnose a childhood psychosis, since the clinical phenomenology is relatively uniform (autistic retreat, negativism, emotional unresponsiveness, motoric states of excitement, emotional frigidity, refusal to speak, disorders in language development, language deterioration, condition of dementia yet intelligent facial expression (‚Prinzengesicht’)). The psychopathological expressions based on heterogeneous causes are apparently relatively uniform in the age-group below 5—6 years. It is therefore difficult to diagnose childhood schizophrenia with sufficient certainty before age 5. Because of this it should be stated quite clearly what is meant by childhood schizophrenia and how it can be distinguished from other forms of childhood psychosis, especially from early autistic disorder. The term childhood schizophrenia should be used only in such cases in which the symptoms, even when modified by age-related specificities, are similar to those shown in adulthood and in which the continuity of the early psychosis into the adult form can be confirmed by longitudinal studies up to early
77. Language and Communicative Behavior in Childhood Psychosis
adulthood. The childhood psychoses, including the infantile autism according to Kanner may share some symptoms, especially negative ones, with adult schizophrenia on a phenomenological level. However, they hardly ever develop into the schizophrenic psychosis found in adults. Also, one does not find in children with so-called childhood psychoses an increased hereditary streak of schizophrenic psychoses, as is the case in childhood schizophrenia (Eggers 1973, 1978 a). Consequently, a separate chapter in this handbook will deal with childhood autism (cf. art. 78). Various forms of infantile psychoses can be described according to the degree of maturation of individual ego functions and defense mechanisms. Taking into consideration the aspects of psychological development, French authors named these illnesses quite pertinently as ‚psychoses de développement’ (Duché 1971, Heuyer 1960, Michaux/Duché 1965). Such conditions would include psychoses of early onset such as the early infantile autism (Kanner 194 3), the psychodefective (Bender 1953) or the no-onset-type (Despert 1938) of childhood psychosis, the pseudoneurotic psychosis (Bender 1953), the acute onset type (Despert 1938), the symbiotic psychosis (Mahler 1954 ) or dementia infantilis (Heller), the dementia praecocissima (de Sanctis 1908), and the syndrome of Kramer-Pollnow (1932). The actual schizophrenic psychoses in childhood, however, require a higher degree of ego-structuring and appear later, after completion of the 5th year of age. They belong to the so-called late-onset psychoses (Kolvin 1971). The reason for the differentiation between various forms of infantile psychosis and childhood schizophrenia is that an already differentiated level of psychological development and a higher degree of ego maturity are prerequisites for the ability to produce psychotic symptoms similar or even identical to those in adults. The ego-structuring achieved allows the genesis of guilt or inferiority feelings and the experience of ego alienation, for instance, which in their turn presuppose the sense of ego identity. Such a level of psychological integration allows only for depressive or schizophrenic psychoses known as late-onset psychoses or ‚psychoses de la phase de latence’ (onset rarely before the age of five) in contrast to the autistic, symbiotic or organic psychoses of early childhood (Eggers 1982).
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2.
Symptomatology
The frequency of childhood schizophrenia lies for under 10-year-olds between 0.5% and 1% and for 10 to 14 -year-olds by 3 to 4 % of total cases of schizophrenic psychoses in the general population. The detection and precise study in early childhood of psychopathological phenomena usually occurring in adults reveal that undoubtedly manic, depressive or schizophrenic symptoms may already appear before the age of 10, and that these correspond positively to adult symptoms although modified by factors related to the phase of development. Thus it is possible to evaluate age-related characteristic features of childhood schizophrenia. It is generally accepted that the younger the child, the poorer the psychopathological symptoms. This view is correct in so far as that at early school age negative, non-productive symptoms predominate, such as poor drive, loss of interests typical for this age, autistic withdrawal from the world of child relations, inability to maintain links with relatives and friends, anxious-paranoid basic mood with a tendency to eruptions of feelings of rage, increased affective blunting and loss of agerelated intentional volitional strivings as well as regressive-atavistic tendencies (encopresis, coprophagy, faecal smearing, eating of waste, fear of toilets, destructive impulses). The personality change is displayed mainly in the emotional, intentional, and social behavior. Previously animal-loving children are unmotivatedly cruel to animals. Children who used to be gentle, sensitive, and affectionate suddenly become unloving, unnaturally cold, hard, wilful, impudent and show no emotional links to previously beloved caregivers. The disturbance in social contact is less marked in childhood schizophrenia than in other childhood psychoses. In their comparative study, Kolvin/Ounsted/Humphrey/ McNay (1971) found that the poor relationships in the late-onset psychoses were “less global and more patchily present” than in the infantile psychoses. The poor relational ability with other people could be confirmed as a central feature of infantile psychosis, and as “an important but not a central feature of late-onset psychosis, with only half of these children mixing poorly or avoiding contact with adults or children” (Kolvin et al. 1971, 387). The social contact disorder in schizophrenic children is closely related to their
V. Pathologies and Disorders of Language Development
796
impoverished drive and impaired ability to react emotionally. In productive forms of childhood schizophrenia the social contact disorder is primarily a result of the child’s preoccupation with often threatening delusions and hallucinatory bodily sensations. Visual and acoustic hallucinations, although seldom in childhood schizophrenia, certainly do occur before the age of 10. For instance among other things a 7-yearold girl heard human voices in her head: “They are always saying something you crab, you dirty slut, they tell me nothing but ugly and indecent things”. The child felt a snake inside her abdomen, believed she was poisoned, felt “persecuted by evil forces” and thought the food was poisoned (Eggers 1982, 84). In contrast, in early childhood psychoses with onset before the age of 5 or in early infantile autism the communication disorder is more elementary and as a rule is not caused by productive-psychotic phenomena such as hallucinations or delusionary symptoms. At most one could suspect such productive symptoms in some of the children with an infantile psychosis on account of their behavior (e. g. a child looks as if he/she is hearing voices), but this cannot be verified. And also at a later stage, children with an infantile psychosis only seldom display true schizophrenic symptoms. The communicative behavior of schizophrenic children is to a great extent the result of age-related delusional and hallucinatory types of experience, including so-called transitivistic depersonalisation phenomena (Eggers 1973, 1982). Children identify themselves with people, animals or even objects in their environment. Other symptoms typical of this age are seemingly delusional-hallucinatory bodily sensations and fears such as those narrated by a 10-year-old boy: “The navel bursts; the heart stops: lightning shoots through me: the sex is broken into two”. Statements like I am not myself anymore or I am div ided into two small persons (Ssucharewa 1967) also indicate that schizophrenic children already have splitting experiences. Moreover, delusional symptoms in children whose illness was manifested before the age of 10 frequently take the form of diffuse and unattached anxiety or cosmic threats: The sun falls from the sky, the rain will never stop and everybody will drown. Later symptoms include paranoid ideas of reference and of being poisoned, and also hypochondriac, religious and depressive
delusional symptoms. Whereas delusional ideas are relatively transient and variable before the age of 10, they become more or less systematized in cases over the age of 12. As a rule these children have an above-average intelligence and are highly sensitive, with early manifested tendencies to brood over metaphysical or religious problems. Thus a boy who became ill at the age of 11 and showing a marked delusional system, already said the following when aged 5: “I consider this life as only a transition period”. Similar expressions were used by a schizophrenic girl at the beginning of her psychosis: “One has to think of the autumn of life”. Hallucinations in psychotic children often take the form of abnormal bodily sensations. The children perceive talking or singing persons within their head or abdomen, feel animals inside their body, have the impression that smoke passes through their body, that their head becomes larger or ‚crooked’, that their navel bursts, their sex is broken into two, lightning shoots through their body, and cornered stones lie in their abdomen. Characteristically, schizophrenic children are more likely to have visual hallucinations than schizophrenic adults (Eggers 1973).
3.
Speech and Language Behavior in Schizophrenic Children
3.1. Clinical Observations The communication disorder is also expressed in language behavior. Although there are no systematic linguistic studies on the language behavior in childhood schizophrenia, we do have, mainly in the older literature, descriptions of language use in these children. However, schizophrenic children’s speech has by no means found the same scientific interest as the speech of children with a childhood psychosis, especially of those with infantile autism. (cf. art. 78). The language disorders in schizophrenic children (between 6—12 years of age) are not uniform, so that at times we find mutism and verbiage even in one and the same child. Some children display an unmotivated change of vocal volume, speaking to themselves loudly or softly. Their utterances appear unmotivated and unrelated, at times with fantastic and incomprehensible content or meaning. We find verbal modifications, word creations (neologisms), stringing together of seemingly meaningless words, senseless repetition of syl-
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lables, words, or phrases (verbigerations). Very typical are eccentricities in expression (e. g. a 12-year-old schizophrenic boy: “Ich bin innerlich so ausgegloist” [“I am so ‚burned-out’ internally”]. Atschkova (1966) reports that sometimes language use stops for no apparent reason, that some children speak to themselves in a whisper but will not answer questions and do not speak to their relatives. Kudrjawzewa (1967) observed in the children she studied neologisms, rhyming, speaking out-of-context, and meaningless talking about technical topics. She describes the monotony and poverty of language in these children. They seldom use language as a tool for communication. Thus, some authors speak of compulsive talking and verbiage in the sense of “fruchtloser Klügelei, in Vorbeireden oder Wiederholungen von Fragen” [“fruitless riddles, missing the point, or repetition of questions”] (Kudrjawzewa 1967, Stutte 1963, v. Stockert 1956). One of the oldest descriptions of language in childhood schizophrenia can be found in L. Voigt (1919, 183). He describes the process of a psychotic language disorder in a 10-year-old girl. When asked to say the Lord’s Prayer, the girl first says: “Das darf man nicht” [“That isn’t allowed”], but then she does begin: “Vater, Vater, Vater, unser, unser, unser, unser, im, im, im, im, Himmel, Himmel, Himmel, Himmel ...” [“Father, Father, Father, our, our, our, our, in, in, in, in, heaven, heaven, heaven, heaven”]. Also in reading she repeats each word several times, her reading being otherwise correct. Three years later, at 13 years, the girl’s speech sounds very clipped, it is over-articulated, monotonous, and slow, as if memorized, the consonants are pronounced very distinctly, each word separated markedly from the following. In between, some utterances are spoken fluently, with normal, natural pronunciation and prosody. The speech content is impoverished, limited to a few short sentences, such as “will brav sein, Verzeihung, will folgen” [“want to be good, excuse me, want to be obedient”], “kann schreiben” [“can write”], “kann lesen” [“can read”], “schön lesen” [“read well”]. At 14 years of age the girl reads fluently with natural prosody and comprehension of the sentence meaning. At 15 years of age we again find verbigeration and the girl repeats stereotypically: “Ich will brav sein, ich will folgen, ich will es noch einmal versuchen” [“I want to be good, I want to be obedient, I want to try once again”].
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3.2. Characteristics of Language Behavior in Schizophrenic Children Schizophrenic children’s language is often characterized by the classic authors as ‚disintegrative speech’. This term covers a whole series of linguistic phenomena such as: 1. Changes in rhythm and rate of speech. Over-articulation, clipped speech, abnormal stressing of consonants in comparison to vowels, unusual stressing of phrases, rapid gabbling, or — on the other hand — abnormal stretching of words and phrases can be found. 2. Changes in speech melody (dysprosody). The children tend to use a singing intonation, which is more or less melodic, but usually at an abnormal pitch. They often fall into a singsong droning, a monotonous mumbling to themselves or they repeat some tune or other in a stereotype litanylike way. Thus a 10-year-old boy played ‚orchestra’, thereby referring to “Hermann” (meaning the Hermann-Hagestedt Radio Orchestra (Eggers 1973, 66)). We can also find meaningless rhyming, as in the case of a 14-year-old schizophrenic boy: “Karl May is vorbei, ach armes, deutsches Mägdelein, es kann ja nimmer sein, Ströme inhaliert, doch nicht imponiert, es ist vorbei, ich bin wie Brei, Gelenke gehören dein, das rechte ist nicht mein, es ist mir einerlei, der Tod eilt herbei” (Voigt 1919, 193). 3. Paragrammatism. This term refers to a series of deviations from normal language, which schizophrenic children have in common with schizophrenic adults, that is, in principle we do not find any differences here between ‚schizophrasia’ in adult and childhood schizophrenias. The language is characterized by abnormal sentence constructions, by unusual word and phoneme relations, by alterations of lexical morphemes or morphemic paraphrasing, by word-finding disorders, by incorrect word ordering, or by verbigerations. These disorders can eventually result in a proper ‚word-salad’. 4. Language disintegration, paraphrasing, distraction of thought, speaking out-ofcontext. Here words and sentences are no longer ordered in meaningful sequences. The sentence segments are incomprehensible to the listener, at least at first hearing or sight. Thereby it must remain open whether these typical schizophrasic phe-
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nomena are the result of a disturbed language production ability or rather of a thought disturbance. — This type of disorder can be demonstrated in the utterances of a 13-year-old acutely afflicted girl with optical and acoustic hallucinations, who developed very impressive delusions: “Sie sind alle mitgefahren, um die Familie zu heilen, schon die ganze Zeit, wie sie den Durchbruch gemacht haben, um mich zu führen, die Freche, die Judenstirne, steckt im Kopf, daß sie mich retten” [“They all came with, in order to heal the family, the whole time already, as they have made the break-through, in order to lead me, the impudent one, the Jewish foreheads, it’s stuck in the head, that they will save me”] (Eggers 1973, 34). Another 13-year-old girl produced typical verbigerations: “Das Feuer, das Feuer, es brennt, es brennt, es brennt ...” [“The fire, the fire, it’s burning, it’s burning, it’s burning ...”]. She displayed a pronounced distraction in speech production. Thus, for example, her answer to the question if she wasn’t feeling well was: “Bei Schlächtern nicht, der himmlische Vater sieht mehr vor Augen als ich. Ich bin schon im Haus zusammengebrochen und gehe ich so, dann sagt die eine so, dann schimpft die Elli so, durch Gottes Weisheit und Gnade ...” [“Not by butchers, the heavenly Father sees more before his eyes than I. I already broke down in the house and if I go like that, then the one will say thus, then Elli will scold so, by God’s wisdom and mercy ...”] (Eggers 1973, 39). The girl’s speech was in part also characterized by derived or composed morphemic paraphrasing (Lecours/Vanier-Clement 1976). She spoke of “Erhaltungsunannehmlichkeit” [“conservation-trouble”], “Ernstlichkeit” [“earnestness”], “Apothekigkeit” [“apothecary-ness”]. Such word-creations (neologisms) can be scattered here and there in the speech productions: “Ich bin verfolgt von den Menschen. Ich will sterben, ich war schon in Vergasung, aber mein Herz wollte nicht sterben. Sie schlachten die Mädels ab. Ich habe gehört von den Leuten. Erhaltungsunannehmlichkeit. Und mir fällt alles auf die Augen” [“I am persecuted by the people. I want to die, was already in the gasification, but my heart didn’t want to die. They kill off the girls. I have heard of the people. Conservation-trouble. And everything falls onto my eyes.”] (Eggers 1973, 39).
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Like schizophrenic adults, schizophrenic children tend to speak out-of-context. This means that a sensible conversation between clinician and patient cannot take place. The children give no context-related answers but rather appear to follow internal ideas and inspirations, that is, they are governed completely internally. Thus their answers appear strangely a-logical, senseless, eccentric, and bizarre as in the following case of a 14 -yearold girl. To the question why she was lying in bed she answered: “Weil ich an die Englein glauben soll. Ich bin ein Backfisch und darum muß ich für die Kinder an die Englein glauben” [“Because I should believe in angels. I am a teenager and so I must believe in angels for the children”]. To the further question if that was a reason not to get up she answered: “Nein, aber weil der Stuhl da so dicht am Tisch steht” [“No, but because the chair is standing so near to the table”]. Asked if she was ill, she answered: “Die sagten, wenn sie von der Kirche kamen, mit dem Handschuh, mit dem Schlüssel” [“They said, when they came from Church, with the glove, with the key”]. The question where she was ailing most elicited the curiously eccentric answer: “An der Zunge” [“My tongue”] (Eggers 1973, 4 9 f.). The combinations in thought and language appear illogical to the listener; they are completely out of context and therefore baffling. However, the girl’s last answer could refer to her thought and language disorder. For, as H. Grimm (1991) indicated, for young children the concepts tongue and language can be identical. Thus, when they are questioned about their language they may refer to their tongue. The three cases of schizophrenic children between 12 and 14 years cited above demonstrate the schizophasic language disorders as manifested at the onset of the psychosis. This contradicts the view of Hoffman/Sledge (1984 ) and Kirov (1985) that “schizophasia occurs primarily in the more advanced stages of schizophrenic illness, and generally is associated with prolonged periods of social isolation and functional deterioration” (cf. art. 54 ). Insofar, although Hoffman’s (cf. art. 54 , 535 f) hypothesis appears plausible that “chronic social isolation, sustained alienation from other human beings, coupled with bizarre ideation, may, over time, cause the schizophrenic to volitionally disregard the constraints of ordinary language” this hypothesis should certainly not be generalized.
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3.3 Language Characteristics in the Further Course of Childhood Schizophrenia As shown by our longitudinal studies with 57 patients suffering from a childhood or prepuberal schizophrenia (onset of illness: 11 children at or before 11 years; 4 6 children between 12 and 13 years), schizophasic language disorders can still be observed after several decades in the course of the illness (mean length of follow-up: 16 years) (Eggers 1973, 1987 b). Thus, during the post-examination of a 30 year old female patient, who had fallen ill at the age of twelve, a curious disorder in the comprehension of meaning was observed, which one could perhaps best refer to as ‚semantic dissociation’ as an expression of a ‚cognitive slipping’. The patient defined the difference between a pond and a river as follows: “Der Teich ist mit Sand besät, der Fluß ist im Wasser und wenn man das Wasser mit dem Feuer zusammentut, ist es dasselbe — beides ist gefährlich, ich weiß was gemeint ist, aber wie das zusammenhängt, weiß ich auch nicht” [“A pond is sown with sand, a river is in water and when one puts the water together with fire it is the same — both are dangerous, I know what is meant, but what the connection is, I don’t know either.”] She was also not able to produce correct and meaningful definitions with the essential characteristics for other terms or to formulate the essential characteristics. When asked to explain the idiom “Morgenstund hat Gold im Mund” [“The early bird catches the worm”] she answered: “Morgens darf man nicht singen oder pfeifen, sonst gibt’s was Schlechtes zu hören.” [“In the morning you may not sing or whistle, otherwise you will get to hear something bad.”] (Why?) “Vom Meister eine verpaßt.” [“Get a clout from the master”]. The word “Gold” meant “Von morgens 5 Uhr bis 7 Uhr bedeute das” [“It means from 5 o‚clock to 7 o‚clock in the morning”] (Eggers 1973, 29). In the answers of this patient we can find a tendency to concretism as well as a tendency to disregard the meaning of the sentence. She ‚hangs on to’ a specific word, and disregards the other words and phrases essential for grasping the overall meaning. In general, what the patients offer are more coincidental, associative ideas and answers which give rise to the impression of irrelevance. 3.4. Language Comprehension Disorder The examples given demonstrate that it is not
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only expressive language which is disturbed in schizophrenic children and adults, but also receptive language or comprehension. This could be attributed to an impairment in the ability to generate hierarchies of individual words and phrases. The comprehension of a sentence does not come about by adding together the words, but by a logical evaluation of words according to their meaning. It seems that the individual words and phrases are seen as being equal in importance and that they are not hierarchically classifiable. This could account for the typically paralogic, strangely confused language of schizophrenic patients. It also accounts for what Beringer (1926) refers to as “der Charakter des Einfallmäßigen, Unverpflichtenden” [“the idea-like, non-committal character”] of schizophrenic utterances as well as the “Bedeutungsverschiebungen” [“shifts in meaning”] which he frequently observed in his patients. The interpretation offered by Grinker/ Holzman (1973) with regard to schizophrenic adolescents and young adults points in the same direction: “The patient may omit ideas essential for the listener to grasp the continuity (ellipsis), as if the patient assumed that the listener must know the full thoughts” (Grinker/Holzman 1973, 171). The tendency of schizophrenic children and adolescents to treat individual words and phrases as equal in importance and to refrain from ordering them hierarchically is in agreement with recent findings by Caplan/Perdue/ Tanguay/Fish (1990) and Caplan/Foy/Asarnow/Sherman (1990). These authors found a significant correlation between the extent of illogical thinking and increased distraction or decreased attentional span. The attentional deficit and the tendency for illogical thinking were evaluated on the basis of a free recall of a previously told story and a free interview. These were based on the Kiddie Formal Thought Disorder Scale (K-FTDS) (Caplan/ Guthrie/Fish 1989). The associative slackening is displayed in unpredictable changes of the topic of conversation towards an unrelated topic, which makes it difficult for the listener to follow the conversation. I have dealt elsewhere (e. g. Eggers 1991) with the difficulties experienced by schizophrenic adolescents as well as by children at high risk for schizophrenia in evaluating on the receptive level the meaning of relevant and irrelevant stimuli and in developing on the expressive level task-related solution strategies (cf. also Bunk 1991). If, like Käsermann (1983), one regards speech as a behavior “das zielgerichtet/funktional zur Lösung der Kom-
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munikationsaufgabe (Realisierung der Intentionen) eingesetzt wird” (“which is applied purposefully/functionally to solve the communicative task (realization of intention)“, then the schizophrenic’s language disorder can be understood as an impairment in the generation and implementation of adequate solution strategies in coping with this communicative task. This view implies the annulment of the contrasts ‚language disorder versus thought disorder’, so that the controversy as to whether the language disorders of schizophrenics are the result of a cognitive disorder or of an independent verbal disorder can be considered closed. 3.5. Linguistic Results Linguistic findings exeeding mere descriptions of the language behavior in schizophrenic children are rare and of recent publication. This is partly due to low incidence rates of childhood and prepuberal schizophrenia (Bunk/Eggers 1990, Eggers 1982). Leaper/Emmorey (1985) performed a comparative case study with 2 schizophrenic and 2 normal children at the ages of 6 and 9 years. They analyzed speech samples from three different situations: an interview, a free picture description and the re-telling of a story. Among others, two psycholinguistic aspects were examined: First, the extent of cohesion with regard to the logical semantic relation between two sentences or sentence segments, and second, the assumed or prerequisite information on which a statement is based. Often the topics of conversation refer to something said earlier (the verbal context) or to something in the immediate environment of the speaker (the nonverbal context). In these instances, the speaker uses a presuming nominal group. With respect to the cohesion in sentence structure over all contexts, no difference was found between the normal and schizophrenic children under study, whereas there are differences between normally healthy and thought disordered schizophrenic adults. Both thought disordered children and thought disordered adults, however, refer during their descriptions and reproductions to irrelevant information and give little explicit reference to what was said previously. The discourse appears fragmentary and logically instable. In a study of a group of schizophrenics ranging in age from 15 to 4 1 years, Morice/ Ingram (1983) found a relationship between
the syntactic complexity in spontaneous speech in the sense of the depth of logically linked clauses and age at onset of illness. The lesser the linguistic complexity, the earlier the onset of illness had been manifested. This relationship was independent of illness duration. The results indicate that there is a common factor responsible for the language disorders as well as for the general phenomenology of schizophrenic symptoms. By those authors concerned with the neuropsychological aspects of information processing in psychotic disturbances, this factor is interpreted as a central regulation factor of attentional processing (Caplan/Foy/Asarnow/Sherman 1990, Cornblatt/Erlenmeyer-Kimling 1985, Nuechterlein/Edell/Norris/Dawson 1986).
4.
Differential Diagnosis
4.1. Differentiation between Language Disorders in Childhood Schizophrenia and in Infantile Autism The fundamental difference is as follows: In autism, language cannot develop, or can only develop partially, probably on account of a serious disorder in social relationships existing from birth. In cases of childhood schizophrenia, language is as a rule at a normal developmental stage since the age levels at illness onset are higher. Language developmental disorders are typical for autistic children, as observed by Kolvin (1971) in 88% of his patients. They are far less often found in childhood schizophrenia. Only when the schizophrenic psychosis has been manifested do changes in language behavior occur. However, in a few cases and at especially early onset (prior to 5—6 years of age) the differentiation from language use in autistic children may prove difficult (Bosch 1972). Changes in language flow, a tendency for echolalia, phonographism, and neologisms can still be observed in schizophrenic children in early school years. A specific language peculiarity characteristic in autistic children is the so-called ‚pronominal reversal’, which is only seldom found in childhood schizophrenia (Kolvin 1971). Sentence fillers, meaningless phrases, and nonsensical words can be found far more frequently in the early childhood psychoses than in childhood and prepuberal schizophrenia. Here, the language deviation most frequently observed by Kolvin/ Ounsted/Roth (1971) was a tendency to answer questions incompletely or only partially.
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Typical are disorders in thought and association (vacuity and withdrawal of thought, incoherence, distraction of thought etc.) whereas they are only rarely found or completely lacking in the early childhood psychoses. One common characteristic of both childhood autism and childhood schizophrenia is the occurrence of echolalia, which, however, occurs more frequently in autistic children. 4.2. Differentiation from the Language Disorders found in Manic Psychoses Manias or manic psychoses are extremely rare in childhood. When they do occur, one usually finds short phases with rapid shifting of phases, often within one or several days. When manic phases occur, they frequently turn into schizophrenic psychoses and then may either merge completely with the schizophrenic process or otherwise the manic-type episodes can remain and be combined with depressive, schizophrenic or schizo-affective episodes. Changes are possible and can alternate before or intermittently during the total course of the psychosis (Bunk/Eggers 1990, Eggers 1986). There are no linguistic studies on manic psychoses and purely manic episodes in the course of a schizo-affective psychosis in children and adolescents. Clinically speaking, however, it appears that the disconnectedness between the verbal utterances is not as marked as in the purely schizophrenic psychoses. This impression is supported by Hoffman/Stopek/Andreasen (1986), who found that manic speech difficulties were due to shifts from one discourse structure to another, while the schizophrenic speech disorder reflects a basic deficiency in elaborating any discourse structure. 4.3. Differentiation from Aphasic and Mutistic Language Disorders The irregularity of language disorders in the schizophrenic child indicates that they cannot be due to an organic defect, i. e., the disorders are distinguishable from sensory or motoric aphasia. However, a small subgroup of schizophrenic adults who were afflicted in childhood can display very serious language disorders in the sense of paraphrasing or paragrammatical speech, as is typical in the aphasic speech disorder. Moreover, the question must remain open whether in the serious dysphasic language disorders in schizophrenics we are dealing with an ‚intentional dysfunction’ in the sense that schizophrenic patients
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are not able to express what they wish to say in a grammatically correct way, or whether we are dealing with a neural deficit corresponding to that of aphasics. Significant correlations between especially seriously disordered schizophrenics and complications due to birth trauma or minor neurological deficits have, however, not been found (cf. art. 54 ). In conclusion, the language disorders of schizophrenic patients are not as marked as in the case of aphasic patients. Also, it is possible with effort and empathy to establish a context of meaning in spite of the scattiness in speech and written language. Among the language disorders of schizophrenic children mutism has been mentioned. This schizophrenic aphrasia is part of a complex psychotic phenomenology in contrast to psychogenic (traumatic or elective) mutism, which is not connected to any psychotic phenomenon.
5.
Relationship between Language Disorders and Communicative Behavior
In human beings, it is the nature of language to serve communication. Language is not an exclusive but an essential part of our communicative behavior: “Wir kommunizieren nicht, weil wir grammatische Regeln und Wortbedeutungen gelernt haben, sondern wir lernen diese, weil wir kommunizieren” [“We do not communicate because we have learned grammatical rules and the meanings of words, but we learn these because we communicate”] (Grimm 1987, 582). Lutz (1938/1939) pointed out the disturbance in the relational characteristic of schizophrenic children’s speech. In fact, he understood schizophrenic language disorders as a specific relational disorder, whereby apart from cognitive and specifically linguistic factors, a motoric disorder (an increase or decrease in motoric activity) certainly is also partly responsible. Even prior to onset of illness, deviations in language and thought can be found as well as in contact behavior, which differentiates subjects with a later manifestation of a schizophrenic psychosis from healthy subjects. In a follow-up study of at-risk children with schizophrenic mothers (Parnas/Schulsinger/ Schulsinger et al. (1982) found that the following items differentiated the schizophrenics from the non-psychotic group: ‚incoherence’, ‚pathology of associations’, ‚incongruent fa-
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cial expression’, ‚difficulties in making friends’. Thus it is also the preverbal, facial expressive behavior which differentiates between healthy subjects and subjects at high risk for schizophrenia. Not only in families with psychotic members, but also in families with disturbed, nonpsychotic adolescents, parental communication deviance seems to be a factor of prognostic significance with regard to the later manifestation of a schizophrenic psychosis, as could be demonstrated in followup studies (Douane/West/Goldstein et al. 1981, Goldstein/Rodick/Jones et al. 1978, Lewis/Rodick/Goldstein 1981). Another high-risk study revealed that children of schizophrenic parents display lower verbal productivity and a decrease in cohesive thought in their spoken utterances, i. e., the formal and the semantic links in their utterances were looser than in healthy peers (Harvey/Weintraub/Neale 1982). The language behavior of these children at risk for schizophrenia was similar to the performance of thought-disordered adult schizophrenics, who also provided fewer links between clauses and used less informative types of cohesive ties (Rochester/Martin 1979). The described language disorders in children at high risk for schizophrenia might be associated with the fact that these children’s flow of speech is more often interrupted by members of the family. The results presented by Waxler/Mishler (1971) appear to indicate this possibility. The described disordered association, illogical thinking and the cognitive slippage in schizophrenic children find their counterpart in the difficulty in maintaining a focus of attention in family transactions, as described by Singer/Wynne (1965). A disorder in adequate focusing in adult schizophrenics can also be linguistically substantiated: Rutter (1985) examined monologues and conversations of schizophrenic patients, of patients with affective disorders, and of normal orthopaedic patients using a variant of the Cloze Procedure. The sentences in the transcribed protocols were separated and presented as a card set to raters who were blind to the subject’s diagnosis and who were to attempt to re-organize the sentences into a meaningful text. The schizophrenic material was more problematic to reconstruct since it was very difficult if not impossible to recognize a reference system according to which the sentences could be ordered. In the conversation situation Rutter observed that the schizo-
phrenic subjects and, in tendency, the affectively disordered subjects would ask questions at inapt points in the conversation and would answer questions with incorrect referential content. Rutter interprets these disorders less as the cause of cognitive deficits or thought disorders but rather as the expression of an impaired ability in taking over social roles during the schizophrenic psychosis.
6.
Conclusions
Language disorders in children and adolescents display a Janus-face from the clinicalphenomenological point of view as well as in linguistic studies: It is not possible to decide whether we are dealing primarily with a cognitive, possibly neurologically caused impairment or rather with a social interaction disorder. The latter would be caused by developmental and communicative impairments. Much seems to support the view that this dichotomous question has been put incorrectly. It is the old controversy ‚nature versus nurture’. Language and behavior per se, as well as schizophrenic behavior, are entirely dependent on a highly complex interaction among genetic, biological, specifically neurological, and social factors. An integrative model of thought and language disorders as well as of communicative behavior in schizophrenics still needs to be developed. An integrative-dynamic model of schizophrenia is described elsewhere (Eggers 1991). Author’s Note: I wish to thank D. Bunk and P. Wiemer for their helpful assistance.
7.
References
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The use of pattern analysis classifying the development of schizophrenia-like illnesses. In A. Marneros & M. T. Tsuang (Eds.), Affectiv e and schizoaffecti v e disorders. 89—101. Berlin/Heidelberg/New York: Springer. Caplan, R.., Foy, J. G., Asarnow, R. F., & Sherman, T. (1990). Information processing deficits of schizophrenic children with formal thought disorder. Psychiatry Research, 31, 169—177. Caplan, R., Guthrie, D., Fish, B., Tanguay, P. E., & David-Lando, G. (1989). The Kiddie Formal Thought Disorder Rating-Scale: Clinical assessment, reliability and validity. Journal of the American Academy of Child and Adolescent Psychiatry 28, 408—416. Caplan, R., Perdue, S., Tanguay, P. E., & Fish, B. (1990). Formal thought disorder in childhood onset schizophrenia and schizotypal personality disorder. Journal of Child Psychology and Psychiatry and Allied Disciplines, 31, 1103—1114. Cornblatt, B. A. & Erlenmeyer-Kimling, L. (1985). Global attentional deviance as a marker of risk for schizophrenia: Specificity and predictive validity. Journal of Abnormal Psychology, 94, 470—486. de Sanctis, S. (1908). Dementia praecocissima catatonica. Folia Neuro-biologica, 2, 9. Despert, L. (1938). Schizophrenia in children. Psychiatric Quarterly, 12, 366. Douane, J., West, K., Goldstein, M. J., Rodnick, E., & Jones, J. (1981). Parental communication deviance and affective style as predictors of subsequent schizophrenia spectrum disorders in vulnerable adolescents. Archiv es of General Psychiatry, 38, 679—685. Duché, D. J., (1971). Psychoses infantiles. Revista portuguesa para o estudo da deficiencia mental, 1, 445. Eggers, C. (1973). Verlaufsweisen kindlicher und präpuberaler Schizophrenien. Berlin/Heidelberg/ New York: Springer. Eggers, C. (1978 a). Zur nosologischen Abgrenzung zwischen frühkindlichem Autismus und kindlicher Schizophrenie. Bibliotheca Psychiatrica, 157, 1—21. Eggers, C. (1978 b). Course and prognosis of childhood schizophrenia. Journal of Autism and Childhood Schizophrenia, 8, 21—26. Eggers, C. (1982). Psychoses in childhood and adolescence. Acta paedo psychiatrica, 48, 81—98. Eggers, C. (1986). Schizoaffective psychoses in children and juveniles. In A. Marneros & M. T. Tsuang (Eds.), Schizo-affectiv e psychoses. 202—224 . Berlin/ Heidelberg/New York/Tokio: Springer. Eggers, C. (1991). Stimulus protection model of schizophrenia: Convergence of neurobiological and developmental psychological factors. In C. Eggers (Ed.), Schizophrenia in youth. 29—40. Berlin/ Heidelberg/New York/London/Paris/Tokio/Hongkong: Springer.
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Christian Eggers, Essen (Germany)
78. Language and Communicative Behavior in Autistic Disorder 1. 2. 3. 4. 5. 6. 7. 8.
1.
Introduction Epidemiology and Classification Differential Diagnosis Etiology of Autistic Disorder and PDD Language and Communications Deficits in Autism Intervention Strategies for Communication Prognosis of Autistic Disorder References
Introduction
Recently renamed Autistic Disorder (AD) in recognition of its life-long duration, Early Infantile Autism (EIA) is one of the most severe and debilitating psychopathologies of childhood and later life. It was first identified as a distinct nosologic entity by Leo Kanner (194 3) in North America who also named it and by Hans Asperger (194 4 ) in Europe who called it ‚Autistic Psychopathy’. Although for a long time the term ‚Kanner’s syndrome’ was used interchangeably with the term EIA, more recently Asperger’s syndrome has been
differentiated from autism by some writers (Wing 1981). Others maintain that Asperger described that subgroup of autistic children who are higher functioning and that no differentiation between high functioning autism and Asperger’s syndrome is warranted at the present time (Schopler 1985). The term EIA was employed interchangeably with such other terms as ‚Psychosis of Childhood’. ‚Childhood Schizophrenia’, ‚Symbiotic Psychosis’ (Mahler 1952) and ‚atypical development’. A major breakthrough in the field was made when the ‚psychoses’ that originate in infancy and early childhood were differentiated from those comparable conditions that appear first in adult life, with very few cases having their origins in childhood. The division was substantiated through studies by Kolvin and his collaborators (Kolvin 1971; Kolvin/Ounsted/ Humphrey/McNay 1971) who were able to show that the ‚early onset’ cases, i. e., prior to age 5, presented different epidemiology and key characteristics than those with later onset. The former are now described as Autism and
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Pervasive Developmental Disorder while the latter are classified using adult criteria for schizophrenia. Although the distinction has been disputed by some writers (Fish 1977), at the present time this is the position of many workers in the field and it is also the position of the DSM III-R.
2.
Epidemiology and Classification
Partly because of the idiosyncratic nomenclature employed by clinicians in different countries to label autistic children, and partly as a result of lack of consensus on etiology, up until 1980 very little agreement existed as to what constituted the key symptoms of the syndrome. This had inevitable repercussions for both assessment and treatment practices. As well, it resulted in diluting and confusing research efforts on the disorder. In fact, many of the early studies employed very different criteria for sample selection than studies do today. Earlier studies have also tended to concentrate on the relatively higher functioning subgroup of children, the ones who did not show any neurological impairment, hence omitted the large number of moderately and severely retarded autistic children. This was not fortuitous since the prevailing etiologic view of the time was psychoanalytic (Bettelheim 1967), postulating that psychogenic factors were responsible for the condition and that autistic children were biologically intact. A rapidly accumulating body of evidence pointing to biological factors in etiology, resulted in a corresponding broadening of the classification criteria to include the lower functioning, mentally retarded subgroup of children (DeMyer/Hingtgen/Jackson 1981). Corresponding restrictions were imposed to exclude other populations of higher functioning children who might be confused with the autistic such as the severely developmentally delayed in receptive language abilities, the attentional deficient and the borderline or atypical cases. The Diagnostic and Statistical Manual III (DSM III) (American Psychiatric Association 1980) was the first effort to adopt an atheoretical, phenomenological approach relying on explicit, operational criteria for the diagnosis (Spitzer/Endicott/Robins 1978). Despite the advantages of this system, however, considerable shortcomings have been identified by a number of writers. To an extent, these problems were remediated in the revised version, the DSM III-R (American Psychiatric Association 1987). For Autistic Disorder (AD) to be diagnosed, at least 8
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criteria must be met, with at least one from each of the three main symptom clusters being present. Cases meeting fewer than the eight criteria, or having no symptom representation in each of the three symptom clusters are diagnosed as Pervasive Developmental Disorder (PDD) Not Otherwise Specified (NOS). The obvious implication is that AD, a form of PDD, represents the more serious expression of the PDD syndrome. The clear advantage of the DSM III-R classification lies in its taking care of all three criticisms levelled against the DSM III just mentioned. The age of onset is no longer crucial, which reflects evidence on the life-long course of the disorder as shown in follow-up studies (Paul 1987). As well, the categories COPDD, Atypical PDD and Residual Autism present in the DSM-III are now observed under one category, PDD, and a more comprehensive and detailed representation of the syndrome has been provided. Despite these advantages, the DSM III-R continues to present difficulties. One of the main ones is that it does not allow for rating the severity of expression of each symptom but requires that information be expressed in a binary YES-NO fashion. This results in issues of severity not being addressed, other than by means of the AD-PDD dichotomy (Konstantareas 1988). Although efforts are under way to take into account and improve the DSM III-R criteria, not only for AD but also for other disorders, researchers and clinicians have to rely on other means to quantitatively determine degree of severity. Checklists have been developed for use over the years with many disorders including autism. Thus the Childhood Autism Rating Scale (CARS) (Schopler/Reichler/DeVellis/ Daly 1980), The Behaviour Rating Instrument for Autistic and Atypical Children (BRIAAC) (Ruttenberg/Dratman/Fraknoi/ Wenar 1966); The Behaviour Observation Scale for Autism (BOS) (Freeman/Ritvo/ Guthrie et al. 1978) have been developed, and their psychometric properties have been reviewed (Parks 1983). The checklists have the advantage of allowing degree of severity and cutoff points for meeting the diagnosis to be addressed, factors crucial for clinical research and administrative purposes.
3.
Differential Diagnosis
The three main symptom clusters to be considered are: (a) Social Interaction Deficits of a qualitative and not merely quantitative na-
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ture, (b) impairment in both nonverbal and verbal communication, and (c) restricted repertoire of activities and interests, along with stereotypical body movements. Insofar as some of the behaviors subsumed under each of these three clusters may be also displayed by children who present with other disorders, there has been a continuous attempt to better define and restrict the boundaries of the syndrome (Rutter/Schopler 1987). Existing differentiation efforts are still a subject of controversy. 3.1. Autism vs Mental Retardation A number of authors have stressed the occurrence of autism and retardation in as many as 80 percent of autistic individuals. Kanner’s (194 3) exclusion of the cognitively delayed and neurologically impaired was in fact partly the result of the scant attention being paid at that time to a careful psychological evaluation of the children (cf. Wing 1989). Aside from this consideration, the crucial question for differential diagnosis is whether or not retardation without autism can be easily differentiated from the far more common retardation accompanied by autism. With the DSM III-R criteria now available, and a better appreciation of the regular and the associated characteristics of autism, it seems that this separation is not difficult for an experienced clinician. (a) With respect to socioaffective ability, one of the key differentiating features is that the social interaction deficits autistic children present are more severe than the corresponding cognitive deficits. This is not true of retardation where the social age of the child is consistent with his/her cognitive ability. Furthermore, the lack of interest in people, inability to appreciate the emotional state of others and obliviousness are absent from the behavior repertoire of mentally retarded children. (b) The qualitative deficit in language and communication so characteristic of autism, along with the severe deficits in the social use of language, are also not displayed by retarded children, and (c) the stereotypical and at times bizarre behavior of the autistic children, including insistence on the maintenance of sameness and sensory and perceptual peculiarities so typical of autism, are minimally present in the retarded-only children. In sum, none of the three main symptom clusters used to identify and define the autistic syndrome are evident in the retarded or, if present, they are much less frequently displayed by them. (d) In addition to
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the above distinctions, autistic children display an uneven profile of cognitive abilities and deficits that is distinct from the even profiles displayed by nonautistic retarded children. Strongest performance in the autistic is for visuospatial and concrete tasks, while weakest for abstractions or sequencing tasks (DeMyer/Hingtgen/Jackson 1981). 3.2. Autism vs Childhood Onset Schizophrenia Since Kolvin’s (1971) early work on the differentiation of the infancy onset versus later onset psychosis of childhood, very little systematic work has been carried out on this particular topic. Yet many writers have agreed, using Kolvin’s work, that the two conditions are distinct (e. g. Rutter/Schopler 1987). It is important to point out that the incidence of schizophrenia appearing in childhood is extremely low. In a statewide epidemiological study in North Dakota, Burd/Kerbeshian (1987) reported an incidence of .19 in 10,000, a rate much lower than that of 4 per 10,000 or even 13.9 per 10,000 for Autistic Disorder. Despite the low incidence, it is important to keep in mind the key distinguishing features between Autistic Disorder and Childhood Schizophrenia. Schizophrenia with onset in childhood does not appear in infancy but in early or middle childhood. Grossly bizarre and disturbed behavior, language and thought disturbance in the form of delusions and hallucinations characterize its appearance. The same criteria employed for diagnosing adulthood onset schizophrenia are used (DSM III-R). In addition, there is a family history of schizophrenia in the backgrounds of such children, the course of their disorder is variable, following remissions and relapses, and they respond to psychotropic medication. 3.3. Autism vs Severe Developmental Language Disorder — Dysphasia Dysphasia shares with autism a major communication deficit which can be receptive or expressive and is most frequently mixed. However, a number of systematic studies have shown that, compared to autism, dysphasia is a less severe and qualitatively different disorder. Dysphasic children can rely on nonverbal communication for expression. Additionally, their social delays, although present, are not as central to their difficulties. Dysphasic youngsters are quite keen on social interaction, are alert to other children’s
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activities and display considerable frustration when unable to use speech effectively. Although socially delayed, they do not display the ‚obliviousness’ and ‚aloneness’ of the autistic child who is particularly indifferent to the peer group. Dysphasic children as well are less likely to employ pronoun reversals such as you for I and to use neologisms and metaphorical language. Finally, more likely than not, these language impaired children are of normal nonverbal intelligence. 3.4. Autistic-like Disorders in Individuals of Normal Intelligence Although Asperger’s (194 4 ) publication of ‚autistic psychopathy’ has been almost contemporaneous to Kanner’s (194 3), only recently has there been interest in describing the characteristics of Asperger’s syndrome children. For many workers in the field Asperger’s syndrome is not really different from the AD expressed in high functioning individuals or PDD (Schopler 1985; Wing 1981). Asperger attributed the characteristics of these higher functioning people to a disturbance in personality or a ‚schizoid personality disorder’. He stressed their increased adaptation with the passing of time, giving an optimistic picture of outcome. As Frith (1989) also points out, Asperger believed that autistic individuals had intelligence of a distinct flavor, opposite to conventional learning and worldly wisdom. Such intelligence he thought might be best represented by the popular view of the ‚mad professor’. More recently, some workers in the field have argued in favor of distinguishing Asperger’s syndrome from PDD or high functioning autism on the basis of deficits in socialization and communication that are milder than those presented by high functioning autistic individuals. As restated by Gillberg (1985) and originally stated by Asperger (194 4 ), the diagnostic features for Asperger’s are: (a) inability to relate normally to others, with social isolation and peculiarities of gaze and social naiveté, (b) pedantic and perseverative speech, (c) deviant nonverbal communication, including reduced facial expression, monotonous intonation and limited or inappropriate gestures, (d) repetitive activities and strong attachments to possessions, and (e) clumsy gross motor movements and poor coordination. Of course why such individuals may not be seen as simply representing the mildest form of the high functioning autism continuum is unclear. For the pres-
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ent no convincing evidence exists that would show qualitative and not merely differences in degree between the two conditions (Schopler 1985). 3.5. Later Onset Autism This issue is only partly resolved. DeLong/ Beau/Brown (1981) have reported three cases of autism following viral infection which occurred well after the third year of life. In one instance the child suffered a herpes simplex infection while in the other two the cause was unknown. There were concomitant EEG and CAT scan findings. The psychophysiological and structural changes apparently dissipated a few months later along with a full psychological recovery from symptoms in two of the three cases. Insofar as these individuals presented a clinical picture of AD after the first 30 months of life, which could be either reversible or continue for a longer period, one wonders how to classify such conditions. Thus far only these few cases have been reported but more may be reported in the future, hence this issue remains unresolved, albeit tantalizing. Deterioration after a period of apparently normal functioning is not uncommon in autism. Roughly 50% of cases assessed in our clinic have presented this clinical picture. However, it is usually between the first and second year of life that this phenomenon appears to occur. Research on this important issue is almost non-existent. 3.6. Rett Syndrome Of greater relevance particularly recently are cases of specific degeneration with a characteristic clinical course in female children who are concurrently or initially diagnosed as autistic. Rett (1966) was the first to describe this syndrome. More recently specific criteria for diagnosis have been published by the Rett syndrome criteria work group (Gillberg 1989). To be diagnosed as Rett’s a child has to mainly show: (a) a normal head circumference at birth and deceleration of head growth between 5 months and 4 years; (b) stereotypic hand movements such as hand wringing/squeezing, mouthing and washing, rubbing automatisms, after loss of purposeful hand skills; (c) appearance of gait apraxia and truncal apraxia/ataxia between 1—4 years of age; (d) an apparently normal prenatal and perinatal period and (e) a tentative diagnosis of Rett syndrome until 2—5 years of age. Supportive criteria include breathing
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dysfunction, EEG abnormalities, seizures, spasticity, growth retardation and scoliosis. Needless to say that as Gillberg (1989) has also shown, not all children meet these criteria. Furthermore, all four cases he reported concurrently with Rett’s syndrome meet criteria for AD. In our own series all 5 children who subsequently showed some of these symptoms and were diagnosed as Rett’s had previously been diagnosed as autistic. The degeneration showed by these children is not ongoing but is rather episodic. Although some writers describe Rett’s as a distinct nostologic entity not to be confused with autism, it is still far from clear if in fact this is the case. Although both AD and Rett syndrome are thought to be due to neurological abnormality, it is unclear whether it is the same abnormality that causes two different variants in phenomenology or whether the two conditions have distinct, or distinct but overlapping underlying neuropathologies (see Gillberg 1989). 3.7. Fragile X Condition Another disorder, that has shown a comparable unclear overlapping phenomenology with AD is Fragile X condition which was first identified by Brown/Jenkins/Friedman et al. (1982), and appears mainly in males. Fragile X individuals are also likely to be cognitively low functioning and male. Many meet the clinical criteria for AD. Gillberg (1983) reported a case of triplets, all showing classic autism, moderate retardation and the Fragile X abnormality. A study by Goldfine and his team (Goldfine/McPherson/Adair et al. 1985) yielded negative results. More recently Hagerman (1989) has argued that Fragile X is the single most prevalent cause of autism in children with documented organic etiology. In view of the fact that as many as 25% of cases of autism have documented organicity (Hagerman 1989) this is a high percentage indeed. With recent improvements in genetic research and DNA technology more autistic individuals who are also Fragile X positive and show retardation will be identified. Hagerman (1989), in reviewing existing evidence, argues that in addition to such physical features as prominent ears, a long face, hyperextensible finger joints, flat feet and macro-orchidism, Fragile X individuals present with a characteristic and unique clinical picture of PDD or autism. Although they meet DSM III-R criteria they tend to show a greater degree of social avoidance with strangers than IQ-
matched non Fragile autistic children. As well, they show an avoidance of social gaze, become easily anxious and such anxiety may escalate into aggressive behavior and episodic violent outbursts, particularly in the adult males. In the area of language, greater jargon, perseveration, echolalia and talking to themselves is displayed by Fragile X males with or without autism.
4.
Etiology of Autistic Disorder and PDD
4.1. Environmental Historically, when Kanner (194 3) first described autism, the prevalent theoretical climate in Child Psychiatry was psychoanalytic. It was therefore understandable that a search for causation would naturally lead towards prevailing assumptions on etiology. In fact, Kanner expressed considerable ambivalence as to where responsibility for autism was to be attributed. He originally felt, on the basis of his highly select sample which consisted of professional or managerial parents, that autistic children were biologically intact. However, they were born into families with fairly rigid, obsessional, dignified and serious dispositions who were not warm, supportive and accepting of their children. Particularly blameworthy for Kanner were the mothers. Coleman/Gillberg (1985) comment on his ambivalence, however, since before his publication on autism, Kanner (194 1) published a book titled In Defence of Mothers in which he sought to absolve them of guilt in relation to their autistic children. An environmental view was also extensively argued by Bettleheim (1967) who in the Empty Fortress claimed that autism was the result of inappropriate mothering. This same view was espoused by a number of other writers. An account of the reasons why the environmental view had so many adherents has been provided by Schopler (1970). He discussed evidence on the social psychology of prejudice and scapegoating which results from ignorance and helplessness and brought it to bear on this issue. It was not until Rimland (1964 ), a parent and professional himself, published his book on a possible Neuronal Theory of Autism that systematic attempts were made to test the environmental view of causation. A number of studies were carried out in which the cognitive, personality, social and communication patterns of
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parents of autistic children were compared to those of normal, dysphoric and other populations. The bulk of the results thus far has failed to support the view that there are systematic differences in the parents of autistic versus those of normal children (Lennox/Callias/Rutter 1977). The findings have not shown them to be noncaring, to lack warmth or to be deviant. Rutter (1978) in fact also remarks that it is rather interesting that the siblings of autistic children should be indistinguishable from other normal children. Had the parents been deviant, it would be difficult to explain how they would be differentially psychonoxious to one but not to the rest of the children. Furthermore, we know that severe social deviation and psychological and physical abuse frequently result in emotional problems in children but that they do not result in autism. In summary, the environmental theories, espoused over the years by a number of writers have failed to receive support. Parents of autistic children are indiscriminable from parents of normals (DeMyer 1979). In fact, in view of the extreme levels of stress many of these parents are subjected to, particularly the parents of the hyperirritable autistic children, it is remarkable how well they function (Konstantareas/Homatidis 1989). Although many of the mothers show reactive depression (DeMyer 1979), they are certainly not otherwise psychiatrically involved. Thus any adverse effects the parents may display appear to be the result rather than the cause of their child’s difficulties. 4.2. Biological There is an extensive body of evidence which clearly supports a biologic view of causation in Infantile Autism. These studies fall into a number of distinct categories, including genetics, pre-, peri- and neonatal complications, EEG, PEG and CAT scan findings, neuropathological and biochemical findings, and the coexistence of autism with a number of other disease entities. Only a brief review of this work is possible here. 4.2.1. Genetics A number of twin studies have been carried out in Britain (Folstein/Rutter 1977), Scandinavia (Gillberg 1983, 1984 ) and the U. S. (Ritvo/Spence/Freeman et al. 1985) in which at least one of the twins was autistic. All studies have been plagued by small numbers since autism is a rare disorder and sex-
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matched twins are difficult to find. Results of the British study (Folstein/Rutter 1977) suggested that autism may require an inheritable cognitive deficit but it could also occur as a result of brain damage by itself. In the Scandinavian study, Gillberg (1983) reported preliminary findings in which high concordance rates were found for monozygotic (MZ) twin pairs and much lower for dizygotic (DZ) twin pairs. Also he found 100% concordance rates in the MZ twins for cognitive deficits of any kind, including retardation, severe speech and language disorders, learning disabilities or autism, compared to 21% for sex-matched DZ pairs. Finally, in the U. S. samples, Ritvo et al. (1985) found 96% concordance for MZ twin pairs and 24 % for DZ pairs. However, his research methodology, involving self-selection, is questionable. Results also show an increased risk rate from 50 to 100% for siblings, suggesting that 2—5% of the siblings of autistic children may themselves be autistic. Finally, there are data suggesting sex differences in the familial transmission of autism. Not only are males more likely to be affected at a ratio of 3 or 4 to 1, but autistic females once affected are more likely to display a more severe general impairment (Konstantareas/Homatidis/ Busch 1989). In conclusion, there is little doubt that at least some cases of autism are genetically caused, although there is a need for more specific evidence as to the transmission pattern or patterns involved. 4.2.2. Preconception, Prenatal, and Neonatal Complications Recently, information has become available suggesting that a greater proportion of parents of autistic, compared to parents of retarded children, have been exposed to chemicals or are professional chemists (Deykin/ MacMahon 1980; Felicetti 1981). An increased incidence of hypothyroidism in the mothers or fathers of autistic children compared to parents of normal controls has also been reported (Coleman/Rimland 1976). Prenatally, viral infections feature prominently, particularly rubella during the first trimester of pregnancy (Chess 1977). But autism related to maternal toxoplasmosis, syphilis, cytomegalovirus, varicella and the mumps and chickenpox viruses has also been reported (Coleman/Gillberg 1985). Mid trimester bleeding is another prenatal complication which is more likely to be associated with the birth of
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an autistic child rather than his/her sibling (Torrey/Hersh/McCabe 1975). As I indicated earlier, prenatal complications in interaction with genetics has been suggested to be associated with autism (Folstein/Rutter 1977). Perinatal complications such as emergency Caesarean section, forceps delivery, prolonged or precipitous labour, cord problems and excess of maternal weight gain are more likely to be present in the births of autistic children than those of their siblings (Deykin/ MacMahon 1980). Of neonatal factors, DeMyer (1979) has estimated that first year illness, followed by behavioral change in the child, was present in 15% of her sample of 33 autistic children, while second year illness accounted for 18% and third year illness for 6% of the cases. 4.2.3. Electrophysiological and Brain Imaging Abnormalities In general, longer brainstem transmission times and abnormal patterns were reported for subgroups of autistic children. A higher proportion of autistic children with abnormal tracings, 50% of them, were found by Tanguay/Edwards/Buchwald et al. (1982). The findings have been interpreted as suggesting that brainstem dysfunction may lead to distortion in auditory input at higher levels, which may account for the autistic child’s cognitive and language deficits. Alternatively, such abnormalities may be incidental to a disease process affecting many parts of the brain, along with the brainstem. Structural brain damage in autism has been examined first through pneumoencephalograms (PEG). Enlargement of the left ventricular system, and especially the left temporal horns, was found by Hauser/DeLong/ Rosman (1975) in 13 of 18 cases with autism. Computerized axial tomography (CAT) scans carried out by Hier/Lemay/Rosenberger (1979) in 16 autistic patients revealed that, although they did not present with localized or diffuse brain injury, they showed a reversal of the left-right brain asymmetry in the parietal occipital region. This was shown by 57% of the autistic patients and by only 25% of other neurological patients. Since some nonautistic children also showed reverse asymmetry, the investigators considered this reversal as a risk factor for autism. Other more recent studies, relying on CAT scans, have yielded negative findings (Tsai/Jacoby/ Stewart 1983). Contradictory results have also been reported for enlargement of the
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lateral and third ventricle. Rumsey/Duara/ Grady et al. (1985) also found substantially elevated utilization of glucose throughout many parts of the brain of 10 autistic adults compared to controls. Thus far, however, no dramatic insights have been gained from the brain imaging research in autism, despite early enthusiasm. Future studies may prove more enlightening. 4.2.4. Neuropathological Research Findings Autopsy studies have been many but poorly controlled and based on incomplete clinical histories. A recent study examined the cortex of four individuals with definite clinical features of autism throughout their lives (Williams/Hauser/Purpura et al. 1980). Although the results from two of the patients did show some abnormalities, these were subtle and limited to dendritic calibre and spine density. The other two patients had essentially no abnormalities, despite many classic clinical autistic features while they were alive. As well, a very detailed autopsy of a 29-year-old man who met criteria for autism and also suffered seizures at 21 years of age, showed lesions in the forebrain and the cerebellum (Bauman/ Kemper 1985). The contradictory results where some autopsies of autistic individuals show brain abnormalities and others do not may be explained by means of the etiological heterogeneity of the syndrome. It is also possible that in some cases of autism brain structure is relatively unremarkable but brain biochemistry is abnormal (Konstantareas 1986). 4.2.5. Biochemical Findings High serotonin levels have been reported for autistic individuals while the reverse was found for others. High serotonin is not unique to autism and has been reported for many other mental retardation syndromes. Studies of platelet monoamine oxidase have yielded essentially negative results thus far, although elevations have been reported in isolated cases (Coleman/Gillberg 1985). A number of other studies have been carried out over the last 15 years including examination of hormones, immune reactions, trace elements, etc. Thus far, no specific biochemical markers have been found. So, although subgroups of children sharing specific biochemical abnormalities may exist, we have not as yet been able to isolate them (Coleman/ Gillberg 1985).
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4.2.6. Autism among Subgroups with Other Diseases Thus far, autism has been demonstrated to occur in some genetic disorders. Some of the possible or definite linkages are with tuberous sclerosis, neurofibromatosis (Gillberg/Forsell 1984 ) and Fragile X or Martin Bell syndrome. In addition, an extra X chromosome is often associated with speech and language difficulties, if not with the entire syndrome of autism (Coleman/Gillberg 1985). Among infectious diseases, exposure of mother to the rubella virus, the virus of mumps, cytomegalovirus, and oral herpes virus (HSV-1) and the genital herpes virus (HSV-2) has been found to be related to autism in the offspring. It is difficult to be certain that autism was directly caused by the given virus in any individual case. Yet for rubella the relationship is more firmly established (Chess 1977). Thus infectious agents acting prematurely or after birth may be at least partly related to the development of autism. Of metabolic diseases, PKU appears to result in a behavior syndrome comparable to autism, if treatment is not instituted in early life. With present screening cutoff levels of 4 mg %, approximately one third of PKU patients may be missed. Of other aminoacidopathies, histidinemia has been reported to coexist with autistic symptoms. Purine autism, with increased secretion of uric acid has also been reported. Autism has also been found in cases of hyperlacticemia or lactic acidosis, with increases in the rate of lactate production relative to rate of lactate utilization (Coleman/Gillberg 1985). Of structural disease entities, hydrocephalus has been frequently associated with autism. Malignant tumours have not been reported but occasionally lesions such as porencephaly and other abnormalities are seen in the CAT scans of autistic patients (Gillberg/Svendsen 1983). As discussed earlier, Rett’s syndrome can also co-exist with autism. Of other degenerative diseases, neurocutaneous disorders such as tuberous sclerosis and neorofibromatosis have also been associated with autism in a number of cases (Lotter 1974; Wing 1975).
5.
Language and Communication Deficits in Autism
That language and communication deficits
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are central to AD is evident in Kanner’s (194 3) first description. Pronominal reversal, i. e., substitution of you for I, delay in speech acquisition, noncommunicative use of speech when speech is available, idiosyncratic and inappropriate or perseverative utterances were among the language characteristics attributed to most of the original 11 cases he described. With the emergence of systematic research in the mid-sixties, particularly work on speech training by Lovaas and his collaborators at UCLA (Lovaas/Berberich/Perloff/ Schaeffer 1966), the centrality of language impairment was emphasized. Since then, an impressive number of research papers and reviews have appeared on this topic. Furthermore, with advances in psycholinguistics and in cognate fields, the issue broadened to encompass both theoretical positions regarding the nature and meaning of language deficits in autism and intervention strategies to remediate them. 5.1. Language Characteristics of Autistic Individuals 5.1.1. Muteness This ranges from total silence to the emission of inarticulate, nonpatterned vocalizations used for vocal play but no recognizable speech. Muteness has also been employed for those vocalizations that are used in a selfstimulatory manner but are devoid of meaning and even for those with minimal functional characteristics. Although rate of muteness reported for autism has varied from 28% to 61% (Fay/Schuler 1980), definition of muteness as well as diagnostic criteria used for the classification of the children and referral practices have varied over the years, hence no conclusive data on it is available. Muteness in the young autistic child has been frequently linked with the suspicion of deafness. This is a very commonly reported phenomenon by parents and one of the first considerations in making a referral to a professional. Hyposensitivity to sound may alternate in the same child with hypersensitivity, particularly under high motivation conditions. In fact, diagnostic checklists such as the Childhood Autism Rating Scale (Schopler/Reichler/DeVellis/Daly 1980) consider this as one of the symptoms of the syndrome. There is little doubt that very rarely is an autistic child concurrently deaf and that the hyposensitivity is functional rather than organic.
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5.1.2. Babbling Babbling, which is reflected in vowel-consonant sound combinations, has adult-like intonational patterns and is repetitious, is also either completely absent or it is distorted in autistic children. In our own sample, a large percentage of children have never babbled while most of those who did have displayed either a delayed or an attenuated form of babble. Very few autistic children seem to develop babbling at the same time as normal children do. Research in this area is of necessity hampered by the retrospective nature of the information collected. Thus to quote exact percentages may be misleading at the present time. Needed is systematic research on normal timing and extent of babbling to provide a basis for the deviant characteristics of the babbling of autistic children. As well, we need to examine more systematically the relationship of the characteristics of babble of those AD children who do produce it and their other presenting characteristics. This will help us determine the relationship of this feature of normal language to the communication and other deficits of autistic children. Some beginnings have already been made in this direction. Ricks (1975) reported that parents in his sample recalled no vocalization in their autistic children during their first year of life. But, between 3 and 5 years of age, some autistic children in his sample did babble. However, the babble was monotonous. Moreover, in contrast to normal babies and Down syndrome children of 3 to 6 years, who ignored their own babbling, the autistics did not ignore it when played back to them. When they responded to the taped babble, however, it was to repeat only their own babbling in a sameness preserving fashion, but not the babbling of other children. These findings suggested to the authors that the babbling peculiarities of autistic children are in keeping with their overall processing and adaptational pattern rather than having unique features of its own. 5.1.3. Echolalia In contrast to babbling, some of which usually occurs before a formal assessment is undertaken, echolalia lends itself to research much more readily. In fact, it is the one key feature best recalled by students because of its striking characteristics. Additionally, it has served well in the psychoanalytic explanation
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of AD over the years because, like Narcissus in the Greek mythology, it reflects the egocentric style and distancing autistic children were thought to choose in an effort to actively separate themselves from others. Echolalia is defined as the meaningless repetition of a word, phrase or sentence, without regard for the communication needs of the interlocutor. It can be immediate or delayed (Kanner 194 3) and mitigated (modified) or unmitigated (Fay/Schuler 1980). Kanner (194 3, 222) described at length the verbal echolalic behavior of 9 of his 11 autistic patients. He appeared to believe that echolalia was not an isolated phenomenon but rather part of the obsessional, perseverative and concrete nature of the disorder. Although some echolalic utterances appear to be routine, mechanical renditions of other people’s speech, most seem to be related to events that are normally affect laden and of significance to the child and/or to his social context. This is an element of echolalia not sufficiently examined in the literature. After years of mere description and benign neglect, and with new data provided from a number of academic disciplines, echolalia started to become a subject of scientific interest and left the realm of enigma and fascination. Since the mid — 70’s, its social aspects are being examined and analyzed, much as they have been studied for other forms of language production (see Prizant 1979). Thus, although behavioral approaches have defined echolalic behavior as inappropriate and have targeted it for elimination, functional approaches have analyzed it for its possible ‚communication intent’. Basing their work on the methodology of pragmatic research on normal language development, Prizant/Duchan (1981) studied immediate echolalia with four autistic children. They arrived at four structural categories: (1) noninteractive echolalia with lack of comprehension, (2) interactive echolalia with no comprehension, (3) echolalia produced noninteractively with comprehension, and (4 ) interactive echolalia with evidence of comprehension, the most advanced category. Of greater interest were the results of the delayed echolalia study (Prizant/Rydell 1984 ) which yielded a variety of functional uses, ranging from relatively automatic, non-intentional utterances to fully communicative and functional. Some of the functions described from least to most communicative were: turn-taking and verbal completion, rehearsal, self-directive, non-interactive labelling, protest, request, interactive la-
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belling, calling, providing information, directive and affirmation (Schuler/Prizant 1985). In analyzing the characteristics of autistic language, these authors have argued that autistic children use a gestalt processing style which contrasts sharply with the more advanced analytic mode necessary for normal language acquisition. In sum, recent developments have provided considerable information on the characteristics and possible functions of echolalia and have linked it to a more general model of disordered information processing in autism. A comparable position has been taken by other cognitive writers in the field (Frith 1989). However, we are still far from understanding why and how such a style has evolved at all and how it precisely relates to other aspects of communication, cognition and social interaction in these children. 5.1.4. Pronominal Reversal and Metaphorical Language Use Although much as with echolalia, pronominal reversal was thought to be the result of the socioaffective impairment and identity problems in autistic children, this is no longer believed to be the case. Of course, it is quite startling to an observer to hear a child address himself as a you or omit the first person pronoun I in using a mand such as asking for juice or a cookie. In our summer camp, for example, Marlene, a 9-year-old girl, would frequently approach us saying “want juice”, omitting the relevant pronoun. On other occasions she would fearfully demand, “You go home now? Come bus, come bus?” The context had allowed us to interpret what she meant to tell us: I want juice and I don’t want the bus to take me home. To the uninitiated, however, the meanings might have been different. Thus, much as with simple, unprocessed S—R connections, pronoun reversal may be interpreted to mean a ‚gestalt’ style of processing or automatic and mechanical repetition rather than be thought as vested with more complex personal meaning. However, this is not to indicate that this style is yet clearly understood. It is only at one level of explanation that one can state that the children’s gestalt processing is responsible for this phenomenon. A number of additional pieces of information need to be explained. First, it is unclear why the child can and does acquire the proper name of the individual whom he addresses as you but cannot say you (see also Frith 1989, 127). Second, it is unclear
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why or when some children completely omit the pronouns while others, or the same child at different times, use a pronoun reversal pattern. Third, we need to know why and under what circumstances do the children use the pronouns correctly and under which they do not. Fourth, we need to examine the interrelationship between echolalia, promonimal reversal and metaphorical language use. Finally, we need to know other important correlates of these three phenomena, such as their relationship to other aspects of the receptive and expressive language of that child. By acquiring additional information, we may be in a better position to arrive at effective remediation. 5.1.5. Phonology, Syntax, Morphology and Prosody For the approximately 50% of autistic individuals who speak, the obvious next question is the nature of their phonologic and syntactic competence. Bartolucci/Pierce/Streiner/Eppel (1976), compared the picture-naming ability of autistic mentally retarded and normal children, appropriately matched on non-verbal M. A. Unexpectedly perhaps, they found the same distribution of error patterns and the same frequency distribution of various phonemes for all three groups. Yet the types of rules the autistic children employed in their constructions may not be as advanced (Cantwell/Baker/Rutter 1978). Tager-Flusberg (1981) also found that autistic children did follow syntactic rules in their comprehension of language. In our own work, we have frequently found a number of autistic children to use syncopated, foreshortened phrases in an effort to terminate the communication as quickly as possible. We have also found them to omit functors (pronouns, prepositions, adverbs, etc.) and have systematically demonstrated how to remedy this through the superimposition of signs on the relevant functors. By progressively fading out the signed functor, once the word is included in the sentence, we were able to assist the children in acquiring the missing word (Konstantareas 1984). Turning to prosodic development, there is little doubt that prosody or ‚speech melody’ is disturbed in the speech productions of autistic individuals. This was identified quite early (Kanner 194 3). Furthermore, the prosodic deficits are apparently in evidence even after considerable improvement in speech production.
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Prosody studies in autism are few, although interest in the topic began early (Goldfarb/ Braunstein/Lorge 1956). In a more recent study by Paccia/Curcio (1982), prosody in echolalic speech was examined in the context of the hypothesis that, if the prosodic contours of an echo changed, that would reflect some degree of comprehension. Results were interpreted to indicate that echolalia did include prosodic restructuring. They also argued that those echolalic children who do not manipulate the prosodic features of their speech may be more impaired linguistically than those who do. More recent work summarized by Baltaxe/ Simmons (1985) suggests that those autistic children who speak may not be prosodically as globally impaired as the earlier studies suggested. Deficits may depend on which aspect of prosody is considered. They believe that most verbal autistic individuals have both delays and abnormalities in mainly their fundamental frequency range and the linguistic information they express. In some instances, they believe the fundamental range may be too narrow or too wide, yet the stress and intonation contour may be appropriate or, conversely, the fundamental frequency range may be close to normal but intonation and stress may be inaccurate. A number of dysphasic children apparently share with the autistic their prosodic abnormalities, including a narrowed frequency range. However, overall the dysphasics in their studies tended to be less extensively impaired in their prosody and to be closer to the normal children. In summary, studies in prosodic development, particularly of autistic children, are not many. We know that normal children reach some prosodic stability by their fourth year, although prosodic maturity is not reached until puberty. The close interrelationships between prosody and other aspects of the autistic child’s language have begun to be clarified. Yet, as Baltaxe/Simmons (1985) also caution, we may find that impairment or delay in prosody and delays in other areas of linguistic functioning may occur independently in the same individual, much as with the adult aphasias. If cross influences between linguistic and prosodic elements do exist, the direction of causation also remains to be specified. Baltaxe/Simmons (1985) speculate that the constructive use of echolalia in autistic children who develop more adequate language may be due to their inability to use prosody in speech reception and expression.
Being unable to break down the speech flow into units, may compel the autistic individual to use larger, unprocessed chunks in an attempt to communicate with others. In that sense, they claim, echolalia may be comparable to the early prosodic ‚frames’, ‚matrices’ and ‚envelopes’ normal children employ to communicate, as discussed by Bruner (1975), among others.
6.
Intervention Strategies for Communication
6.1. The Speech Training Approach Early attempts to treat autistic children were predicated on the psychoanalytic model. No special emphasis was placed on speech and language remediation. It was not until the 1960s with Ferster (1961), that learning difficulties were perceived to be crucial to the autistic child’s deficits. Ferster (1961) stressed the non-existence of generalized reinforcers in these children, e. g., praise, approval and warm bodily contact, despite the children’s obvious responsiveness to primary reinforcers such as food, drink, etc. Thus the learning therapists emphasized the need to build social skills, and particularly language, from scratch. The first systematic study using operant principles to build speech or to modify the echolalic speech of autistic children was published by Lovaas/Berberich/Perloff/Shaeffer (1966). The central tenet of this position, further elaborated and modified over the years, was that speech, because of its obvious social and symbolic aspects, should be given priority in treatment attempts with this population. Elsewhere (Konstantareas 1981), the behaviorist position to speech training is presented in some detail. To summarize, a two-stage sequence was followed with the mute children. In the first, speech sounds, syllables and words were shaped through imitation, discrimination, and reinforcement out of context. Thus the child could acquire, through chaining, words such as baba, mama, data, etc. Additional words such as juice, cookie, giv e and so on, were introduced for imitation. Once these spoken but context-free utterances could be emitted by the child, the second stage, involving speech in context, was introduced. Here words were reinforced if emitted in response to the relevant object or in the context of an activity. Progressively phrases and sentences correctly related to the context
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were introduced and, when correct, were reinforced. The systematic, well-documented and orderly application of the principles has made them very appealing to educators and therapists over the years. Thus the operant paradigm has established its credibility in a field that tended to be predominated by descriptive accounts or clinical case presentations of general efforts to help the autistic child. The quantitative and evaluative stance of the behaviorists compelled them to re-evaluate and modify their earlier expectations that, once speech was acquired, the autistic child would become ‚normal’. In an elegantly reported follow-up, Lovaas/Koegel/Simmons/ Long (1973) acknowledged some of the limitations of their procedures, particularly the fact that maintenance of hard-won gains required continuation of intervention. Stimulus and response generalization and maintenance were not automatic, not only for the behaviorist technology, but for any therapeutic intervention. As well, they implied, but did not outrightly state, that the child’s presenting characteristics may be crucial for his ability to acquire speech. But these were not the only difficulties. Some workers in the field complained of the wooded, flat and robot-like quality of the speech acquired through operant training. Others were also concerned about the lack of spontaneity evident in the speech of this population (Bonvillian/Nelson 1978), while still others were unable to help autistic children produce speech at all, despite extensive efforts. Hingtgen/Churchill (1969), for example, reported that after 6 hours per day five weeks, three of their four autistic children had acquired 60, 25 and 16 words each, while a fourth child could not acquire anything but sounds. A mixed outcome was also obtained by Mack/Webster/Goksen (1980) in the Clarke Institute in a follow-up of 54 autistic or autistic-like children exposed to a program akin to that developed by Lovaas/Berberich/Perloff/Schaefer (1966). Although many children acquired spoken language, others could not. This might have been surprising then but, as we shall see, it is not at all surprising now if one takes into account the child’s cognitive and other deficits which may preclude speech acquisition. Speech training strategies based on the behavioral paradigm have been increasingly directed at the very young children. The rationale behind this development, as described by Lovaas (1987), is twofold: (a) That treatment
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gains with the older children originally employed “have been specific to the particular environment in which they were treated, substantial relapse has been observed at followup, and no client has been reported as recovered” (Lovaas 1987, 3). (b) With children younger than 4 years of age, treatment for most of their waking hours for many years, and including all significant persons in all significant environments, would result in extensive gain maintenance. In addition, the possibility of successful mainstreaming into the primary school would be higher for the younger children. A significant assumption made was that very young autistic children are less likely to discriminate between environments and therefore more likely to generalize and maintain their treatment gains. Space precludes a detailed account of experimental design, assessment and treatment procedures and outcome of this intensive intervention (cf. Lovaas 1987; Lovaas/Smith 1988). In brief, three groups of children participated: (a) An experimental, intensive behavioral group exposed on average for 4 0 hours per week to communication and behavior training for 2 or more years. (b) Control group 1, consisting of children with comparable characteristics to the experimental but exposed to training for less than 10 hours per week for a comparable length of time. This group was used to examine spontaneous recovery. (c) Control group 2, not exposed to specific intervention but comparable in characteristics to the other two, was used to guard against the possibility that the experimental group was particularly selected to be higher functioning or different from the usual autistic population. No random assignment was employed. Results revealed that 4 7% of the experimental treatment group achieved normal intellectual and educational functioning, with IQs in the normal range and successful performance in first grade in public schools. Another 4 0% were mildly retarded and assigned to special classes and 10% were profoundly retarded and assigned to classes for autistic and retarded children. Children in control group 1, by contrast, fared much worse. Only 2% of them achieved normal functioning, 4 5% were mildly retarded and 53% were severely retarded and placed in classes for autistic and retarded children. Control group 2 was not significantly different from Control group 1. Lovaas (1987) interpreted these data as providing strong support in favor of early intensive behavioral
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intervention. Furthermore, he argued that, for all intents and purposes, teachers could not distinguish the experimental group subjects from normal children, although he conceded that on “closer psychological assessment, particularly as these children grow older, certain deficits may remain ...” (Lovaas 1987, 8). In a commentary and critique of this report and the success claims for the intensive behavioral approach, Schopler/ Short/Mesibov (1989) argued that it is impossible to determine the effects of the intervention Lovaas (1987) reported because of: (a) inappropriate choice of outcome measures, (b) subject selection bias, and (c) inadequate control groups. 6.1.1. Critique of Speech Training The behavioral approach to speech training has been quite productive and effective, and continues to enjoy considerable popularity. It has provided a technology for assistance with speech shaping and word and phrase acquisition. However, it has not been without its criticism. The following have been the main criticisms that have been levelled against it: (1) It has tended to be mechanistic and simplistic in that it has concentrated on speech only, ignoring by and large the necessity for helping the children achieve spontaneous, functional speech (Goetz/Schuler/Sailor 1979; Konstantareas 1986). (2) Perhaps because of its emphasis on repetition and drilling, it results in stilted and flat verbal output with poor pitch, intonation and stress and the other prosodic elements of normal speech production which reflect intention. (3) It is attempted, with minor exceptions such as work by Carr and his group who use sign language (Carr 1979), with all dysfunctional children rather than a select group for which it may be more relevant (Konstantareas 1981). This may be responsible for the inability of some children to profit from it despite repeated efforts (cf. Creedon 1973; Hingtgen/ Churchill 1969). (4 ) Perhaps because of ignoring new knowledge in the fields of developmental psychology, psycholinguistics and communication theory, it has not taken into account the crucial relevance, among other factors, of cognitive growth, information processing, socio-affective development and communication acquisition in normal children. Such information would have allowed for the development of a richer and more flexible approach to language intervention.
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6.2. Simultaneous Communication Training Partly because of the limitations of speech training with particularly the mute and the lower functioning subgroup of autistic children and partly as a result of its effectiveness once attempted with those subgroups but also with the verbal and higher functioning, speech and sign language training (simultaneous communication) has become one of the main alternatives to speech only training. It was first attempted by Creedon (1973) and by Webster/McPherson/Sloman et al. (1973) but shortly thereafter its use acquired something of a momentum, which it continues to enjoy until now. Elsewhere we reported the rationale for its use (Konstantareas 1986). In brief, among the reasons that have been considered to be important for its success have been: (1) The information processing characteristics of autistic children. Autistic children have been shown to be impaired primarily in auditory sequential processing (Hermelin/O’Connor 1970). Interestingly, in one of our studies we found the lower functioning subgroup to have suffered a greater number of and more prolonged ear infections than matched for CA normal children or functioning autistic children (Konstantareas/Homatidis 1987). Autistic children are also generally better able to code visually, spatially and kinesthetically and have most of their difficulties in encoding temporal-sequential input. Processing speech, which requires decoding and recoding, may tax their capacities to such an extent that they may not deal with it at all. Further evidence for the auditory peculiarities of these children has been provided by Condon (1975) who has reported deficits in ‚self-synchrony’ and ‚interactional synchrony’ in autistic children. Self-synchrony refers to ‚entrainment’ between one’s vocalizations or speech and his/ her body movements and interactional synchrony to the precise correspondence between the listener’s movements and the articulatory structure of the speaker’s utterances. Upon microkinesic analysis, Condon (1975) found delays of up to a full second, i. e., twenty-four frames of moving film. Furthermore, for many children the body movement repeated itself in a reverberatory fashion two or more times, to a single auditory signal, a phenomenon Condon calls ‚multiple entrainment’. Attempts to replicate the ‚Condon effect’ have met with only partial success. If replicated, these findings may provide important clues to the apparently disturbed auditory universe
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of these children as reported by themselves (Volkmar/Cohen 1985). (2) Developmental and motivational features of the children also appear relevant to the effectiveness of sign language use with them. Interventions thus far have rarely taken into account the child’s cognitive ability. Speech training techniques have been employed, for example, regardless of the child’s mental age. Thus an 8-year-old child with a mental age of 11 months may be asked to speak, an activity above his cognitive competence. Although gestures, shared attention, imitation and turntaking may be highly recommended in his case, systematic speech training may be premature. Information on normal child development and the relevance of action and gesture in early communication acquisition (cf. Lock 1978) are of particular relevance in guiding intervention with the very young and/or low functioning children. If spoken language evolves phylogenetically and ontogenetically from gestures, we may need to focus our attention on these forerunners of verbal communication. Following the constructivist approach of Piaget (1963) to normal language acquisition, and regardless of the primacy given to cognition, the correspondences between the two domains are compelling (Ingram 1978). One can therefore hardly afford to ignore the relevance of cognition to intervention with autistic children. Thorough assessment of it through sensorimotor intelligence testing with the younger children and nonverbal intelligence tests, such as the Leiter International Performance Scale, for those above the mental age of 2 years, has been our practice. It is only after we have carefully assessed the children’s various cognitive, communication and social abilities that we can decide on the communication system best suited to any given child (Konstantareas 1990). A comparable view has been expressed by other clinicians (cf. Watson 1985). Aside from cognition, motivational factors are very crucial. What is reinforcing for an autistic child is frequently impossible to decide upon in advance. Also how these children avail themselves of desirable objects is very important to consider. Many autistic individuals satisfy need states by goal-directed movements aimed at the coveted object rather than use conventional linguistic means to obtain it. This goal-directed reaching has, in fact, been considered by us and by others (Schaeffer 1978) to be one of the key factors underlying spontaneity in communication by means of sign language. They frequently touch oth-
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ers as well when unable to obtain an object and to pull or push them toward a desired location. They use their hands to ‚ask’ for help in achieving their goals. This tendency of autistic individuals to be motoric and active, much as younger and immature organisms tend to be, has direct relevance to their ability to employ a system based on hand and motor movement. As well, autistic individuals tend to be impatient with small visual detail, such as the printed word, hence, their reluctance to engage in desk-related behavior. (3) Finally, certain features of sign language render it particularly well-suited to the information processing and special characteristics of this population. For Hewes (1973), protolanguage was likely gestural. Vocalization, originally a mutation present in some individuals, became progressively selected for. The socially shy autistic children may therefore feel more comfortable with the more natural and spontaneous manner sign language affords them to express intent. Signs, being an extension of body movements, may also be easier for them to use since many of them, particularly the younger and lower functioning, do not vocalize spontaneously. The signs for come, go, giv e and want are examples of natural extensions of reaching or approaching others. Another feature of sign language, iconicity, has been shown to be of relevance in early sign acquisition. With normal children, Brown (1977) demonstrated that perceived iconic signs are easier to learn than non-iconic. Such signs which are ‚timebound’, ‚age-bound’, ‚culture-bound’ and ‚experience-bound’ are perceived as similar to their referents. Using ‚translucency’ as a test of iconicity, Bellugi/Klima (1976) found that 50% of the 90 signs shown to their subjects could be seen as having some connection to their references. Translucency refers to the degree to which a subject can discern a relationship between a sign and its referent, after having been presented with both. With autistic children, Konstantareas/Oxman/Webster (1978) were able to demonstrate that iconic signs of the Ontario sign language for the deaf were easier to acquire than were noniconic signs. This was especially the case for verbs and adjectives which tend to have extensive sensorimotor elements associated with them. Another characteristic of sign language relevant to its ease of acquisition by lower functioning and lower speed language processors, such as the autistic children, is the rate of its presentation. Signs were shown to
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be at least twice as long as speech to process by fluent users of both signs and speech (Bellugi/Fischer 1972). A third characteristic is lack of redundancy. Sign language retains content words such as nouns, adjectives and verbs but omits functors such as the copula, articles and prepositions. Because it is an economical, low redundancy language, it may be better suited to the needs of children who have difficulty in processing information. Finally, sign language training has distinct advantages over speech training in terms of it being amenable to direct manipulation. Compared to the tongue, lips, mouth and oral cavity, the inaccessible internal structures on which we rely to produce speech, one can mold the child’s hands into signs. Thus, by virtue of its reliance on accessible parts of the body, sign language seems easier to employ in early training compared to speech. 6.2.1. Implementation Studies Creedon’s (1973) paper on implementation of simultaneous communication training has constituted a basic model for interventions in this area. Since 1973, with a study by Webster et al., our group has embarked upon a series of studies aiming at clarifying intervention issues. Konstantareas/Oxman/Webster (1977) reported on a demonstration project with 6 children who were able to acquire signs over a brief, five-week summer camp period. Konstantareas/Webster/Oxman (1979) provided the outcome of a systematic effort at organizing and carrying out a simultaneous communication program with five children. Intensive and detailed evaluation of changes in social interaction and communication, as well as in a variety of other behaviors, was attempted. Results were quite promising, particularly for communication acquisition, both receptively and expressively. Spontaneous social interaction, however, did not substantially increase as a result of the intervention. However, self-help skills improved and unoccupied behavior decreased. Once the feasibility of application was established, we examined a variety of issues which appeared to require attention. One obvious question was parental concern as to possible reduction of vocalizing and speech as a result of exposure to simultaneous communication. Oxman/Konstantareas/Leibovitz (1979) provided a negative answer to this question. Although children in our experimental group began the program with fewer vocalizations than an untreated control, they
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vocalized more by the program’s end. The issue of whether simultaneous two-modality training (signing and speaking) would be inferior to single modality (signing and mouthing) was also examined (Konstantareas/Leibovitz 1981). Results showed that, on average, the two-modality intervention was superior. Gain maintenance and generalization for simultaneous communication was shown to be quite good, particularly for the higher functioning children who continued to be exposed to simultaneous language training after they left an intensive program (Konstantareas 1987). 6.2.2. Evaluation of Simultaneous Communication Training Since 1973, more than 30 studies have appeared in the literature on this alternative to speech training. Most are either case studies or involve small groups of children. For selective reviews, see Bonvillian/Nelson (1978), Carr (1979), Kiernan (1983) and Konstantareas (1986). The older, mute and minimally vocal autistic children have appeared to be the best candidates for this technique but we have no evidence on best predictors for its success. Some workers in the field have proposed that children with vocal imitation skills are best suited to speech training (Carr 1979). However, a more recent study by Barrera/ Sulzer-Azaroff (1983) found that echolalic autistic children benefited more in acquiring expressive labels from a simultaneous than an oral only training approach. Van Wagenen/ Jensen/Worsham/Petersen (1985) also recommend the use of this approach with verbal children as a result of their own work in this area. Thus, although by default the mute and older children have been traditionally and successfully exposed to simultaneous communication, perhaps as a last resort, this need not be valid. The review of evidence presented earlier as to the goodness of fit between the presenting characteristics and needs of autistic children and the characteristics of this strategy, as well as recent work, suggest that the superimposition of signs on words may be useful with a fair number of this group and indeed other language impaired groups, as we have shown (Konstantareas 1984 ). Furthermore, even blind autistic and mute children can benefit (Konstantareas/Hunter/Sloman 1982). Research is required to examine the relevance of at least the following child characteristics as predictors of effectiveness of the simultaneous communication ap-
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proach: receptive and expressive speech, ability to imitate words and signs, ability to respond to gestures and to words, mental age and IQ and degree of interactive ability. Only by systematically engaging in this effort can we arrive at valid predictors of communication medium, i. e., words only versus words and signs. Some efforts in examining this issue have already been made by us (Konstantareas/Blackman 1978) and by others (Yoder/ Layton 1988) but much more is needed. Aside from type of medium, one may have to consider using both approaches but successively. In our clinical work we have frequently recommended graduating from simultaneous to speech only communication, once word production had increased. We, Konstantareas (1987) and Layton/Stutts (1985) have shown that, regardless of modality of training, high verbal imitators prefer to use speech while low imitators prefer to communicate by sign. Specifically on pragmatic usage, Layton/Stutts (1985) also found that the high verbal imitators outperformed the low imitators on all communicative functions while the low imitators used mostly requests as their sole communicative function. In conclusion, simultaneous communication training appears to be an approach well suited to many autistic children and can lead either to speech or, in those children with poor vocalization ability, to the use of signs to express basic needs. Children who, in the past, would be completely unable to communicate through speech, now have a viable, alternative means of communication, the use of elementary signs. We have found that as many as 50% of children who did not speak prior to simultaneous communication training begin to speak after exposure to this technique. This result has also been reported by others (e. g., Creedon 1973). Furthermore, this approach is not uniquely suited to autistic individuals but has been successfully attempted with retarded children and even children with severe reading disabilities (Blackburn/Bonvillian/Ashby 1984). 6.3. Other Interventions In addition to the two main approaches to training, a variety of techniques have been employed but evidence on their effectiveness is chiefly anecdotal. Pictures of real life objects have been used with very low functioning autistic children or with those unable to shape their hands into even gross approximations to signs. Picture boards have been constructed
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and used well with those autistic children who respond poorly to either speech or simultaneous communication training. The Bliss Symbol System, particularly relevant to the needs of individuals with neuromuscular disorders, has also been attempted with autistic children. In one of the very few studies available on this issue, Hurlbut/Inata/Green (1982) compared the use of Bliss symbols and an iconic picture-drawing system with three cerebral palsied adolescents who had severe physical and mental disabilities and were nonambulatory. No other diagnostic information is provided in the report. Probe data were taken to assess maintenance, stimulus and response generalization, and spontaneous usage of each system. Results revealed that all students required approximately four times as many trials to acquire the Bliss symbols as the corresponding iconic drawings. As well, they retained all drawings while they required retraining in almost all Bliss symbols. This is not surprising in view of the similarities between the representational drawings and their corresponding objects, and the much less obvious similarities between the more abstract Bliss symbols and the objects. In fact, one suspects that one of the reasons for the unavailability of published studies on the use of the Bliss system with autistic individuals may be its limited usefulness with this population. In view of the well-documented difficulties autistic children show in abstracting information and in light of our previous discussion on their processing difficulties, even the higher functioning subgroup may find the system difficult. Furthermore, the higher functioning subgroup is also likely to be verbal. More recently, considerable interest has been expressed in Facilitated Communication. Originally discovered by Crossley and her colleagues in Australia, this technique involves helping individuals with poor verbal abilities to express themselves with the aid of the touch of another person, the facilitator. An alphabet board, a hand-held typewriter or a computer are used. The children type or point to letters aided by the touch of the facilitator who gently holds or touches the individual’s arm at the elbow, wrist or the hand. The facilitator mainly assists the person not by moving his/her hand to the correct letter, but by ensuring that the person does not perseverate in hitting the same key more than once. The main published account of this technique by Biklen (1990) challenges
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existing theoretical views on the limited literacy abilities of particularly the mute and apparently low functioning autistic children. He reports some striking conversations with such low functioning individuals using facilitated communication. Answers to even complex questions pertaining to feeling states and requiring social reasoning capacity were spelled correctly and were logically correct in individuals thought to be cognitively quite limited and nonliteral. There has already been some controversy related to whether the facilitators merely facilitate or actually manipulate and influence the process (Crossley/ McDonald 1980). As well, it was difficult for students to communicate with more than one or two facilitators, especially early on in the process. Furthermore, Biklen (1990) concedes that the method is not a uniform approach to teaching or supporting communication that can be used with each person but depends on the specific attitudinal characteristics of the facilitator, such as a non-patronizing attitude, self-effaciveness, being apologetic for asking simplistic questions, etc. Some of the descriptions provided by Biklen (1990) are suggestive of a population with considerable symbolizing and representational capacities not frequently encountered even in high functioning autistic individuals. In some instances, insofar as no information on diagnosis is provided to us, we cannot judge the relevance of the work to autism. It is at present unclear who may benefit from this approach. As well, it has, of course, not been found that facilitated communication will cure autism, although Crossley apparently believes that considerable improvement after facilitated communication is possible in terms of the behavioral characteristics of children (Biklen 1990). As to the explanation for the apparent success of this new approach, the current hypothesis offered by its proponents is that it overcomes the apraxia many of these minimally verbal or mute individuals suffer from. How this is achieved and whether one can assess in advance who is apraxic, hence will benefit, have not yet been clarified. In some respects, however, the technique resembles sign language with mute individuals since it, too, once it is provided, allows the expression of thoughts and feelings previously blocked due to the unavailability of an expressive capacity. Remarkably, even 6-year-old autistic youngsters can apparently spell out correctly words no one explicitly taught them. They seem to have incidentally acquired them from looking at television programs and commer-
cials. In sum, in addition to speech and simultaneous communication training, the use of real pictures of objects or drawings of objects hold promise with some autistic children. As well, facilitated communication holds considerable promise and may turn out to be one of the most useful means of interacting with minimally verbal autistic children. We require, however, much research into the neurological underpinnings of the facilitated communication process. We also need to examine who of the autistic children, and under what conditions will benefit from any augmentative communication system.
7.
Prognosis of Autistic Disorder
Considerable information on prognosis has been collected, which spans the last forty to fifty years, but much more is needed before we can fully understand the life-long characteristics of the disorder. In general, autism continues well into adulthood, although developmental changes have been documented (Paul 1987). In middle childhood there is already a movement towards tentative, albeit still deviant, social interaction. Level of functioning may determine the degree of involvement. As well, some speech may appear in those previously completely mute as well as improvement in hyperactive behavior, although stereotypical ritualistic and compulsive behavior persist. In adolescence an estimated 10—35% of autistic children undergo regression and some become seizuring with a peak between 11 and 14 years of age. Paul (1987) reports that once regression is present, return to normal functioning may await until the individual reaches his/her late twenties. With increasing age social skills and language may improve somewhat. In addition, there is further improvement to the point that as many as 14 % of autistic individuals no longer meet social deviance criteria for the condition. No recent studies on this issue are available, however. The language characteristics of autistic adults with typical autism may resemble those seen in schizophrenia, with loose associations, preoccupation with particular topics and semantic concreteness (Paul 1987).
8.
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of perceptual limitations in mute autistic children. Archives of General Psychiatry, 21, 68—71. Hurlbut, B. I., Inata, B. A., & Green, J. D. (1982). Nonvocal language acquisition in adolescents with severe physical disabilities: Bliss symbol versus iconic stimulus formats. Journal of Applied Behav ior Analysis, 15, 241—258. Ingram, D. (1978). Sensori-motor intelligence and language development. In A. Lock (Ed.), Action, gesture and symbol: The emergence of language. 261—290. London: Academic Press. Kanner, L. (194 1). In defense of mothers. Springfield, Ill.: Charles C. Thomas. Kanner, L. (194 3). Autistic disturbances of affective contact. Nervous Child, 2, 217—250. Kiernan, C. (1983). The use of nonvocal communication techniques with autistic individuals. Journal of Child Psychology and Psychiatry, 24, 339— 395. Kolvin, I. (1971). Studies in the childhood psychoses. I. Diagnostic criteria and classification. British Journal of Psychiatry, 118, 381—384. Kolvin, I., Ounsted, C., Humphrey, M., & McNay, A. (1971). II. The phenomenology of childhood psychoses. British Journal of Psychiatry, 118, 385— 395. Konstantareas, M. M. (1981). Developing new avenues of communication. In M. M. Konstantareas, E. G. Blackstock, & C. D. Webster (Eds.), Autism: A primer. 95—106. Montreal: The Quebec Society for Autistic Children. Konstantareas, M. M. (1984 ). Sign language as a communication prosthesis with language-impaired children. Journal of Autism and Dev elopmental Disorders, 14 (1), 9—25. Konstantareas, M. M. (1986). Manual language: its relevance to communication acquisition in autistic children. In H. T. A. Whiting & M. G. Wade (Eds.), Themes in motor dev elopment. 159—179. Dordrecht: Martinus Nijhoff. Konstantareas, M. M. (1987). Autistic children exposed to simultaneous communication training: A follow-up. Journal of Autism and Dev elopmental Disorders, 17 (1), 115—131. Konstantareas, M. M. (1988). Autism: Recent developments in its assessment and treatment. Psychiatry, 2, 19—26. Konstantareas, M. M. (1990). A psychoeducational model for working with families of autistic children. Journal of Marital and Family Therapy, 16, 59—70. Konstantareas, M. M. & Blackman, A. (1978). Assessing preferred communication training modalities in non-verbal autistic children. Paper presented at the Research Symposium of the Canadian Society for Autistic Children, Vancouver, B. C. Konstantareas, M. M. & Homatidis, S. (1987). Brief report: Ear infections in autistic and normal
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children. Journal of Autism and Dev elopmental Disorders, 17 (4), 585—594. Konstantareas, M. M. & Homatidis, S. (1989). Assessing child symptom severity and stress in parents of autistic children. Journal of Child Psychology and Psychiatry, 30, 459—470. Konstantareas, M. M., Homatidis, S., & Busch, J. (1989). Cognitive, communication, and social differences between autistic boys and girls. Journal of Applied Developmental Psychology, 10, 411—424. Konstantareas, M. M., Hunter, D., & Sloman, L. (1982). Training a blind autistic child to communicate through signs. Journal of Autism and Dev elopmental Disorders, 12, 11—11. Konstantareas, M. M. & Leibovitz, S. F. (1981). Early communication acquisition by autistic children: Signing and mouthing versus signing and speaking. Sign Language Studies, 31, 135—154. Konstantareas, M. M., Oxman, J., & Webster, C. D. (1977). Simultaneous communication with autistic and other severely dysfunctional nonverbal children. Journal of Communication Disorders, 10, 267—282. Konstantareas, M. M., Oxman, J., & Webster, C. D. (1978). Iconicity: Effects on the acquisition of sign language by autistic and other severely dysfunctional children. In P. Siple (Ed.), Understanding language through sign language research. 213—237. New York: Academic Press. Konstantareas, M. M., Webster, C. D., & Oxman, J. (1979). Manual language acquisition and its influence on other areas of functioning in autistic and autistic-like children. Journal of Child Psychology and Psychiatry, 20, 337—350. Layton, T. L. & Stutts, N. (1985). Pragmatic usage by autistic children under different treatment modes. Australian Journal of Human Communication Disorders, 13, 127—142. Lennox, C., Callias, M., & Rutter, M. (1977). Cognitive characteristics of parents. Journal of Autism and Childhood Schizophrenia, 6, 163—173. Lock, A. (1978). The emergence of language. In A. Lock (Ed.), Action, gesture and symbol: The emergence of language. 3—20. London: Academic Press. Lotter, V. (1974 ). Factors related to outcome in autistic children. Journal of Autism and Childhood Schizophrenia, 4, 263—277. Lovaas, O. I. (1987). Behavioral treatment and normal educational and intellectual functioning in young autistic children. Journal of Consulting and Clinical Psychology, 55 (1), 3—9. Lovaas, O. I., Berberich, J. P., Perloff, B. F., & Schaeffer, B. (1966). Acquisition of imitative speech by schizophrenic children. Science, 151, 705—707. Lovaas, O. I., Koegel, R., Simmons, J., & Long, J. S. (1973). Some generalization and follow-up measures on autistic children in behaviour therapy. Journal of Applied Behavior Analysis, 6, 131—166.
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Tanguay, P. E., Edwards, R. M., Buchwald, J., Schwafel, J., & Allen, V. (1982). Auditory brainstem evoked responses in autistic children. Archives of General Psychiatry, 39, 174—180. Torrey, E. F., Hersh, S. P., & McCabe, K. D. (1975). Early childhood psychosis and bleeding during pregnancy. Journal of Autism and Childhood Schizophrenia, 5, 287—297. Tsai, L., Jacoby, C. G., & Stewart, M. A. (1983). Morphological cerebral asymmetrics in autistic children. Biological Psychiatry, 18, 317—327. Van Wagenen, L., Jensen, W. R., Worsham, N., & Petersen, B. P. (1985). The use of simultaneous communication to teach difficult verbal discriminations to an autistic and developmentally disabled child. Australian Journal of Human Communication Disorders, 13, 143—152. Volkmar, G. R. & Cohen, D. J. (1985). The experience of infantile autism: A first person account of Tony W. Journal of Autism and Dev elopmental Disorders, 15, 47—54. Watson, L. R. (1985). The TEACCH Communication Curriculum. In E. Schopler & G. Mesibov (Eds.), Communication problems in autism. 187— 206. New York: Plenum. Webster, C. D., McPherson, H., Sloman, L., Evam, M. A., & Kuchar, E. (1973). Communicating with an autistic boy by gestures. Journal of Autism and Childhood Schizophrenia, 3, 337—346. Williams, R. S., Hauser, S. L., Purpura, D. P., DeLong, G. R., & Swisher, C. N. (1980). Autism and mental retardation. Archiv es of Neurology, 37, 749—753. Wing, L. (1975). Clinical and therapeutic approach to early autistic psychosis in children: The point of view of the research worker. (French) Rev ue de Neuropsychiatrie Infantile et d’Hygiene Mentale de l’Enfance, 23 (12), 803—818. Wing, L. (1981). Asperger’s syndrome: a clinical account. Psychological Medicine, 11, 115—129. Wing, L. (1989). The diagnosis of autism. In: C. Gillberg (Ed.), Diagnosis and treatment of autism. 5—22. New York: Plenum. Yoder, P. J. & Layton, T. L. (1988). Speech following sign language training in autistic children with minimal verbal language. Journal of Autism and Developmental Disorders, 18, 217—229.
M. Mary Konstantareas, Toronto (Canada)
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79. Speech Disordered Children 1. 2. 3. 4. 5. 6.
1.
Introduction Describing Phonological Errors Associated Underlying Deficits Causal Factors Psycholinguistic Implications of Phonological Disorder References
Introduction
Speech disordered children are not a homogenous group. However, they all share the frustration of not being able to express their needs and thoughts intelligibly, often failing academically and being socially isolated. Speech disorders can be classified into a number of subtypes. Perhaps the most important dichotomy is that between articulatory/phonetic disorders and phonological disorders. Articulation disorder refers to an impaired ability to physiologically produce speech sounds. Phonological disorder refers to an impaired ability to use speech sounds linguistically (Grundy 1989). Every language has a set of phonemes (speech sounds) that are combined in sequences to form words. Phonemes are the minimal linguistic units that differentiate meaning e. g. /r/ and /l/ are two phonemes in English because they distinguish word pairs like lip and rip. A phoneme is a linguistic abstraction, not an acoustic or articulatory entity. While the acoustic phonetic properties of /l/ in lip and ball vary greatly, English speakers nevertheless perceive them both as the phoneme /l/. Every language also has constraints governing how phonemes may be combined. The cluster /sv/ is illegal in English, but legal in Swedish. Most phonologically disordered children can articulate all their native language’s speech sounds. Their difficulty lies in selecting and combining phonemes into sequences that constitute words in their native language. While the incidence of developmental phonological disorder is unknown, because surveys failed to differentiate types of speech disorder, estimates range from 3 to 10% of the normal school population (Enderby/Philipp 1986). To these children, who have a specific disorder, must be added those whose speech disorder is part of a more general handicap such as hearing impairment or intellectual disability. One survey of a clinical
population found that up to 60% of children referred to community speech pathology clinics are phonologically disordered (Dodd 1982). However, children diagnosed as phonologically disordered vary in terms of: the type of errors made; the detectable underlying deficits in the speech processing chain from perception to production; associated linguistic disorders; the causal and maintenance factors of their disorder; and consequently, their response to different therapeutic approaches.
2.
Describing Phonological Errors
The description of mispronunciations, whether those of young children acquiring language or those of speech disordered children, was initially taxonomic or phonemic. Phonetic inventories for speech sounds appropriately produced in particular positions within word structures were listed (Fletcher 1990). Such phoneme repertoires, while valuable for articularly assessment, are limited because they provide no information about how a phoneme might be produced or omitted in a given phonetic context. For example, while a child might produce /s/ correctly in sun, /s/ might be deleted in consonant clusters e. g. [top] for stop. Unlike taxonomic theory, generative phonology viewed phonology as an integral part of the grammar of a language (Chomsky/Halle 1968). One of the concerns of generative phonology is to explain the relationship between abstract mental representation of words and their actual pronunciation. Adult’s underlying mental representations are assumed to contain all the phonemic contrasts needed to distinguish one word from another, but the minor non-distinctive (redundant) features, such as aspiration, are specified by phonological output rules (Hyman 1975). Generative phonological theory provided the impetus for the description of mispronunciations in terms of phonological processes and rules (e. g. Compton 1970). Stampe (1972) defined a phonological process as the mental operation that results in the substitution of a class of sounds or sound sequences presenting a specific difficulty to the speech capacity. In Stampe’s view, the child’s task in learning phonology is to suppress those processes that do not occur in the adult language. For example, the following productions illus-
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trate the phonological process of cluster reduction: [tp] stop; [kIp] skip; [sip] sleep; [sI] swing. A taxonomic analysis would conclude that /s/ is in error for 50% of occurrences. A phonological rule analysis would state: in /s/ + consonant clusters, if the consonant is a plosive, then the /s/ deletes, but if the consonant is a continuent, then the consonant deletes. The latter analysis allows prediction of how words not contained in the language sample will be pronounced. Both taxonomic and phonological rule analyses depend crucially on the accuracy of detailed phonetic transcriptions of disordered speech and this limitation is not always acknowledged (Carney 1979). Instrumental analyses of speech errors have shown that even skilled transcribers cannot perceive all the phonological contrasts marked. For example, Hardcastle/Morgan/Clarke (1987) used electropalatography to demonstrate articulatory differences in the pronunciation of ‘heard’ [t] for /ʃ/ in [tip] sheep as opposed to [t] in tent. The role of instrumentation in the description of phonological errors will obviously grow. However, our current understanding of speech errors is derived from observers’ transcriptions of their perceptions. 2.1. Developmental Patterns Most children begin to use recognisable words at about 12 months of age. By 18 months they often have a vocabulary of 50 words. The phonology of the first 50 words is often inconsistent and in some instances children render better (i. e. more adult-like) pronunciations of particular words than they do when they are slightly older and have larger vocabularies (Leopold 194 7). For example, one child produced Gladys perfectly at 12 months. This may have been an example of protolanguage (Halliday 1975) because the word was used to elicit attention whether or not Gladys was within auditory range. However, once the child had a larger vocabulary Gladys was pronounced as [dædIs], conforming to current phonological processes (Dodd 1975). In one early study of normal development Smith (1973) described the phonological acquisition of his son. He assumed that the child’s underlying representation of words corresponded directly to the adult surface form and postulated realisation rules that mapped these forms to the child’s own surface (output) forms. Smith later revised his model
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to include a perceptual filter to account for any miscoding of words. The realisation rules implemented major strategies: (1) consonant cluster reduction e. g. /l, r, w, j/ delete postconsonantally as in [bu] blue; /s/ deletes preconsonantally as in [pun] spoon. (2) consonant harmony or assimilation e. g. [lεloʊ] yellow. (3) systemic simplification e. g. fricatives and affricates are realised as plosives as in [tIp] for ship and chip. The number and type of realisation rules implementing these strategies varies according to the level of phonological development which is loosely related to chronological age, and level of cognitive development (Macken/ Ferguson 1983). Individual children can abstract idiosyncratic rules that are not common in normal development e. g. the s + consonant cluster rule described earlier. However, most children share similar sets of phonological rules and apply them consistently (Aitchison 1987) and similar normal developmental speech error phenomena have been observed across languages, e. g. Magnusson (1983) observed cluster reduction in Swedish. Children usually attain a phonological system that is consistent with that of the adults in their environment between 4 and 6 years of age. 2.2. Phonological Disorder Phonologically disordered speech has been described in terms of features, phoneme repertoires, rule statements contrastive analyses and/or phonological processes (Fletcher 1990). Reviews of such error data from children diagnosed as phonologically disordered have led to a range of conclusions about what distinguishes disorder from normal developmental errors. Some reviewers hold that disorder merely reflects varieties of delayed development. Fletcher’s (1990) review concluded that disorder arises when normal phonological development becomes delayed or ‘frozen’ relative to other aspects of language development. Ingram (1976) asserts that phonological disorder occurs when normal developmental processes fail to be eliminated, resulting in early processes co-existing with later ones. Others argue that disorder reflects severity in terms of the number of errors made, rather than the type of errors made (Shriberg/Kwiatowski/Best et al. 1986). These three conclusions differ in detail but have as their basic tenet that the types of phonological processes used by the population diagnosed
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as disordered can also be observed in the normal population. Other researchers argue that phonologically disordered children use processes that are different from those observed during normal development. Leonard (1985) described a variety of unusual and subtle phonological behaviours associated with disorder. These included: (1) the replacement of speech sounds that occur early in development by speech sounds that are usually acquired later e. g. substitution of [s] for all word final consonants except /p, b, and m/. (2) additions to adult surface forms e. g. addition of syllabic nasals to word final voiced plosives: [badn] bad, [bIgn] big. (3) use of sounds or suprasegmental features not occuring in the child’s native language e. g. marking consonant clusters with a bilabial fricative [ßes] dress (Leahy/Dodd 1987); marking plurality suprasegmentally by rising tone, higher fundamental frequency, longer duration and higher intensity. Another frequently observed characteristic of phonologically disordered children’s errors is strict word structure constraints (Dunn/Davis 1983). For example, most children delete some consonants word finally during normal development, but some disordered children may mark most word final consonants with a glottal stop (Leahy/Dodd, 1987). There are also phonologically disordered children whose speech appears to be characterised by inconsistent errors. Speech pathologists often regard inconsistency as one indicator of developmental dyspraxia, a motor programming deficit rather than a linguistically based problem (Hall 1989). Alternatively, apparently inconsistent phonological behaviour may, on closer inspection of phonetic context, be consistent. Leonard (1985) reviews some interesting examples. One 4 .0 year old child demonstrated a constraint that prevented nasals and plosives from occuring in the same word e. g. [pedi and meni] penny (Willbrand/Kleinschmidt, 1978). Grunwell (1981) reported a 6:3 year old child who used an extremely complex rule: all adult forms containing stressed syllable initial fricatives, liquids, glides, bilabial plosives or nasals that were followed by a front vowel were realised with an apical place of articulation e. g. [bu] blue, but [di] bee, [f] four, but [θit] feet. However, there are also reports of children whose speech is fluent but characterised by inconsistent errors both within and between
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words and who show no associated dyspraxic groping, repetition or soft neurological signs (Spencer 1986). The speech of children with Down Syndrome is often described as inconsistent, with children producing a variety of pronunciations for many words e. g. [h t, ti, si, ʃi] horse in one 15 minute language sample (Dodd/Leahy 1989). As these examples show, vowel errors may co-occur with inconsistency of consonant production (Murdoch/Porter/ Younger/Ozanne 1984 ). While little is known about the acquisition of vowels by children developing phonology normally, Reynolds (1990) concluded that most children over 24 months of age make few vowel errors. More detailed rule analysis of apparently inconsistent errors might reveal that some children use complex, bizzare/phonological rules. Alternatively, those making inconsistent errors may constitute a distinct sub-group of phonologically disordered children.
3.
Associated Underlying Deficits
Textbook overviews of articulation and phonological disorders invariably have a section where they review research which has sought correlations between speech related abilities (e. g. speech sound discrimination, motor skills) and disorder. Reviewers (e. g. Sommers 1984 ; Winitz 1969) usually stress that conflicting findings are the rule rather than the exception. There are two major factors contributing to these contradictory findings. Researchers employ widely differing methodologies to assess the same skills. For example, when Bountress (1984 ) compared the results of a single group of non-communication disordered children on three different standard assessment of speech perception, he found statistically significant differences in performance between the tests. The other, perhaps more important, factor is that many studies have assumed, incorrectly, that speech disordered children are a homogenous population. Thus different populations of speech disordered children have varied in their performance on identical tasks. Multivariate analyses of speech disordered children indicate that subgroups exist: some perform within normal limits on measures of perception, cognition or language, and some do not (McNutt/Hamayan 1982). The need to classify subgroups of phonological disorder is now generally agreed. What remains controversial is the criteria that should be
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used. Grundy (1989) suggests a psycho-linguistic perspective: phonological disorder may result from the impaired operation of mental processes serving “either the productive, or the perceptive, or the organizational mechanisms of speech” (Grundy 1989, 257). However, no information is given concerning the phonological behaviours indicating the site of these three deficits. Research studies investigating classification systems based on linguistic typologies have yielded little information. Both Arndt/ Shelton/Johnson/Furr (1977) and Winitz/ Darley (1980) tested large groups of children seeking associations between speech error patterns and independent variables such as measures of language, motor skills, auditory discrimination and oral stereognosis. No reliable associations were found. One plausible explanation for this failure to find any relationship between types of errors and other speech related abilities is that the linguistic typologies employed focused on speech sounds rather than phonological processes, failing to distinguish between articulatory and phonological disorders. In the discussion above (2.2) three categories of error types emerged in the description of what constituted a phonological disorder: delay (Fletcher 1990); consistent but unusual (non-developmental) phonological errors (Leonard 1985); and inconsistent phonological errors (Dodd/ Leahy 1989). Perhaps these three categories may reflect the nature of the deficits underlying subgroups of phonologically disordered children. Dodd/Leahy/Hambly (1989) tested this possibility by comparing the performance of three groups of subjects, selected according to the nature of their surface phonological errors: children using normal developmental processes that were inappropriate for their chronological age — ‘delayed’; children using some consistent but nondevelopmental processes — ‘deviant consistent’; and children who exhibited many apparently non-rule-governed errors — ‘deviant inconsistent’. In one experiment their production errors in imitation, picture naming and spontaneous speech were evaluated. In imitation there is no need to access internal lexical representations, picture naming requires accessing the internal representation as well as generating a production plan, and spontaneous speech requires planning long utterances phonologically and syntactically and involves communicative intent. The results distinguished between the three
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subgroups of phonologically disordered children, providing an initial validation of the classification. The delayed group made fewer errors than the other two groups but had stable performance across the three production tasks. The inconsistent group were better in imitation than in elicited or spontaneous production. The deviant consistent group’s errors increased with the complexity of the production task, indicating that the domain of some phonological processes extends across words e. g. use of one consonant to mark all consonants in an utterance (Leahy/ Dodd 1987). Other experiments comparing these three subgroups of phonological disorder have revealed that the deviant consistent group performs poorly on tasks involving detection of phonological legality of spoken nonsense words, recognition of their own phonological forms (Dodd/Leahy/Hambly 1989) and awareness of alliteration and rhyme (Brierly 1987). These findings suggest that the use of consistent but unusual phonological rules might be attributed to an impaired ability to abstract knowledge from the mental lexicon about the nature of the phonological system to be acquired. Leonard (1985) views children as active learners of their phonological system, who seek to mark, in their speech output, the contrasts between words they perceive. Consistent but bizarre solutions to the problem of marking differences might result from selecting the wrong parameters of the perceived speech signal as salient in their native phonology. If this were so, these children’s deficit could be labelled cognitive and lie in Grundy’s (1989) organisational level of the speech chain. Phonologically disordered children who make inconsistent errors appear to have intact knowledge of their phonological system, not differing from controls on tasks distinguishing the deviant consistent sub-group (Dodd/Leahy/Hambly 1989; Brierly 1987). However, their performance on a series of fine motor tasks suggests that their deficit may lie in motor programming (Bradford 1990). The three subgroups of phonologically disordered children plus a matched normal control group were assessed on four tasks measuring: repetitive use of a simple motor programme (pegboard task); motor accuracy involving both perceptual and motor programming abilities; kinæsthetic memory; and, learning to pronounce novel words. The kinæsthetic memory task was the only one
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that failed to discriminate the inconsistent subjects from the other subgroups of phonological disorder and the normally speaking controls. These findings are in agreement with those of Sommers (1984 ) who concluded that the severity of speech disorder was associated with poor fine motor skill — children with inconsistent errors are perceived as particularly unintelligible. A deficit at the level of speech production (Grundy 1989), specifically motor planning, might, then, account for children who produce inconsistent phonological errors. Children whose errors are due to the use of normal developmental processes that are inappropriate for their chronological age did not appear to have any specific deficit on the tasks that discriminated the two other subgroups of phonological disorder. This is not surprising, since they are following the normal course of development, albeit slowly. The factors underlying their delay may be more general: impoverished language learning environment, slower neurological maturation, or general cognitive delay (Powers 1971). This point leads to the question of the aetiology underlying the deficits in the speech processing chain that have been identified. Localising subgroups of phonologically disordered children’s deficit is useful for planning assessment and intervention. However, it is also important to consider the origin of the deficits.
4.
Causal Factors
Most speech disorders are considered to be ‘functional’, i. e. no established cause (Sommers 1984 ). However, a great deal of research effort has been spent seeking correlations between speech disorders and a wide range of factors e. g. family history of communication disorder, neurological assessment, sensory deficit and socio-economic status. This reflects the assumptions that causal factors exist and are clinically relevant. For example, Robinson’s (1987) survey found that disordered children frequently had a family history of communication disorder, indicating a genetic component; and, that a range of plausible medical ‘causes’ (e. g. neurological illness such as meningitis, low birth weight) were recorded for a quarter of the children studied. Such diagnoses can be associated with persistent neurological deficits, although this is not invariably so. Two other frequently mentioned
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causes of phonological disorder are fluctuating hearing loss due to otitis media (Dickson 1984 ), and psychopathology (Prizant/Auder/ Burke et al. 1990). A number of more controversial proposed causes of phonological disorders are discussed below. 4.1. Familial Phonological Disorders Parents of phonologically disordered children often report other communication disordered family members who have received remediation for impaired speech or literacy. Reports of the number of children who have a family member who is also communication disordered vary between 24 % (Ingram 1959) and 4 5.9% (Neils/Aram 1986). These studies are limited by their inclusion of a wide range of types of communication disorder. However, Neils/Aram (1986) found that ‘articulation disorder’ was the most common type of communication disorder reported for relatives (54 .9%). More recent studies have established a familial basis for some phonologically disordered children (Lewis 1990). While description of the mode of inheritance awaits further research, Lewis’ (1990) analysis suggests “either an autosomal dominant or multifactorial-polygenic mode of transmission [with] a sex-specific threshold for expression” (Lewis 1990, 168). 4.2 Language Learning Environment Phonological acquisition is obviously dependent upon adequate exposure to the language to be learned. Current theory holds that language acquisition is the result of the process of social interaction (Halliday 1975). These interactions occur around shared activities that are appropriate for the child’s focus of attention and interest in a natural situation. The adult provides language models and feedback about the child’s speech. Language use is thus taught alongside form (phonology, grammar and vocabulatory). There are two major ways in which this crucial language learning experience can be disrupted. (1) Communication Disordered Caretakers Children acquire the language in which they are immersed. If their language model is disordered, it is likely that they will learn that disorder. As examples: many children who lisp also have mothers who lisp (Blanton 1936); hearing children of hearing impaired parents are at risk of communication impairment, particularly phonological disorder
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(Schiff/Ventry 1976). The long-term effects of initial exposure to disordered language depend upon other available language learning experiences and intervention. (2) Inadequate Exposure to Language Individual differences between children’s language learning potential preclude definition of what constitutes ‘adequate exposure’ for language acquisition. Nevertheless some language learning environments are associated with delayed or disordered acquisition of phonology. The one that has received most research attention is that of multiple birth children (MBC). They have been reported to have delayed communication development compared to singletons in terms of age of speech onset, syntax, vocabulary, pragmatics and phonology (Savic 1980). Their unintelligibility has led some authors to conclude that twins often share an autonomous language (Luria/Yudovich 1959). An opposing view is that twin’s unintelligible speech is unintentionally disordered rather than a deliberately autonomous language (Savic 1980). Rather, their disordered speech may result from their language learning environment. Three-way communicative interactions (one adult and two children) are their norm for adult-child interactions, reducing the amount of adult modelling and feedback (Savic 1980). Further, MBC spend more time interacting with another child, reducing their exposure to adult language. A similar language learning environment can exist for siblings close in age or for children in day care. Nevertheless, many children whose primary communication partners are children of a similar age evidence normal phonological development. It would, then, be premature to draw conclusions about the contribution of the language learning environment to the acquisition of disordered phonology. 4.3. Auditory Sensation and Perception It is a common assumption that children make speech errors because they misperceive adult speech. The misperception may be attributed to hearing impairment or an impaired ability to process auditory information. In either case, a child may store incorrect or incomplete mental representations of words which in turn give rise to spoken errors. There is no doubt that permanent hearing impairment affects speech development. Even a mild bilateral hearing loss across the speech
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frequency range has serious implications for speech and language development; and, children with a specific high frequency hearing loss have particular difficulties with fricatives. A more controversial causal relationship is that between phonological disorder and fluctuating hearing loss. Many phonologically disordered children have a history of otitis media which may be associated with periods of impaired hearing. There are a number of plausible explanations that may account for this relationship: — During episodes of hearing loss, children are likely to misperceive words. Mental representations of these misperceived words may not be corrected when normal hearing is restored (Katz/Illmer 1972). — Children who experience frequent episodes of impaired hearing may learn to rely primarily on vision for information about the world and not attend to auditory information, even when their hearing is unimpaired (Katz/Illmer 1972). — During the first year of life infants learn to discriminate between the phonemes of their native language. Even if no further episodes of hearing loss occur after infancy, their knowledge of their native language’s system of phonemic contrasts may be impaired (Kirkwood/Kirkwood 1983). However, the evidence concerning a causal link between episodes of otitis media and phonological disorders is far from clear-cut. Most children (75%) experience at least one episode of otitis media with effusion (OME), and well over ten percent will have recurrent episodes (Teele/Klein/Rosner 1984 ). Not all these children become communication disordered. While retrospective studies have consistently shown a relationship between OME and communication disorder, they are flawed because they fail to document the number and length of episodes of OME. Prospective studies of infants enrolled in early infancy should be more reliable since hearing status can be monitored throughout development. However, recent prospective studies report conflicting evidence. One study (Teele/Klein/ Rosner 1984 ) suggested that the receptive language ability of high socio-economic status children declined with increasing number of episodes of OME, but this relationship did not hold for children from low socio-economic backgrounds. In the Wright/Sell/ McConnell et al. (1988) study children’s re-
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ceptive and expressive language scores were considered in relation to three variables: age of first OME episode; number of episodes; and presence of hearing loss at time of testing. None of these variables significantly affected speech and language performance. The results of these studies suggest that while fluctuating hearing loss may be an important contributing factor to phonological disorder, it is rarely a sole cause. In the absence of any sensory impairment, central auditory processing impairments are often cited as a major cause of phonological disorders (Sommers 1984 ; Tallal 1987). Early researchers stressed the need for assessing speech discrimination ability and ‘ear training’ in therapy. More recently, sophisticated assessment procedures for identifying auditory processing deficits have been devised (Willeford 1985). Katz (1983) reviewed the literature concerned with the relationship between speech disorders and phonemic synthesis (the ability to ‘blend’ distorted speech sounds into words). He found that children who made speech errors performed more poorly than age matched controls. However, children identified as having such a central auditory processing problem are most often described as having a wide range of impairments including receptive language, attention and memory as well as speech (Katz 1983). There is, then, little evidence for central auditory processing deficits being a cause of phonological disorders in the absence of more general learning disability. The literature reviewed in this section leads to the conclusion that in most cases it is impossible to attribute phonological disorder to a single causal factor (see also Robinson 1987). For example, one case (Leahy/Dodd 1987) had a family history of phonological disorder, but had also suffered a series of ear infections in early childhood that may have been associated with fluctuating hearing loss. This little girl also had a highly verbal older sibling who ‘interpreted’ for her, contributing to the maintenance of her disorder. Perhaps a predisposition to phonological disorder can be inherited, but its emergence may be dependent on co-occurence of certain medical or language learning environment conditions. A phonologically disordered child’s assessment should, then, include not only a description of the characteristics of the linguistic disorder, but also case history and psychosocial information.
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5.
Psycholinguistic Implications of Phonological Disorder
5.1. One Lexicon or Two? One controversial issue in the study of children’s speech errors is the number and nature of their mental representations of a word. Since phonologically disordered children have been shown to perceive differences between minimally paired words that they cannot produce, a number of researchers have proposed that children have two lexicons: one serving word recognition and the other word production (e. g. Chiat 1983). Other researchers claim that only one lexicon need be posited (e. g. Hughes 1983). Analyses of phonologically disordered children’s errors led Spencer (1986) to support a modified version of Dinnsen/Elbert/Weismer’s (1981) proposal that there are two main categories of disorder, distinguished according to the nature of their output representations of words. Both groups have largely intact input representations. One group have output representations that underspecify phonemes resulting in children’s surface errors. For example, sandal might be represented as /fricative + ændǝl/ allowing variable surface realisations such as [fændǝl], θændǝl or sændǝl]. A second group’s output representations are fully specified but simpler than the adult forms e. g. /tænǝl/ for candle resulting in consistent errors. However, the relationship between word’s underlying representations and their surface realisations is difficult to determine (Hughes, 1983). For example, one child deleted or realised consonants variably according to phonetic context — [d o:] for dog but [d ogi] for doggie (Weismer/Dinnsen/Elbert 1981). These data suggest that children’s surface errors do not always reflect their ‘output’ lexicon’s specifications for words. Rather, output constraints may be imposed subsequent to lexical retrieval of words. In the case of the previous example dog would be fully specified in the lexicon but a phonological process deleting word-final plosives would result in [d], whereas intervocalic /g/ in [dgi] would be realised since it would not be constrained by the process governing word-final consonants. This hypothesis is consistent with data from treatment efficacy studies focusing on phonological processes showing generalisation from taught to untaught lexical items. For example, treatment aimed at teaching a child
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to produce word-final /p/ and /k/ generalised to all appropriate word final consonants (Leahy/Dodd 1987). Such evidence casts doubt on the need to posit two entirely different lexicons. 5.2. Relationships Between Speaking, Spelling and Reading Children who have a current spoken phonological disorder are also reported to have a spelling disorder (Ham 1958). However, the spoken error is not reflected by the spelling error i. e. children don’t spell words the way they say them. A correctly pronounced word is just as likely to be spelled incorrectly as a mispronounced word (Robinson/Beresford/ Dodd 1982). The words most frequently spelled in error by phonologically disordered children are those where a spelling rule needs to be applied e. g. /k/ is represented orthographically by ck after a short vowel as in back but by ke after a long vowel as in bake. In contrast, words that have a strict one sound-one letter correspondence (e. g. adopt) and words that have unusual spellings (e. g. ocean) are spelled equally well by phonologically disordered children and reading age matched controls (Dodd/Cockerill 1985). In this study the most common error type for the non-speech disordered group was plausible misspellings e. g. sittee for city, whereas the phonologically disordered children most often produced errors that contained illegal sequences of letters e. g. zroor for zebra. Thus, while there is no one-to-one correspondence between speech and spelling errors, the two disorders are linked in that both reflect an impaired ability to derive and use phonological and orthographic rules. There is also a link between reading disability and impaired phonological processing. Reading disabled children perform poorly on tasks assessing phonological awareness (Lencher/Gerber/Routh 1990). Tests of preschool children’s phonological awareness are predictive of their later success in acquiring literacy (Bradley/Bryant 1983) and speech disordered children are reported to perform poorly on standard reading tests (Snowling/ Stackhouse/Rack 1986). Recent evidence suggests that if either speech, spelling or reading is identified as being disordered, then some impairment also exists for the other two abilities (Dodd/Sprainger/Oerlemans 1989). These results are consistent with the hypothesis that a central impairment in processing phonological information leads to problems
in speaking, spelling and reading. Identification of patterns of disorder across the three skills would provide valuable information for the construction of psycholinguistic models of children’s processing of verbal information as well as providing insights into the nature of phonological disorder. Authors note: My thanks to V. Duggirala, A. Ozanne and P. McCormack for their valuable insights. The NHMRC provided financial assistance.
6.
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Powers, M. (1971). Functional disorders of articulation: Symptomatology and etiology. In L. Travis (Ed.), Handbook of Speech Pathology and Audiology. 837—876. Englewood Cliffs NJ: Prentice Hall. Prizant, B., Audet, L., Burke, G., Hummel, L., Maher, S., & Theodore, G. (1990). Communication disorders and emotional stroke behavioural disorders in children and adolescents. Journal of Speech and Hearing Disorders, 55, 179—192. Reynolds, J. (1990). Abnormal vowel patterns in phonological disorder. British Journal of Disorders of Communication, 25, 115—148. Robinson, R. (1987). Introduction and overview. In Proceedings of the First International Symposium on Specific Speech and Language Disorders in Children. 1—19. London: AFASIC. Robinson, P., Beresford, R. & Dodd, B. (1982). Spelling errors made by phonologically disordered children. Spelling Progress Bulletin, 12, 19—20. Savic, S. (1980). How Twins Learn to Talk. London: Academic Press. Schiff, N. & Ventry, I. (1976). Communication problems in hearing children of deaf parents. Journal of Speech and Hearing Disorders, 41, 348—358. Shriberg, L., Kwiatowski, J., Best, S., Hengst, J. & Terselie-Weber, B. (1986). Characteristics of children with phonologic disorders of unknown origin. Journal of Speech and Hearing Disorders, 51, 140—161. Smith, N. (1973). The Acquisition of Phonology. Cambridge: The University Press. Snowling, M., Stackhouse, J., & Rack, J. (1986). Phonological dyslexia and dysgraphia: A developmental analysis. Cogniti v e Neuropsychology, 3, 309—339. Sommers, R. (1984 ). Nature and remediation of functional articulation and phonological disorders. In S. Dickson (Ed.), Communication Disorders: Remedial Principles and Practices. 118—172. Glen-
view IL: Scott Foresman & Co. Spencer, A. (1986). Towards a theory of phonological development. Lingua, 68, 3—38. Stampe, D. (1972). A Dissertation on Natural Phonology. New York: Garland. Tallal, P. (1987). The neuropsychology of developmental language disorders. In Proceedings of the First Symposium on Specific Speech and Language Disorders in Children. 36—47. London: AFASIC. Teele, D. W., Klein, J. D., & Rosner, B. A. (1984 ). Otitis media with effusion during the first three years of life and development of speech and language. Pediatrics, 74, 282—287. Weismer, G., Dinnsen, D. A., & Elbert, M. (1981). A study of the voicing distinction associated with omitted word-final stops. Journal of Speech and Hearing Disorders, 46, 320—327. Willbrand, M. & Kleinschmidt, M. (1978). Substitution patterns and word constraints. Language, Speech and Hearing Serv ices in Schools, 9, 155—161. Willeford, J. (1985). Assessment of central auditory disorders in children. In M. Pinheiro & F. Musiek (Eds.), Assessment of Central Auditory Dysfunction. 239—255. Baltimore: Williams & Wilkins. Winitz, H. (1969). Articulatory Acquisition and Behaviour. New York: Meredith. Winitz, H. & Darley, F. (1980). Speech production. In F. Lassman, R. Fisch, D. Vetter, P. LaBenz, & E. LaBenz (Eds.), Early Correlates of Speech, Language and Hearing. 232—265. Littleton, MA: PSG Publications. Wright, P., Sell, S., McConell, K., Sutton, A., Thompson, J., Vaughan, W., & Bess, F. (1988). Impact of recurrent otitis media on middle ear function, hearing, and language. Journal of Pediatrics 113, 581—586.
Barbara Dodd, St. Lucia, Queensland (Australia)
80. Developmental Dysarthria 1. 2. 3. 4. 5. 6. 7.
1.
Introduction Etiology and Behavioral Pathology Speech Pathology Clinical Evaluation Treatment Summary References
Introduction
Developmental dysarthria, a disorder of speech associated with neuropathologic con-
ditions occurring in children, is a relatively new term in the communication disorders literature, although the disorder has existed for a very long time. Historically the term ‚dysarthria’ has referred to acquired neuromotor speech deficits seen in adults and has only recently come into use to describe speech disorders of children associated with disturbances in muscular control of the speech mechanism, such as is seen in cerebral palsy. Because ‚developmental’ neurogenic speech disorders result from insult or lesion to the
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brain occurring prior to or during the course of speech development, developmental and acquired speech disorders are not directly comparable. Lesions to the developing brain disrupt systems as they develop, whereas, lesions to the adult brain disrupt systems that are fully developed anatomically and physiologically. What is known today as cerebral palsy was first described by Little in the ‚Lancet’ in the 19th century (Little 184 3) and it was labelled Little’s disease. Little’s description indicated that children with the disease had neuromotor involvement of the upper and/or lower extremities and that some had involvement of the speech musculature. Later writers noted variability in the type of motor problems seen. For example, hypertonic muscles were seen in some children, whereas flaccidity and/or tremors were present in others. By the late 1800s and early 1900s, there was some agreement that several types of cerebral palsy existed, and, not long after that, classification systems began to appear in the literature (Minear 1956; Phelps 1956). For example, Minear (1956) summarized the results of a survey of the American Academy of Cerebral Palsy, indicating that at least eight different types of cerebral palsy were being observed at the time. These included (1) spasticity, (2) athetosis, (3) rigidity, (4 ) ataxia, (5) tremor, (6) atonia, (7) mixed, and (8) unclassifiable cerebral palsy. Recognizing the variety of neurologic problems associated with cerebral palsy, Crothers/Paine (1959) streamlined classifications into three subtypes including spasticity, involuntary motion disorders (dyskinesia, extrapyramidal cerebral palsy), and mixed. They further differentiated spastic patients based on the topographic distribution of neuromotor signs (e. g., hemiplegia, paraplegia). These classifications of cerebral palsy continue to be used at the present time (Hardy 1983), and they remain problematic because patients within each classification are heterogeneous. Given this heterogeneity, it is not surprising that speech disorders or dysarthrias seen in children vary as they do in adults. That is, Darley/Aronson/Brown (1969 a; 1969 b) reported the existence of several types of dysarthria, in adults, correlated with underlying neuropathology. Although the types of dysarthria seen in children with neurologic disorders have not been studied extensively, clinicians can predict with some reliability
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whether or not the speech musculature will be involved based on information concerning the type of cerebral palsy and the motor systems involved based on information concerning the type of cerebral palsy and the motor systems involved. For example, in spastic quadriplegia involving the upper and lower extremities of the body, speech is more likely to be involved than in spastic diplegia involving only the lower extremities because of the topographic arrangement of cortical motor control. However, the pattern of speech disruption is much more difficult to predict based upon this information. Further, not all children with neuromotor problems carry a diagnosis of cerebral palsy; that is, dysarthria may be present in children with a variety of neurologic disorders. Perhaps research with children similar to that conducted by Darley/ Aronson/Brown (1969 a; 1969 b) with adults presenting with a variety of neurological impairments may lead to a better understanding of the relationship between neuropathology and speech disorders in children.
2.
Etiology and Behavioral Pathology
There are many conditions that interfere with neurologic development that may occur before birth (prenatal), during or immediately following birth (perinatal), or later during early childhood (postnatal). Any of these conditions may result in dysarthria depending upon which brain mechanisms are involved. Prenatal problems include genetic factors such as blood incompatibilities of mother and child (e. g., Rh incompatibility), metabolic disturbances, and others. Problems that disrupt oxygen supply to the fetus, maternal infections, exposure to roentgenograms, chemicals, and other problems occurring during early pregnancy also may cause damage to the neurologic system of the fetus. As well, perinatal head trauma may occur in difficult deliveries either from the use of forceps during delivery or from cranial pressure exerted by contact between the baby’s head and the mother’s pelvis. Premature and rapid deliveries also may be problematic in that they do not allow for gradual adjustment of the fetal circulatory system to extrauterine conditions. Respiratory problems that occur during and following birth may also result in brain damage. Other problems may occur after birth. These include infections such as encephalitis and meningitis, brain abscesses, tumors,
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stroke, and other encephalopathies resulting in disorders such as Reye’s syndrome (Holzhauer/Campbell/Hall/Halpin 1986). Head injuries among children also are common. It has been estimated that the annual braininjury rate per 100,000 children in the USA is 185 and that major causes of pediatric brain injury are falls, recreational activities, and motor vehicle accidents (Kraus/Fife/Cox et al. 1986). Any of the aforementioned conditions and others may result in developmental dysarthria, depending upon the site and extent of brain damage. The neurologic basis for developmental dysarthria found in children is similar to that described for acquired adult disorders. That is, dysarthria results when, during the course of development, damage to the motor cortex, direct and indirect motor pathways, basal ganglia, cerebellum and/or peripheral nerves occurs. Brain injury in any of these areas disrupts information communicated via the final common pathway to and from the muscles involved in speech production. We should point out that brain damage affecting the motor system occurring prenatally and perinatally is often labelled cerebral palsy. When damage occurs postnatally, it may or may not be labelled cerebral palsy. For example, some head-injured children evidence motor disorders similar to those seen in cerebral palsy, but may not be labelled as such. There are two major types of dysarthria that are commonly discussed with regard to developmental neuromotor disorders. These include spastic dysarthria and dyskinetic dysarthria. Spastic dysarthria results from infarction of the upper motoneuron system (motor cortex and/or direct and indirect motor pathways), whereas dyskinetic dysarthria results from primary involvement of the basal ganglia and connections. Mixed dysarthrias among neurologically impaired children also occur when aspects of both the upper motoneuron system and the basal ganglia are involved (Pruszewiez/Obrebowski/Zgorzalewicz 1977). Other types of dysarthria (e. g., ataxic dysarthria resulting from cerebellar infarction and flaccid dysarthria resulting from lower motoneuron involvement) appear to be less common in children than in adults (Hardy 1983). 2.1. Abnormal Movement Patterns When the neurologic system is damaged prior
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to completion of its development abnormal movement patterns — not seen in adults — may be present. In a normal child, some components of the motor system develop before others and therefore dominate motor behavior until other systems are completely developed. For example, excitatory motor components develop before inhibitory ones. When the normal motor system has completely developed, some of the early motor patterns disappear, some remain but are no longer dominant, and some continue as in infancy throughout life. When the neurologic system is damaged developmentally, early patterns of behavior that normally disappear do not. Other early dominant movement patterns that normally become nondominant, remain dominant or become exaggerated. To overcome these problems, compensatory motor patterns often develop. These retained, exaggerated, and/or compensatory behaviors result largely because normal inhibitory mechanisms do not develop. Therefore, excitatory muscle activity remains unchecked as the brain matures following a lesion. For example, the Moro embrace reflex may persist, and tonic neck reflexes and other postural reactions may become overly dominant and exaggerated. Several writers, including Ingram (1962), Sheppard (1964 ), Alexander (1987) and McDonald/Chance (196 4 ) have described specific infantile oral reflexes that involve aspects of speech production including labial, lingual, velar, pharyngeal, mandibular, laryngeal, respiratory, and others. Table 80.1, taken from McDonald/Chance (1964 ) provides a list of some of these reflexes involving structures used in articulation of speech. Abnormal and compensatory oral motor behaviors seen in neurologically impaired children are listed in Table 80.2, which is taken from Alexander (1987). Researchers have suggested that these and other infantile reflexive behaviors may be critical to the development of speech production in neurologically impaired children. Mysak (1963), Sheppard (1964 ; 1987) and others have suggested that abnormal oral motor reflex patterns may interfere with speech production. However, this assertion has been questioned. For example, Hixon and Hardy indicated that nonspeech and speech movement patterns are controlled by different neurologic mechanisms and therefore are unrelated (Hixon/Hardy 1964). Love/Hagerman/Taimi (1980) studied the relationship between infantile oral reflexes
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Reflex Cephalic reactions Facial response Rooting reflex Mouth opening Lip reflex Biting reflex Sucking reflex Chewing reflex Laughing
Swallowing (Oral) Swallowing
Stimulus Stroking the lobe of the ear or the nostril Sharp tapping around mouth
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Response Turns head away from stimulus Rounding and protrusion of lips as in pouting Movement of the head as if trying to get a nipple into the mouth Lowering of the mandible and separation of lips
Repeated light stroking of the cheek or around the mouth Sight of an object such as a nipple, finger, or tongue depressor, which is usually associated with mouth opening Tapping around the angle formed at Involuntary movements of the lips — lip closure and pouting the corner of the mouth Object placed between teeth (or gums) Strong, sustained elevation of the mandible Gentle pushing and pulling on a nippleAlternating protruding and retracting or finger placed in mouth movement of the tongue, often with elevation of the tip Tapping with teeth or gums with a Alternating elevations and depressions of tongue blade the mandible Light stroking or tickling, particularly Involuntary twitching of the body, opening of the mouth, disruption of breathing of the sides of the thorax rhythm, often accompanied by sound production on both inhalation and exhalation Presence of food or liquid in oral cavityWaveline motion of tongue to propel food into oropharynx Contact of food or fluid with mucosa Contraction of faucial pillars and walls of of faucial pillars and pharyngeal wall pharynx, elevation and closing of larynx, and momentary suspension of respiration
After McDonald ET & Chance B. Cerebral palsy. Englewood Cliffs, NJ: Prentice-Hall, 1964, 123. In Thompson (1988). Neurogenic articulation disorders in children. In McReynolds & D. Yoder (Eds.), Handbook of speech-language pathology and audiology. 548—591. Philadelphia: B. C. Decker Inc. Table 80.1: Infantile Oral Reflexes Observed in Neurologically Impaired Children
and speech performance in 60 individuals, and speech performance in 60 individuals, with cerebral palsy and found that only 25 percent of the subjects presented with infantile oral reflexes. This finding contrasted with data reported by Shepard, who found that 4 3 of 52 dysarthric subjects (84 percent) displayed abnormal reflex patterns (Sheppard 1964 ). When Love/Hagerman/Taimi examined speech performance of the 15 subjects displaying abnormal oral reflexes, eight of the children demonstrated no speech, and all but one of the remaining seven evidenced some articulatory impairment. However, a clear pattern between the number of abnormal reflexes present and the level of articulatory proficiency was not found. These data indicate that the presence of abnormal reflexes and dysarthria varies greatly across neurologically impaired children.
2.2. Spastic Disorders Children with spastic dysarthria may have a wide range of speech problems resulting from damage to the neuromotor system. In general, hyperreflexia and hypertonia of muscle groups involved in speech production is seen. Variability across children with spastic dysarthria is common, however, because of subtle variations in patterns of brain injury. Many children with spastic dysarthria also evidence spastic involvement of the upper and lower extremities and are classified as such. These classifications include s p a st i c h e m ip l e g i a, s p a st i c p a r a p l e g i a, s p a st i c d ip l e g i a, and s p a st i c q u a d r i- p l e g i a. All of these motor disorders result from impairment of portions of the upper motoneuron system. It is important to understand the extent of neurologic involvement found in children carrying these classifications because they pro-
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Behavior Cheek-lip retraction Exaggerated jaw closure Exaggerated tongue protrusion Jaw thrusting Jaw thrusting with protrusion Jaw thrusting with retraction Lip pursing Tongue retraction Tongue retraction with anterior elevation Tongue thrusting Tonic biting
Description Abnormal pulling back of cheeks; lips appear thin and form a tight line across mouth; often seen head and neck hyperextension and tongue retraction Abnormal jaw closure on objects such as feeding utensils Forward-backward suckling movement with exaggerated forward motion; tongue appears thick Strong depression of lower jaw; jaw may be stuck in open position; position occurs with head-neck hyperextension Compensatory strong depression of lower jaw occurring in an attempt to close jaw Strong depression and retraction of lower jaw seen concomitant with head and neck hyperextension and tongue retraction Lips pursed and protruded with tension extended to the cheeks; corners of lips retracted slightly Posterior movement of tongue into oropharyngeal area occurring with head and neck hyperextension; back of tongue appears humped; the tongue is thick Tongue assumes posterior position in oral cavity with tongue tip elevated and pushing against hard palate and alveolar ridge; compensatory for tongue instability Strong forward pushing of the tongue; tongue appears thick Strong jaw closure in response to tactile stimulation of biting surface of teeth or gums; jaw is stuck in closed position; increased head, neck, trunk extension occurs in attempt to overcome abnormal pattern
After Alexander (1987) Oral-motor treatment for infants and young children with cerebral palsy. Sermin Speech Lang, 8, 87—100. In Thompson (1988). Neurogenic articulation disorders in children. In L. McReynolds & D. Yoder (Eds.), Handbook of speech-language pathology and audiology. 548—591. Philadelphia: B. C. Decker Inc. Table 80.2: Abnormal and Compensatory Oral Motor Behaviors of Infants and Young Children with Cerebral Palsy
vide information on the distribution of brain damage. Because of the close proximity of corticobulbar and corticospinal tracts at the cortical level and during their course to the brain stem and spinal cord, damage to one system often occurs concomitant with the other. Therefore, classifications may be helpful in predicting the extent to which muscles involved in speech production are affected. In s p a st i c h e m i p l e g i a, the upper and lower extremities of one side of the body are involved, resulting from unilateral lesion of the corticospinal system. The corticobulbar system may or may not be involved; but when it is involved, dysarthria may result from hemiparesis and spasticity in the lower half of the face and oral musculature. S p a st i c p a r a p l e g i c children present with involvement of both lower extremities while the upper extremities remain unaffected. In addition, the muscles of the torso walls may be
involved, resulting in respiratory involvement and possible mild dysarthria. In a large study of speech patterns in dysarthric children, Kamalashile (1975) found only two paraplegic children with dysarthria probably because respiratory impairment often does not affect speech production, unless other aspects of the speech musculature also are affected. The extent of neuromotor involvement in s p a st i c d i p l e g i a exceeds that of hemiplegia and paraplegia in that the muscles of both the upper and lower extremities and the torso are involved. The spastic involvement in diplegia also often extends to the neck musculature; however, involvement of the arms and neck area are less severe than that of the legs. In children with spastic diplegia, speech production may or may not be impaired. Some children may evidence rather mild speech problems such as dysprosody resulting from involvement of the respiratory system coupled
80. Developmental Dysarthria
with impairment of the extrinsic laryngeal musculature. But other children may evidence severe dysarthria resulting from involvement of the oral, laryngeal, and respiratory musculature. As pointed out by Hardy (1983), oral and laryngeal motor involvement may not be extensive in these cases. However, when a marked reduction in respiratory support is present, coupled with mild dysfunction of oral and laryngeal mechanisms, significant dysarthria may result. S p a st i c q u a d r i p l e g i a is the most severe. In children with quadriplegia, both the upper and lower extremities are involved with equal severity and motor involvement often extends to the oral and laryngeal musculature. Therefore, developmental dysarthria is often seen, and often it is severe. Speech production problems were reported in 63 of the spastic quadriplegic children studied by Kamalashile (1975). 2.3. Dyskinetic Disorders In children with dyskinetic dysarthria, as in spastic dysarthria, variability exists with regard to the various dimensions of speech production that may be disrupted. Movement of the lips, tongue, mandible, soft palate, laryngeal mechanism, and the respiratory mechanism may be impaired secondary to involvement of the thoracic wall, laryngeal, and orofacial musculature. In children with dyskinetic dysarthria, all four extremities often are involved; therefore, they may be labelled quadriplegic, with the upper extremities being more seriously involved than the lower extremities. In general, movement patterns in impaired muscle groups are lacking in coordination, and involuntary movements such as athetosis and chorea, may be seen. Atethoid movements are usually described as slow and writhing; whereas, chorea is characterized by rapid, flailing, and jerking movements of the extremities.
3.
Speech Pathology
Review of the literature focused on identification of speech pathology associated with the developmental dysarthrias is limited. Although several studies have compared performance of dyskinetic and spastic children on certain speech and nonspeech tasks, many parameters of speech production have not been studied extensively. Further, research methodologies employed in many studies have been problematic. For example, some
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studies have not controlled for important variables such as hearing ability and intelligence, and children presenting with wide ranges of severity have been included for study in a single group. These sources of uncontrolled variability make it difficult to draw conclusions about specific speech patterns occurring in children with dysarthria. In addition, it is interesting to note that most studies focusing on speech production problems associated with developmental dysarthria were published in the mid to late 1960s. By the 1970s, a shift in focus to prespeech, oral motor behaviors, feeding, and positioning was noted, with little discussion of speech production behavior. This shift was perhaps influenced by factors such as (1) changes in legislation affecting delivery of services in the USA to younger and more severely impaired children; (2) popularity of neurodevelopmental theories and approaches to treatment (K. Bobath 1966; 1971; 1976; B. Bobath 1967; 1971 a; 1971 b); and (3) concern with early feeding programs for neurologically impaired children (Morris 1977). Hardy (1983) appears to be the first to refocus on speech production problems in these children, specifically in children with cerebral palsy. The following discussion will focus primarily on speech production problems. Each of the subsystems involved in speech production (respiration, phonation, resonance, and articulation) will be discussed separately and, where possible literature will be cited comparing the performance of spastic and dyskinetic dysarthric children. 3.1. Respiration Studies of respiration in children with dysarthria have shown that breathing patterns often are disrupted in children with spastic, athetoid, and ataxic cerebral palsy. However, athetoid children appear to evidence more severe involvement than others. Athetoid children with dyskinetic dysarthria present with “varying gradations of a pattern of irregular, shallow, and noisy breathing” (Berry/Eisenson 1956, 358) resulting in disruption in volume, rate, and rhythm of speech. Some abnormal breathing patterns include rapid breathing (McDonald/Chance 1964 ), shallow breathing (Palmer 1952), involuntary movement of the respiratory musculature (McDonald/Chance 1964 ) and “reversed breathing” (Davis 1982). In a study in which the breathing patterns of 58 children with athetoid cerebral palsy were studied, Palmer (1952) re-
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ported that every subject had at least one breathing abnormality. In contrast, children with spastic dysarthria presented with relatively better respiratory control, although these children evidenced reductions in chest movement and greater abdominal breathing movement than did normal children. There are several speech problems that may result from these and other impairments of respiratory functioning in children with dysarthria, however, malfunctioning of the respiratory system alone does not often result in significant speech production problems. It is when other subsystems of speech production are impaired along with respiration that the repiratory component becomes important. Some abnormal speech patterns that have been noted include short phrasing (Hardy 1983), frequent inspiration (Hardy 1983), reduced syllabic repetitions (Schliesser 1982) decreased rate, (Clark/Hoops 1980), and uncontrolled phonation (McDonald/Chance 1964). 3.2. Phonation A variety of phonation problems may be seen in children with dysarthria, some of which result from impairments in respiratory functioning. Phonation problems also commonly result from abnormal body postures and reactions. For example, when hyperextension of the head occurs in the symmetrical tonic neck reflex, breathy vocal quality may result. As explained by Davis (1982), head “hyperextention biomechanically facilitates vocal fold abduction” (Davis 1982, 103). Other phonation problems result from involvement of the vagus (tenth cranial) nerve. In this case, strained vocal quality may be seen because of hypertonicity and spasticity of the intrinsic laryngeal musculature. This problem is common in spastic dysarthria. Reactions to decreased lung volume and other compensatory learned behaviors also may contribute to hypertension of the vocal folds. For example, children with low vital capacity may use increased body tension to push expiratory air for speech production. This causes an increase in general tension in the laryngeal mechanism, and the child with dysarthria sounds as if she or he is using residual air phonation (Davis 1982). There are three general dimensions of phonation that may be disrupted in dysarthric speakers. These include (1) pitch, which is determined by the longitudinal tension of the vocal folds, (2) loudness, which is determined by the amount of medial compression of the
V. Pathologies and Disorders of Language Development
folds, and (3) periodicity, which is determined by patterns of vocal fold vibration. In children with dysarthria, any of these dimensions may be impaired. Pitch may be high or low, and reduced pitch range may be evident. Loudness often is reduced, and breathiness and aperiodicity may occur. Few studies are reported in the literature that have attempted to describe phonation problems in developmental dysarthria. Early studies by Rutherford (194 4 ) and Leith/Steer (1958) indicated, based on listener judgements, that pitch, loudness, and rate are often affected in dysarthria. Examining aspects of phonation in 4 8 children with athetoid cerebral palsy and 74 with spastic cerebral palsy, Rutherford reported a greater degree of impairment in the children with athetoid as compared to those with spastic cerebral palsy. Specifically, Rutherford found decreased pitch range, increased loudness, breathiness, slow speech and abnormal rhythm. Laryngeal dysfunction noted in the athetoid children included dilator spasm, constrictor spasm, and phonation out of phase with articulation. Structural and functional abnormalities of the vocal folds were less often noted in the children with spastic dysarthria, however, many phonation problems were seen in the spastic children as well. Further study is needed in this area such that phonatory problems in developmental dysarthria can be better understood. Manifestations of phonation problems that have been reported, but that have not been well studied in children are listed in Table 80.3. In addition, possible reasons for each phonatory characteristic are listed. 3.3. Resonance Children with dysarthria also may evidence resonatory and other articulatory problems because of insufficient velopharyngeal functioning. In one study, the authors estimated that approximately 30 percent of children with dysarthria secondary to cerebral palsy have velopharyngeal closure problems (Dawes 1958). In another study, 34 of 54 children presented with nasality (rhinophonia) (Pruszewics/Obrebowski/Zgorzalewicz 1977). These problems may result from malfunction in timing, range of motion, changes in muscle tone, reduced movement (unilateral or bilateral paresis), and/or random reflexive behaviors of the soft palate and/or posterolateral pharyngeal walls. For example, Pruszewicz/Obrebowski/Zgorzalew-
80. Developmental Dysarthria
Phonatory problem Decreased sustained phonation (Pruszewicz/Obrebowski/Zgoralewicz 1977) Breathy vocal quality (Hardy 1963; Rutherford 1944) “Strained” vocal quality (Davis 1982) Decreased loudness (Hardy 1983) Bursts of loudness (Davis 1982) Increased loudness (Rutherford 1944) Monoloudness; decreased loudness range (Hardy 1964) Sudden changes in pitch (Davis 1982) Monopitch; decreased pitch range (Davis 1982) Slow rate (Rutherford 1944) Abnormal rhythm (Rutherford 1944) “Residual air phonation” (Davis 1982)
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Laryngeal abnormality Decreased medial compression of vocal folds Decreased medial compression of vocal folds Hypertension, spasticity of laryngeal musculature Decreased medial compression of vocal folds Aperiodicity resulting from involuntary activity of laryngeal musculature Constrictor spasm; hypertension of laryngeal musculature Decreased medial compression of vocal folds and immobility of vocal folds Changes in longitudinal tension resulting from involuntary activity of laryngeal mechanism Decreased longitudinal tension and immobility of vocal folds Out of phase phonation and articulation Out of phase phonation and articulation Hypertension of vocal folds
After C. Thompson (1988). Neurogenic articulation disorders in children. In L. McReynolds & D. Yoder (Eds.), Handbook of speech-language pathology and audiology. 548—591. Philadelphia: B. C. Decker Inc. Table 80.3: Phonation Problems Seen in Children with Developmental Dysarthria and Possible Laryngeal Abnormalities
icz reported that ten of 54 children with dyskinetic dysarthria had disordered velar functioning resulting in hypernasality; four presented with distinct velar asymmetry, and six presented with reduced bilateral movement. Physiologic problems causing perceived hypernasality were undetermined in another 22 children in the study. Netsell (1969) discovered five abnormal velopharyngeal movement patterns seen among cerebral palsy speakers by studying simultaneous recordings of intraoral air pressure, the rate of nasal air flow, and the speech signal. Patterns noted included gradual opening, gradual closing, anticipatory closing, retentive opening, and premature opening. In children with gradual opening patterns, early segments of connected speech were produced normally, with the onset of nasal airflow occurring in later segments. In gradual closing, the opposite was observed. In anticipatory opening, nasal airflow was seen as speech was initiated and subsided thereafter, and, in children with retentive opening patterns, slow closure of the velopharyngeal port occurred
during the formation of individual consonants. Finally, in premature opening, the velopharyngeal seal was broken at inappropriate times during consonant production, thereby disrupting the acoustic form of the consonant. Other patterns of velopharyngeal functioning also may be observed in children with dysarthria. For example, Kent/Netsell (1978) reported instability of velar elevation in athetoid children. Disruptions in velopharyngeal functioning result in abnormal intraoral breath pressure needed for production of all speech sounds except nasals. Therefore hypernasality and/or nasal emission may be detected during speech production. Other speech problems such as slow rate of speech also may be noted secondary to velopharyngeal incompetence, when children compensate for slow palatopharyngeal movement. 3.4. Articulation Articulation errors occurring in children with dysarthria have been reported by several investigators including Byrne (1959), Clark/
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Hoops (1980), Irwin (1968), and Rutherford (194 4 ). These data have indicated that children with dysarthria have complex articulation problems because of weakness, decreased range of motion, alterations in timing, changes in muscle tone, abnormal oral movement patterns such as extensor jaw thrust and tongue thrust, and other neuromotor problems of the lips, jaw, and tongue. In general, studies have shown that dyskinetic dysarthric speakers present with more severe articulation problems than do spastics (Byrne 1959; Irwin 1968; Farmer 1980; Platt/ Andrews/Howie 1980; Platt/Andrews/Young/ Quin 1980). That is, spastic dysarthric speech is generally more intelligible and less articulatorily impaired than athetoid dysarthric speech. This finding is perhaps due to the many aberrations in tongue, mandibular, and lip control seen in children with extrapyramidal damage. As pointed out by Palmer (1952) athetoid children evidence difficulty in elevation of the tip of the tongue, gross clumsy tongue movement, bizarre lip closing and facial grimacing. Studies describing articulatory errors seen in children with dysarthria have pointed out a number of error patterns, some of which appear to remain consistent as these children mature (Platt/Andrews/Young/Quin 1980). Specifically, in terms of manner of articulation, children with dysarthria evidence great difficulty with production of fricatives, affricates, and liquids in both initial and final word positions, and stops, nasals, and glides are somewhat easier at least in the initial word position. As pointed out by Byrne (1959) in a study of 61 children with developmental dysarthria with cerebral palsy aged 2 to 7 years, 75 percent of the children produced /w/, /b/, /j/, /m/, and /d/ correctly, and at least 60 percent of the children produced /n/, /h/, /g/, /k/, and /t/ correctly in the initial word position. However, these sounds were produced correctly in the final position in less than 50 percent of contexts as were fricatives and affricates in both initial and final positions. In a similar study with older dysarthric speakers, Platt/Andrews/Young/Quin (1980) indicated that these individuals continue to evidence problems with fricatives and affricates, although productions in the initial position become more accurate with age. With regard to place of articulation, most errors are noted in production of postdental fricatives (/ð/, /θ/), alveolar fricatives and affricates (/s/, /z/, and /dʒ/), palatal liquids (/r/),
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and labiodental fricatives (/f/, /v/) but bilabial and velar articulations are more often produced accurately. These patterns, again, are consistent in older children and adults with developmental dysarthria although final word productions of postdental fricatives remain particularly difficult. Phonemic errors made by children with developmental dysarthria also have been studied and classified (Byrne 1959; Farmer 1980; Platt/Andrews/Howie 1980). The most comprehensive phonemic analysis reported in the literature was completed by Platt/Andrews/Howie on their data derived from 50 congenitally dysarthric adults. Findings indicated that most errors consisted of withinmanner (place and voicing errors) as compared to between-manner errors. Vowel production errors also are common, particularly in attempts to produce those in extreme positions of the vowel diagram (Byrne 1959; Platt/Andrews/Young/Quin 1980; Irwin 1968; Kent/Netsell/Bauer 1975). This is not surprising given reductions in range of motion of the tongue and other oral structures found in dysarthric children, Kent/Netsell (1978). Difficulty performing diadochokinetic tasks (both speech and nonspeech) also has been noted among children with dysarthria (Hixon/Hardy 196 4 ; Platt/Andrews/Young 1980; Schliesser 1982). However, mixed findings have been reported with regard to the correlation between these activities and speech production. That is, alternate motion rates using speech stimuli have correlated highly with speech intelligibility in several studies; (Hixon/Hardy 1964 ; Platt/Andrews/ Young/Quin 1980; Schliesser 1982) whereas, conflicting results have been reported with regard to correlations between nonspeech alternate motion rates and speech intelligibility. In a study of 50 children with developmental dysarthria, Hixon/Hardy (1964 ) reported that of five nonspeech activities including (1) opening and closing of the lips and teeth together, (2) retracting and rounding the lips, (3) raising the tongue to the alveolar ridge and lowering it, (4 ) lateralizing the tongue from one corner of the mouth to the other, and (5) opening and closing the jaw, only one (lateralizing the tongue) correlated with speech production ability. In a similar study of 15 adults with developmental dysarthria aged 16 to 51 years, Schliesser (1982) found three nonspeech activities to be strongly related to severity of dysarthria. These included opening and closing the jaw, retracting the
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tongue to the alveolar ridge, and retracting and rounding the lips. These conflicting findings may indicate differences between younger and older individuals with dysarthria and/or reflect the great heterogeneity seen in developmental dysarthria. Whatever the source(s) of variability in these studies, one can say that most children with developmental dysarthria evidence difficulty in performance of both speech and nonspeech diadochokinetic tasks and that these problems may or may not relate to the severity of dysarthria.
4.
Clinical Evaluation
Clinical assessment of dysarthria in children includes evaluation of all subsystems of speech production including respiration, phonation, resonance, and articulation. As well, evaluation of intelligibility and prosody are important. The major goals of the evaluation are to (1) identify physiologic deficits of the speech production system, (2) identify the involved speech production subsystems, (3) estimate the severity of dysarthria based on a variety of factors including intelligibility scores and ratings of speech naturalness, and (4 ) establish the modifiability of speech through stimulability testing and identification of compensatory strategies that may improve speech. In testing for neuromotor speech problems the evaluation may be approached from three different levels: physiologic, acoustic, and perceptual. Each level of analysis provides different information that assists the clinician in achieving the aforementioned goals. At the physiologic level, measures of muscle activity, kinematic parameters, muscle strength, muscle endurance (fatigue), muscle tone, and aerodynamic factors are considered, whereas, acoustic analyses examine the components of the speech waveform which include frequency, intensity and duration. Perceptual measures, which are most often used clinically, provide information based on auditory judgements relevant to all subsystems of production, prosody and intelligibility. The evaluation of dysarthria typically examines muscle function during both speech and nonspeech activities. However, the importance and meaning of data derived from the nonspeech measures is controversial as was discussed earlier. Similarly, both maximal and submaximal performance measures are taken, even though the usefulness of maximal performance measures have been questioned
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(Kent/Kent/Rosenbek 1987). Nonetheless, certain nonspeech maximal performance measures may be useful to the clinician (Luschei 1991; Robin/Somodi/Luschei 1991). The following sections present a speech subsystem approach to the evaluation of developmental dysarthria. 4.1. Evaluation of the Respiratory System 4.1.1. Physiologic Analyses Evaluation of respiration in children with neuromotor speech problems should include measures of subglottic air pressure and maintenance of subglottic pressure across the vital capacity. If an individual is able to maintain a subglottic pressure of 5 cm H2O for 5 seconds, then one can rule out the contribution of the respiratory system as the primary source of the speech production problem (Netsell/Hixon 1978). A commonly used method to measure subglottic airflow is the U-tube manometer with a leak tube to simulate glottal resistance (Netsell/Hixon 1978). A simple version of this test, using a glass of water and straw is described by Hixon/Hawley/Wilson (1982). A second area of assessment involves the examination of respiratory movements. Dysarthric speakers may exhibit altered respiratory patterns which include exaggerated use of certain muscles, or ‚paradoxic’ movements in which the circumference of the abdomen is decreased (Yorkston/Beukelman/Bell 1988). The most commonly used instrument to assess chest wall movements in dysarthric speakers is the magnamometer (Hixon/Mead/ Goldman 1976; Putman/Hixon 1984 ). Other measures of respiratory function include the vital capacity, the consistency of the lung volume level and the overall lung volume level. 4.1.2. Perceptual Measures Perceptual observations discussed by Darley/ Aronson/Brown (1975) are useful indicators of respiratory involvement in dysarthric speakers (although they may be indicative of problems at other levels of the system as well). Observations including monoloudness, excess loudness variation, loudness decay, alternating loudness, forced inspiration-expiration, and short phrases alert the clinician to possible involvement of the respiratory system. The advantage of these observations is that they can be made during conversational
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speech. However, taken alone, perceptual observations are often unreliable and perhaps invalid (Yorkston/Beukelman/Bell 1988). 4.2. Evaluation of the Phonatory System 4.2.1. Physiologic measures One important indicator of phonatory function is airflow. The most common method of measuring airflow is with a pnemotachographic device (Folkins/Moon 1990), a noninvasive procedure that measures the pressure drop across a resistance that is placed in the airstream. Dysarthric speakers may have inconsistent phonatory control and, therefore, an average measure of air flow may not be reflective of the integrity of their system (Netsell/Lotz/Shaughanessy 1984 ). However, by using a computer to digitize the data, allowing for examination of resistance over time, inconsistencies may be quantified. Other methods to evaluate vocal function include the stroboscope, the electroglottograph (EGG), and electromyography (EMG). A strobe is a light that flashes at a specific frequency which allows for observations of the vocal folds in various positions. The EGG is a device that measures vocal fold contact by a technique that detects current flow through tissue. Measures derived from this device reflect the opening and closing of the vocal folds and their temporal pattern. The EMG signal is a measure of the electrical activity of muscles. The muscle activity can be obtained from electrodes placed on the surface or by placing needle electrodes in the muscle. 4.2.2. Acoustic measures Acoustic measures of vocal performance are becoming commonplace in speech pathology clinics in so much as technological advances now allow for inexpensive and easy to use instruments. The measurement of fundamental frequency can be made rather easily and clinicians can obtain objective data on habitual frequency, fundamental frequency range, and frequency variability in connected speech. Measures of vocal intensity and cycle-to-cycle change in amplitude or frequency during phonation also can be made. Spectrograms also provide information about the acoustic components of speech. For example, during vowel production tasks, noise or weakness in patients with vocal involvement can be identified by examining spectral changes compared to normal spectra.
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Likewise, the acoustic spectrum, a plot of the energy contained in each of the frequencies of a complex sound (i. e., a Fourier transformation), may provide useful information about the presence or absence of vocal fold neuropathology. 4.2.3. Perceptual Measures Darley/Aronson/Brown (1975) suggest a variety of perceptually based parameters that may be observed when diagnosing phonatory deficits in adults with dysarthria. These include pitch level, pitch breaks, monopitch, voice tremor, monoloudness, excessive loudness variation, loudness decay, alternating loudness, harsh voice, hoarse voice, breathy voice, strained-strangled voice, and short phrases. Ability to sustain steady phonation, produce reflexive sounds, and alter pitch and loudness are all indicative of phonatory function and are among the most common means of assessing vocal pathology. Poor performance on these tasks may be indicative of neurological involvement affecting one or more aspect of phonatory function including the ability to produce adequate subglottic pressures, ability to control exhalatory efforts during phonation, and hyperadduction of the folds. Impairment of the respiratory system also can reduce maximal phonation time. The s/z ratio is another common measure of phonatory and respiratory integrity. Unlike the maximal phonation time, the s/z ratio is thought to differentiate respiratory involvement from phonatory impairment (Boone 1977). The patient is asked to sustain first an /s/, and then a /z/, for as long as possible. Individuals with normal phonatory systems should be able to sustain /s/ for as long as /z/; if there is some laryngeal abnormality, the subject should be able to produce a normal length unvoiced sound (/s/), but have a reduction in the voiced cognate. If there is respiratory insufficiency, the overall times may be reduced for both sounds. 4.3. Evaluation of the Resonatory System 4.3.1. Physiologic Measures Because the velopharyngeal system acts as a valve upon the airstream, measures of air flow and air pressure serve as indicators of its functional adequacy. These measures are considered indirect in that the clinician must extrapolate from the aerodynamic measures velar resistance or orifice size. One easy, commonly used method for detecting air flow is
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to place a mirror below the nose. If there is nasal air flow, the presence of humidified air should fog the mirror. Quantitative measurement of airflow requires the placement of a tube, with known resistance, in the airstream. The pressure drop across the constant resistance is linearly related to flow. This is the same methodology noted above for testing respiratory airflow. Aerodynamic measures also may be used to estimate orifice size. One such method, described by Warren/DeBois (1964 ) does so by assuming that the area of the orifice can be determined if the differential pressure across the orifice is measured. Another method (Hixon/Bless/Netsell 1976), supplies forced oscillatory airflow simultaneously to the nasal and oral cavities (with a mask) and to a rigid walled model of the nasal and oral cavity having an adjustable orifice which mimics the VP port. The two outputs are balanced and the size of the patient’s VP orifice can be inferred from the size of the model’s. Radiographic techniques still are used to examine VP function. Lateral still radiography is the oldest form of assessment of the velar port. However, these are static representation of the velum, (one picture taken at a time), and therefore are limited in usefulness for understanding speech problems. In contrast, motion picture radiography and videofluoroscopy provide useful information about the functioning and integrity of the VP port. Multiview videofluoroscopy (Skolnick 1969) allows for examination of the VP mechanism from separate views (sagittal, frontal, and base). Computerized tomographic (CT) scans also may be used to examine the soft palate. For instance, Moon/Smith (1987) recorded a series of scans of the palate, of which each scan represented a single frame that could be viewed on a video monitor. Ultrasound is a technique used to study articulation, but has recently been applied to the study of pharyngeal wall movement as many instrumental techniques are limited in their ability to view this aspect of VP functioning. By placing a transducer on the skin below the earlobe and behind the ramus of the mandible, visualization of the pharyngeal wall is possible (Parush/Ostry 1986). A very useful and commonly used clinical technique for visualizing the palate and its movement is endoscopy. An endoscope is an optical instrument that allows one to visualize internal body structures under a light source (part of the stroboscope described above for
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phonatory assessment), using fiberoptic fibers to illuminate an area of interest. Nasal endoscopy is quite popular. Using a nasal endoscope (a) the presence or absence of an adenoidal pad, (b) the extent of velar movement, (c) the size and shape of the VP port, and (d) the contribution of lateral wall movement to closure may be evaluated. 4.3.2. Acoustic Measures The spectrograph provides information about oral-nasal coupling. However, the changes related to such coupling are subtle and may not be of clinical utility in that spectographic analysis is time consuming and requires a great deal of training. The Oral Nasal Acoustic Ratio (TONAR) is a device used to measure the relative magnitudes of oral and nasal pressure. This is an instrument that has received relatively little attention, yet the procedure is simple and highly reliable. 4.3.3. Perceptual Measures Of course the clinician’s ear is an important aspect of diagnosis. Judgments of nasality are used by the majority of clinicians to assess VP structure and function. However, even here a number of approaches exist. Visual intraoral examination is another common method of VP assessment. However one can discern movement of soft palate, but still perceive hypernasality. More than 90% of clinicians use perceptual judgement to assess the adequacy of the VP port (Schneider/Shprintzen 1980). Some approach the task by having the patient prolong the vowels /a/ and /i/ with nostrils open and closed, with change in quality across the two phonemes indicating an adequately functioning mechanism. Others use the Iowa Pressure Articulation Test (Morris/Spriestersbach/Darley 1961) which allows for assessment of pressure consonants which may be particularly troublesome for individuals with VP incompetence. Other clinicians use multidimensional scaling techniques. 4.4. Evaluation of the Articulatory System 4.4.1. Physiologic Measures The most common form of evaluation is the oral motor examination. The oral motor examination includes evaluation of the peripheral speech structures at rest and during nonspeech activities, as is common in an oral peripheral examination (Dworkin/Culatta 1980). Signs of lips and facial weakness include parting of the lips at rest and asymmetry
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of the angles of the mouth. In addition, there may be flattening of the nasolabial fold on one or both sides and mandibular weakness may be suspected when the mandible hangs lower than normal in a resting position. The size of the tongue in relation to the oral cavity also should be checked, with a shrunken appearance of one or both sides indicating unilateral or bilateral involvement, respectively. Abnormal patterns also may be noted at rest such as anterior or posterior tongue elevation. As well, observation of the palatopharyngeal mechanism should be accomplished with the child’s tongue relaxed on the floor of the mouth and with the mouth open wide. With bilateral involvement, both sides of the soft palate rest near the posterior aspect of the tongue; whereas with unilateral damage, only the weak side appears lower than normal. However, keep in mind that many normal children present with asymmetry of the soft palate; therefore, neurologic impairment cannot be inferred from this observation alone. Other observations that may be made when the oral structures are at rest include any pocketing of food in the anterior or lateral sulci, indicating abnormal oral motor functioning. In addition, the child’s ability to control oral secretions should be noted. Finally, structural relationships of the lips, jaw, tongue, and palate should be checked (e. g., tongue size, palatal arch, and maxillary arch). Children with dyskinetic dysarthria often present with a high palatal arch and narrow maxillary arch that, coupled with restricted mobility of the tongue, influences articulatory precision. In assessment of nonspeech movement of the articulators, strength, range of motion, coordination, and accuracy of movement are assessed. Symmetry of structures is also assessed, and the presence of abnormal oral reflexive or compensatory behaviors as listed in Table 80.2 are noted. Lip-pursing also may be noted during these activities. To assess mandibular control, range of motion is tested as the child opens and closes the mouth and moves the mandible from side to side without resistance. Movement with imposed resistance is checked to determine the strength of muscles that open and close the mandible. The examiner tests the muscles involved in opening the jaw by attempting to close the child’s mouth when the child is given instructions to open the mouth as widely as possible and to try to prevent the examiner from forcing it closed. Muscles involved in
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closing the mouth are evaluated as the child attempts to overcome resistance when closing the mouth. This time, the examiner exerts force to keep the jaw open as the child attempts to close it. The tongue also is checked to evaluate strength and range of motion, the latter by testing tongue protrusion, elevation, and lateralization. Upon tongue protrusion, weakness may be observed on one or both sides, and, with a unilateral weakness, the tongue deviates toward the side of weakness. Exaggerated tongue protrusion and/or tongue thrust may be observed. In tongue elevation to the upper lip and alveolar ridge and in lateralization from side to side, weakness is noted when the child is unable to move the tongue in desired directions and when slowness or irregularity of movement is noted. Tongue strength is tested by exerting pressure against it upon protrusion with a tongue blade or by observing the child’s ability to place the tongue in the cheek and resist the examiner’s attempts to force it inward. Diadochokinesis is often used to test oral motor coordination. Although the usefulness of this procedure has been questioned (Kent/ Kent/Rosenbek 1987; Luschei 1991) most clinicians still use this measure. Activities performed in assessment of rapid alternating motion of the lips, jaw, and tongue include (a) productions of /u/ and /i/ and repetition of /p/ for observation of the lips; (b) repetition of /t/ for observation of tongue tip articulation; (c) repeated productions of /k/ for evaluation of posterior tongue activity; and (d) repetitions of /p t k/ for evaluation of sequential motion. Syllables per second of /p1/, /t1/, /kA/, and /p1 t1 kA/ repetitions are calculated was well as duration of sustained repetitions. Slowness (decreased number of syllables per second) and short duration of syllabic repetition often indicate neuromuscular weakness of the lips, tongue, and/or mandible. However, they also may be seen secondary to respiratory insufficiency, velopharyngeal incompetence, and/ or laryngeal involvement. Observable incoordination of the articulators and abnormal rhythm (e. g., pauses between syllables or words, variable rate) also indicate neuromuscular involvement. One measure of articulatory muscle function is the EMG (described above). As previously noted, EMG activity can be observed using surface electrodes placed on the skin of the lips, jaw or even tongue (Somodi/Robin/Luschei 1990).
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There are a number of instruments used to measure articulatory movement, the most common being stain gauge transducers which provide information about the displacement and velocity of a given structure. This method is most applicable to the measurement of upper and lower lip and jaw during speech and nonspeech activities. Examination of the tongue typically requires the use of X-ray or ultrasound techniques. Force transducers have been used to examine the strength of certain oral structures or the amount of force used during given activities. The forces used during speech are estimated to be below 20% of the maximal strength of a given articulator. Fine force control has been examined in both dysarthric and apraxic adults who show differences from normal speakers (McNeil/Weismer/Adams/ Mulligan 1990). Robin and Luschei recently developed a device to measure the strength and fatigue of oral structures (Robin/Somodi/Luschei 1991). By examining the amount of pressure a person can generate while pressing on a bulb, muscle strength is estimated; whereas, fatigue is examined by calculating the duration of sustained pressure equal to 50% of maximal. 4.4.2. Acoustic Measures Acoustic measures of articulation involve the use of the sound spectrograph. Data obtained from spectrographic recordings has been used to gain an understanding of intelligibility of dysarthric speech (Ansel/Kent 1986) and to provide insight into the underlying problems giving rise to dysarthric speech (Kent/Rosenbek 1983). Acoustic measures, like many instrumental measures, require training to use and interpret. However, they can provide useful information about the speech waveform to augment data derived from perceptual tests. 4.4.3. Perceptual Measures Articulation tests are used to assess the sound inventory. There are several commercially available articulation tests that may be used with children with dysarthria. For many children, a single-word articulation test is appropriate; however, analysis of speech in a sentence articulation task also should be undertaken for children with sentence production ability. One test that can be recommended for testing both single words and sentences is the Screening Deep Test of Articulation (McDon-
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ald 1964 ). Because it is designed to sample sound production in a variety of phonetic contexts, it is particularly useful for children with dysarthria. These children present with restrictions in motor function; therefore, production of some sound combinations may be possible, whereas others may not be. Regardless of the test instrument chosen, consonant errors should be analyzed with regard to place of articulation (bilabial, labiodental), manner of articulation (stop, fricative) and voicing, error type (substitution, omission, distortion), and word position of errors. A place-manner-voicing analysis provides a method for identification of patterns such as substitution of linguovelar by linguoalveolar sounds (place errors), substitution of fricatives by stops (manner errors), and substitution of voiceless by voiced sounds (voicing errors). In addition, an analysis of vowel production errors should be undertaken with regard to place (front, central, back), height (high, mid, low), tension, and lip rounding. These analyses are well described in other sources focused primarily on articulation (Bernthal/Bankson 1981). Sound productions also should be analyzed phonetically by means of narrow phonetic transcription. Because sound distortion is common in dysarthria, resulting from weakness and incoordination of the articulators, this analysis may be particularly useful for children with dysarthria. For example, children with dysarthria may produce bilabials as fricatives instead of as stops because of incomplete lip contact. Phonologic process analysis also may be useful in assessment of dysarthria. This analysis has been discussed by several writers (Compton 1975; Ingram 1976; Weiner 1978; Hodson 1980; Shriberg/Kwiatkowki 1980). Using phonologic process analysis, one may identify modifications or simplifications of adult phonology. 4.5. Speech Intelligibility Speech intelligibility is commonly estimated in assessments of speech production in children and is particularly important in assessment of dysarthria. Intelligibility measures are useful for estimating the severity of speech deficits (Platt/Andrews/Young/Neilson 1978); they provide a method for evaluating the extent to which neurophysiologic impairments and abnormal systems of speech production influence speech. And they provide a functional dependent variable or outcome meas-
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ure for use in evaluating the effects of treatment for some children. Intelligibility in developmental dysarthria has received little attention, as have other aspects of speech production in this population. However, methods used to estimate intelligibility in adult dysarthric speakers may be used with children. The Assessment of Intelligibility of Dysarthria Speech (Yorkston/ Beukelman 1984 ) provides a set of word and sentence stimuli that when read or produced imitatively are analyzed to yield indices of speech intelligibility. Although normative data have not been gathered for children, this test could easily be adapted for assessment of developmental dysarthria. 4.6. Prosody Individuals with dysarthric speech often have impairments in prosody and, therefore, assessment of prosody is recommended with dysarthric children (Robin/Eliason 1991). In assessing prosody, it is recommended that emotive intonation patterns such as happy, sad, and angry be tested as well as linguistic distinctions such as interrogative versus declarative forms or sentence level stress. A detailed review of stimuli used in assessing prosody can be found in Robin/Klouda/Hug (1991). It is recommended that both perceptual judgments of prosody be made as well as acoustic studies if possible to isolate which aspect of the speech waveform (frequency, duration or intensity) is creating the prosodic disruption. 4.7. Compensatory Strategies and Stimulability Testing A final aspect of assessment is focused on evaluation of the modifiability of abnormal speech production. This activity, sometimes referred to as diagnostic therapy (Rosenbek/ La Pointe 1985), provides a basis for making prognostic statements and for planning treatment. Although the direction of this portion of the evaluation is guided by the presenting behaviors of an individual child, a few guidelines can be offered. One major adjustment that often improves speech production is posture. The best posture for efficient speech production for most people is when the spine is straight and the head is held at midline. Therefore, attempts should be made to position children in this posture. Other compensatory techniques are directed toward specific subsystems and overall
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intelligibility of speech. First, alterations in breath support may be made. For example, instructions to inhale more deeply before speaking may improve overall speech production by providing a greater amount of air volume for driving the system. Forced laryngeal adduction may also compensate for respiratory (Nober 1987) weakness and facilitate loudness variation (Rosenbek/LaPointe 1985). Next, alterations in vocal intensity might be tested. For children presenting with hypertonic muscle tone and strain strangled vocal quality, instructions to speak with reduced intensity may improve vocal quality. Conversely, for children with generalized muscular weakness and breathy vocal quality, but who appear to speak with minimal effort, instructions to speak more loudly may improve vocal quality. Finally, attempts to modify articulatory precision should be made. For example, slowing the speech rate may facilitate better articulation. Rate modification may be extremely useful for improving intelligibility. Even though dysarthric speakers typically speak at a slower rate than normal, further rate reduction may be necessary. Yorkston/Beukelman/Bell (1988) provide an in depth review of specific motor control techniques used with adult dysarthric speakers that may also be useful with children. Attempts also should be made to modify articulatory placement for production of errored phonemes, both in isolation and in CV segments. Given simple placement instructions, some articulatory contacts may be relatively easy for a child to accomplish. However, some articulatory postures may be more difficult because of motoric constraints. Attempts to approximate these more difficult postures should be made so that an acoustically acceptable signal is produced. For example, a child who has difficulty with the tongue tip elevation necessary for production of /t/, may be able to produce an acoustically acceptable /t/ by coupling the blade of the tongue and the alveolar ridge. 4.8. Other Assessment Considerations Children with dysarthria, like children with other types of speech disorders, often present with a variety of additional problems. These include auditory processing, intelligence, language development, and other neuropsychologic factors (Wilson/Davidovicz 1987); visual perception; and somatosensory impairments (Hardy 1983). These factors will not
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be discussed here; however, it is necessary that they be considered in both assessment and treatment of these children.
5.
Treatment
Treatment for developmental dysarthria is based upon the age of the child being treated, presenting behavioral deficits, severity, the clinician’s theoretical framework for the development of speech in neurologically impaired children and other factors. Developed largely as an outgrowth of theories of neuromotor speech development and the clinical experience of authorities in the field, three major orientations to treatment are available, including (1) neurodevelopmental treatments focused on motor development and prespeech behavior (Alexander 1987; Bobath 1967; Bobath/Bobath 1972; Morris 1987; Mysak 1980; 1987) (2) treatments for disrupted subsystems of speech production (Hardy 1983), and (3) provision of nonspeech, alternative and augmentative communication systems (Ferrier/ Shane 1987). It is necessary to point out, however, that experimental data documenting the effects of these treatments are lacking. As observed by Jaffe (1984 ), “treatment for dysarthria is not researched in the most recent literature” (Jaffe 1984 , 163). Data are unavailable to indicate the extent to which treatment improves communicative functioning; data on subject variables important for successful application of a particular treatment have not been reported; and many treatments have not been well described. Therefore, central to this discussion is the need for applied, clinical research documenting the effects of these and other treatments for developmental dysarthria. 5.1. Neurodevelopmental Approaches Neurodevelopmental treatment approaches such as oral motor treatment (Alexander 1987) feeding treatment (Morris 1987), and neurospeech therapy (Mysak 1980), have been developed largely for intervention with infants and young, preverbal children with cerebral palsy, emphasize positioning, handling, and sensory stimulation in an attempt to inhibit development of abnormal postures and reactions. Treatments of this type have derived from neurodevelopmental theory, suggesting that special posturing and handling inhibits abnormal movement patterns and allows facilitation of more normal move-
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ment patterns prerequisite for speech development (Bobath/Bobath 1964). Although it is beyond the scope of this chapter to provide a detailed description of these treatment approaches, they are based on common premises that are summarized in the points below: a. The overall goal of treatment is to facilitate normal motor development as much as possible because the development of coordinated oral motor behavior is directly influenced by movement patterns of the body. b. Abnormal movement patterns reduce opportunity for normal movement and sensory feedback and so are inhibited through special posturing and handling techniques. c. Normal movement patterns are facilitated by means of visual, auditory, tactile, and other stimulation methods. d. Facilitation of normal oral motor reflexive and volitional movements provides a basis for speech production. e. Training techniques are implemented throughout the day and are emphasized during activities of daily living such as feeling. f. Early intervention is essential. g. Family involvement is encouraged. Neurodevelopmental treatments are comprehensive, encompassing a wide range of activities which are described elsewhere (see Alexander 1987; Davis 1978; Morris 1977; 1982; Mysak 1980). Specialized training is, however, necessary before implementing certain aspects of it (i. e., positioning and handling) and, several components of this treatment are controversial with regard to their effect on speech production. For example, some treatments utilized reflexive activity and as printed out earlier the relationship between reflexive activity and volitional speech behavior has been questioned. Further, data are unavailable to indicate that the accomplishment of some aspects of treatment is possible, such as training selective responding to auditory stimuli or modifying abnormal respiratory patterns. Advocates of neurodevelopmental approaches to treatment have not published data to support these or any other aspects of this treatment. These data are badly needed. 5.2. A Subsystems Approach A perhaps more traditional approach to intervention for developmental dysarthria involves modification of disrupted subsystems of speech production identified during assess-
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ment. Treatment is focused on respiration, phonation, resonance, and articulation with the overall goal of treatment being facilitation of the best possible speech given the neuromotor limitations of a particular child. This approach to treatment is most appropriate for preschool and school-age children. Younger children and infants probably do not present with the ability to participate in treatment of this nature. Like neurodevelopmental treatment, posture and positioning are emphasized. Suggestions for posturing children and adults have been described in several sources (Hardy 1983; Morris 1987; Mysak 1980). A subsystems approach to treatment has been recommended for both acquired and developmental dysarthria (Hardy 1983; Rosenbek/LaPointe 1985). In the following discussion, suggestions taken from the adult and child literature are summarized. Many of these interventions were borrowed from those used with other speech impaired populations (e. g., methods for managing resonance are similar to those used with individuals with cleft palate and methods for managing phonation are similar to those used with children with voice disorders). Suggestions for both speech and nonspeech training will be discussed where appropriate for each subsystem. One should keep in mind that these are only suggestions and that data supporting their use are unavailable. In fact, not one treatment study evaluating the efficacy of intervention for dysarthric children has been published to our knowledge. 5.2.1. Respiration The major goals of intervention concentrated on respiration include (1) modification of inspiration to provide sufficient air intake for speech production, (2) modification of expiratory patterns to facilitate controlled exhalation, (3) modification of inspiration and expiration relationships, and (4 ) production of speech within respiratory limits. Inspiration training consists of tasks designed to gradually increase air intake. The mean duration of inhalation is measured, and a target duration is set. The child is instructed to breathe deeply, and air intake is monitored using a variety of methods: tactile monitoring of torso movement; visual monitoring of the movement of a light-weight object (such as a feather) attached to a string and suspended in front of the child’s mouth, visual feedback using a spirometer. When air intake has been
V. Pathologies and Disorders of Language Development
modified in nonspeech activities, inspiration is monitored during speaking tasks with a gradual increase in the length of spoken utterances. Finally, the optimum length of phrase produced per breath is identified, and the child is trained to inhale at these intervals. Some caution is warranted with regard to inhalation training. This training is inappropriate for children for whom increased effort results in increased dysfunction. Further, deep inspiration prior to speech production is an atypical speech-breathing pattern; for some children, it may disrupt coordination of inspiration, expiration, and phonation. For these children, concentration on controlled exhalation may be more appropriate. Exhalation training also often begins with nonspeech tasks, with the major goal of such training being facilitation of controlled exhalation. Blowing is one such task that has been suggested. Blowing exercises are implemented to increase the pressure and/or duration of expired air in an attempt to improve the strength and coordination of respiratory muscles. A variety of devices are available for measuring air pressure and duration during blowing such as the simple device described above by Hixon/Hawley/Wilson (1982) using a water glass and a straw. Whether or not blowing exercises improve respiratory support for speech production is, however, an empirical question, and, as pointed out be Hardy (1983) there may be no relationship between these activities. As soon as possible, controlled exhalation training should involve speech production. A logical beginning point is sustained vowel phonation with the goal being to increase the duration of phonation. Consonant productions are incorporated in strings of CV productions. During these activities, pitch and loudness should be kept constant, and consonants and vowels chosen for practice should be in the sound repertoire of the child. The Visipitch may be useful for providing visual feedback regarding pitch and loudness variation during this training. Modification of inspiratory and expiratory relationships involves a combination of inspiration training activities and expiration training activities. Maximum inspiration is facilitated followed by controlled expiration. As with other aspects of respiratory treatment, this training may begin during nonspeech tasks and then move to speech tasks (e. g., deep inhalation followed by controlled vowel prolongation and deep inhalation followed by consonant repetitions, CV repeti-
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tions, and so on). The final aspect of respiration training is focused on connected speech production and training the child to talk within the physiologic limits of her or his mechanism. 5.2.2. Phonation Intervention focused on improved phonation is applied in accordance with the type of laryngeal pathology seen in a particular child. As discussed in the assessment section, there are three major aspects of phonation that may be disordered, which include loudness, quality, and pitch. In children with dysarthria, any of these may be impaired. The voice may be too soft (breathy) or too loud, vocal quality may be abnormal, or pitch may be too high or too low. Treatment methods used to improve laryngeal problems secondary to neurologic involvement (dysarthria) are similar to those used to improve laryngeal problems secondary to other problems. A few of the more common treatment methods will be discussed here, keeping in mind that no data exist to support their use. For other methods, a textbook on voice disorders may be consulted (Aronson 1985). Common problems seen in children with dysarthria concern the intensity, or loudness, dimension of phonation. Specifically, laryngeal weakness and hypo-adduction result in breathy phonation, whereas hypertonicity and hyper-adduction result in overly loud phonation. Breathy phonation may be modified by means of exercises used to increase speaking effort. These include various ‚pushing’ exercises as originally advocated by Froeschels/Kastein/Weiss (1955). This method simply requires simultaneous pushing with the arms and phonating. This method may not be used with some children with dysarthria, however, because in addition to weakness of the larynx, they also may evidence upper extremity weakness that precludes pushing activity. Children may also be instructed to tighten the muscles of the abdomen and oral mechanism prior to and during speech production in the hope that this effort will generalize to the laryngeal mechanism. Voiced bilabial plosives and labiodental fricatives are good speech sounds for use in practicing this activity because of the visible articulatory contact inherent in their production and a Visipitch may be utilized to evaluate any changes in intensity. Methods to decrease loudness or adduction involve maneuvers that decrease effort and
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muscle tension. General muscular relaxation techniques may in some cases be helpful; however, most neurologically impaired children are probably unable to undergo procedures necessary to accomplish this (e. g., progressive muscular relaxation [Jacobsen 1976], the chewing method [Froeschels 1952]). A technique that may be useful for more children is laryngeal massage done either manually or with vibration. Aronson (1985) presents instruction in manual laryngeal message. Once relaxation has been induced, vowels, CV sequences, words, and phrases are practiced. The effects of the yawn-sigh (Boone 1977) and other easy-onset techniques also may be evaluated. For some children, reduced laryngeal tension and concomitant reduced loudness may result from use of these techniques. Similar techniques may be used for altering vocal quality (e. g., strained or strangled vocal quality seen in spasticity). When pitch is targeted for treatment, attempts to raise pitch, lower it, or increase its variability are often therapeutic goals. This may be done by means of visual feedback such as is possible with the Visipitch. Using this type of biofeedback, the targeted pitch or pitch pattern is displayed along with the child’s production. In this manner, immediate feedback is provided. Closely related to pitch and loudness training and perhaps more important with regard to intelligibility is stress and intonation. Children presenting with monopitch and/or monoloudness also evidence reduced stress patterns or flat intonation contour in speech production. Therefore, treatment focuses on improving stress patterns. This training may begin as soon as the child is able to prolong vowels. During vowel prolongation, intonation variation is introduced. The clinician simply models a down, up, down pattern while phonating /a/ and the child imitates. Visual feedback using a Visipitch, voice light, or other instrument is also helpful during this training. As soon as the child has learned to produce a few consonants, these are incorporated into training, and when production of words and short phrases in possible, contrastive stress drills may be implemented (Rosenbek/LaPointe 1985). 5.2.3. Resonance Treatment of abnormal resonance for children with dysarthria is approached in a manner similar to that for children with cleft palate, although some unique considerations
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are involved in managing dysarthria. One major treatment strategy is prosthetic or surgical management. In children presenting with significant hypernasality and nasal emission, a palatal lift or pharyngeal flap surgery may be recommended. Deciding whether or not this type of management is appropriate requires some special considerations: a. Prosthetic or surgical management is contraindicated when other subsystems of speech physiology are severely involved such that speech production remains unintelligible even with decreased hypernasality. b. In cases of disproportionately severe hypernasality relative to other speech subsystems, prosthetic or surgical management may be recommended to improve physiologic support for development of speech. c. Some children may be unable to tolerate a palatal lift, for example, if a hyperactive gag reflex is present. d. Palatal lifts may be difficult to manage for some children with dysarthria because motor involvement of the upper extremities precludes independent insertion and removal. When prosthetic or surgical intervention is recommended and when mild to moderate cases of hypernasality are present, which preclude the use of the management strategies just described, treatment procedures may be applied to improve resonatory functioning. Nonspeech procedures include the use of whistling and blowing exercise for facilitation of oral airflow (Shprintzen/McCall/Skolnick 1975), elicitation of the gag reflex with simultaneous production of /a/ (Mysak 1980) and palatal massage (Cole 1971; Lubit/Larsen 1969; Yules/Chase 1969) for improving velopharyngeal closure. Speech tasks for improving resonance in dysarthria have not been specifically described. A logical progression of activities might begin with nonnasal vowel training, followed by nonnasal CV training, CVC, word, phrase training, and so on. During these tasks, instructions to overarticulate (open mouth wider, exaggerate oral contacts) may be given to improve oral airflow. As with treatment focused on respiration and phonation, incorporation of visual feedback techniques is recommended during resonance activities. These may range from simple devices such as a mirror or feather placed under the child’s nose to sophisticated equipment such as The Oral Nasal Acoustic Ratio (TONAR).
V. Pathologies and Disorders of Language Development
5.2.4. Articulation Treatment to improve articulation in developmental dysarthria may include (1) training of nonspeech behavior in an attempt to increase strength, range of motion, and/or tone of the lips, tongue, and mandibular musculature and (2) speech training to improve speech sound production. Because oral exercises involve individual muscle groups, the practice may not improve speech production which involves the integration of several muscle groups. Further, it has been suggested that many oral exercises require movements not needed in speech production (e. g., tongue lateralization) and so are probably unnecessary. Two types of oral exercises have been discussed: isotonic and isometric (Rosenbek/ LaPointe 1985). Isotonic exercises simply involve repetitive movement of the articulators without resistance, and isometric exercises involve movement of specific structures with imposed resistance. Of course, when this type of activity is included in treatment, only those structures that appear weak need to be treated, and often only one or two movements per structure may be necessary (e. g., tongue elevation, but not protrusion and retraction). In the accomplishment of this treatment, visual (e. g., mirror work) and tactile stimulation (e. g., tactile manipulation) may be required to facilitate desired movement patterns. Once the movements have been approximated, treatment is focused on increasing the number of repetitions of a particular movement and on increasing the duration of sustained movement with imposed resistance. It may be possible to incorporate instrumentation into this training. Netsell (1975) reported a biofeedback technique using EMG feedback in which muscle potentials were converted to audible tones. With electrodes attached to a patient’s upper lip, for example, muscle activity was monitored and modified with instructions to keep the tone within a specified frequency range. Speech training proceeds much like articulation training in other populations with regard to target selection and training activities. However, some additional considerations in treatment for developmental dysarthria are necessary. These pertain largely to the presenting neurophysiologic limitations of children with dysarthria. That is, it may be impossible for certain articulations to be accomplished due to restrictions in movement and/
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or abnormal movement patterns. For example, a child who cannot accomplish linguovelar coupling is likely unable to produce /g/ or /k/. Therefore, /g/ and /k/ would be inappropriate targets for treatment. This is not to say that this child should never be trained to produce these sounds. However, postponing treatment that focuses on them may be indicated, with treatment instead focused on sounds that are within the neurophysiologic limits of the child’s system. Another, perhaps unique, aspect of target selection with children with dysarthria pertains to training compensatory articulations. In many cases of developmental dysarthria, when normal articulatory coupling cannot be accomplished, compensatory placements may be trained to yield an acceptable acoustic product. The example provided earlier with regard to production of /t/ with more anterior placement of the tongue than is normal is salient here. Although training of this nature should be attempted only when attempts to train normal articulations have failed, these compensatory patterns often become targets with children with developmental dysarthria. Articulation treatment in this population utilizes a variety of stimuli such as tactile positioning of the child’s articulators, visual models of articulatory placement (e. g., pictures, drawings, and/or the clinician’s model), and auditory cues (e. g., spoken models, tape recorded feedback). As soon as target behaviors are produced successfully in isolation, sound production training is done in syllable and word contexts, incorporating production in utterances of increasing length as soon as possible. During this phase of training, attention should be given to generalization to untrained sounds, word positions, and linguistic contexts. Treatment probes designed to assess such generalization may be helpful in guiding treatment and in understanding speech acquisition in children with dysarthria. The process of generalization has not been studied in this population. Data are unavailable that indicate whether or not training in the initial position, for example, facilitates transfer to the final and medial position in words. Clinicians also do not know whether generalization occurs across sounds similar in place, manner, voicing, or a particular process. As well, the extent to which generalization from phrases to sentences to conversational speech occurs is unknown as is the extent to which trained responses are used in nontraining situations or the natural environment. In chil-
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dren with functional articulation disorders, articulation generalization is variable (Bankson/Byrne 1972; Powell/McReynolds 1969), therefore, it is likely to be in children with dysarthria as well. Another focus of treatment that is related to articulation is the rate of speech production. As mentioned earlier about assessment of compensatory strategies, articulation is often improved when children are given instructions to reduce their rate of speech. When such is the case, rate reduction treatment might be incorporated into articulation training using devices such as a metronome, a flashing light, or a pacing board with the goal of treatment to facilitate production of one word per beat of the metronome, flash of the light, or touch of the pacing board. It is important to point out here that rate reduction often produces changes in pitch and loudness variation. Therefore, the clinician must decide which abnormal prosodic variable is the least disruptive to speech intelligibility: rate or intonation. 5.2.5. Intelligibility The final consideration in a subsystems approach is concerned with speech intelligibility. Speech intelligibility reflects the interworkings of all subsystems of speech production and, therefore, provides an index for evaluating the effects of training one or several aspects of speech production. Because improved speech intelligibility is the ultimate goal of treatment, it is suggested that periodic assessment of intelligibility be undertaken to evaluate treatment effectiveness and to modify treatment when appropriate. 5.3. Nonspeech Alternative or Augmentative Communication Another major treatment approach for dysarthria pertains to provisions of an alternative or augmentative communication system or device. These devices often are used with children with dysarthria and range from simple to complex, depending upon the presenting behaviors and abilities of the child (Ferrier/Shane 1987; Cook/Coleman 1987; McDonald/Schultz 1973). For example, simple picture communication boards may be used with some children (Vanderheiden/Harris-Vanderheiden 1976), whereas, with others, computer based systems may be provided. Selection of a nonspeech communication system is based on the child’s physical ability,
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level of cognitive functioning, visual processing ability, and other considerations such as the communicative environment in which the system will be used. Based on the data, a system is prescribed with appropriate symbols (Clark/Woodcock 1976; Carlson 1984 ), vocabulary size, access mechanism, and output ability. Cook/Coleman (1987), Shane/Bashir (1980), Vanderheiden/Harris-Vanderheiden (1976) and others have discussed matching nonspeech communication systems to children. As with other treatments for dysarthria, little data have been published indicating the benefits of providing nonspeech communication systems to nonspeaking children. Although several authors have presented case studies (Buzolich 1987; Glennen/Calculator 1985), the need for controlled experimental research in this area is apparent. Culp presents a review of outcome research, indicating that there is a high percentage of communication board rejection and a low percentage of communication board use among nonspeaking individuals and suggests specific directions for research (Culp 1987). Research evaluating the usefulness of specific alternative or augmentative communication systems and treatment methods for facilitating optimum use of these systems is badly needed.
6.
Summary
This chapter has reviewed developmental dysarthria and has highlighted significant needs for research. Specifically, needs for further research to identify neuropathological disorders, other than cerebral palsy, that result in dysarthria and to delineate types of dysarthria that can be reliably identified in children have been highlighted. For example, children presenting with a variety of disorders, such as Reye’s syndrome, need to be studied using neuroimaging techniques to document the site and extent of brain damage, and physiological, acoustic, and perceptual techniques to assess speech production deficit patterns. With data such as these, we may begin to better understand the relationship between neuropathology and speech pathology in brain damaged children. This chapter also has pointed out the need for better assessment tools. For dysarthria, standardized tests designed to evaluate the various subsystems of speech production are needed. In addition, data regarding dysarthric and normal children’s performance on many physiologic and acoustic measures are
needed. Finally, this chapter has pointed out that a paucity of research exists which has evaluated the effects of treatment for developmental dysarthria. We strongly suggest that single-subject experimental research designs be used to demonstrate the effects of treatment strategies summarized in this chapter. The advantages of using these designs in clinical research and guidelines for using them have been discussed in several sources including Connell/Thompson (1986), Kearns (1986), McReynolds/Kearns (1983) and, McReynolds/Thompson (1986). Clinicians and researchers working with children with developmental dysarthria are encouraged to consult these sources and to begin gathering scientific data to document the effects of treatment for these disorders.
7.
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Morris, S. E. (1982). The pre-speech assessment scale. Clifton, N. J.: Preston. Morris, S. E. (1987). Therapy for the child with cerebral palsy: interacting frameworks. Seminars in Speech and Language, 8, 71—85. Mysak, E. (1963). Dysarthria and orthopharyngeal reflexology: a review. Journal of Speech and Hearing Disorders, 28, 252—260. Mysak, E. (1980). Neurospeech therapy for the cerebral palsied. A neuroev olutional approach. 3rd Edition. New York: Teachers College Press. Netsell, R. (1969). Evaluation of velopharyngeal function in dysarthria. Journal of Speech and Hearing Research, 34, 113—122 (a). Netsell, R. (1975). Instrumentation in the rehabilitation of dysarthria. Presented at the Veterans Administration Workshop on motor speech disorders, Madison, WI. Netsell, R. & Hixon, T. J. (1978). A noninvasive method for clinically estimating subglottic air pressure. Journal of Speech and Hearing Disorders, 43, 326—330. Netsell, R., Lotz, W., & Shaughanessy, A. (1984 ). Laryngeal aerodynamics associated with selected voice disorders. American Journal of Otolaryngology, 5, 397—403. Nober, E. H. (1987). Assessment of auditory processing in cerebral palsy. Seminars in Speech and Language, 8, 19—39. Palmer, M. F. (1952). Speech therapy in cerebral palsy. Journal of Pediatrics, 40, 514—524. Parush, A. & Ostry, D. (1986). Superior lateral pharyngeal wall movements in speech. Journal of the Acoustical Society of American, 80, 749—756. Phelps, W. M. (1956). Classification of athetosis with special reference to the motor classification. American Journal of Physical Medicine, 35, 24—31. Platt, L. F., Andrews, G., Young, M., & Quin, P. T. (1980). Dysarthria of adult cerebral palsy. I. Intelligibility and articulatory impairment. Journal of Speech and Hearing Research, 23, 28—38. Platt, L. F., Andrews, G., Young, M., & Neilson, P. D. (1978). The measurement of speech impairment of adults with cerebral palsy. Folia Phoniatrica, 30, 50—58. Platt, L. F., Andrews, G., & Howie, P. M. (1980). Dysarthria of adult cerebral palsy. II. Phonemic analysis of articulation errors. Journal of Speech and Hearing Research, 23, 41—55. Powell, J. & McReynolds, L. (1969). A procedure for testing position generalization from articulation training. Journal of Speech and Hearing Disorders, 12, 625—645. Pruszewicz, A., Obrebowski, A., & Zgoralewicz, B. (1977). Selected problems in the hearing, voice, and speech disturbances in the extra-pyramidal form of cerebral palsy. Folia Phoniatrica, 29, 302—310.
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Putman, A. & Hixon, T. J. (1984 ). Respiratory kinematics in speakers with motor neuron disease. In M. McNeil, J. Rosenbek, & A. Aronson (Eds.), The dysarthrias. San Diego: College Hill. Robin, D. A. & Eliason, M. (1991). Speech and prosodic problems in children with neurofibromatosis. In C. Moore, K. Yorkston & D. Beukelman (Eds.), Recent advances in motor speech disorders. 137—144. Baltimore: Paul H. Brooks. Robin, D. A., Klouda, G., & Hug, L. (1991). Neurogenic disorders of prosody. In M. P. Cannito & D. Vogel (Eds.), Treating disordered speech motor control: For clinicians by clinicians. 24 1—271. Austin, TX: Pro-Ed. Robin, D. A., Somodi, L., & Luschei, E. S. (1991). Measurement of tongue strength and endurance in normal and articulation disordered subjects. In C. Moore, K. Yorkston, & D. Beukelman (Eds.), Dysarthria and apraxia of speech: Perspectiv es on management. 173—184. Baltimore: Paul H. Brooks. Rosenbek, J. C. & LaPointe, L. L. (1985). The dysarthrias: description, diagnosis, and treatment. In D. L. Johns (Ed.), Clinical management of neurogenic communicativ e disorders. 97—152. Boston: Little Brown. Rutherford, B. (194 4 ). A comprehensive study of loudness, pitch, rate, rhythm, and quality of children handicapped by cerebral palsy. Journal of Speech and Hearing Disorders, 9, 263—271. Schliesser, H. F. (1982). Alternate motion rates of the speech articulators in adults with cerebral palsy. Folia Phoniatrica, 34, 258—264. Schneider, E. & Shprintzen, R. (1980). A survey of speech pathologists: current trends in the diagnosis and management of velopharyngeal insufficiency. Cleft Palate Journal, 17, 249—253. Shane, H. C. & Bashir, A. S. (1980). Election criteria for the adoption of an augmentative communication system: preliminary consideration. Journal of Speech and Hearing Disorders, 45, 408— 414. Sheppard, J. (1964 ). Cranio-oropharyngeal motor patterns in dysarthria associated with cerebral palsy. Journal of Speech and Hearing Research, 7, 373—380. Sheppard, J. (1987). Assessment of oral motor behaviors in cerebral palsy. Seminars in Speech and Language, 8, 57—70. Shprintzen, R. J., McCall, G. N., & Skolnick, M. D. (1975). A new therapeutic technique for the treatment of velopharyngeal incompetence. Journal of Speech and Hearing Disorders, 40, 69—83. Shriberg, L. & Kwiatkowski, J. (1980). Natural process analysis. New York: Jon Wiley & Sons. Skolnick, M. L. (1969). Video velopharyngography in patients with nasal speech, with emphasis on lateral pharyngeal wall motion in velopharyngeal closure. Radiology, 93, 747—755.
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Somodi, L., Robin, D. A., & Luschei, E. S. (1990). An inexpensive means of assessing strength and fatigue. Paper presented at the Annual Meeting of the American Speech, Language, and Hearing Association, Seattle, Washington. Thompson, C. K. & McReynolds, L. V. (1988). Neurogenic articulation disorders in children. In L. McReynolds & D. Yoder (Eds.), Handbook of Speech-Language Pathology and Audiology 548— 591. Philadelphia: B. C. Decker, Inc. Vanderheiden, G. C. & Harris-Vanderheiden, D. (1976). Communication techniques and aids for the nonvocal severly handicapped. In L. Lloyd (Ed.), Communication assessment and interv ention strategies. 607—652. Baltimore: University Park Press. Warren, D. & DeBois, A. (1964 ). A pressure-flow technique for measuring velopharyngeal orifice area during continuous speech. Cleft Palate Journal, 1, 52—71.
81. 1. 2. 3. 4.
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Weiner, F. (1978). Phonological process analysis. Baltimore: University Park Press. Wilson, B. C. & Davidovicz, H. M. (1987). Neuropsychological assessment of the child with cerebral palsy. Seminars in Speech and Language, 8, 1—18. Yorkston, K. M. & Beukelman, D. R. (1984 ). Assessment of intelligibility of dysarthric speech. Tigard, OR: CC Publications. Yorkston, K. M., Beukelman, D. R., & Bell, K. R. (1988). Clinical management of dysarthric speakers. Boston: Little, Brown and Company. Yules, R. B. & Chase, R. A. (1969). A training method for reduction of hypernasality in speech. Plastic Reconstruction Surgery, 43, 180—185.
Cynthia K. Thompson, Evanston, Illinois (USA) Donald A. Robin, Iowa City, Iowa (USA)
Effects of Congenital Malformations on Speech Development Introduction Cleft Lips and Palate Apert Syndrome and Crouzon Disease References
Introduction
Congenital craniofacial malformations constitute “experiments of nature” (Pruzansky 1973) which offer as much of a challenge to the fields of linguistics and speech science as they do to surgery, speech pathology, dentistry, psychology and other clinical specialties. These experiments often include perturbations of the speech production mechanism due to aberrant supralaryngeal vocal tract structure, and are most informative to the linguistic researcher when the associated speech is organized by a normal cognitive system possessed of a mature or developing linguistic system. Such speakers permit investigation of (a) the plasticity of the speech production mechanism for the successful realization of a phonological system, and (b) the anatomical requirements for accomplishing this task. Children with congenitally aberrant supralaryngeal vocal tracts provide an opportunity to explore the adequacy of linguistic theories in accounting both for their speech production and for the role of speech production in language acquisition.
Only rarely do congenital craniofacial malformations affect single structures. Historically, even the relatively common defect of cleft palate was diagnosed and treated without recognition of either (a) alterations in the anatomy contiguous to the cleft, such as abnormalities of the cervical spine which can affect the configuration of the pharynx, or (b) the fact that over 50% of individuals born with clefts have associated malformations, many presenting with syndromes which alter both the vocal tract and the auditory system. In such conditions as Crouzon disease and Apert syndrome, the linguist is presented with multiple perturbations of the ‘normal’ mechanism.
2.
Cleft Lip and Palate
2.1. Introduction Comprehensive reviews of effects of cleft lip and palate on articulation, with exhaustive literature citations, are found in Bzoch (1989), McWilliams/Morris/Shelton (1990), and Peterson-Falzone (1988). Improved surgical techniques have markedly increased the number of children with clefts who demonstrate normal development of communication skills, and there has been a recent surge of studies on the optimum age of surgical closure of the
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palate to prevent abnormal speech development. Based on current data on motor development, speech-motor control, and sensorimotor feedback, Kemp-Fincham/Kuehn/ Trost-Cardamone (1990) suggested that there seems to be a sensitive period for development of speech motor control, and consequently phonetic development, occurring between 4 and 6 months, and that it may therefore be important to close the palate prior to or during this period. Their theoretical discussion concurs with recent reports of better speech development in babies operated within the first six months of life as opposed to babies operated at later ages (e. g., Copeland 1996). 2.2. Prelinguistic Vocalizations and Early Childhood Studies Several recent studies have investigated prelinguistic vocalizations and the early stages of phonetic and phonologic development in children with clefts. Philips/Kent (1984 ) discussed weakening of the second formant by nasalization in the cries of cleft infants, but reported acoustic evidence of rhythmically organized vocalizations in their reduplicated babbling, with reduced acoustic consonant-vowel contrasts. The authors hypothesized that the reduced contrast could cause delays in acquisition of the vowel system. Salas-Provance/ Kuehn (1990) compared fundamental frequency, utterance duration and syllable duration in 4 cleft palate babies and and 4 noncleft babies from 13 to 15 months. The cleft palate babies exhibited higher mean fundamental frequencies and a restricted range of F0. Utterance durations were longer as compared to the non-cleft babies, but syllable durations were similar. O’Gara/Logemann (1988; 1990) analyzed the vocalizations of 51 cleft palate babies periodically between 3 and 36 months of age. The babies were divided into an ‘earlier closure/greater tissue group’ whose clefts were closed prior to 12 months of age (average 9.3 months) and a “later closure/lesser tissue” group who were closed after 12 months (average 14 .5 months). All of the babies showed a higher frequency of use of glottal and labial place features than of intraoral place features, with the earlier closure group showing greater use of intraoral place features than the later closure group and an earlier decrease in the use of glottal placements. At 6 months of age, none of the babies in either group showed the ‘alveolar takeover’ (predominance of alveolar
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productions over labials or velars) noted to occur in normal babies. The earlier closure group showed oral stop predominance at 18 to 19 months of age, while the later closure group never showed this predominance even through 36 months of age. Pharyngeal placements occurred only sporadically in both groups. Stops exceeded fricatives in both groups at all ages studied. Both groups showed a spurt in the use of nasal fricatives (discussed below) at 30—31 months of age, possibly related to the increased language requirements for fricative differentiation. The earlier closure group showed an early preference for front vowels, similar to normal babies, while the later closure group was slower to develop this preference. Both groups showed a consistent preference for mid-vowels rather than high or low vowels across all ages studied. Philips (1989) reported that surgical closure of the cleft produced a spontaneous increase in what had been limited phonetic repertoires and a concomitant decrease in the use of atypical phonological processes in toddlers with clefts. Grunwell/Russell (1987) analyzed the ‘speech-like’ pre- and postoperative vocalizations of 3 cleft palate infants operated between 11 and 14 months. None were using plosives other than ‘glottal plosives’ prior to surgery. Post-operatively, all were using some plosive articulations but only one was using apical/laminal plosives. The authors felt that the predominance of glottal contoids and velar approximants and a marked lack of bilabial and apical/laminal contoids replicated the results of O’Gara/Logemann (1988). Lynch/Fox/Brookshire (1983) reported that two cleft palate toddlers between the ages of 2:5 and 3:1 produced a disproportionate number of words beginning with glides and nasals, despite the fact that both reportedly had adequate velopharyngeal closure. Estrem/Broen (1989) studied 5 cleft palate toddlers, only one of whom had adequate velopharyngeal closure at the time the data was collected. These children chose and produced more words beginning with velars and glottals, and also targeted and produced more words beginning with labials and targeted fewer words beginning with alveolars. In short, the children with clefts selected words that contained sounds they were capable of producing, and they selected and produced more posterior sounds and labial sounds than did normal toddlers.
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Powers/Dunn/Erickson (1990) similarly found limited phonetic inventories in 4 males aged 3:2 to 3:11 with good velopharyngeal closure. Fricatives and affricates were rarely used, and stops were limited primarily to the word-initial position. Liquids and glides, other than /w/, were also infrequently used. Glottal and pharyngeal substitutions were rarely heard. The most common phonological processes were cluster reduction, liquid simplification, final consonant deletion and backing. The authors pointed out that not all of the articulatory problems could be explained solely on the basis of present or past structural deficits. Their results coincided with those of a longitudinal study by Van Demark/Morris/VandeHaar (1979), who found that their subjects were considerably behind normal children in mastering sounds that do not require velopharyngeal closure. 2.3. Analysis of Articulation Analysis of articulation problems in children with clefts has been approached in two ways which could be broadly termed ‘cause’ and ‘effect.’ In the former, errors have been classified according to the apparent physical etiology, i. e., labial, dental, palatal, velopharyngeal. In the latter approach, errors have been categorized both according to the normal mode of production of affected phonemes, and according to the mode of production of replacement phonemes. When replacement phonemes are studied, the relationship to observations of early vocalizations becomes apparent. Categorization of errors based on presumed structural bases becomes inexorably tied to categorization by place of production, the exception being the structural deviation viewed as the primary culprit in ‘cleft palate speech,’ namely the velopharyngeal mechanism. Labial defects typically have little impact (see Peterson-Falzone 1988). Dental/occlusal anomalies and reduced width of the maxillary arch may affect linguadental, linguoalveoar and linguapalatal phonemes, although these are typically recognizable even if distorted (Peterson-Falzone 1988) unless nasal air loss is predominant or the use of compensatory articulations obscures the phonemic contrasts. Abnormal tongue carriage and deviant lingual contacts in articulation were often viewed in the older literature as indicative of defective lingual structure or innervation; current investigators view these problems as secondary to abnormal structure
V. Pathologies and Disorders of Language Development
and function of the velopharyngeal system. Inadequate velopharyngeal closure produces nasal air loss on consonants requiring the build-up of intraoral pressure, and hypernasal resonance on vowels and vocalic segments. Children in whom such inadequacy is present during acquisition of speech motor control often develop one or more maladaptive ‘compensatory articulations’ (discussed below) which may persist even after an adequate velopharyngeal system has been provided through surgical or prosthetic care. Clearly the articulatory errors found in school-age children and adults with clefts are dictated in part by the adequacy of their early care and by the status of their oral and velopharyngeal systems at the time they are tested. Bearing in mind the consequent heterogeneity of subjects in studies of ‘cleft palate speech,’ these studies have repeatedly shown (1) more problems with fricatives and affricates than with plosives; (2) more problems on voiceless than voiced consonants, probably related to differences in aerodynamic requirements; (3) difficulty in suppressing voicing on voiceless consonants, interpreted as a result of leakage of air through the velopharyngeal port and a consequent inability to equalize air pressure above and below the vocal folds; (4 ) better production of single consonants than of the same consonants occurring in clusters, possibly reflecting the effect of impaired oral structures on the ability to make rapid articulatory adjustments; (5) substitution of either nasal phonemes or ‘backed’ productions, the latter being an apparent attempt to make use of the vocal airstream before it escapes through an open velopharyngeal port; (6) a tendency for articulation skills to continue to improve well past the age when these skills plateau in non-cleft children; and (7) a higher than normal frequency of problems with consonants not dependent upon adequate velopharyngeal closure. (For references, see McWilliams/Morris/Shelton 1990; PetersonFalzone 1988; Philips/Kent 1984). The literature on cleft palate is replete with descriptions of ‘compensatory articulations.’ Most of these seem to represent a sacrifice of the place feature for the retention of the manner feature (Trost 1981), although the child with severely disordered articulation may substitute glottal stops for continuants and even for liquids and glides, as well as for stops. Trost (1981) listed six compensatory articulations heard in English-speaking patients: glottal stops, pharyngeal stops, pha-
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ryngeal fricatives, velar fricatives, mid-dorsum palatal stops and ‘posterior nasal fricatives,’ the latter being Trost’s term for what older literature often called ‘nasal snort’. Trost also noted that some of these articulations, particularly glottal stops, can occur simultaneously with articulatory gestures in other parts of the vocal tract, an example being bilabial closure produced simultaneously with a glottal stop. Trost-Cardamone (1985) later added “pharyngeal affricates” to the list of compensatory articulations. There are references to palatal fricatives occurring as compensatory gestures (Philips/Kent 1984 ; McWilliams/Morris/Shelton 1990), and there is a growing body of evidence that many, if not most, of the productions classified as “pharyngeal” fricatives may actually be laryngeal fricatives (Kawano/Isshiki/Harita/ Tanokushi 1985; Witzel/Brown/Laskin/Margar-Bacal 1990). Philips/Kent (1984 ) pointed out that both pharyngeal and laryngeal articulations contribute to relatively low-frequency acoustic structure for consonants, with weakened or absent cues in some spectral regions and additional (abnormal) cues in other spectral regions. In severely nasalized speech, the lowfrequency nasal formant may be nearly continuously present, the effect of which is to obscure segment boundaries normally marked by changes in source excitation, manner, or place of articulation. Basic acoustic feature contrasts that are weakened or eliminated by velopharyngeal inadequacy include periodic versus aperiodic energy source, nasal versus nonnasal resonance, occluded versus nonoccluded vocal tract, voiced versus voiceless excitation, and a variety of contrasts related to place of articulation. 2.4. Timing One of the most productive areas of research in recent years has been that of timing or motor speech coordination in speakers with repaired clefts. Aerodynamic, spectrographic, radiographic and combined photodetectornasopharygoscopic studies have shown differences not only between cleft and non-cleft speakers in timing of speech segment durations (D’Antoni 1982; Forner 1983), but also between cleft speakers with apparent velopharyngeal competency versus those with varying degrees of incompetency on various measures of timing and coordination of the action of the laryngeal and articulatory mech-
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anisms (Karnell/Folkins/Morris 1985; Warren/Dalston/Morr et al. 1989). It has been conjectured that these differences may be attributable, in part, to an abnormally tight mechanical linkage between the tongue and velum in speakers with repaired clefts. Forner (1983) suggested that the backing of articulatory gestures may alter the aerodynamic interaction of labial, lingual, velar, and laryngeal valving. There is an obvious cause-effect question in considering compensatory articulations and the temporal differences shown in these studies: Do compensatory articulations cause the temporal disruptions, or do the demands of attempting to coordinate laryngeal, velopharyngeal, lingual and labial activity in the presence of velopharyngeal inadequacy cause the development of compensatory articulations?
3.
Apert Syndrome and Crouzon Disease
Apert syndrome (acrocephalosyndactyly Type I) and Crouzon disease (craniofacial dysostosis) are two of a large family of syndromes of “premature craniofacial synostosis.” In both Apert and Crouzon, premature closure of multiple sutures of the face and skull results in significant distortions of the craniofacial complex, including a malformed neurocranium and hypoplasia of the middle third of the face contributing to decreased space in the nasal, oral and pharyngeal airways. The hypoplastic maxilla is displaced posteriorly with respect to the mandible, and the oral airway is further crowded by (a) accumulations of soft tissue along the lateral palatine shelves, and (b) a long and thick soft palate (see Peterson-Falzone 1988, for a more complete description of the features of these syndromes and for references). The supralaryngeal structures in subjects with these syndromes may be described in brief as (a) a normal-sized tongue in severely constricted oral and pharyngeal cavities, limiting the tongue’s configurational possibilities within the vocal tract, and (b) malalignment of the labial and dental articulators due to the malocclusion. While the syndromes of Apert and Crouzon are rare, affected individuals have provided important information about the use of anomalous anatomy for achieving the vowel space of a language. It is not possible to obtain comparable information by perturbing a model of the vocal tract, because it is not possible to predict how the
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human cognitive system will respond to the perturbations. Because speakers with Apert syndrome or Crouzon disease must learn the phonology of their language with a vocal tract potentially restricted in its ability to achieve articulatory maneuvers, a series of acoustic and perceptual studies was undertaken to explore the ability of such speakers to maintain the normal set of vowel contrasts in English. The results of these studies may be summarized as follows: (1) A spectrographic study of the formant structure of vowels produced in a constant /hVd/ frame by six subjects with Apert syndrome and three with Crouzon disease (all adolescents with the exception of one unoperated Apert adult) showed a marked tendency for the F1-F2 plots to collapse into the “schwa” or neutral vowel region (Landahl/ Peterson-Falzone/Lieberman 1978). However, within this compact acoustic vowel space, the vowel tokens showed spatial organization with regard to their expected phonetic categories. The intervowel formant relationships reflected the relationships seen in normal speakers (Peterson/Barney 1952): That is, /i/ /a/ and /u/ appeared to serve as point vowels for these subjects despite the constricted vowel tracts. However, divergences and convergences between mean formant values were either too great or too small. In no subject was there a normal distribution of mean formant values for any vowel. In summary, the general relational nature of the vowel space was realized, but the vowels were not as contrastive as in normal speakers. (2) In an in-depth study of vowels produced in a wide variety of phonetic contexts by the unoperated Apert adult male speaker, Fourier analysis and Linear Predictive Coding showed the same compact vowel space when compared to the norms of Stevens/ House (1963) (Landahl/Butler/Lieberman/ Peterson-Falzone 1981). In all contexts, /u/ was the most deviant vowel. (3) Two studies of the intelligibility of the words and the identifiability of the vowels produced by the unoperated Apert adult yielded similar results (Landahl/Robinson/ Peterson-Falzone 1979; Varley/Landahl/ Gould 1986). Linguistic students were able to identify the words used in the study described above at the 95% level and the vowels excised from those words at the 75% level. No /u/ tokens were correctly identified, corresponding to the highly aberrant formant structure. When the excised vowel tokens were submit-
V. Pathologies and Disorders of Language Development
ted to a discriminant function analysis based on data produced by nine randomly selected adult male speakers from the Peterson/Barney study of 1952, the results indicated that the listeners did much better at vowel identification that did the discriminant function analysis, suggesting that the listeners used more information than F1 and F2 in figuring out the speaker’s vowel system. The discriminant function analysis did not do significantly better when information on F3 was added. Durations of two short/long pairs of vowels were studied in an attempt to determine whether durational cues were assisting the listeners in identifying the excised vowels, but the results were not definitive. (4 ) A vocal tract modeling study (Landahl/Gould 1987) was undertaken to investigate whether it should be physically possible for the speaker used in the above studies to produce a different type of vowel space other than the one revealed in the acoustic measurements. The results were essentially negative, that is, the vowel space computed by the programmed model was even more compact than had been observed in the previous studies with the exception of the fact that the model indicated that the speaker should have been able to produce /a/ within the normal region. The authors concluded that it may have been more important for the speaker to keep his /a/ in proper relation to the rest of his vowel space than to imitate a ‘normal’ /a/. (5) A developmental study of the F1-F2 vowel spaces of a male and a female child with Apert syndrome (Hasner/Landahl 1987) was undertaken for comparison to the vowel spaces of normal infants (Lieberman 1980). At approximately one year of age, the vowel spaces of the Apert children did not exhibit obvious abnormal qualities. The formant frequency ranges were consistent with those reported by Lieberman (1980). The authors felt that these findings were due to the fact that the physical development of the vocal tract in Apert children is not grossly different from that of normal children at this early stage. However, longitudinal data derived from the female Apert child indicated a compact vowel space by the age of two years. In summary, this series of studies has indicated that the experiments of nature represented by Apert syndrome and Crouzon disease do not totally preclude the articulation of human language but do have deleterious effects on the production system for realizing the linguistic system in speech.
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4.
References
Bzoch, K. R. (1989). Communicativ e Disorders Related to Cleft Lip and Palate (3rd edition). Boston: College-Hill. Copeland, M. (1990). The effects of very early palatal repair on speech. British Journal of Plastic Surgery, 43, 676—683. D’Antonio, L. L. (1982). An investigation of speech timing in individuals with cleft palate. Unpublished doctoral dissertation, University of California, San Francisco. Estrem, T. & Broen, P. A. (1989). Early speech production of children with cleft palate. Journal of Speech and Hearing Research, 32, 12—23. Forner, L. L. (1983), Speech segment durations produced by five and six year old speakers with and without cleft palates. Cleft Palate Journal, 20, 2, 185—198. Grunwell, P. & Russell, J. (1987). Vocalisations before and after cleft palate surgery: a pilot study. British Journal of Disorders of Communication, 22, 1—17. Hasner, A. & Landahl, K. (1987). Development of vowel space in children with Apert syndrome. Unpublished manuscript, Department of Linguistics, The University of Chicago. Karnell, M. P., Folkins, J., & Morris, H. L. (1985), Relationships between the perception of nasalization and speech movements in speakers with cleft palate. Journal of Speech and Hearing Research, 28, 1, 63—72. Kawano, M., Isshiki, N., Harita, Y., & Tanokushi, F. (1985). Laryngeal fricative in cleft palate speech. Acta Otolaryngologica, Supplement 419, 180—188. Kemp-Fincham, S. I., Kuehn, D. P., & Trost-Cardamone, J. E. (1990). Speech development and the timing of primary palatoplasty. In J. Bardach & Hl. Morris (Eds.), Multidisciplinary management of cleft lip and palate. 736—745. Philadelphia: W. B. Saunders. Landahl, K., Butler, J., Lieberman, P., & PetersonFalzone, S. J. (1981). Fourier and linear predictive analyses of aberrant vowel formants. In B. J. Urban (Ed.), Proceedings of the 18th Congress of the International Association of Logopedics and Phoniatrics. 113—118. Landahl, K. & Gould, H. (1987). Congenital malformation of the speech tract in humans and its developmental consequences. In R. J. Ruben, T. R. Van de Water, & E. W. Rubel (Eds.), The Biology of Change in Otolaryngology. 131—149. Amsterdam: Excerpta Medica. Landahl, K., Peterson-Falzone, S., & Lieberman, P. (1978). Formant frequency patterns in anomalous supralaryngeal vocal tracts. Presented before the annual convention of the American SpeechLanguage-Hearing Association, San Francisco. Landahl, K., Robinson, J., & Peterson-Falzone, S.
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(1979). Vowel durational cues in speakers exhibiting aberrant formant frequency patterns. Presented before the American Speech-Language-Hearing Association, Atlanta. Lieberman, P. (1980). On the development of vowel production in young children. In G. Yeni-Komshian & D. Ferguson (Eds.), Child Phonology — Volume I: Production. 113—142. New York: Academic Press. Lynch, J. L., Fox, D. R., & Brookshire, B. L. (1983). Phonological proficiency of two cleft palate toddlers with school-age follow-up. Journal of Speech and Hearing Disorders, 48, 274—285. McWilliams, B. J., Morris, H. L., Shelton, R. L. (1990). Cleft palate speech (2nd edition). Toronto: B. C. Decker. O’Gara, M. M. & Logemann, J. A. (1990). Early speech development in cleft palate babies. In J. Bardach & H. Morris (Eds.), Multidisciplinary management of cleft lip and palate. 717—721. Saunders, 1990. O’Gara, M. M. & Logemann, J. A. (1988). Phonetic analyses of the speech development of babies with cleft palate. Cleft Palate Journal, 25, 2, 122— 134. Peterson, G. E. & Barney, H. L. (1952). Control methods used in a study of the vowels. Journal of the Acoustical Society of America, 24, 175—184. Peterson-Falzone, S. J. (1988). Speech disorders related to craniofacial structural defects, Part 2. In N. J. Lass, L. V. McReynolds, J. L. Northern, & D. E. Yoder (Eds.), Handbook of speech-language pathology and audiology. 477—547. Toronto: B. C. Decker. Philips, B. J. & Kent, R. D. (1984 ). Acoustic-phonetic descriptions of speech production in speakers with cleft palate and other velopharyngeal disorders. In NJ. Lass (Ed.), Speech and language: Adv ances in basic research and practice, Volume 11. 113—168. New York: Academic Press, 1984. Philips, B. J. (1989). Phonological development of children with palatal clefts (abstract). Folia Phoniatrica, 41, 203—204. Powers, G. R., Dunn, C., & Erickson, C. B. (1990). Speech analyses of four children with repaired cleft palates. Journal of Speech and Hearing Disorders, 55, 542—549. Pruzanksy, S. (1973). Clinical investigation of the experiments of nature. ASHA Reports, 8, 63—94. Salas-Provance, M. & Kuehn, D. P. (1990). Nonsegmental characteristics in prespeech utterances of babies with cleft palate. Presented before the American Speech-Language-Hearing Association, Seattle. Stevens, K. & House, A. (1963). Perturbation of vowel articulation by consonantal context: an acoustical study. Journal of Speech and Hearing Research, 6, 111—128.
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Trost, J. E. (1981). Articulatory additions to to the classical description of the speech of persons with cleft palate. Cleft Palate Journal, 18, 3, 193—203. Trost-Cardamone, J. E. (1985). From diagnosis to treatment: Speech remediation for persons with cleft palates and related velopharyngeal disorders. Short course presented before the California Speech-Language-Hearing Association, Anaheim. Van Demark, D. R., Morris, H. L., & Vandehaar, C. (1979). Patterns of articulation abilities in speakers with cleft palate. Cleft Palate Journal, 16, 3, 230—239. Varley, D., Landahl, K., & Gould, H. (1986). Perceptual categorization of a compressed vowel space. Journal of the Acoustical Society of America,
79, Suppl. No. 1, 58. Warren, D. W., Dalston, R. M., Morr, K. E., Hairfield, W. M., & Smith, L. R. (1989). The speech regulating system: Temporal and aerodynamic responses to velopharyngeal inadequacy. Journal of Speech and Hearing Research, 32, 566—575. Witzel, M. A., Brown, S., Laskin, R. L., & MargarBacal, F. (1990). The laryngeal fricative in cleft palate speech: Description and diagnosis. Presented before the American Speech-Language-Hearing Association, Seattle.
Sally J. Peterson-Falzone, San Francisco, California (USA)/Karen L. Landahl, Chicago, Illinois (USA)
82. Stuttering: Physiological Correlates and Theoretical Perspectives 1. 2. 3. 4.
1.
Introduction Physiological Correlates of Stuttering Conclusion References
Introduction
The purpose of this chapter is to summarize the results of investigations of the physiological bases of stuttering. Many different methodologies have been employed to assess the physiological correlates of stuttering, and the different methodologies often were motivated by distinct theories of the etiology of the disorder. Thus, this review will also discuss theoretical perspectives in relation to the physiological findings. Stuttering is a disorder of speech with a prevalence estimated to be 1% of the world’s population (Bloodstein 1981; Van Riper 1982). It is a disorder in the rhythm or natural flow of speech “... in which the individual knows precisely what he wishes to say, but at the same time is unable to say it ...” (WHO 1977, 202). The disruptions of speech or disfluencies that characterize stuttering are easily recognized by the naive listener. There are sound and syllable repetitions, silent pauses, voiced pauses, and interjections that disrupt the flow of speech. The normal flow of sound production is the acoustic consequence of movement, which in turn is the result of an organized neural input to the motoneuron pools that innervate the muscles involved in speech. Speech re-
quires coordinated activity in many different muscles, including orofacial, laryngeal, and respiratory muscles. Thus an organized synaptic input must be distributed over a large number of muscles, so that appropriate forces are developed in the appropriate muscles at the right time. A universal symptom of stuttering is that the distributed input to muscles is disrupted, and inputs appropriate for the continuation of speech are not generated or are overtaken by other sources of neural drive. What are the factors that produce breakdowns in speech motor processes in stuttering? Historically, theories of the etiology of stuttering emphasized a single aspect of the disorder as the major explanatory variable. For example, stuttering has been explained as arising primarily from faulty laryngeal control (Kenyon 194 3), the negative evaluations of children’s speech by their parents (Johnson 194 2), or as a learned anticipatory struggle response (Bloodstein 1981). Theories of stuttering proliferated, and battles were waged in the stuttering literature with a major division between those who believed in a ‘physiological cause’ and those who believed stuttering was ‘entirely learned’. The futility of this debate has been recognized in recent years (e. g., Smith/Weber 1988), and evidence has accumulated that there is a genetic component underlying the development of stuttering (e. g., Howie 1981) and that environmental factors and learning also play important roles in the development and maintenance of disfluent behavior (e. g., Bloodstein 1981).
82. Stuttering: Physiological Correlates and Theoretical Perspectives
Currently on the theoretical front, many authors argue that single factor approaches cannot provide a complete explanation of stuttering, because many factors converge to produce the conditions we associate with this disorder. Thus, several multifactorial models of stuttering (e. g., Starkweather 1987; Wall/ Meyers 1984 ; Van Riper 1982; Zimmermann/ Smith/Hanley 1981) have appeared and are receiving widespread acceptance. Central to these models are the assumptions that (1) many different types of variables play a role in the development and maintenance of stuttering, and (2) there is considerable variation between individuals who stutter on the relative importance of each factor in the development of the disorder. The present review of physiological factors correlated with stuttering is grounded in the integrative, multifactorial approach to stuttering that we have described in earlier papers (Zimmermann 1980 c; Zimmermann/Smith/ Hanley 1981; Smith 1990). A key aspect of this multifactorial framework is that it recognizes that disruption of speech motor performance is a universal symptom of the disorder. Therefore, the long list of complex factors involved in the etiology of the disorder, e. g., psychosocial, linguistic, and cognitive factors, can be viewed as ultimately either directly or indirectly interacting with speech motor processes to produce the kinds of breakdowns characteristic of stuttering. This approach recognizes that many different kinds of measurements will contribute to our attempt to understand stuttering, e. g., sociocultural, behavioral, acoustic, and physiological measures, but that all of these levels of measurement must be integrated into a comprehensive explanation of stuttering. This approach leads us to examine linkages between different levels of measurement and to determine how various factors contribute to a disruption in speech motor processes. For example, experimental results suggest that stuttering is correlated with linguistic complexity (Bloodstein 1981). Under the proposed multifactorial model, the challenge is to determine the link between linguistic complexity and speech motor breakdown. In summary, we believe that a theory of stuttering must be a multifactorial theory with integration of these factors accomplished through an understanding of their effects on the operation of neuromotor systems.
2.
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Physiological Correlates of Stuttering
Cognitive, emotional, and linguistic processes influence the planning and execution of speech motor behavior. Investigations exploring the physiological bases of stuttering have employed diverse methodologies to assess central and peripheral physiological processes underlying the various stages of speech production, including preparation and execution. In addition, a number of investigations of the physiological bases of stuttering have assessed the status of sensorimotor, autonomic, and other systems in stutterers during performance of a wide range of nonverbal motor tasks. A complete review of this literature is beyond the scope of this chapter. Therefore the following sections will outline major themes that have emerged in the search for the physiological correlates of stuttering. 2.1. Measures of CNS Function The Orton-Travis theory that stuttering develops because normal patterns of cerebral dominance are absent (Orton 1928; Travis 1931) has had a major impact on investigations of central nervous system (CNS) processes and stuttering. Thus, investigations have focused on the search for differences in hemispheric laterality between stutterers and normal speakers. Electroencephalography (EEG) has been widely used to study human brain function. Early EEG investigations, using necessarily crude methods of data analysis (for example, the percent time of alpha), reported left/right alpha ratios that seemed to support the Orton-Travis theory (e. g., Douglass 194 3). In later studies, signal averaging was used to study the laterality of eventrelated potentials of the brain. By measuring slow changes in the EEG, specifically the contingent negative variation (CNV), investigators attempted to obtain an index of cognitive, linguistic, and motor planning processes preceding speech production in stutterers. Results of these studies (Zimmermann/Knott 1974 ; Pinsky/McAdam 1980) are not consistent. Zimmermann/Knott reported that a majority of stutterers showed larger shifts over the right hemisphere preceding speech production, while the stutterers tested by Pinsky/ McAdam showed the normal pattern of a larger CNV over the left hemisphere preceding speech. Other methodologies for assessing CNS function also have produced mixed results.
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Andrews/Quinn/Sorby (1972) found that three adult stutterers showed normal unilateral left cerebral dominance for speech on the intracarotid sodium amytal test. Some investigations reporting tests of dichotic listening on groups of stutterers and nonstutterers have yielded significant group differences in ear advantage, while other studies report no group differences (e. g., Curry/Gregory 1969; Dorman/Porter 1975). In summary, there may be some deficit in the central nervous system processes subserving speech production and associated functions in individuals who stutter. The proposal that such a deficit may be found does not imply that the deficit(s) must be the same in all individuals who stutter, nor does it imply that the differences between stutterers and nonstutterers are causally related to stuttering. At this point, however, we simply do not know anything about the precise nature of these deficits nor of the significance of the differences that are reported. Our lack of understanding in this area is no doubt due to the difficulty of studying brain functions in intact, behaving human subjects and the limits of current theories of brain-behavior relationships. Advances in technologies for studying human brain functions, for example, quantitative analysis of EEG and SPECT (single photon emission computed tomography), may aid in understanding stuttering if the measures can be integrated into a general theoretical account of brain-behavior relationships. 2.2. Electromyography (EMG) In general, investigations of muscle activity and movement (reviewed in section 2.3 below) in stutterers have been undertaken with the goal of describing abnormal activity and have not been explicitly theory driven. Activity of articulatory and laryngeal muscles has been recorded with surface and indwelling electrodes during speech production in stutterers. These investigations report that stuttered speech is characterized by excessive activity in articulatory and laryngeal muscles, oscillations of muscle activity at frequencies characteristic of normal tremor, and coactivation of antagonistic orofacial and laryngeal muscles (e. g., Fibiger 1971; Freeman/Ushijima 1978; Kalotkin/Manschreck/O’Brien 1979; McClean/Goldsmith/Cerf 1984 ; Smith 1989). These descriptions are widely accepted, but there are many issues that remain to be re-
V. Pathologies and Disorders of Language Development
solved before the significance of these observations to a theory of stuttering can be understood. For example, of the investigations reporting excessive muscle activity during disfluent behavior, only two include a quantitative analysis of the EMG data (Freeman/Ushijima 1978; Kalotkin/Manschreck/O’Brien 1979); and Kalotkin/Manschreck/O’Brien failed to normalize values for comparisons across subjects. In a recent study by Smith/Denny/ Wood (1991), EMG amplitude was found on average to be larger during 500 ms intervals of perceptually fluent speech following the disfluencies compared to the EMG during the disfluencies. Thus, despite the widespread impression that stuttering is associated with abnormally high levels of muscle activity, the degree, distribution across muscles, time course, and consistency across subjects of excessive muscle activity related to stuttering is not well established. It is well established that, in stutterers, abnormal oscillations of muscle activity occur. This finding has been replicated in a number of laboratories and has led to specific hypotheses concerning the neural sources producing motor instability in stuttering (e. g., Smith 1989). The third result, listed above, co-activation of antagonistic muscles has also been a consistent finding, however the interpretation of this result often has been confused by the erroneous assumption that co-activation of antagonistic muscles is always an abnormal pattern of muscle activation. In fact, depending on the task demands, co-activation can be a preferred strategy of recruitment of muscles. For example, Smith (1989) applied a cross-correlational analysis and reported coactivation of antagonistic muscles of the jaw during disfluencies of stutterers, but this was not abnormal. The normal subjects tested demonstrated coactivation of these muscles to a similar degree during speech. The existing EMG data on stuttering provide some clues concerning the nature of aberrant inputs to motoneuron pools innervating muscles involved in speech production. The next step is to apply more detailed methods of signal analysis to test specific hypotheses about (1) the time course of muscle activity in fluent and disfluent speech, (2) the sources in the nervous system that generate the aberrant activity, and (3) the age at which these abnormal aspects of speech motor activity develop.
82. Stuttering: Physiological Correlates and Theoretical Perspectives
2.3. Kinematic Events Measurement of kinematic events has indicated that stuttering is characterized by abnormal chest wall movements, including increased durations of expiratory and inspiratory phases, halted movements, unusual, oppositional movements of the abdomen and rib cage, speaking on inspiration, and chest wall tremor (Fossler 1930; Seth 1934 ); abnormal or ‘nonpredicted’ positioning of the vocal folds (Conture/McCall/Brewer 1977); tonic positioning, oscillatory movements of the articulators, and a disruption in inter-articulator timing (McClean/Goldsmith/Cerf 1984 , Zimmermann 1980 a; b). Caruso/Abbs/Gracco (1988) reported that normal speakers showed an invariant sequence of peak velocities of upper lip, lower lip, and jaw movements measured for a single speech gesture within a single utterance, while stutterers’ fluent productions of the utterance showed reversals of this pattern. From this finding they speculated about the role of the supplementary motor area in stuttering. McClean/Kroll/ Loftus (1990) replicated the methods of Caruso/Abbs/Gracco, but did not find that normal speakers demonstrated invariant velocity sequencing of these structures. For stutterers, McClean et al. reported that velocity sequencing was strongly dependent on the therapeutic history of the subject. Kinematic analysis of articulatory events in stutterers’ fluent and disfluent speech produced the important observation that even the perceptually fluent speech of stutterers is characterized by abnormal sensorimotor organization (Zimmermann 1980 a; b). This observation has been confirmed in a number of subsequent studies (e. g., Peters/Boves 1988). This is a significant result, because it led to the insight that, although perceptual judgments of stutterers’ speech are dichotomous (e. g., fluent or disfluent), the processes underlying stuttering are continuous. 2.4. Measures of Autonomic Activity In our multifactorial theoretical approach to stuttering and in many other theories of stuttering (e. g., Brutten/Shoemaker 1967), a significant factor thought to contribute to speech motor breakdown is the emotional state of the speaker. Scientists have long recognized that the physiological changes underlying emotional experience, for example, changes in heart rate, blood flow, and sweat-
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ing, are mediated by activity of the autonomic nervous system (ANS). Furthermore, autonomic processes are integrated with somatic sensorimotor processes at many levels of the nervous system (Pick 1970). Therefore, investigation of ANS activity may provide important clues as to how the emotional state of the individual affects speech motor processing. A major goal of studies of ANS activity in stuttering has been to determine if stutterers have higher levels of autonomic arousal compared to normal speakers. ANS function has been assessed in stuttering by measuring heart rate, blood flow, blood pressure, electrodermal activity, and biochemical assays. In many early studies only one autonomic measure was used, while later studies have used multiple measures, making them more sensitive to group differences and better able to distinguish sympathetic and parasympathetic influences. Results of earlier investigations produced mixed results concerning the role of the ANS in stuttering (see Weber/Smith (1990) for a review). In contrast, two recent studies employing large numbers of subjects and simultaneous measurement of a variety of autonomic indices have produced consistent findings. Peters/Hulstijn (1984 ) recorded heart rate, pulse volume, and tonic and phasic skin conductance while 24 stutterers and 24 nonstutterers performed tasks including writing, mirror writing, responding to intelligence test items, silent reading, and spontaneous speech. They found no between-group differences on any autonomic measure, but they reported that for both groups, speaking was associated with relatively large increases in autonomic arousal when compared to that observed in the other tasks. Weber/Smith (1990) recorded tonic and phasic skin conductance, peripheral blood flow, and heart rate in 19 stutterers and 19 normal speakers with matched group distributions of age, sex, and educational background. Autonomic measures were recorded during jaw movements, a strenuous breathholding task, reading, and spontaneous speech. Weber/Smith reported no group differences on any of the measures recorded for any of the tasks. They, like Peters/Hulstijn, found that speaking, for both groups of subjects, was characterized by high levels of autonomic arousal. Weber/Smith further analyzed the fluent and disfluent utterances within the stuttering subjects and found that increased sympathetic arousal was correlated
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with the occurrence and severity of disfluent speech. The results reported by Peters/Hulstijn and Weber/Smith are remarkably similar. They suggest the following conclusions regarding autonomic activity and stuttering: (1) stutterers, even when engaged in disfluent speech, do not experience autonomic arousal that is outside the range of that experienced during speech by nonstutterers; (2) for both stutterers and nonstutterers, speaking is characterized by large increases in sympathetic arousal, even when compared to a strenuous physical maneuver or difficult cognitive tasks; and (3) within individuals who stutter, higher levels of sympathetic arousal tend to co-occur with speech that is perceived as disfluent. In view of these conclusions, research now needs to be directed at discovering if increased sympathetic arousal in stutterers is correlated with specific characteristics of instability in speech motor processes. 2.5. General Motor Performance in Stutterers and Nonstutterers Many different theories of stuttering have provided impetus for investigations comparing stutterers’ and nonstutterers’ performance, usually by measuring aspects of timing control, on various motor tasks. The OrtonTravis theory of inadequate cerebral dominance in stuttering triggered numerous investigations by researchers in the 1920’s and 30’s. In many of these studies rapid, repetitive movements or reproduction of a temporal pattern by subjects moving hands, oral structures, and/or the chest wall were analyzed. In many cases, stutterers were found to perform more poorly (e. g., Blackburn 1931; Hunsley 1937), while in other studies, no differences were found (e. g., Cross 1936; Seth 1934 ). Recent investigations suggest that stutterer/ nonstutterer differences may emerge more consistently when the task requires that the subjects generate (rather than reproduce) a rhythm (e. g., Brown/Zimmermann/Linville/ Hegmann 1990), or that he plan and execute movements that involve complex temporal and spatial coding (e. g., Webster 1989). The idea that stuttering is primarily the result of a deficit in control of the larynx led investigators to test whether stutterers differed from nonstutterers in voicing control. A study by Adams/Hayden (1976), reporting that stutterers were slower than nonstutterers in phonating the vowel /a/ in response to an auditory cue, was the first in a long series of
reaction time (RT) investigations of stuttering in the 1970’s and 80’s. These investigations have included tests of auditory-voice reaction time, visual-voice reaction time, and tests of manual reaction time. The results of the many RT studies cannot be summarized in detail, but in general, they strongly suggest that stutterers’ have longer RT’s than normal speakers when the response required is a speech utterance, but that group differences with manual or other nonspeech RT responses are less consistent (Peters/Hulstijn/ Starkweather 1989). Although often motivated by distinct theories of the ‘cause’ of stuttering, these studies address a question central to our understanding of the disorder: Is stuttering a speech disorder that arises in part from a generalized deficit in sensorimotor organization, or is it speech specific, with no relation to other motor skills? The positive findings of the studies reviewed in this section are adequate to sustain the viability of the hypothesis that stuttering is often accompanied by a generalized sensorimotor deficit. The precise nature of such a deficit remains to be discovered.
3.
Conclusion
Historically, researchers and clinicians who work in the area of stuttering have been divided into a multitude of camps with almost no agreement on what the goals of theory should be or on what data should be regarded as significant. Physiological data were dismissed by those with a behavioral approach, and behavioral data were rarely incorporated into narrow, ‘physiological’ explanations of stuttering. In the past few years, some degree of consensus has emerged concerning both theory and data. Both researchers and clinicians are beginning to agree that a multifactorial approach to stuttering is essential and that both behavioral and physiological data must serve as the building blocks for an integrated, multifactorial theory. From the present review of the physiological correlates of stuttering, it can be seen that our knowledge is far from complete. In particular, information on central nervous system processes in stuttering is lacking. Much more progress has been made in understanding autonomic nervous system activity in relation to stuttering. These data are congruent with the results of many investigations that, through administration of standard personality tests, failed to find a “stuttering person-
82. Stuttering: Physiological Correlates and Theoretical Perspectives
ality” (Bloodstein 1981). Taken together, these results weigh strongly against the hypothesis that stutterers have generally high levels of emotional reactivity (e. g., Brutten/ Shoemaker 1967). What emerges instead, is the view that stuttering is a disorder that arises when a variety of factors, including normal levels of emotional stress, impact on a sensorimotor system that is vulnerable to breakdown. Acknowledgement: Preparation of this review was supported by grant DC00559 from the NIH’s National Institute on Deafness and Other Communication Disorders.
4.
References
Adams, M. & Hayden, P. (1976). The ability of stutterers and nonstutterers to initiate and terminate phonation during production of an isolated vowel. Journal of Speech and Hearing Research, 19, 290—296. Andrews, G., Quinn, P., & Sorby, W. A. (1972). Stuttering: an investigation into cerebral dominance for speech. Journal of Neurology, Neurosurgery, and Psychiatry, 35, 414—418. Blackburn, W. (1931). A study of the voluntary movements of the diaphragm, tongue, lips and jaw in stutterers and normal speakers. Psychological Monograph, 41, 1—13. Bloodstein, O. (1981). A Handbook on Stuttering. Chicago: National Easter Seal Society. Brown, C., Zimmermann, G., Linville, R., & Hegmann, J. (1990). Variations in self-paced behaviors in stutterers and nonstutterers. Journal of Speech and Hearing Research, 33, 317—323. Brutten, E. & Shoemaker, D. (1967). The Modification of Stuttering. Englewood Cliffs: Prentice Hall. Caruso, A., Abbs, J. & Gracco, V. (1988). Kinematic analysis of multiple movement coordination during speech in stutterers. Brain, 111, 439—455. Conture, E., McCall, G., & Brewer, D. (1977). Laryngeal behavior during stuttering. Journal of Speech and Hearing Research, 20, 661—668. Cross, H. (1936). The motor capacities of stutterers. Archives of Speech, 1, 112—132. Curry, F. & Gregory, H. (1969). The performance of stutterers on dichotic listening tasks thought to reflect cerebral dominance. Journal of Speech and Hearing Research, 12, 73—82. Dorman, M. & Porter, R. (1975). Hemispheric lateralization for speech perception in stutterers. Cortex, 11, 181—185. Douglass, L. (194 3). A study of bilaterally recorded electroencephalograms of adult stutterers. Journal of Experimental Psychology, 32, 247—265.
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Fibiger, S. (1971). Stuttering explained as a physiological tremor. Speech Transmission Lab-Quarterly Program & Strategy Report, 1—2, 1—23. Fossler, H. (1930). Disturbance in breathing during stuttering. Psychological Monograph, 40, 1—32. Freeman, F. & Ushijima, T. (1978). Laryngeal muscle activity during stuttering. Journal of Speech and Hearing Research, 21, 538—562. Howie, P. (1981). Concordance for stuttering in monozygotic and dizygotic twin pairs. Journal of Speech and Hearing Disorders, 24, 317—321. Hunsley, Y. (1937). Disintegration in the speech musculature of stutterers during the production of nonvocal temporal pattern. Psychological Monograph, 49, 32—49. Johnson, W. (194 2). A study of the onset and development of stuttering. Journal of Speech Disorders, 7, 251—257. Kenyon, E. (194 3). The etiology of stammering: The psychophysiologic facts which concern the production of speech sounds and of stammering. Journal of Speech Disorders, 8, 347—348. Kalotkin, M., Manschreck, R., & O’Brien, D. (1979). Electromyographic tension levels in stutterers and normal speakers. Perceptual and Motor Skills, 49, 109—110. McClean, M., Goldsmith, H., & Cerf, A. (1984 ). Lower-lip EMG and displacement during bilabial disfluencies in adult stutterers. Journal of Speech and Hearing Research, 27, 342—349. McClean, M., Kroll, R., & Loftus, N. (1990). Kinematic analysis of lip closure in stutterers’ fluent speech. Journal of Speech and Hearing Research, 33, 155—160. Orton, S. (1928). A physiological theory of reading disability and stuttering in children. New England Journal of Medicine, 199, 1046—1052. Peters, H. & Boves, L. (1988). Coordination of aerodynamic and phonatory processes in fluent speech utterances of stutterers. Journal of Speech and Hearing Research, 31, 352—361. Peters, H. & Hulstijn, W. (1984 ). Stuttering and anxiety: The difference between stutterers and nonstutterers in verbal apprehension and physiologic arousal during the anticipation of speech and nonspeech tasks. Journal of Fluency Disorders, 9, 67— 84. Peters, H., Hulstijn, W., & Starkweather, C. (1989). Acoustic and physiological reaction times of stutterers and nonstutterers. Journal of Speech and Hearing Research, 32, 668—680. Pick, J. (1970). The Autonomic Nerv ous System: Morphological, Comparativ e, Clinical and Surgical Aspects. Philadelphia, Toronto: J. B. Lippincott Company. Pinsky, S. & McAdam, D. (1980). Electroencephalographic and dichotic indices of cerebral later-
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ality in stutterers. Brain and Language, 11, 374— 397. Seth, G. (1934 ). Psychomotor control in stammering and normal subjects: An experimental study. British Journal of Psychology, 49, 139—143. Smith, A. (1989). Neural drive to muscles in stuttering. Journal of Speech and Hearing Research, 32, 252—264. Smith, A. (1990). Factors in the etiology of stuttering. ASHA REPORTS, Research Needs in Stuttering: Roadblocks and Future Directions, 18, 39— 47. Smith, A., Denny, M., & Wood, J. (1991). Instability in Speech Muscle Systems in Stuttering. In H. Peters, W. Hulstijn, & W. Starkweather (Eds.), Speech Motor Dynamics. New York: Springer-Verlag, 231—242. Smith, A. & Weber, C. (1988). The need for an integrated perspective on stuttering. ASHA, 30, 30—32. Starkweather, C. (1987). Fluency and Stuttering. Englewood Cliffs, NJ: Prentice-Hall. Travis, L. (1931). Speech Pathology. New York: Appleton-Centruy-Crofts. Van Riper, C. (1982) The Nature of Stuttering. Englewood Cliffs, NJ: Prentice Hall. Wall, M. & Myers, F. (1984 ). Clinical Management of Childhood Stuttering. Baltimore: University Park Press. Weber, C. & Smith, A. (1990). Autonomic correlates of stuttering and speech assessed in a range
of experimental tasks. Journal of Speech and Hearing Research, 33, 690—706. Webster, W. (1989). Sequence initiation performance by stutterers under conditions of response competition. Brain and Language, 36, 286—300. World Health Organization (1977). Manual of the international statistical classification of diseases, injuries, and causes of death. Geneva: World Health Organization. Zimmermann, G. (1980 a). Articulatory dynamics of fluent utterances of stutterers and nonstutterers. Journal of Speech and Hearing Research, 23, 95— 107. Zimmermann, G. (1980 b). Articulatory behaviors associated with stuttering: A cineradiographic analysis. Journal of Speech and Hearing Research, 23, 108—121. Zimmermann, G. (1980 c). Stuttering: A disorder of movement. Journal of Speech and Hearing Research, 23, 122—136. Zimmermann, G. & Knott, J. (1974 ). Slow potentials of the brain related to speech processing in normal speakers and stutterers. Electroencephalography and Clinical Neurophysiology, 37, 599—607. Zimmermann, G., Smith, A., & Hanley, J. (1981). Stuttering: In need of a unifying conceptual framework: Journal of Speech and Hearing Research, 24, 25—31.
Anne Smith, West Lafayette, Indiana (USA)/ Gerald N. Zimmermann, Iowa City, Iowa (USA)
83. Linguistic Phenomenology in Stuttering 1. 2. 3. 4. 5. 6. 7. 8.
1.
Introduction Stuttering Accompanied by Language Disorders Stuttering is a Language Disorder Language Systems Cognitive Grammar The Competition Model Research Implications References
Introduction
Interpretations of the stuttering-language disorder interaction fall into two broad categories. Historically, the most prominent view has been that stuttering is often a c c o m p an i e d by l a n g u a ge d i s o r d e r. More recently, the perspective that stuttering i s a
l a n g u a ge d i s o r d e r has been expressed by various authors. After a consideration of the motivation for each interpretation, some current and controversial issues in psycholinguistics will be advanced as particularly germane to stuttering research development.
2.
Stuttering Accompanied by Language Disorders
From approximately 194 0—1965 psychodynamic and learning theory explanations for the onset and nature of stuttering were in favor. During that period there were frequent reports that many children who stutter also have language and articulation disorders, and attempts were made to explain why these separate disorders might appear in one client. The typical interpretation invoked the
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construct of fear of speech. The child who stutters might be less inclined to talk for this reason, thereby retarding speech development. A more popular argument was one that is still preferred by Bloodstein (1987, 355—359); the child with a language or speech problem is more likely to receive help (formal or informal) that produces fear of speech difficulty, thereby causing stuttering. There is a substantial literature verifying the observation that several linguistic deficits often accompany stuttering — deficits in phonology, prosody, syntax, semantics, and pragmatics. Nippold (1988) has provided a comprehensive review of this research. Because evidence accumulated that stuttering could not be explained adequately as a psychodynamic or learned behavior, the interpretations for these findings have shifted toward physiology. In addition, there is a growing interest in providing therapy for stuttering and the ‚additional’ language deficits as early as possible (despite Bloodstein’s warning).
3.
Stuttering is a Language Disorder
Several authors have developed the thesis that stuttering represents a deficit in language processing, and our view is that this perspective is more coherent than the one which suggests that stuttering may be accompanied by language disorder. The most thorough treatment of this perspective has been supplied by Wingate (1988). Our discussion will also draw heavily on an excellent review of the evidence by Duckworth (1988) and Hamre’s (1984) review of language models. Wingate (1988, ch. 3) dates the formal study of language factors to the work (1935—194 5) of Spencer Brown under Wendell Johnson at the University of Iowa. Based on Brown’s (194 5) summary of these linguistic influences on stuttering loci, subsequent references are frequently made to ‚ B r ow n’s fo u r fa ct o r s’. In short, these represent (a) a phonetic factor — more stuttering on consonants than vowels; (b) a grammatic factor — more stuttering on nouns, adjectives, adverbs, and verbs; (c) a length factor — more stuttering on words longer than five letters; and (d) a sentence position influence — more stuttering on the first three words than subsequent words. Brown’s interpretation was compatible with the preferred view of stuttering at that time, namely, that these four features likely conspire to render such words more salient (fear-inducing). For unknown reasons
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— perhaps because this psychological view seemed to ‚settle the matter’ — interest in pursuing linguistic correlates of stuttering was meager for two decades. Renewed interest in the 1960’s seems to correspond with a growing dissatisfaction with psychological theory and more general interest in the biology of language embodied in a ‚new’ discipline, p s ych o l i n g u i s t i c s. That is, if it is clear that one cannot defend more stuttering on nouns than prepositions because nouns induce fear, then it is reasonable to ask whether nouns are more physiologically complex as they operate in conversation. As it turns out, Brown’s data have been a rich source for recent investigators. On our view, Wingate’s (1988) reanalysis of this work is particularly useful for three reasons. First, he provides a rational psycholinguistic explanation for Brown’s ‚four factors.’ Second, he presents compelling evidence that two additional factors (discovered but ignored by Brown) have a more immediate and pervasive influence on stuttering occurrences than the other four; stutters inevitably occur during the production of s y l l a b l e i n i t i a l p h o n e s a n d st r e s s e d syllables. Third, Wingate’s development of phonetic and prosodic influences is heuristic beyond theoretic implications for stuttering. His discussion also provides evidence from stuttering that may clarify several linguistic phenomena in human language (syllable structure, propositionality, sonority hierarchy and its development, nature of normal hesitation patterns, entry of prosodic decisions in a speech plan hierarchy). From reviews of the research (cited above) it is clear that certain of Brown’s six factors have been investigated moreso than others. Acoustic and physiologic phonetic studies have revealed evidence of instability in stutterers’ stuttered (and fluent) articulatory gestures. Research on prosodic and syntactic complexity lends credence to the view that both influence stuttering frequency and loci. Currently, of course, conceptualization of linguistic factors is considerably different from earlier views (cf. 5. & 6.). It is likely that future research on stuttering will be fruitful to the extent that current and changing linguistic theory is applied. To advance an understanding of linguistic influences, then, students of stuttering bear a substantial cross-disciplinary burden. As evidence accumulates, explanations for the acquisition, accomplished use, and impairment
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of language change. On the view that stuttering is a language disorder, it is expected that developments in psycholinguistics have potential for clarifying the acquisition, nature, and treatment of stuttering. After outlining a rather accepted view of language systems (and their hypothesized interaction with stuttering) we will present two new interpretations, Cognitive Grammar theory and the Competition Model, v is-a-v is their implications for stuttering research.
4.
Language Systems
As a general outline, linguistic phenomenology can be grouped into five systems: Phonology, prosody, syntax, semantics, and pragmatics. Figure 83.1 illustrates one view on the relationship between these systems and stuttering.
guage production “...defect that extends beyond the level of motor execution.” 4.1. Spread-of-Effect If stuttering is a language disorder then it is reasonable to hypothesize that systems beyond the core (phonology and prosody) are also vulnerable to impairment. For each client, then, one might ask, “How pervasive is this person’s language impairment?” The basic argument is that each of the systems is relatively isomorphic, contributing its unique complexity to the ultimate ease with which an utterance is rendered phonetically. This isomorphism (autonomy) of systems argument is compatible with current applications to stuttering, but it contrasts sharply with developing psycholinguistic theory (cf. 5. & 6.). 4.2. Syntax
Fig. 83.1: Language Systems Model
This perspective characterizes a deficit in phonology and prosody as the sine qua non of stuttering. In short, each stutter verifies that. As a succinct summary of the evidence on the phonetic transition difficulty in stuttering, Wingate (1988, ch. 6) presents a ‚fault line’ thesis that captures the regular occurrence of stutters in transition from the i n i t i a l p h o n e (‚onset’) to the remainder (‚rime’) of the st r e s s e d syllable. This approaches an observable answer to Duckworth’s (1988, 67) important question: “How might deficits in language structure be related to language function?” Although Duckworth seems to suggest that ‚function’ relates to communicative interaction (one dimension of the ‚pragmatic’ system), we must also address this question in terms of (a) linguistic function for a hierarchical speech plan and (b) neurologic function for a cogent account of a stuttered event; e. g. Wingate’s (1988, 239) neurolinguistic summary is that stuttering is a lan-
As we have mentioned, stuttering loci and frequency appear to be positively related to syntactic complexity when MIT-Style grammar is used to construct or analyze simple vs. complex sentences. That is, the traditional grammar from which Brown (194 5) extracted “parts of speech” is inadequate for parsing natural language and categorizing stutters (Wingate 1988). Cognitive grammar, a recent development, will be presented later with comment on how this might be applied to a refined clarification of the role of syntax in stuttering. 4.3. Semantics To our knowledge, there have been no published applications of formal or generative semantic theory to investigations of stuttering. If we use the more vague construct, ‚meaning,’ as our referent for semantics, then there are two variables of relevance to an understanding of stuttering: P r o p o s i t i o na l i t y and l ex i c a l a c c e s. Reviews of the language literature inevitably cite the classic study by Eisenson/Horowitz (194 5) which revealed that significantly more stuttering occurred during the reading of meaningful (compared to meaningless) connected prose. They employed Hughlings Jackson’s seminal discovery that ‚propositionality’ characterizes natural language commerce and is at the nexus of what aphasics cannot do with words. Eisenson and Horowitz suggested that increments in propositionality may correlate positively with increments in stuttering frequency
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— and, we would add, may be associated with duration/other indices of severity. Lexical access difficulty may contribute to those occasions when a word is only partially available and a stutter results. There is some evidence of ‚word-finding’ difficulty in children who stutter and this needs to be explored further. More recently, Wingate (1988) used the standard Word Fluency task — “write as many words as you can think of that begin with the letter S.” Twenty adult stutterers generated significantly fewer words than the twenty nonstutterers. While he also used other tasks that suggested word access difficulty, it was the Word Fluency deficit that he found most commensurate with his “fault line” hypothesis. That is, in both stuttering and the Word Fluency task, the word-initial phone is in place but lexical access and assembly are not readily available. With respect to investigating the semantic integrity of stutterers’ language and/or determining the effects of semantic complexity on stuttered events, it may be revealing to apply lexical acquisition models for hypothesis testing. One might predict, for example, that the expression of semantic relations acquired early would be associated with less stuttering than those acquired later. It is clear that the semantic system(s) is integrated with prosodic decisions at a very early stage in utterance planning; often a word receives primary stress for purely semantic reasons. Such rich integration among systems has been captured by the recently developed cognitive grammar theory and the Competition Model (cf. 5. & 6.) These present serious challenges to the argument that each system functions autonomously.
5.
Cognitive Grammar
The theory of cognitive grammar, developed by linguist Ronald Langacker (1987), presents a radical reorientation to the characterization of linguistic structures. A number of contemporary theoretical approaches characterize grammatical structures as autonomous from other levels of language (e. g., semantics). One consequence of this imposed separation is the assumption that grammatical structures are semantically empty or arbitary. E. g., it is widely assumed that active and passive forms of a simple sentence are semantically equivalent representations of a single underlying ‚deep structure.’ Langacker proposes instead that grammar consist of units that are inher-
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ently symbolic. That is, syntactic structures represent conventionalized forms of meaning, as do words and inflections. Thus syntax, the lexicon, and morphology are all characterized similarly as consisting of symbolic units. A s y m b o l i c u n i t can be reduced to a s e m a n t i c u n i t that stands in a symbolic relationship with a p h o n o l o g i c a l u n i t. On this view, there is no need to posit the existence of linguistic elements that are not present in the overt expression (e. g., the well-known dummy do). Cognitive grammar theory posits that active and passive sentence forms are available in a language because of the capacity of speakers to c o n st r u e a situation in alternate ways. Similarly, simple past and past-progressive forms of verbs allow speakers latitude in describing actions from a particular perspective. This characterization of the interaction between speakers’ cognitive capabilities and linguistic structures represents a shift away from idealized models of grammar toward models that are based upon human performance. Speakers’ employment of figurative language and so-called ‚rote’ expressions is of interest in a cognitive grammar framework. These elements are frequently discarded from orthodox linguistic analyses because they do not appear to be amenable to description in terms of rules. Yet they constitute much of what is produced when speakers speak. A cognitive grammar orientation accords these expressions the status of u n i t. As a consequence, units can vary from a single word to a phrase to an entire utterance. Investigations of stuttering and language variables have implicitly assummed a traditional linguistic model (cf. MIT-Style grammar, 4 .2.). Consequently, investigators have counted stuttered words, classified stuttered words by grammatical category, and performed transformational analyses upon samples of stuttered speech. Cognitive grammar theory has the potential to profoundly alter our view of what constitutes the unit of analysis in linguistic investigations of stuttering.
6.
The Competition Model
The Competition Model (Bates/MacWhinney 1987; MacWhinney 1987) represents an attempt to ground language acquisition and language processing in biology. Its authors describe it as a model of linguistic p e r fo r m a n c e rather than of linguistic c o m p e t e n c e.
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As such, it seems more likely to accommodate instances of language breakdown than models that posit abstract representations of grammatical competence based upon formal logic. It represents an attempt to deal with individual differences among children acquiring language as well as with differences that exist among natural languages. A major goal of the Competition Model is to “... delimit a set of fundamental processing mechanisms whose strength at a given point in development varies across learners in a way that can eventually be linked to fundamental differences between the learners” (Bates/ MacWhinney 1987, 159). Toward this end, investigations have been carried out to determine whether various measures of linguistic performance gathered from very young children correlate with each other and with measures taken at a later age. Additional studies have been aimed at language processing skills in individuals with aphasia. These studies of children and of brain-injured adults may shed light on the cognitive abilities that underlie language use: which of these abilities develop in synchrony, and which are potentially dissociable? The authors have explored the extent to which factors at one level of linguistic structure (e. g., phonology) influence the acquisition of forms at another level (e. g., syntax). They have observed that the distinctive patterns of language style that emerge in children can be seen in phonology, grammar, the lexicon, and even in non-linguistic social and cognitive domains. That is, there seems to be a spread-of-effect (cf. Fig. 83.1 & 4 .1.) across all levels of language, brought about by the differential strength or activation of the mechanisms underlying language use. An impressive body of evidence has accrued that suggest that some children tend to favor nominal forms in early language development while others use pronominal forms. Furthermore, the nominal users tend to be referential, expanding noun phrases, while the pronominal users have more heterogeneous vocabularies and develop more elaborate verb phrase morphology. This nominal/referential versus pronominal/expressive finding suggests a link between lexical and morphological development. Of special interest to the present work is the additional finding that the children who seem to follow a pronominal/expressive style have a greater tendency to imitate words and sentences. However, the imitation is often imprecise, leading Bates/
MacWhinney to speculate that these children may be “... focussing on the suprasegmental/ intonational ‚packaging’ of a target rather than its phonetic details” (Bates/MacWhinney, 184 ). Thus, a link seems to exist between phonological-prosodic development and lexical and morphological development.
7.
Research Implications
In this section, reference will be made to Cognitive Grammar (CG) and the Competition Model (CM). Direction for research of four types will be presented (descriptive, developmental, comparative, and clinical). 7.1. Descriptive What do CG & CM offer for refining our understanding of the nature of stuttering? First, they suggest caution for isolation of systems in research designs. Second, they portend novel means of approaching ex p l a n at i o n of linguistic phenomenology in stuttering. That is, because they focus on linguistic p e r fo r m a n c e rather than an idealized competence, research designed in accord with CG & CM will more likely clarify the relationship between language structure and function (cf. Duckworth’s question, 4 .) Consider the merits of Wingate’s “fault line” hypothesis (cf. 4 .3.). While his evidence supports the inference that phonetic transition difficulty is tied to a problem of lexical access and assembly, a CG analysis might explain the loci variability of such difficulty in discourse. Research might reveal that stutters co-occur with certain combinatorial properties of s y m b o l i c u n i t s of various sizes. On the apparent (but unexplained) deviance of stutterers’ spoken stories (Wingate 1988, 217), it may be that stutterers do not possess the normal repertoire or ready availability of c o n st r u a l options. One might predict, then, that stutterers’ stories will contain a more limited array of larger units resulting in the frequent appearance of ‚rote’ or conventional phrases. More generally, both CG&CM offer a direction for further research on the alleged influences of syntactic complexity, lexical access, and propositionality on stuttering. 7.2. Developmental To our knowedge, CG is a linguistic theory without published application to first language acquisition. However, if partial explanation on the nature of stuttering derives
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from CG generated studies (such as those suggested in 7.1.), it will be logical to apply such findings to the stuttering acquisition issue. Of course, this issue can be addressed now; there is f u n c t i o n a l i s t i c correspondence between CG & CM on core constructs, and CM has been rigorously applied to language development questions. For example, children favoring pronominal forms (cf. 6.) use substantially more different words, and this was one characteristic of adult stutterers’ spoken stories reported by Wingate (cf. 7.1.). At what age does this appear and are young stutterers more likely to be pronominal than nominal users? CM has derived considerable support from longitudinal studies seeking correlations betwen levels of analysis (semantic, syntactic, etc.). This is probably the design of choice to investigate stuttering developmental interactions between various s y m b o l i c u n i t s or levels of analysis. E. g., Menyuk/Liebergott/ Schultz (1986, 79—93) reviewed their study of 53 children over the first 3 years. They found significant positive correlations between age of achieving (a) structured CV’s, (b) closed syllables, and (c) 50 different words. The longitudinal design also identifies a sound approach for comparing these correlations from normal children to correlations from children who demonstrate e a r ly dysfunction (stuttering) in phonologic-prosodic production. One logical extension of this approach would be to determine if there are earlier (than stuttering) indices of phonologic difficulty (i. e. ‚protostuttering’). Considering the stages of vocal development (Vihman 1988, 72—77), there is reason to suspect a correlation between difficulty in achieving canonical babbling (6—8 months) and later stuttering — and, perhaps, later ties to lexical acquisition and access. Canonical, or reduplicated babbling (dadada), “constitutes the chief production milestone in the first year” (Vihman 1988, 74 ). It represents the first evidence of mastery of articulatory-laryngeal control to the extent that repeatable and smooth CVC p h o n e t i c t r a n s i t i o n s are available for subsequent elaboration. It may not be a coincidence that a basic failure of phonetic transition has often been described as the essence or core feature of stuttering. Are children who deviate from the typical 6—8 month achievement of canonical babbling more likely to stutter later? The development of vocal control usually refers to modifications within a child over time (‚ontogenetic’). Jason Brown (1988) has
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proposed a “microgenetic” (within milliseconds) account of “vocal development” that is coherent with (a) phases of childhood vocal development and (b) characteristics of different aphasias. As it turns out, his microgenetic theory can also be viewed as a neural version of CM and it may emerge as a useful neurolinguistic model for stuttering. 7.3. Comparative Both CG & CM support a suspicion that errors in phonetic transition (stuttering; apraxia of speech, cf. Hamre/Harn 1979) might share with other production errors (e. g. misarticulations, slips of the tongue) a sensitivity to influences from (a) other CM l eve l s and (b) CG c o n st r u a l and s y m b o l i c u n i t decisions. That is, evidence concerning one disorder might clarify the nature of another that is phenomenologically related. It would seem heuristic to apply d e s c r i p t i ve research (cf. 7.1. for examples) for such a cross-disciplinary purpose. Finally, it is common for evidence from disorders to serve a c o m p a ra t i ve function to contribute to an understanding of normal language use and acquisition. 7.4. Clinical One might view the clinical enterprise as hypothesis testing in the truest sense of that experimental construct (Hamre 1972). As knowledge develops concerning linguistic phenomenology in stuttering, determining the operation of such correlates in a single client can extend and focus diagnostic explanation, treatment planning, and measures of progress.
8.
References
Bates, E. & MacWhinney, B. (1987). Competition, variation and language learning. In B. MacWhinney (Ed.), Mechanisms of language acquisition. 157—193. Hillsdale, NJ: Lawrence Erlbaum Associates. Bloodstein, O. (1987). A handbook on stuttering. Chicago: National Easter Seal Society. Brown, J. (1988). The life of the mind. Hillsdale, NJ: Lawrence Erlbaum Associates. Brown, S. (194 5). The loci of stutterings in the speech sequence. Journal of Speech Disorders, 10, 181—192. Duckworth, M. (1988). Stuttering and linguistics. In M. Ball (Ed.), Theoretical linguistics and disordered language. 51—79. San Diego: College-Hill.
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Eisenson, J. & Horowitz, E. (194 5). The influence of propositionality on stuttering. Journal of Speech Disorders, 10, 193—197. Hamre, C. (1972). Research and clinical practice: a unifying model. ASHA, 14, 542—545. Hamre, C. (1984 ). Stuttering as a cognitive-linguistic disorder. In R. Curlee & W. Perkins (Eds), Nature and treatment of stuttering: New directions. 237—259. San Diego: College-Hill. Hamre, C. & Harn, W. (1979). The effect of masking on apraxia: Evidence from spectrographic data. In H. Hollien & P. Hollien (Eds.), Current issues in the phonetic sciences. 1057—1063. Amsterdam: Benjamins. Langacker, R. (1987). Foundations of cognitiv e grammar, v ol. 1: Theoretical prerequisites. Stanford: Stanford University Press. MacWhinney, B. (1987). The competition model. In B. MacWhinney (Ed.), Mechanisms of language acquisition. 249—308. Hillsdale, NJ: Lawrence Erl-
baum Associates. Menyuk, P., Liebergott, J., & Schultz, M. (1986). Predicting phonological development. In B. Lindblom & R. Zetterstrom (Eds.), Precursors of early speech. 79—93. Basingstoke, Hampshire (UK): MacMillan. Nippold, M. (1988). Concomitant speech and language disorders in stuttering children: A critique of the literature. Journal of Speech and Hearing Disorders, 55, 51—60. Vihman, M. (1988). Early phonological development. In J. Bernthal & N. Bankson (Eds.), Articulation and phonological disorders, 2nd ed. 95—109. Englewood Cliffs, NJ: Prentice Hall. Wingate, M. (1988). The structure of stuttering: A psycholinguistic analysis. New York: Springer-Verlag.
Curt Hamre/William Harn, Lubbock, Texas (USA)
84. Psychological Aspects and Theories of Stuttering 1. 2. 3. 4. 5.
1.
Introduction Psychological Aspects of Childhood Stuttering Psychological Aspects of Adulthood Stuttering Discussion References
Introduction
The controversy which carried on into the 70s as to whether stuttering should be considered either a manifestation of a psychological disorder or an organic/physiological or linguistic one, has today shifted in favour of an integrative multimodal view (Gregory 1986). The integrative models and the various accents they set, assume that stuttering in early childhood is influenced by multiple, coexisting, interacting factors of a physiological/organic, linguistic and psychological nature, which can change individually in the course of a lifetime (Friedler/Standop 1986; Peters/Starkweather 1989). Since the disorder is not assumed to be homogenous, this view of the phenomenon of stuttering can be regarded as a more restricted, idiosyncratic view with the discussion differentiated according to age groups and degrees of chronicity (Schulze/ Johannsen 1986).
Since current research is concerned with delivering more and more individual, empirical proof of the importance of the different variables associates with the three bundles of factors already mentioned, it is necessary to gain a better understanding of the way the different factors interact together and with general developmental psychological processes. The extent to which the factors are etiologically important, the extent to which they influence the speech disorder qualitatively and quantitatively and the influence they have on features marking the development of the disorder and on the probability of remission must also be more fully understood. Current trends in research and theoretical discussions show that interest now revolves around the organic/physiological and linguistic bundles of factors (Peters/Hulstijn 1987; Schulze/Johannsen 1986). In contrast, the psychological aspects, which are sometimes referred to as ‚traditional’ factors, are nowadays taken less systematically into consideration in terms of models and research themes (Schulze/Johannsen 1990). This development together with a paradigmatic change in favour of modular research strategies does not mean that the psychological factor has been adequately investigated or scientifically ex-
84. Psychological Aspects and Theories of Stuttering
hausted. The problems of developing models capable of showing the nature and the functioning of psychological variables of influence, would suggest that the opposite is more likely to be the case and illustrates the general scientific problems of dealing with psychological partial aspects of complex phenomena. The theoretical notions and the empirically substantiated findings relating to the importance of psychological factors of influence for childhood stuttering are reviewed synoptically below.
2.
Psychological Aspects of Childhood Stuttering
With the emergence of the social and behavioral sciences (psychoanalysis, behaviourism, social psychology, communication sciences, linguistics), an increasing interest in psychosocial variables began to develop at the beginning of the 30s with a focal point in the period 194 5—1970. The most widely differing models and research paradigms of these disciplines were also applied to the investigation of stuttering. The concepts which evolved during this period formed an antipole to the purely organic/physiological models and methods of treatment which had prevailed up to this time (Shames/Rubin 1986). The focal point of research has particularly influenced the practice of prevention and early treatment of stuttering or treatment concepts for childhood stuttering and it has even dominated in some countries. As already mentioned, since the beginning of the 80s we have been able to observe a renewed focusing of research and theory formation on organic/physiological (Curlee/Perkins 1985) and linguistic variables (Wingate 1988), although the amount of research into psycho-social variables must be regarded as very small in comparison to the total research effort (Schulze 1989, 55 ff). Although, in my opinion, a definite move away from purely psychological interpretation models has become apparent in current scientific discussion, stuttering still tends to be considered a purely psychological problem by many practioners and in terms of public opinion. The patient’s or the parents’ anticipatory attitude is often connected with this. The aim of therapy is subsequently to change in the personality of the patient and possible organic or linguistic factors are not often taken into account.
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2.1. Models: Psycho-Social Factors The theoretical concept relating to the importance of psycho-social factors (Schulze 1989) can be subdivided into two groups: A. The model of the psychopathological personality containing two fundamental assertions. (a) Stuttering is basically a behavioral manifestation of a neurosis. b) the child’s personality disorder is closely linked to pathological features of the parents’ personalities. This leads to a dialogic loss of confidence in the child and results in stuttering. B. The model of the effectiveness of unfavourable interactional variables does not assume a fundamental psychological disorder in the child or his reference person, although the importance of individual dimensions of behavior and attitude must be regarded as central to the aetiology and course. We shall refer to more behaviorally oriented models of social interaction with a focus on immediate, open and directly observable interactional behaviors. Examples are: (1) The diagnosogenic theory of the genesis of stuttering which was postulated as early as the 4 0s and which is still popular today. This attributes stuttering causally to a parental misinterpretation of normal speech disfluencies in the child (Johnson 1959). (2) The operant conditioning concept based on learning theory which explains the onset and, in particular, the maintenance of stuttering in terms of operant conditioning processes alternating between the parents and the child (Costello 1984). (3) Finally, the concept of the efficiency of communicative stressors which assumes powerful interaction between stutter-specific personal factors in the child and external communicative stressors (Starkweather 1987). The systematic examination of these theoretical concepts makes it clear that we are not dealing with completely different thought models, but that most of the concepts overlap to a great degree with regard to content even though some accentuation may be different. Apart from the use of completely different terminologies and the reference to different personality theories (e. g. trait versus state model of personality; Amelang/Batussek 1990), the main difference is, in may opinion, just how fundamental the personality disorder is assumed to be in the child and the parents, and to what extent the concepts can be interpreted as etiological and to what extent they can be generalized. These theoretical
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contributions are to be regarded as hypothetical attempts to examine the extremely complex interrelationship of the personal, interactional and environmental conditions in which stuttering is to be found. The following illustration shows how intricate and complex such relationship can be. It contains the variables classified as meaningful in the theoretical and clinical discussion. If we assume that childhood stuttering takes place within the framework of the infrafamilial styles of communication and interaction, it becomes clear that these can be affected by various psychosocial factors of influence. Different kinds of personal factors relating to the parents and the child are also as important as factors relating to family structure or socio-cultural parameters. A. Personal factors relating to parents and child (A.1) Previous socialization experiences (special socialization conditions e. g. growing up in a children’s home or in a foster family, growing up when parents often move home) (A.2) Intrapsychic structures (e. g. high level of aspiration; ambition; coping with success or failure; basic affective mood; self-control; self-assertiveness; self-confidence; strength of ego). (A.3) Life and stress management (e. g. threshold of tolerance of everyday stress; ways of coping with critical life events such as training, re-training, illness, separation from important reference persons. (A.4 ) Verbal and non-verbal communication styles of relevant reference persons (e. g. competitive communication styles: ‚time pressure’, ‚listener loss’, ‚interruption’, ‚high speech rate’, high communicative responsibilitiy; discrepancy between verbal and nonverbal behavior; multilingualism). (A.5) Organic-physiological and psychological disorders (e. g. motoric disorder of the mouth; cognitive or linguistic retardation, stress resulting from chronic illness and rehabilitation measures, medical operations, behavior and performance disorders). B. Family life style (B.1) Social environment (e. g. lack or excess of external contacts, constant change of reference person, e. g. children of publicans, children of parents in migration; children whose parents often move home). (B.2) Leisure behavior (e. g. adult-oriented leisure behavior, excessive television or video
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viewing; lack of separation between leisure and work spheres). (B.3) Housing conditions (cramped, noisy living accomodation, house-building situation, frequent changes of home and locality when child is looked after while both parents are at work). (B.4 ) Job satisfaction and working conditions (job/professional stress affecting family; unemployment; early retirement; irregular working hours due to shift change or duty). (B.5) Socio-economic conditions (e. g. high level of financial stress, distraint). C. Family structure (C.1) Inter-generative relationship (e. g. blurring of generation boundaries; multi-generation household with conflict arising from distribution of responsibility in household and child-rearing matters). (C.2) Intrafamilial power and role distribution (e. g. competitive or unclear role distribution in the nuclear family). (C.3) Marital relationship (e. g. hidden or open continuous crisis; marital separation). (C.4 ) Parent-child relationship (e. g. inner rejection of child or one parent; predominantly negative, punishment oriented guidance of children; frequent daily power struggles relating to everyday routine; moral overtaxing of children; coalition forming). (C.5) Brothers-sisters relationship (hidden or open competitive relationship). Hypothetically, these factors can influence the child’s fluency directly or indirectly via such mediator variables as stress and anxiety. The high level of individual variability of relevance of such psycho-social and environmental stimuli for the development of stuttering suggests that individual vulnerability due to certain stressors is more important than the nature of the stressor (Bloodstein 1987; Van Riper 1982). — The way that children cope with such stressors on an experimental psychological level has not been well researched. In the light of recent results of stress research in adults, it must be assumed that there is a complex stress process with information processing (primary appraisals, secondary appraisals etc.) playing an important part on various levels (Jerusalem 1990). Moreover, it must be assumed that individual vulnerability and coping behavior in the child is not only determined by cognitive processes (attitudes, appraisals), but also by interrelated organic/physiological and linguistic variables which cause the stress experienced by the
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child to promote stuttering rather than the development of another psycho-physiological disorder. One of the problems of such descriptive models is that not much is known about the psycho-physiological processes that underlie these psychosocial variables, although their effect on fluency can be reliably determined and the individual pattern of the variables concerned can be worked out by functional analysis in individual cases (Starkweather/Gottwald/Halfond 1990). 2.2. State of Research The enormous complexity of the factors involved in the development of stuttering makes it necessary to restrict the variables to be examined and complicates investigation. A serious problem for the interpretation of research data is that many research approaches do not clearly distinguish which of the following are to be examined: dispositional factors (e. g. heredity, pre-, peri-, postnatal influences or developmental conditions in early childhood), immediate causal factors: (factors and events immediately preceding the initial manifestation of stuttering in time or coinciding with it) or factors responsible for stabilization, chronification, generalization: (factors promoting chronification or barriers preventing remission; chronification factors reinforcing frequency and intensity or contributing to the generalization of the disorder in other areas of life). — This often results in a lack of interpretational clarity and in interpretative arbitrariness because, for example, the important process of differentiating between the cause and the psycho-social consequences of stuttering when interpreting the data can only be carried out inadequately. The current state of research into the importance of psycho-social and interactional variables can be summarized as follows. 2.2.1. Scope of Research The results of about 70 empirical studies have been published in the last 4 5 years. These aimed at specifying psycho-social variables: (parental variables, intrafamilial constellations, styles of interaction). About 3200 families have been investigated up to now. About 600 families were allocated to studies which were concerned with the issue of the typical personality features of stutterers’ parents. In addition, there are several studies on mainly adult stutterers and occasional studies on children examining personal psychological variables in the stutterers themselves (Schulze 1989).
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2.2.2. Research Methods Two main methods of research are used. a) Interviewing or testing the parents of stutterers or the stutterer him-/herself using informal and standardized test procedures (e. g. clinical depth interviews; psychometric personality tests such as MPI, MMPI, 16-PF, FPI; projective tests such as Rorschach, TAT, CAT, SCENO, Family in Animals). — In terms of life history, most studies proceed from the current situation of the stutterer and a few employ the method of retrospective questioning of adult stutterers on early childhood events or on their experience of upbringing and family climate in early childhood. b) Direct behavioral observation of parentchild interaction in dyadic or triadic play situations (naturalistic, semi-naturalistic, experimental) recorded on video. The evaluation is carried out using methods of systematic behavioral observation (e. g. with special systems of categories or signs). 2.2.3. Study Designs The predominant study design is the crosssectional study with control group comparison. As a rule, a control group is formed from a non-impaired total population. The inclusion of a further control group e. g. as a control for a general factor such as ‚disability’ or ‚language disorder’ is rare. Study and control groups are normally matched according to one variable (e. g. age or sex). Other important variables such as duration of stuttering, severity of stuttering, therapy and counselling experience, developmental status, completeness of family, number of brothers or sisters etc. are seldom included as a control. As a result, the differences of variance in relevant features cannot be taken into account in such post-hoc analyses in spite of control group design. Because of the levelling of possible group differences due to the heterogenity of the disorder or the subject number which is usually low, there is an increasing demand for research to be carried out on a sub-group specific basis (Cooper 1990; Yairi 1990). A similar research strategy contains the socalled “high density” design (Cox/Seider/ Kidd 1984 ). Families in which stuttering occurs frequently are investigated (e. g. 5 family members must have stuttered for at least 6 consecutive months) and are compared with non-stuttering control families. This special
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study design makes it possible to compare stutterers and their non-stuttering relatives and stutterers and their families with nonstuttering families. The logic of this investigation approach is that the factors which are relevant to the development of stuttering should occur in a higher concentration in families containing many stutterers. These could include perinatal, medical, developmental-psychological, linguistic factors or factors associated with upbringing, social factors, personality factors and interactional factors within the family. This method is therefore very important because it enables the investigation of the multivariate conditions of stuttering in a relatively small sample and can contribute to the clarification of stutter-specific constellations of variables. The individual case study (n = 1) and the methods of comparative casuistics are being increasingly employed as a research method, particularly in the investigation of atypical conditions associates with the onset and course of stuttering (Barlow/Hersen 1984; Jüttemann 1990). 2.2.4. Variables Investigated Early studies were primarily aimed at the empirical detection of global, static-structural personality features (e. g. neuroticism, extraversion, overprotection). However, later studies were increasingly concerned with the functional-dynamic effects of individual aspects of attitude, experience and behavior (e. g. readiness to label, level of aspiration, childrearing and communication styles, self-confidence, perceived difference in status). 2.2.5. Results The results of the previous empirical studies on the etiological importance of parental and interactional variables for childhood stuttering can be summarized as follows (Schulze 1989, 74 ff). 2.2.5.1. Findings Relating to Psychopathology of the Personality of the Parents Various methods have been used to investigate hypotheses contained in some theoretical concepts and, above all, those derived from clinical descriptions. According to these hypotheses, stuttering, when considered etiologically, is the result of a personality disorder of the parents and, in particular, of the mother. There is an entire series of control group studies which use mainly standardized
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personality tests (MPI, MMPI, 16-PF, FPI). According to the data obtained from about 580 families, the parents of stutterers can be no more readily distinguished as a group by typical personality features or a higher occurrence of personality disorders than the nonstuttering control groups. One study without control group comparison of a group of 50 families of stutterers diagnosed 20 to 30 mothers to be neurotic, but these results could not be confirmed. The factorial analytical study of Riley and Riley (1984 ) suggested that in 5% of that 56 parents investigated, the parents had a psychological need for the stuttering symptoms. On the basis of this study it would appear that parental psychological disorders are involved only to a slight extent in the genesis and manifestation of childhood behavioral disorders and that the role they play is only small for stuttering. 2.2.5.2. Specific Attitudinal Characteristics of Parents There are a series of findings suggesting that the parents of stuttering children are very demanding, over-exact, dominant and critical. Furthermore, they also show an increased tendency to diagnose ‚stuttering’, have a low level of tolerance of disfluency and differ according to the individual dimensions of their child-rearing styles, e. g. with respect to being consistent, their affective participation, their readiness to communicate, their conformity to norms. Although there are differences between these and the normal control groups, they cannot be considered completely certain because of the inconsistency of the findings and they should also not be interpreted as stutter specific features because of the absence of further control groups in the study designs. These differences could also be due to a general factor ‚disability’ since disordered behavior in children brings about a change of attitudes, feelings and behavior in the parents (e. g. concern, feelings of guilt, ambivalence of action) (Lerner/Spanier 1978). Taking into consideration the scope of the variables examined (the questionnaire in the study of Johnson (1955) contained 84 6 items) and the many psycho-social dimensions in which no differences were ascertained, the findings should be considered particular since they have not been confirmed in any other duplicate studies. Moreover, in some studies there were no differences in the dimensions of attitudes which were investigated in relation to the control families. In the factorial analytical study of the clinical population of Riley and
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Riley (1984 ), the anticipatory attitudes of 5% of the parents (when measured multidimensionally) were found to be unrealistic. This also means, however, that the anticipatory attitudes of 4 9% of the parents of stuttering children were appropriate. 2.2.5.3. The Way Stuttering Children See Their Parents The results of these studies show that stutterers view their parents very differently. In contrast to the control groups the following differences could be ascertained: The way the child perceives his/her parents acceptance, overprotection and control, love. Moreover, stutterers characterize their fathers retrospectively as “less cooperative and accepting stricter less fair and loving, less interested, more dictatorial”. Other studies show no significant differences in the children’s perception of upbringing or domestic environmental influences. 2.2.5.4. Parent-Child Interaction in Observational Studies As a result of criticism of extremely reactive diagnostic procedures (retrospective self-reports) and measuring techniques and because of the improvement of recording and evaluation techniques (film, video, tape-recorder, computer), an increasing number of methods of direct behavioral observation have been developed for use in interactional diagnostics. Widely differing dimensions of verbal and nonverbal interactional behavior have been investigated so far with the main focus of interest on verbal interactional styles. In contrast to the results of early interactional studies which showed that parents of stutterers considerably had more negative interactional styles, there are other studies which in no way can support this. Some studies allow hypotheses which assume differences in thematic coherence, flexibility of dialogue and initiative. Other differences relate to questioning and instructional behavior, speed of mothers’ speech, divergence of speech rate between mothers and fathers. However, it is necessary to point out that there has not yet been a thorough experimental investigation of these hypotheses, although some of the partial results are already considered substantiated and play an important role in prevention and early treatment (Conture 1990). As a whole, the results of available observational studies can only be considered con-
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tradictory. Faults in study designs (lack of suitable control groups, inadequate matching) restrict the interpretation of the data considerably. However, the interactional climate must not be considered to be more negative in general terms. It is more probable to assume that interactional parameters which can generate communicative stress occur more frequently and are of a different nature in families of stutterers than in normal control families. The systematic investigation of such interactional parameters and the proof of their stutter specificity or etiological importance are still at an early stage and must be intensified before general therapeutic principles can be developed (Cooper 1990). 2.2.5.5. The Position of the Stutterer Within the Family The findings concerned with the question of whether stutterers occupy a particular position in the family in comparison to brothers and sisters are inconsistent. — Some studies suggest that stutterers often occupy ‚only child’ status in the family, but other studies cannot support this. The significance of the age difference between the stutterer and his/ her elder brothers and sisters could also not be confirmed.
3.
Psychological Aspects of Adulthood Stuttering
Stuttering is characteristically a disorder of early childhood and is generally closely associated with motoric and linguistic developmental processes. However, in the case of stuttering in adulthood the following questions relating to psychological aspects are of importance: A. What are the psychosocial consequences of stuttering for the sufferer and do these give rise to certain personality features or certain attitudes, feelings and behavior? A series of surveys (Baumgärtel 1984 ; Cox 1986; Schulze/Johannsen 1990) comparing psychological variables in the case of adult stutterers and non-stuttering control groups show that adult stutterers are slightly more anxious, more sensitive, more insecure and less selfconfident in social situations. Despite considerable individual variability, group differences emerge which are interpreted as secondary psychosocial symptoms of the disorder. Because of assumed or actual social stigmatization and because of discrimination against the stutterer in terms of his/her
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achievement (as exemplified by ‚stutterer jokes’), increased levels of self-observation and communicative self-control can arise as a result of avoiding stuttering and concealing the disorder. Consequently, the anxiety level in the stutterer is generally slightly raised. As a result of experiencing the occasional ineffectiveness of the chosen coping strategies, the area of verbal communication, over the years and decades, becomes a constant source of failure, helplessness and injury in terms of expectation and experience and these give rise to widely varying coping mechanisms (e. g. resignation, social withdrawal, aggressiveness) (Carlisle 1986). The psychological consequences of the disorder probably increase in proportion to their significance for the overall psychosocial situation of the patient. In addition, there are also psychological problems originating in other areas (e. g. life, marital, professional crises) or psychological disorders which are independent of stuttering. Moreover, the effectiveness of stuttering therapy (fluency shaping or stuttering modification) is dependent on the successful transfer to other life situations beyond therapy. Although this transfer often takes place spontaneously in the case of young stutterers, it can actually be considered to be the problem itself in the case of juvenile or adult stutterers who have had the disorder for many years. — Under laboratory conditions basal fluency can be established quite easily with the help of various methods (Ham 1986). — For transfer and generalization, additional psychological transfer strategies must be activated (Boberg 1983; Edelstein 1989; Webster/Poulos 1989). These are taken from various branches of clinical psychology (behavioral psychology, cognitive psychology, client-centred therapy, rational-emotive therapy). Stuttering therapy for adults should employ methods of psychological change without the therapy basically being conceived as psychotherapy. If psychological problems are predominant, psychotherapy is indicated as treatment or it should precede stuttering therapy. B. Is there a psychogenic form of stuttering which can be interpreted etiologically and which is comparable to so-called neurogenic stuttering (Helm-Estabrooks 1986)? Dysfluency occurring unequivocally as a result of emotional trauma or within the framework of a primary psychological/psychiatric disorder is rare and is nowadays distinguished from stuttering by differential diagnostics.
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The etiological proof of ‚psychogenic’ stuttering is difficult since it is necessary to exclude a history of stuttering in the patient which existed before the sudden initial manifestation of stuttering in adulthood. A neurological disorder must also be excluded. In practice, the psycho-genesis of stuttering described by the patient and his reference persons is often questionable. Plausible explanations for certain phenomena (e. g. intraindividual variation of symptoms) are put forward out of psychological necessity and physical and emotional traumas in the family (e. g. accident, illness, separation) are considered to be the concepts causing the disorder. Although such concepts undoubtedly fulfil an important psychohygienic function (e. g. exculpation of guilt, resistance to change), they are usually not relevant as an etiological interpretation. Psychogenic stuttering is also rarely reported in the literature (Freund 1966). Individual clinical cases are documented in the context of a war neurosis and in relation to anxiety attacks, depression and other somatic complaints lacking an organic basis and in relation to schizophrenia and manic depressive psychosis. The current main differential diagnostic criteria are: (1) a sudden initial manifestation in youth or adulthood which is closely associated with the experience of chronic stress or with the onset of an acute emotional crisis, (2) a predominantly monosymptomatic dysfluency pattern, (3) the dysfluency extends beyond the specific situations and is relatively independent of them, (4 ) the patient has only a slight perception of the dysfluency and (5) there is usually no stutter-specific distress (Schulze 1989; St. Louis 1986). Using methods of differential diagnosis, it is necessary to distinguish the rare psychogenic form of stuttering and true stuttering from transitory dysfluencies which occur as a reaction to specific stress situations, in particular, situations involving communication and speech. — Interruptions to the speech flow which are closely associated with objectively and subjectively identifiable stress situations (e. g. examination situation, television interview, marriage proposal, multilingual conversation, reporting an accident e. g. from an emergency telephone) can contain the whole spectrum of severe stuttering symptoms (sentence inversions, interjections such as “ahh, ahh”, word/part-word repetitions, prolongations, blockages, secondary motoric phenomena). In clinical terms, there are the
84. Psychological Aspects and Theories of Stuttering
following relatively consistent, typical features: The cause is known and when the stress phase is over, the fluency pattern is reestablished. There is usually no generalized speech fear or generalized speech avoidance. The distress which is often referred to as ‚speech anxiety’ or ‚insecurity’ can be very great, but it is usually limited to certain stress situations. The sufferer doesn’t usually consider him-/ herself to be a stutterer although he perceives his speech to be ‚stuttered’ or ‚disjointed’ in the situation. These differential diagnostic distinctions and the development of chronic stuttering in response to psychological stress are important in terms of choosing a therapy approach. It is necessary to ascertain to what extent therapeutic work would be useful or possibly sucessful on the level of speech/speaking (speech pattern, fluency, disfluency behavior) and to what extent psychological variables (attitudes, feelings, open behavior) and the current life situation of the patient are important
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for treatment. It is also necessary to decide if the stutterer-therapeutic (multimodal) approach should be replaced by basic psychotherapeutic/psychiatric treatment.
4.
Discussion
Although the state of research is sketchy and to some extent contradictory there exists no doubt among experts that psychosocial aspects play a certain role in the development, chronification and remission of stuttering. According to the earlier theories and the views which are still held today by laymen and the public, the main causes of stuttering are to be found in psychological traumas or psychopathological personality features. In contrast, the dynamics of the development of stuttering and the characteristically inconsistent pattern of the disorder are explained today in terms of the effectiveness of such moderator variables as stress and emotional agitation together with organic and linguistic
Fig. 84.1: Hypothetical variables (factors of influence) creating and changing intrafamilial styles of com-munication and interaction in relation to the onset and development of childhood stuttering (Schulze 1989).
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factors. The heterogeneity of the findings would suggest that there are neither stutter specific factors in the child, his environment nor in the mutual relationship between the two. The breadth of the possible psychosocial factors (cf. figure 84 .1) and the enormous variety of the stutter-relevant variables occurring individually in clinical practice, would seem to suggest the existence of an unspecific psychosocial context of influence. This means that each psychosocial factor can be relevant to stuttering if it contributes to the destabilization of the equilibrium of the capacities and demands which are necessary for fluent speech (Adams 1988; Starkweather 1988). On the basis of the previous findings, it is impossible to speak in terms of typical stutterers or typical families of stutterers or typical fathers or mothers of stutterers. The extent to which psychosocial factors are involved can vary widely individually and only individual diagnostics can ascertain the importance of these in the functional analysis of behavior and in the treatment concept. It must also be decided to what extent psychological therapy elements should be integrated into the therapy approach for stuttering. On the basis of the state of research it is impossible to justify treatment for childhood stutterers that is basically oriented around family therapy, analytical child psychotherapy or client-centred play therapy. In the case of juveniles and adults the therapy design should be in accordance with the basic or predominant disorder. A psychogenesis of stuttering which is unequivocal is extremely rare and psychotherapy is necessary. As a rule, however, stuttering therapy includes multimodal procedures and procedures based on combined methods. It combines methods of speech therapy and psychological modification methods and these should be applied and dosed carefully by the therapist in accordance with the needs of the individual case (Wendlandt 1984).
5.
References
Adams, M. R. (1988). The “Demands and capacities” model: Theoretical elaborations. Paper presented at the Second International Oxford Dysfluency Conference. Sommerville, College Oxford, England. August 24—26, 1988. Amelang, M. & Batussek, D. (1990). Differentielle Psychologie und Persönlichkeitsforschung. Stuttgart: Kohlhammer. 3rd Ed. Barlow, D. H. & Hersen, M. (1984 ). Single case
experimental designs. Strategies for studying behav iour change. New York: Pergamon Press. 2nd Ed. Baumgärtel, F. (1984 ). Ein Beitrag zur Persönlichkeitsdiagnostik von Stotterern. Bremer Beiträge zur Psychologie, 33. Bremen: Universität Bremen. Bloodstein, O. (1987). A handbook on stuttering. Chicago: National Easter Seal Society. 4th Ed. Boberg, E. (Ed.) (1983). Maintenance of fluency. New York. Elsevier 1981. Carlisle, J. A. (1986). Tangled tongue. Liv ing with a stutterer. Reading: Addison-Wesley Publishing Comp. Conture, E. (1990). Stuttering. Englewood Cliffs: Prentice Hall. 2nd Ed. Cooper, J. A. (Ed.) (1990). Research needs in stuttering: Roadblocks and future directions. Rockville, Maryland: Asha Reports No. 18. Costello, J. M. (1984 ). Operant conditioning and the treatment of stuttering. In W. H. Perkins (Ed.), Stuttering disorders. 107—127. New York: ThiemeStratton Inc. Cox, M. D. (1986). The psychological maladjusted stutterer. In K. O. St. Louis, (Ed.), The atypical stutterer. Principles and practices of rehabilitation. 93—122. Orlando: Academic Press. Cox, N. J., Seider, R. A., & Kidd, K. K. (1984 ). Some environmental factors and hypotheses for stuttering in families with several stutterers. Journal of Speech and Hearing Research, 27, 543—548. Curlee, R. F. & Perkins, W. H. (Eds.) (1985). Nature and treatment of stuttering. London: Taylor & Francis. Edelstein, B. A. (1989). Generalization: Terminological, methodological and conceptual issues. Behaviour Therapy, 20, 311—324. Fiedler, P. & Standop, R. (1986). Stottern. Ätiologie, Diagnose, Behandlung. München: Uban & Schwarzenberg. 2nd Ed. Freund, H. (1966). Psychopathology and the problems of stuttering. With special consideration of clinical and historical aspects. Springfield, III.: C. C. Thomas. Gregory, H. H. (1986). Stuttering: A contemporary perspective. Folia Phoniatrica, 38, 89—120. Ham, R. (1986). Techniques of stuttering therapy. Englewood Cliffs: Prentice Hall. Helm-Estabrooks, N. (1986). Diagnosis and management of neurogenic stuttering in adults. In K. O. St. Louis, (Ed.), The atypical stutterer. Principles and practice of rehabilitation. 193—218. Orlando: Academic Press. Jerusalem, M. (1990). Persönliche Ressourcen, Vulnerabilität und Streßerleben. Göttingen: Hogrefe. Johnson, W. (1955). A study of the onset and development of stuttering. In W. Johnson & R. R. Leutenegger (Eds.), Stuttering in children and
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adults. 37—73. Minneapolis: University of Minnesota Press. Johnson, W. (1959). The onset of stuttering. Minneapolis: University of Minnesosta Press. Jüttemann, G. (Ed.) (1990). Komparativ e Kasuistik. Heidelberg: Asanger. Lerner, R. M. & Spanier, G. B. (Eds.) (1978). Child influences on marital and family interaction. New York: Academic Press. Peters, H. F. M. & Hulstijn, W. (Eds.) (1987). Speech motor dynamics in stuttering. Wien: Springer. Peters, H. F. M. & Starkweather, C. W. (1989). Development of stuttering throughout life. Journal of Fluency Disorders, 14, 303—321. Riley, G. D. & Riley, J. (1984 ). A component model for treating stuttering in children. In M. Peins (Ed.), Contemporary approaches in stuttering therapy. 123—172. Boston: Little, Brown & Company. Schulze, H. (1989). Stottern und Interaktion. Vergleichende Untersuchung der v erbalen Interaktionsstile v on Eltern und ihren stotternden Kindern. Ulm: Universität, Phoniatrische Ambulanz. Schulze, H. (1989). Dysfluency — Syndrome. In G. Kittel (Ed.), Kursbuch für Phoniatrie und Pädaudiologie. 103—118. Köln: Deutscher Ärzte-Verlag. Schulze, H. & Johannsen, H. S. (1986). Stottern bei Kindern im Vorschulalter. Theorie, Diagnostik, Therapie. Ulm: Universität. Phoniatrische Ambulanz. Schulze, H. & Johannsen, H. S. (1991). Importance of parent-child interaction in the genesis of stutter-
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ing. Folia Phoniatrica, (43, 133—143). Shames, G. H. & Rubin, K. (1986). Stuttering then and now. Columbus: C. E. Merrill Publ. Company. St. Louis, K. O. (Ed.) (1986). The atypical stutterer. Principles and practices of rehabilitation. Orlando: Academic Press. Starkweather, C. W. (1987). Fluency and stuttering. Englewood Cliffs: Prentice Hall. Starkweather, C. W. (1988). Upgrading the demands and capacities model. Paper presented at the Second International Oxford Dysfluency Conference. Sommerville College, Oxford, England. August 24 —26, 1988. Starkweather, C. W., Gottwald, S. R. & Halfond, M. M. (1990). Stuttering prev ention: A clinical method. Prentice Hall: Englewood Cliffs. Van Riper, C. (1982). The nature of stuttering. Englewood Cliffs: Prentice Hall. 2nd Ed. Webster, W. G. & Poulos, M. G. (1989). Facilitating fluency. Transfer strategies for adult stuttering treatment programs. Tucson: Communication Skill Builders. Wendlandt, W. (1984 ). Zum Beispiel Stottern. Stolperdrähte, Sackgassen und Lichtblicke im Therapiealltag. München: Pfeiffer. Wingate, M. E. (1988). The structure of stuttering. A psycholinguistic analysis. New York: Springer. Yairi, E. (1990). Subtyping child stutterers for research purpose. In J. A. Cooper, (Ed.), Research needs in stuttering: Roadblocks and future directions. 50—57. Rockville, Maryland: ASHA Reports No. 18.
Hartmut Schulze, Ulm (Germany)
85. Therapy of the Stuttering Child 1. 2. 3. 4.
1.
Introduction The Direct Treatment of Stuttering The Indirect Treatment of Stuttering References
Introduction
A particularly vibrant area of stuttering treatment activity in the past two decades has been treatment of young children who stutter. Many modern clinicians have rejected Wendel Johnson’s (1959) diagnosogenic theory and Bloodstein’s (1987) anticipatory struggle theory so that now treatment for young children is condoned and even enthusiastically endorsed. The purpose of this chapter is, then, to review the current status of therapy for the
young stuttering child (up to the age of 8 or so).
2.
The Direct Treatment of Stuttering
2.1. Introduction Direct treatments are those that attempt to change stuttered speech by methods aimed in a straightforward manner towards reducing moments of stuttering and increasing durations of nonstuttered speech. Their ultimate goal is usually the complete elimination of stuttering, resulting in normal-sounding and normal-feeling stutter-free speech. Direct treatments are essentially the only treatments
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that have been evaluated empirically, although there is much room for criticism of the amount and quality of that body of research. Perhaps research efforts are lacking here because researchers have believed that ‚spontaneous recovery’ will eliminate stuttering in many young children, although this belief has been seriously challenged (R. Ingham 1983; Martin/Lindamood 1986). Further, research aimed at discriminating which stutterers will and will not recover without formal treatment is essentially nonexistent. 2.2. The Basics of Direct Treatment with Young Stutterers Elsewhere this writer (Costello 1983) has described the basics of direct treatment to consist of “... the most simplistic and uncomplicated kind of treatment format: ... arranging differential consequences for the occurrence of fluent utterances and moments of stuttering.” The application to stuttering of these basic principles of behavior change has been thoroughly described and documented (cf. Costello 1980; 1982; Costello/Ingham 1984 a; Ingham 1984). The first published study to test these principles with preschool-aged stutterers was the seminal study of Martin/Kuhl/Haroldson (1972). Two young children individually conversed with a puppet named Suzibelle. During these conversations a child’s moments of stuttering were immediately followed by a 10-s period during which the lights illuminating Suzibelle were turned off and Suzibelle stopped talking to the child (e. g., timeout). This treatment eliminated the stuttering of both children, and a new era of stuttering treatment for children was underway. Subsequent studies used another form of timeout, wherein the stutterer is required to stop speaking for a brief period whenever a stutter occurs. This procedure has been repeatedly shown to serve as a functional negative consequence for stuttering in older children and adults (e. g., Costello 1975; Ryan 1974 ) and is also quite useful for young stutterers from about the age of five. Other events that have been used with young children to consequate moments of stuttering are: saying slow down (Reed/Godden 1977), requiring the child to repeat the word or utterance that contains stuttering (Onslow/Costa/Rue 1990), applying response cost (removal of a token reinforcer) (Salend/Andress 1984 ), and clinician remarks such as uh oh or there’s a bumpy word (using the child’s label for stuttering).
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As is always the case, different stimuli will serve as functional negative stimuli for different children. The methods described above emphasized the controlling effects of negative feedback for moments of stuttering. Other versions of the basics have concentrated on the application of positive reinforcement for nonstuttered utterances, such as stutter-free speech of a minimum duration (Peters 1977; Shaw/ Shrum 1972). Myriads of stimuli are useful as positive reinforcers in such procedures: clinician praise, stickers, ‚plus’ marks on data sheets, etc. Token reinforcement systems are also quite powerful, as long as the exchange rate for ‚back-up’ reinforcers isn’t too sparse. Of course, as in treatments for all other kinds of behaviors, reinforcement schedules become progressively more intermittent, and reinforcing stimuli gradually more natural, as treatment continues. As well, most clinicians design treatments that combine feedback for both nonstuttered utterances and occurrences of stuttering. Interesting and effective applications of the basics were reported by Johnson (1984 ) and Onslow (1990) wherein parents were the treatment agents and the home environment was the treatment setting. Johnson taught parents to attend selectively to their children’s stutterfree utterances and to ignore utterances that contained stuttering during ongoing daily activities. Onslow/Costa/Rue trained mothers of young stutterers to reinforce stutter-free utterances with praise and tangible reinforcers during formalized treatment sessions at home and during natural daily activities. In the above examples basic contingency management was applied to the nonstuttered and stuttered speech of young children during spontaneous conversation. For some young children, however, production of a substantial amount of conversational speech may be unlikely. Stuttering severity, stutterers’ reactions to their stuttering, general shyness, or even the existence of a concurrent language disorder could make stutter-free utterances of reinforceable length infrequent. Another disadvantage of conversation as a treatment medium is highlighted by research suggesting that disfluency is exacerbated by increases in sentence complexity (Gaines/Runyan/Meyers 1991; Ratner/Sih 1987) and length (Brundage/Ratner 1989; Gaines/Runyan/Meyers (1991) — variables that can fluctuate in children’s spontaneous conversation. Therefore, a treatment task that is spontaneous and nat-
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ural but less conversational, and that can control utterance complexity and length, would seem beneficial. This concept has become almost standard in the treatment of young children. 2.3. Extended Length of Utterance as a Treatment Strategy The concept of designing treatment so that only very short stutter-free utterances are required in the beginning and progressively longer stutter-free utterances are gradually introduced was first described by Ryan (1974 ; Ryan/Ryan 1983). Ryan’s program is referred to as GILCU (gradual increase in length and complexity of utterance) and adds to the basics the principles of programmed instruction and successive approximation (Costello 1977). Ryan’s work with older children showed that this program was not only highly successful but was relatively simple for clinicians to learn to administer. Johnson/Coleman/Rasmussen (1978) also successfully applied the GILCU program to children in the public schools. For use with younger children, the principles of GILCU have been operationalized in detail in a highly successful version referred to as Extended Length of Utterance (ELU) (Costello 1983). Children’s stutter-free utterances are very gradually extended from 1 syllable through 2, 3, 4 , 5, and 6 syllables (spontaneously generated words and phrases evoked by pictures), to connected speech utterances progressing from 3 s through 5, 10, 20 ... seconds, ultimately to 5 min of stutterfree conversation with the clinician in the clinic. Throughout the program stutter-free and stuttered responses are consequated with positive reinforcement and negative feedback, respectively. 2.4. Summary Several characteristics of direct treatment that applies the basics with young children should be highlighted. First, the hallmarks of this kind of treatment are the use of child-appropriate response contingent differential consequences for stutter-free utterances and moments of stuttering, most often combined with requirements for the production of progressively longer stutter-free utterances (ELU). Second, this kind of treatment appears to be appropriate for all young children who stutter, irrespective of (a) the child’s level of awareness or concern about stuttering; (b) the severity of stuttering; (c) who serves as treat-
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ment agent: clinician, parent, or teacher; or (d) where treatment takes place: clinic, home, or school. Third, this kind of treatment includes no instructions to the child regarding how to produce stutter-free speech. Children are left to their own devices, which may mean that they build upon their existing fluent speech or independently develop an acceptable speech pattern that meets the clinician’s standards for natural-sounding, stutter-free speech at normal speaking rates. 2.5. Treatments Founded on ‚Additives’ Many direct treatments described for young children add to the basics the requirement that children alter their habitual speech pattern in specific ways so as to approach speech differently and thereby reduce the occurrence of stuttering (Cooper 1987; Culp 1984 ; Runyan/Runyan 1986; Shine 1984 ). Such additives have become fundamental in the treatment of adult stutterers, which is apparently why they are suggested for use with children as well. Although additives are described by a variety of labels, certain characteristics appear to be common among them. They are: decreased speaking rate, oftentimes paired with prolongation of vowels and continuant consonants; gentle/easy onset of vocalization; control of air flow/breath management; light articulatory contacts; reduced loudness. Coppola and Yairi (1982) added rhythmic speech to this list. Most of the reports of these procedures are based on little or no data. Among the questions in need of study are the following. (1) Would additives be required if treatment began with only the use of the basics? In most reports, speech pattern changes are introduced into the treatment at the outset. Further, many of the treatments that use additives introduce several at the same time, and in combination with the basics. In such cases the role of the additives cannot be isolated nor can their necessity be demonstrated. (2) Is it possible to adequately operationalize and measure the use of additives? Although speaking rate is often measured, different conventions for its measurement abound. Even more problematic: how does one measure prolongation? light contact? easy onset? airflow? And if measurement of these characteristics can be developed and agreed upon, will such measurement be able to be applied online by clinicians during treatment? This would appear to be mandatory for treatments that require children to use such additives.
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(3) Are young children able reliably to manipulate their speech production so as to include alterations required by additives? Ryan (1974 ) mentioned that it was difficult to get young children to produce the kind of prolonged speech required by DAF treatment regimes. It is likely that this is true for other unusual manners of speaking as well, perhaps due to young children’s immature motor control systems or to their lack of metalinguistic awareness (Cooper 1987). Conture (1990) attempts to deal with this problem by using elaborate analogies to “provide essential insight for the young client into what he or she does that interferes with speech and what is necessary to change in order to speak more fluently.” (4 ) What is the quality of children’s speech at the end of treatment that uses additives? Reports of the outcomes of these techniques have not included assessment of the naturalness of children’s posttreatment speech (cf. Martin/Haroldson/Triden 1984 ). If children continue to use additives to control stuttering, noticeable abnormalities in speech naturalness would be expected. In summary, while many direct treatments with young children recommend inclusion of additives to the basic treatment paradigm, the necessity of such additions and the quality of their effect on fluency have not yet been well documented.
3.
The Indirect Treatment of Stuttering
3.1. Introduction Indirect treatments are those that attempt to change stuttered speech by methods (generally referred to as counseling) aimed at behaviors of others in the child’s environment (particularly parents) and at other aspects of the child’s behavior. Broadly, indirect therapies are based on the belief that certain conditions — those that provoke stress for the child (communicative or otherwise), or make the child feel generally insecure or anxious, or produce uncertainty about the ability to communicate, or that make demands beyond the child’s capacities — aggravate, if not cause, the child’s stuttering (e. g., Gregory 1987; Prins 1983; Starkweather/Gottwald 1990; Starkweather/Gottwald/Halfond 1990; Williams 1984 ). Such conditions are, then, considered to be the targets for treatment. Most indirect therapies, although perhaps
compelling in their underlying logic, are completely unsupported by empirical evidence regarding their effects (cf. Costello 1983; Ingham/Ingham 1990; Guitar 1984 ). This unfortunate state of affairs appears to exist for several reasons. (a) The treatments are illdefined and suggest multitudes of potentially independent variables in need of modification. (b) Objective measurement of the amorphous independent and dependent variables dictated by these viewpoints is difficult (e. g., see Ulliana/Ingham 1984 ), although some efforts have been made in this direction (Cooper 1987; DeNil/Brutten 1991). (c) Outcomes of these treatments are usually confounded by accompanying direct treatments (e. g., Conture 1990; Cooper 1987; Gregory 1984 ; 1987; Guitar/Peters 1980; Johnson 1984 ; Prins 1983; Riley/Riley 1984 ; Rustin 1987; Rustin/Cooke 1983; Starkweather/Gottwald/ Halfond 1990; Wall/Myers 1984 ). In the several cases where direct treatment follows a period of indirect treatment, the inference can be made that indirect treatment did not produce a completely satisfactory outcome. However, it is not possible to discern whether the preceding indirect therapy was expeditious, detrimental, or irrelevant to the eventual outcome of the direct treatment. 3.2. Indirect Therapy Directed Toward Parents Recently, it has been suggested that rapid parental speech may aggravate a child’s stuttering, perhaps by inducing fast speech in the child. This suggests that modification of parent speech rate should be a target of treatment (Johnson 1984 ; Gregory 1984 ; Prins 1983; Starkweather/Gottwald/Hanson 1990; Wall/ Myers 1984 ). Meyers/Freeman (1985b) found that mothers of stuttering children did, indeed, speak more rapidly than mothers of nonstutterers; however, their stuttering children did not speak faster than nonstuttering children. Stephenson-Opsal/Ratner (1988) found that reductions in mother’s speech rates were accompanied by decreases in their children’s stuttering, but not via speech rate reductions. These researchers suggested that reduced parent speech rates may prompt changes in other aspects of the child-parent conversational interaction such as rate of turn-taking, change in demand-structure of child-directed speech, and reduced language complexity, thus allowing the child more time to ‚preprogram’ utterances.
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Another variable suggested as a treatment target (Gregory 1984 ; Riley/Riley 1984 ; Rustin 1987; Rustin/Cooke 1983; Williams 1984 ) is interruptions. Meyers/Freeman (1985a) found that mothers of stuttering and nonstuttering children were more likely to interrupt a child during a disfluency than during a fluent utterance and that both children’s own interruptions of mothers’ speech were more likely to be disfluent than fluent. These data, however, offer no direct evidence regarding the functional relationship between stuttering and interruptions. Therefore, the recommendation that interruptions of the stuttering child’s speech should be reduced appears premature as a treatment procedure. Table 85.1 provides a partial list of other u n d o c u m e n t e d variables suggested in the literature as potential treatment targets for indirect treatments aimed at altering parent behaviors. Both hypothesized f l u e n c y i n t e r r u p t o r s and f l u e n c y fa c i l i t a t o r s are listed. In an overview of the concept of indirect treatment for young stuttering children, Costello (1983) raised two questions that have yet to be answered satisfactorily. First, do clinicians have the right to ask families to change certain aspects of their relationship with the stuttering child, and to infer by this that the family is at least partially responsible for the child’s stuttering, when little or no evidence exists that these variables do, in fact, influence the child’s stuttering? Second, are clinicians effectively able to affect changes in family members’ behaviors, when many of those behaviors occur in environments and under conditions not accessible to the clinician? Given the known effects of direct treatments with young children, it continues to seem reasonable to contend that “a more suitable strategy for treatment of stuttering in young children is to directly teach them to produce fluent, nonstuttered speech no matter what is going on in their natural environment” (Costello 1983). 3.3. Indirect Therapy Directed Toward the Stuttering Child Most indirect therapies also address characteristics of the child — other than fluency and stuttering — under the assumption that modification of such characteristics produces or facilitates fluency. Suggested targets have been communication attitudes and feelings (Cooper 1987), speech avoidance and fear (Wall/Myers 1984 ), unduly high self-expec-
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tations (Riley/Riley 1984 ), and overall psychological adjustment (Wall/Myers 1984 ). Also suggested has been treatment of any existing concomitant communication disorder including auditory processing and oral motor discoordination (Conture 1990; Riley/ Riley 1984 ). Changing the child’s language use and pragmatics has been mentioned in terms of encouraging use of less complex vocabulary and syntax and reducing questionasking (Williams 1984 ), teaching the child to be a good listener and good conversationalist (Conture 1990; Gregory 1984 ) and to use contentional turn-taking rules — that is, not to interrupt (Conture 1990; Gregory 1984 ; Meyers/Freeman 1985a; Rustin/Cooke 1983; Starkweather/Gottwald/Halfond 1990; Wall/ Myers 1984 ; Williams 1984 ), and helping the child develop appropriate social skills, especially in reaction to being teased (Rustin 1987; Wall/Myers 1984 ). Also mentioned has been instruction in relaxation skills (Rustin 1987). Yet again the major problem with this kind of indirect treatment (aside from the absence of common theoretical underpinnings, which is made obvious by the hodgepodge assortment of behaviors recommended for treatment) is that its effects are entangled with concurrent employment of the above-described parent counseling and even direct treatment of the child’s stuttering. Therefore, the extent to which attention to these variables influences the eventual outcome of treatment has not been determined. 3.4. Generalization and Measurement. Two remaining issues, either of which could fill its own chapter, remain to be briefly mentioned. First, the ultimate evaluation of the outcome of any kind of stuttering treatment rests on information regarding the generalization and maintenance of treatment effects across all aspects of the child’s daily environment. Many of the reports cited herein suggest that across-settings generalization occurs spontaneously among young children, as an outgrowth of treatment; yet most of the same reports provide little more than anecdotal evidence in this regard. A review of the relevant literature by Ingham/Onslow (1987) highlights this deficit and describes the few procedures that have been used to promote generalization. They conclude that ‚Train and Hope” (Stokes/Baer 1977) is the method (or n o nmethod) most often relied upon. Lastly, much has been written regarding the kind of measurement required to docu-
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Fluency Interruptors telling the child to slow down, relax, think before talking (Asha 1990) calling attention to child’s speech (Asha 1990) correcting child’s stuttered speech (Asha 1990) quickly changing topics (Gregory 1984) asking too many questions without waiting for reply (Gregory 1984; Rustin 1987; Rustin/Cooke 1983) making too many verbal demands that require complex verbal responses (Prins 1983) finishing child’s statements and filling in words or guessing what child is about to say (Gregory 1984; Williams 1984) not listening to the child (Prins 1983; Rustin 1987; Williams 1984) smiling or frowning at inappropriate times while child is talking (Williams 1984) hurrying the child when the child is talking (Riley/Riley 1984; Williams 1984) making conversation unrelated to the current activity (Rustin 1987) constantly correcting or criticizing child’s verbal and nonverbal behavior (Gregory 1984; Riley/ Riley 1984) using ambiguous nonverbal communication (Rustin 1987) allowing the child to speak in competition with others (Prins 1983; Williams 1984) being too directive regarding child’s conversation or play (Rustin 1987) being a passive parent (Rustin 1987) allowing child to use stuttering to manipulate parents (Riley/Riley 1984) being inconsistent or making extreme changes in disciplinary practices (Rustin/Cooke 1983; Williams 1984) being erratic in planning and conducting routine daily activities (Gregory 1984; Prins 1983) arranging activity schedules that create time pressure for the child (Gregory 1984; Prins 1983) making behavioral demands the child is unable to meet (Prins 1983) having disagreements between parents (“verbal bickering”) of any kind, in the child’s presence (Williams 1984) having disagreement between parents regarding whether or not child is a stutterer, in the child’s presence (Conture 1990) discussing how much fun parents will have when child has begun preschool or kindergarten, in the child’s presence (Williams 1984) being separated/divorced (Williams 1984) showing negative reactions to the child’s stuttering (Starkweather/Gottwald/Halfond 1990) imposing high standards (Conture 1990; Gregory 1984; Starkweather/Gottwald/Halfond 1990; Williams 1984) having an abnormal need for the child to stutter (Riley/Riley 1984) bringing a sibling into the world or otherwise creating a family crisis (Gregory 1984; Williams 1984) allowing siblings or peers to tease the child (Riley/Riley 1984; Williams 1984) Fluency Facilitators regularly spending more (talking) time with the child (Conture 1990; Prins 1983; Starkweather/ Gottwald/Halfond 1990) simplifying language used with child (Conture 1990; Prins 1983; Starkweather/Gottwald/Halfond 1990; Wall/Myers 1984) reading more often to the child (Conture 1990) directly discussing child’s stuttering with the child (Starkweather/Gottwald/Halfond 1990) enhancing child’s degree of independence and self-reliance (Rustin/Cooke 1983) enhancing child’s ability to problem solve (Rustin/Cooke 1983) increasing child’s self-confidence and self-acceptance (Gregory/Hill 1984) Table 85.1: Hypothesized fluency interruptors and fluency facilitators postulated in the literature
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Selection of valid dependent variables Reliable measurement of dependent variables Periodic measurement of treatment effects throughout pretreatment, treatment, and posttreatment phases Multiple measures of natural conversational speech across settings beyond the treatment environment At least occasional use of nonreactive (covert) measures Use of a potent treatment method for the establishment/acquisition of stutter-free speech Inclusion of transfer activities (if necessary) Inclusion of maintenance activities (if necessary) Table 85.2: Features to be addressed in research on stuttering treatment effects, especially in regard to acrosssetting generalization (Ingham 1989)
ment stuttering treatment effects with validity and reliability (e. g., Costello/Ingham 1984 b; Ingham/Costello 1984 ). Table 85.2 lists eight features suggested by Ingham (1989) that should be addressed in studies purporting to demonstrate stuttering treatment effects. The conduct of such research obviously requires a major commitment of time and resources, but the last word on stuttering treatment with young children — irrespective of the approach entertained — won’t be written until such research has been conducted, reported, and replicated.
4.
References
ASHA (1990). Let’s Talk (No. 19). Asha, 32. Bloodstein, O. (1987). A handbook on stuttering. Chicago: National Easter Seal Society. Brundage, S. B. & Ratner, N. B. (1989). Measurement of stuttering frequency in children’s speech. Journal of Fluency Disorders, 14, 351—358. Conture, E. G. (1990). Stuttering (2nd ed.). Englewood Cliffs, NJ: Prentice Hall. Cooper, E. B. (1987). The Cooper Personalized Fluency Control Therapy. In L. Rustin, H. Purser, & E. Rowley (Eds.), Progress in the treatment of fluency disorders. 124 —14 6. London: Taylor and Francis. Coppola, V. A. & Yairi, E. (1982). Rhythmic speech training with preschool stuttering children: An experimental study. Journal of Fluency Disorders, 7, 447—457. Costello, J. M. (1975). Time-out procedures for the modification of stuttering: Three case studies. Journal of Speech and Hearing Disorders, 40, 216—231. Costello, J. M. (1977). Programmed instruction. Journal of Speech and Hearing Disorders, 42, 3—28. Costello, J. M. (1980). Operant conditioning and the treatment of stuttering. In W. H. Perkins (Ed.), Strategies in stuttering therapy. Seminars in Speech,
Language, and Hearing, 1, 311—325. Costello, J. M. (1982). Techniques of therapy based on operant theory. In W. H. Perkins (Ed.), Current therapy of communication disorders. General principles of therapy. 3—11. New York: Brian C. Decker Division of Thieme-Stratton. Costello, J. M. (1983). Current behavioral treatments for children. In D. Prins & R. J. Ingham (Eds.), Treatment of stuttering in early childhood. Methods and issues. 69—112. San Diego: CollegeHill Press. Costello, J. M. & Ingham, R. J. (1984 a). Stuttering as an operant disorder. In R. F. Curlee & W. H. Perkins (Eds.), Nature and treatment of stuttering: New directions. 187—213. San Diego: College-Hill Press. Costello, J. M. & Ingham, R. J. (1984 b). Assent strategies for child and adult stutterers. In R. F. Curlee & W. H. Perkins (Eds.), Nature and treatment of stuttering: New directions. 303—333. San Diego: College-Hill Press. Culp, D. (1984 ). The preschool fluency development program. In M. Peins (Ed.), Contemporary approaches in stuttering therapy. 39—71. Boston: Little-Brown. De Nil, L. F. & Brutten, G. J. (1991). Speechassociated attitudes of stuttering and nonstuttering children. Journal of Speech and Hearing Research, 34, 60—66. Gaines, N. D., Runyan, C. M. & Meyers, S. C. (1991). A comparison of young stutterers’ fluent versus stuttered utterances on measures of length and complexity. Journal of Speech and Hearing Research, 34, 37—42. Gregory, H. H. (1984 ). Prevention of stuttering: Management of early stages. In R. F. Curlee & W. H. Perkins (Eds.), Nature and treatment of stuttering: New directions. 335—356. San Diego: CollegeHill Press. Gregory, H. H. (1987). The treatment of stuttering: Recent history and contemporary issues. In L. Rus-
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tin, H. Purser, & E. Rowley (Eds.), Progress in the treatment of fluency disorders. 105—123. London: Taylor & Francis. Gregory, H. H. & Hill, D. (1984 ). Stuttering therapy for children. In W. H. Perkins (Ed.) Current therapy of communication disorders: Stuttering disorders. 77—94. New York: Thieme-Stratton. Guitar, B. (1984 ). The indirect treatment of stuttering. In J. M. Costello (Ed.), Speech disorders in children: Recent adv ances. 291—312. San Diego: College-Hill Press. Guitar, B. & Peters, T. J. (1980). Stuttering: An integration of contemporary therapies. Memphis, TN: Speech Foundation of America. Ingham, J. C. (1989). Generalization in the treatment of stuttering. In L. V. McReynolds & J. E. Spradlin (Eds.), Generalization strategies in the treatment of communication disorders. 63—81. Toronto: B. C. Decker. Ingham, R. J. (1983). Spontaneous remission of stuttering: When will the emperor realize he has no clothes on? In D. Prins & R. J. Ingham (Eds.), Treatment of stuttering in early childhood. Methods and issues. 113—140. San Diego: College-Hill Press. Ingham, R. J. (1984 ). Stuttering and behav ior therapy: Current status and experimental foundations. San Diego: College-Hill Press. Ingham, R. J. & Costello, J. M. (1984 ). Stutterers treatment evaluation. In J. M. Costello (Ed.), Speech disorders in children: Recent adv ances. 303—346. San Diego: College-Hill Press. Ingham, R. J. & Ingham, J. C. (1990). Let’s talk about stuttering. Asha, 32, (12), 42. Ingham, R. J. & Onslow, M. (1987). Generalization and maintenance of treatment benefits for children who stutter. Seminars in Speech and Language, 8, 303—326. Johnson, G. F., Coleman, D., & Rasmussen, K. (1978). Multidays: Multidimensional approach for the young stutterer. Language, Speech, and Hearing Services in Schools, 9, 129—132. Johnson, L. J. (1984 ). Facilitating parental involvement in therapy of the preschool disfluent child. In W. H. Perkins (Ed.), Current therapy of communication disorders: Stuttering. 29—39. New York: Thieme-Stratton. Johnson, W. (1959). The onset of stuttering. Minneapolis: University of Minnesota Press. Martin, R., Haroldson, S., & Triden, K. A. (1984 ). Stuttering and speech naturalness. Journal of Speech and Hearing Disorders, 49, 53—58. Martin, R., Kuhl, P., & Haroldson, S. (1972). An experimental treatment with two preschool stuttering children. Journal of Speech and Hearing Research, 15, 743—752. Martin, R. & Lindamood, L. P. (1986). Stuttering and spontaneous recovery: Implications for the
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speech-language pathologist. Language, Speech, and Hearing Services in Schools, 17, 207—218. Meyers, S. C. & Freeman, F. J. (1985a). Interruptions as a variable in stuttering and disfluency. Journal of Speech and Hearing Research, 28, 428—435. Meyers, S. C. & Freeman, F. J. (1985b). Mother and child speech rates as a variable in stuttering and disfluency. Journal of Speech and Hearing Research, 28, 436—444. Onslow, M., Costa, L., & Rue, S. (1990). Direct early intervention with stuttering: Some preliminary data. Journal of Speech and Hearing Disorders, 55, 405—416. Peters, A. D. (1977). The effect of positive reinforcement on fluency: Two case studies. Language, Speech, and Hearing Services in Schools, 8, 15—22. Prins, D. (1983). Continuity, fragmentation, and tension: Hypotheses applied to evaluation and intervention with preschool disfluent children. In D. Prins & R. J. Ingham (Eds.), Treatment of stuttering in early childhood. Methods and issues. 21—4 2. San Diego: College-Hill Press. Ratner, N. B. & Sih, C. C. (1987). The effects of gradual increases in sentence length and complexity on children’s dysfluency. Journal of Speech and Hearing Disorders, 52, 278—287. Reed, C. G. & Godden, A. L. (1977). An experimental treatment using verbal punishment with two preschool stutterers. Journal of Fluency Disorders, 2, 225—233. Riley, G. D. & Riley, J. (1984 ). A component model for treating stuttering in children. In M. Peins (Ed.), Contemporary approaches in stuttering therapy. 123—171. Boston: Little-Brown. Runyan, C. M. & Runyan, S. E. (1986). A fluency rules therapy program for young children in the public schools. Language, Speech, and Hearing Services in Schools, 17, 276—284. Rustin, L. (1987). The treatment of childhood dysfluency through active parental involvement. In L. Rustin, H. Purser, & E. Rowley (Eds.), Progress in the treatment of fluency disorders. 166—180. London: Taylor & Francis. Rustin, L. & Cooke, F. (1983). Intervention procedures for the disfluent child. In P. Dalton (Ed.), Approaches to the treatment of stuttering. 4 7—75. London: Croom Helm. Ryan, B. P. (1974 ). Programmed therapy for stuttering in children and adults. Springfield, IL: Charles C. Thomas. Ryan, B. P. & Ryan, B. V. K. (1983). Programmed stuttering therapy for children: Comparison of four establishment programs. Journal of Fluency Disorders, 8, 291—321. Salend, S. J. & Andress, M. J. (1984 ). Decreasing stuttering in an elementary-level student. Language, Speech, and Hearing Services in Schools, 15, 16—21.
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Shaw, C. & Shrum, W. (1972). The effect of response-contingent reward on the connected speech of children who stutter. Journal of Speech and Hearing Disorders, 37, 75—88. Shine, R. E. (1984 ). Direct management of the beginning stutterer. In W. H. Perkins (Ed.), Current therapy of communication disorders: Stuttering disorders. 57—76. New York: Thieme-Stratton. Starkweather, C. W. & Gottwald, S. R. (1990). The demands and capacities model II: Clinical applications. Journal of Fluency Disorders, 15, 143—157. Starkweather, C. W., Gottwald, S. R., & Halfond, M. M. (1990). Stuttering prev ention. A clinical method. Englewood Cliffs, NJ: Prentice Hall. Stokes, T. F. & Baer, D. (1977). An implicit technology of generalization. Journal of Applied Behav ior Analysis, 10, 349—367.
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Stephenson-Opsal, D. & Ratner, N. B. (1988). Maternal speech rate modification and childhood stuttering. Journal of Fluency Disorders, 13, 49—56. Ulliana, L. & Ingham, R. J. (1984 ). Behavioral and nonbehavioral variables in the measurement of stutterers’ communication attitudes. Journal of Speech and Hearing Disorders, 49, 83—93. Wall, M. J. & Myers, F. L. (1984 ). Clinical management of childhood stuttering. Baltimore: University Park Press. Williams, D. E. (1984 ). Prevention of stuttering. In W. H. Perkins (Ed.), Current therapy of communication disorders: Stuttering disorders. 21—28. New York: Thieme-Stratton.
Janis Costello Ingham, Santa Barbara, California (USA)
86. Therapy of the Stuttering Adult 1. 2. 3. 4. 5. 6.
Speech Therapy and Fluency Training The Combination of Speech and Social Therapy Measures Multimodal Therapy Therapy Success and Prognosis Conclusion References
Since the 1850s, the treatment of stuttering has focused on prosthetic, early pedagogic, homeopathic approaches, and, above all, practice (see Fiedler/Standop 1986; Rieber/ Wollock 1977, for an historical overview). Most of the methods concentrate directly on remedying or improving the speech disorder. If, however, one shares the view that stuttering has a neuropsychological basis which is significantly influenced by psychosocial factors, then it follows that speech training procedures address only a limited area of stuttering symptomatology. Speech techniques are meaningful only when they are integrated as elements in a comprehensive treatment plan. Such a plan should also adress the psychosocial disturbances which affect the stuttering and can seriously impair the stutterer’s psychosocial well-being.
1.
Speech Therapy and Fluency Training
Apparently there is no fluency training technique or speech therapy that can permanently eliminate stuttering (Andrews/Howie/Dozsa/
Guitar 1982). Nevertheless, systematic practice of new speech habits and speech patterns are indispensable to speech disorder treatments. The form of speech training employed and its relative importance within the total treatment plan depends, among other factors, upon the severity of the stuttering. With regard to the introduction of new speech habits, it is important to distinguish between speech therapy and fluency training. 1.1. Speech Therapy As subgroup of treatment methods speech therapy methods demand a controlled therapeutic setting and generally lead directly to noticeable improvement in speech. However, in most cases, these methods call for the support of another (trained) person, which makes the transfer of therapeutic progress into daily life difficult. 1.1.1. Simultaneous Speech and Shadowing Here, the stutterer and the therapist (or another person) read a text aloud simultaneously. Alternatively, the stutterer repeats with a slight delay, material from a text that is read aloud or recited by another person (like a shadow). Simultaneous speaking is also known as the Unisono-method (already presented by Liebmann in 1914 ). The symptom reduction during such practice is considerable. It is not, however, significantly maintained outside of the experimental or practice
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setting. The efficacy of both methods can be explained by the hypothesis that stuttering is caused by a defect of perceptive awareness and that this kind of aid to speech diverts the attention of the stutterer from his/her own speech to that of the other person doing the talking (see Cherry/Sayers 1956). The application of these procedures is justified, for one, by the possibility of demonstrating to a severrely speech-disturbed stutterer that his/her stuttering can be influenced. 1.1.2. Masking The presence of a strong sound (or strong white noise) over earphones, can prevent the stutterer from engaging in an auditory control of his/her articulation. Theoretically, this explains the considerable symptom reduction and supports the perceptive awareness hypothesis (Cherry/Sayers 1956; Van Riper 1973). A therapeutic goal of this procedure can also be the systematic practice of new speech pattern accompanied by white noise (the reestablishment of neuromotor autoregulation; Fiedler/Standop 1986). Of course, this method is impractical in daily life. This led to the development of aids which mask hearing and which can be worn in the ear outside of the therapy situation. Evidently, these masking devices help only very few stutterers; therefore, the effectiveness of using extremely costly speech aids must necessarily be thoroughly considered (see Ingham/Southwood/Horsburgh 1981). 1.1.3. Reinforcement and Feedback In the 1970s many operant procedures were tried individually or in combination to treat stuttering. For example: response contingent positive and negative verbal reinforcement, as well as other operant techniques (such as time-out and token economy) were intended to have an effect on the frequency of stuttered verbal behavior (e. g. Ingham/Andrews 1973; Shames/Egolf 1976; James 1976). Likewise, biofeedback using electromyographic feedback for relaxation during reading and spontaneous speech, was introduced (e. g. Guitar 1975; Lanyon 1977). The application of operant techniques does lead to significant progress in speaking. Surprisingly, though, the successes that usually occur immediately do not follow the typical learning curves and thus cannot be explained in terms of classical learning theory. These results lead to the interesting assumption, among others, that attention must be brought back to a conscious
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concentration on speech and, above all, on an associated gradual slowing of the style of speaking (Becker/Kessler/Fuchsgruber 1975; Fiedler 1991). Unfortunately, the hoped-for therapeutic effect of this procedure does not last long outside of the therapy situation. Therefore, the application of operant techniques and biofeedback can only be recommended in conjunction with other methods. 1.2. Fluency Training Systematic rehearsal of newly acquired fluency stands in the center of goal-directed fluency training. The wide variety of fluency training methods is almost impossible to thoroughly describe. Most of them, however, involve techniques and ‚tricks’ which were first ‚discovered’ by stutterers themselves during their attempts to overcome their speech difficulties. Subsequently they were systematically studied and further developed by therapists. These styles of speech are incompatible with stuttering and the majority of them help stutterers to speak fluently (in the therapy situation) within less than hours, sometimes after only minutes (e. g. Howie/Andrews 1984 ). Fluency techniques can usually be applied without mechanical devices and thus offer a good premise for the transfer of learning to daily situations. They should, therefore, take priority over speech therapy techniques in the treatment of stuttering. 1.2.1. Changing the Sound of the Voice: Gentle Onset “Gentle onset” (changing the volume level of the voice) is a so-called “starter” (Widlak 1977) typically used in self-help techniques and at the same time is one of the most troublesome stuttering symptoms. Starters are parts of words that by and large can be produced without errors and are easy for the stutterer to pronounce. They serve as regular starting aids for articulation of difficult words and word-beginnings. One type of the therapy using starters reqirers stutterers to concentrate on the modification of their breathing and their speech habits, as described by Schwartz (1976). In Schwartz’s blowing technique aimed at preventing tension in the laryngeal region, in particular spasms of the vocal band (lanryngospasm), speaking is precede by an inaudible aspirate. This recalls the breathing method proposed by A. Gutzmann (1879). In this procedure the client begins talking with ‚audible’ sigh which is gradually replaced
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by a voiceless ‚blowing’. The aim of blowing is to set the vocal bands into vibration by ‚gently’ emitting a stream of air before starting to say difficult words and then to maintain it in speaking a sentence. Using a silent /h/ as a starting aspirate is the most common example of this technique. Also common is the ‚bridging’ of stuttering by means of sounds like /e/, /w/ or /m/. In therapy, this technique is first practiced with obvious exaggeration which is reduced until the client is able to employ the technique without listeners discerning it. Because the danger exists that this technique could lead to the development of a new secondary symptom in the stuttering syndrome, it should not be used as the sole treatment approach (see Van Riper 1973). 1.2.2. Changing the Prosody: Accentuation and Intonation The key principle lies in the conscious addition of speech intonation features directed towards changing ones prosody (for rationale, e. g. Wingate 1979; Bergman 1987). Better known forms of this approach are: (a) expanding vowels and “vocal” binding of successive words (until the whole sentence is articulated as one word; Bluemel 1913; H. Gutzmann, as early as 1898), (b) the conscious emphasis of syllables (“syllable-timed-speech”; Andrews/Harris 1964 ), and (c) monotonous speaking (“monotoned speech”; Adams/Sears/Ramig 1982). We recommend the latter less because it belongs to the stuttering symptom constellation. In contrast, speech is accent optimally by introducing learned gestures to accompany speech (Calavrezo 1965; mimic exercises, Krause 1981; gesture exercises, Fiedler/Standop 1983; 1986). 1.2.3. Rhythmic Speaking This procedure belongs to every approach that attempts the most obvious reduction of speech errors possible. Even though it is not exactly one of the most popular procedures due to its prosody-changing quality, it is nonetheless one of the central components of many behavior therapy programs (e. g. Beech/ Fransella 1971; Andrews/Ingham 1972; Öst/ Götesham/Melin 1976; Helps/Dalton 1979; Wendlandt 1980). Normally the pronunciation of syllables, words, or sentence parts follows acoustic (metronome, ear-metro-
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nome), tactile (haptometronome), or visual stimuli. The goal of the therapy exercises is to gradually move from a very slow speech rhythm, which is oriented towards errors-free speech, to a more normal speed and intonation. 1.2.4. Prolonged Speech At this point, prolonged speech may be one of the most effective speech techniques (see Andrews/Guitar/Howie 1980). In practice, it is built into supposedly different approaches which are in fact similarly structured: for example, as “smooth motion speech” (Howie/ Tanner/Andrews 1981), as “systematic slowed speech” (Resick/Wedinggesen/Ames/Meyer 1978), or within the well-known so called “Lagato”-technique (Gutzmann 1879). The previous use of delayed auditory feeedback (DAF) to support prolonged speech (e. g. Perkins 1973a; 1973b) is not necessary or helpful in every case. Today most authors work with prolonging-instructions and observation learning (e. g. Howie/Tanner/Andrews 1981). Typically, prolonged speech begins at a rate of 50 syllables per minute. When the stutterer can produce error-free speech at this rate, the tempo is increased in steps of 5 syllables per minute until it approaches that of normal speech. 1.3. Other Aspects of Speech Therapy and Fluency Training At present, prolonged speech is one of the fluency training methods which can best be supported empirically and which has proven most reliable in short-term, as well as longitudinal, studies (Fiedler 1988). Experience has shown that if fluency training is to be effective in the long run, a very long period of systematic practice (significantly more than 50 practice hours) is necessary. Accomplishments through treatment can be maintained in various ways. Of these, the systematic construction of a training program seems particularly useful. Further suggested measures include: — symptom recognition exercises (self-monitoring: Van Riper 1973, 24 5—265; Ingham 1982), — breathing exercises (e. g. “regulated breathing approach”: Azrin/Nunn, 1974 ; for critique, see Rohjahn/Pesta 1977), — autogenic training (Krech 1963) and relaxation techniques (especially, the direct relaxation of the muscles and body parts involved in speaking; Lanyon 1977), and above all the use of — sound and video recordings as speech feed-
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back (Datiles 1977; Toups 1979; Fiedler/Standop 1986). The adjunct use of medication in stuttering treatment, such as the occasionally recommended low dosage of a neuroleptic (Haloperidol), strikes us as counterindicated for numerous reasons (Andrews/Dosza 1977; Murray/Kelly/Campbell/Stefanik 1977; Prins/ Mandelkern/Cerf 1980): First of all, the possible reduction in stuttering rate made possible with Haloperidol remains far behind the possibilities of other speech therapies and it contaminates their effectiveness. Furthermore, the use of neuroleptics can lead to serious side-effects (concentration disturbances, lethargy, extrapyramidal dyskinesia, nausea). Previous therapy studies have shown that this has regularly led to premature termination of therapy by over one third of the patients.
2.
The Combination of Speech and Social Therapy Measures
By now it is accepted therapy practice to combine speech and fluency training with social therapy measures. Exactly when and to what degree this occurs in treatment depends upon the severity of the speech disturbance and the extent of the stigmatisation caused by the stuttering. 2.1. Training Social Skills and Assertiveness Most authors agree that social training should begin as early as possible in the treatment. Role-playing of socially relevant skills is most often recommended (Van Riper 1973; Wendlandt 1980; 1984 ). Here, video and acoustic feedback play an important role. The goal in every case is to test the fluency training and new social strengths which were gained in the protected therapy setting under ‚reallife’ conditions. 2.2. Group Treatment In general, it appears common to extend treatment to a group format at an appropriate time (Fiedler 1986; 1990): Fluency skills such as social competence are more easily gained in a group setting, to some extent through modeling without the therapist having to lead or prompt each individual. Overall, a group offers the most promising prerequisite for a transfer of therapeutic progress, especially when group members exchange their strategies with one another and support such a
transfer. People who are similarly affected by stuttering can observe the outbreak of factors which may help to maintain stuttering: the secondary disturbances and anticipation anxiety (as well as the secondary gains which may possibly develop in these processes). The goal of social therapy often extends to an examination of the daily life of the stutterer. Participation in group therapy can facilitate the establishment of a self-help group. The therapy can be continued by the clients more independent of therapists: the clients can mutually control and support their therapy regime; they can also maintain regular telephone contact, organize activities together outside of therapy, and found self-help groups for others who are affected.
3.
Multimodal Therapy
Current therapy practice calls for the combination of speech and social therapy components in a thorough treatment program. Such multimodal treatment concepts generally emphasize the following four aspects (these examples are taken from the Fiedler/ Standop 1986, 225—230, treatment program): (1) Speech therapy and accompanying measures: The fluency training is pursued by prolonged speech (via direct instructions, modeling, and video-feedback). Additionally, the following are introduced: an exact self-evaluation of speech behavior via symptom-/selfmonitoring, then specific relaxation of muscles in the head, neck and upper body, as well as speech variation exercises (such as intended fluent stuttering as in the nonavoidance approaches; see Sheehan 1970, 269 ff). (2) Social skills training: We prefer training social competency through role-play and the use of video-feedback. The use of one of the standard behavior therapy procedures is not meant here, rather the training is individually planned for each client specifically in regards to his/her particular social deficits in his/her private life and occupation. (3) Transfer: This therapy step is primarily concerned with the transference of newly learned speech methods and social skills to daily life situations. Stuttering groups are formed in which the skills learned in therapy are practiced in the most realistic daily life situations possible (for example, executing important telephone conversations in front of a video-camera or the videotaping and subsequent evaluation of a therapeutic excursion
86. Therapy of the Stuttering Adult
of the group in the city interviewing people; Fiedler 1990). (4 ) Self-modification and relapse prev ention: Since relapses amongst adults are still more the rule than the exception, the therapy group developes detailed plans to deal with possible crises and relapses, enabling individual clients to handle them independently. Criteria are also established for the event that renewed help from a therapist is advisable. There has long been a selection of multimodal therapy programs, and recently concrete therapy manuals have appeared which well suit he needs of speech pedagogy (e. g. Perkins 1973a; b; Van Riper 1973; Böhme 1977; Ryan/Van Kirk 1978; Wendlandt 1984 ). They vary according to the technical execution of the speech therapy or the fluency training.
4.
Therapy Success and Prognosis
Spontaneous remission, often observed in stuttering children, is noticeably less frequent as they age, rarely occuring in adults. Quarrington (1977) found that spontaneous remission in adults depends upon an arduous self-therapy by the stutterer. The success in such selftherapy efforts does not ever, however, occur ‚spontaneously’, rather, it was, as a rule, obtained after one to five years. The number of relapses amongst adults has remained an unsolved problem. Although the speech therapy possibilities in the last decades have improved considerably, only few adult stutterers today dare hope to be completely ‚cured’ of their stuttering. This stands in marked contrast to the beginner’s success that one often sees in stuttering treatment. Most of the measures described above lead within the controlled therapy situation to a near complete reduction of stuttering frequency — often after only a few hours of practice. Relapses usually arise first after therapy ceases, and unless a catamnesis takes place, they will remain hidden from the therapist. This problem, thus, earns special attention. Most of the therapy studies carried out up to now were based upon catamnesis studies from 6 to 12 months (see Jehle 1982). Based on available knowledge about the individual nature of relapses, however, it seems highly necessary that a follow-up catamnesis after at least 2 years take place (see Bloodstein 1975). For several reasons, many of the success stories found in therapy reports should be viewed cautiously (Fiedler 1988): The number
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of drop-outs in therapy studies ranges at least between 4 and 25 percent, the problems associated with this rate are hardly discussed. Examinations of the maintained success of improved speaking behavior are usually administered under standardized conditions which do not greatly tax the speaker. The general transfer of the treatment effect to daily life is only seldom checked, even though this is exactly the area where the reasons for the variability of the speech disturbance are to be found. The findings of the simple follow-up measure via a telephone conversation only a few weeks after therapy termination (which is unfortunately too seldom executed), have been distinctly discouraging (e. g. Resick/Wediggensen/Ames/Meyer 1978). Among other factors which influence the treatment process are the age and gender of the stutterer. In general, girls have better therapeutic prognosis than boys. In adulthood, however, this situation reverses: woman have significantly less success-chances than men (Case 1960). The length of treatment also plays a role. 100 sessions or more promise a better prognosis (Andrews/Guitar/Howie 1980). It appears to be of only secondary importance whether this treatment is stretched over several months or wether it is concentrated intramurally in a block of several weeks. Finally, unrealistic high and low success expectations appear to correlate with lower therapeutic success (Guitar/Bass 1978).
5.
Conclusion
The majority of authors today feel that the treatment of stuttering in adult patients demands setting of multidimensional goals achieved by an eclectic treatment approach. Such an approach should carefully select treatment measures which take into consideration both the individual’s unique speech impediments (stuttering, articulation, prosody, mimic, gesture, etc.), and his/her current conditions and resulting problems (above all, speech anxiety and possible limitations in behavior and performance within his/her private and occupational interpersonal relationships). The variation range and effectiveness of the possible treatment steps is now so diverse that a satisfactory impact on the current degree of speech disturbances may be made. In view of the persistent relapse rate, however, it appears advisable that the success prognosis in therapy of adult stutterers should be realistically modest, so that they can really be
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actualized within the therapy. Furthermore, ‚freedom from symptoms’ is rarely a realistic prognosis. In the therapy of the stuttering adult we find ‚flowing speech’ or “more fluent stuttering than at the beginning of therapy” to be much more realistic. Since there are almost no predictors of therapy success known as of yet, the beginning of therapy should not raise any inappropriate expections, especially not too high or too low of success expectations, since these can impede therapy.
6.
References
Adams, M. R., Sears, R. L., & Ramig, P. R. (1982). Vocal changes in stutterers and nonstutterers during monotoned speech. Journal of Fluency Disorders, 7, 21—35. Andrews, G. & Dosza, M. (1977). Haloperidol and the treatment of stuttering. Journal of Fluency Disorders, 2, 217—224. Andrews, G., Guitar, B., & Howie P. (1980). Metaanalysis of the effects of stuttering treatment. Journal of Speech and Hearing Disorders, 45, 287—307. Andrews, G. & Harris, M. (1964 ). The syndrome of stuttering. London: Heinemann. Andrews, G., Howie, P. M., Dozsa, M., & Guitar, B. E. (1982). Stuttering: Speech pattern characteristics under fluency-inducing conditions. Journal of Speech and Hearing Research, 25, 208—216. Andrews, G. & Ingham, R. J. (1972). Stuttering: An evaluation of follow-up procedures for syllabletimed speech / token system therapy. Journal of Communication Disorders, 5, 307—319. Azrin, N. H. & Nunn, R. G. (1974 ). A rapid method of eliminating stuttering by a regulated breathing approach. Behav ior Research & Therapy, 12, 279—286. Beech, H. R. & Fransella, F. (1971). Research and experiments in stuttering (2nd ed.). New York: Pergamon. Becker, P., Keßler, B., & Fuchsgruber, K. (1975). Ein vergleichendes Therapieexperiment zur Theorie und Effizienz der Stotterbehandlung auf operanter Grundlage. Archiv für Psychologie, 127, 78—92. Bergmann, G. (1987). Stuttering as a prosodic disturbance: A link between speech execution and emotional processes. In: H. F. M. Peters & W. Hulstijn (Eds.), Speech motor dynamics in stuttering 393—407. New York: Springer. Bloodstein, O. (1975). A handbook on stuttering (2nd ed.). Chicago: National Easter Seal Society for Crippled Children and Adults. Bluemel, C. S. (1913). Stammering and cognate defects of speech (Vol. 2). New York: Stechert. Böhme, G. (1977). Das Stotter-Syndrom: Aetiologie, Diagnostik und Therapie. Bern: Huber.
Calavrezo, C. (1965). Die Behandlung des Stotterns durch die Sprachgebärden. De Therapie Vocis et Loquelae, 1, 399—401. Case, H. W. (1960). Therapeutic methods in stuttering and speech blocking. In H. J. Eysenck (Ed.), Behav ior therapy and the neuroses. 207—220. Oxford: Pergamon. Cherry, E. C. & Sayers, B. M. (1956). Experiments upon the total inhibition of stammering by external control, and some clinical results. Journal of Psychosomatic Research, 1, 233—246. Datiles, U. P. (1977). The effects of v ideotape feedback on the modification of stuttering behav ior through self-confrontation and analysis. Educ. Diss. Illinois: Northern University. Fiedler, P. (1986). Verhaltenstherapie in Gruppen: Überblick und Perspektiven. Gruppendynamik, 17, 341—360. Fiedler, P. (1988). Sprechstunde oder Psychotherapie? Wege und Umwege in der erfolgreichen Behandlung erwachsener Stotternder. In F. Hinteregger & F. Meixner (Eds.), Stottern — aus der Sicht der Betroffenen und der Therapeuten. 51—60. Wien: Jugend & Volk. Fiedler, P. (1990). Aktuelle Entwicklungen in der therapeutischen Gruppenarbeit: Konzepte, Wirkfaktoren und Indikationen. Forum des Zentralv erbandes für Logopädie, 2/90, 1—6. Fiedler, P. (1991). Neuropsychologische Grundlagen des Stotterns. In M. Grohnfeld (Ed.), Handbuch der Sprachtherapie. Band 5: Störungen der Redefähigkeit (43—60). Berlin: Edition Marhold. Fiedler, P. & Standop, R. (1983). Stuttering: integrating theory and practice. Rockville, Maryland: Aspen. Fiedler, P. & Standop, R. (1986). Stottern, Ätiologie, Diagnose, Behandlung (2nd ed.). München: Psychologie Verlags Union. Guitar, B. (1975). Reduction of stuttering using analog electromyographic feedback. Journal of Speech and Hearing Research, 18, 672—685. Guitar, B. & Bass, C. (1978). Stuttering therapy: the relation between attitude change and longterm outcome. Journal of Speech and Hearing Disorders, 43, 392—400. Gutzmann, A. (1879). Das Stottern und seine gründliche Beseitigung durch ein methodisch geordnetes und praktisch erprobtes Verfahren. Berlin: Med. Diss.. Gutzmann, H. (sen.) (1898). Das Stottern. Eine Monographie für Ärzte, Pädagogen und Behörden. Frankfurt/M.: Rosenheim. Helps, R. & Dalton, P. (1979). The effectiveness of an intensive group speech therapy programme for adult stutterers. British Journal of Disorders of Communication, 14, 17—30. Howie, P. & Andrews, G. (1984 ). Treatment of adult stutterers: managing fluency. In: R. F. Curlee
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& W. H. Perkins (Eds.), Nature and treatment of stuttering: new directions. 425—446. San Diego: College-Hill. Howie, P. M., Tanner, S., & Andrews, G. (1981). Short- and long-term outcome in an intensive treatment program for adult stutterer. Journal of Speech and Hearing Disorders, 46, 104—109. Ingham, R. J. (1982). The effects of self-evaluation training on maintenance and generalization during stuttering treatment. Journal of Speech and Hearing Disorders, 47, 289—301. Ingham, R. J. & Andrews, G. (1973). Behavior therapy and stuttering: A review. Journal of Speech and Hearing Disorders, 38, 405—441. Ingham, R. J., Southwood, H., & Horsburgh, G. (1981). Some effects of the Edinburgh Masker on stuttering during oral reading and spontaneous speech. Journal of Fluency Disorders, 6, 135—154. James, J. E. (1976). The influence of duration on the effects of time-out from speaking. Journal of Speech and Hearing Research, 19, 206—215. Jehle, P. (1982). Zur Problematik des Rückfalls in der Stottertherapie. In D. Nord-Rüdinger, I. Graudenz, N. Barth, R. S. Jäger, P. Jehle & R. Kühn (Eds.), Beiträge zu Theorie und Praxis in Psychologie und Pädagogik. 51—74. Frankfurt: Deutsches Institut für Internationale Pädagogische Forschung. Krause, R. (1981). Sprache und Affekt: Das Stottern und seine Behandlung. Stuttgart: Kohlhammer. Krech, H. (1963). Das Entspannungstraining. In H. Jacobi (Ed.), Phoniatrie. 148—153. Leipzig: Barth. Lanyon, R. I. (1977). Effects of biofeedback-based relaxation on stuttering during reading and spontanous speech. Journal of Consulting and Clinical Psychology, 45, 860—866. Liebmann, A. (1914 ). Vorlesungen über Sprachstörungen. (Heft 9: Die psychische Behandlung von Sprachstörungen). Berlin: Coblentz. Motsch, H. J. (1983). Problemkreis Stottern: Theoretische und therapeutische Neuorientierung (2nd ed.). Berlin: Marhold. Murray, T. J., Kelly, P., Campbell, L., & Stefanik, K. (1977). Haloperidol in the treatment of stuttering. British Journal of Psychiatry, 130, 370—373. Öst, L., Götesham, K., & Melin, L. (1976). A controlled study of two behavioral methods in the treatment of stuttering. Beha v ior Therapy, 7, 587—592. Perkins, W. H. (1973a). Replacement of stuttering with normal speech: I. Rationale. Journal of Speech and Hearing Disorders, 38, 283—294. Perkins, W. H. (1973b). Replacement of stuttering
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with normal speech: II. Clinical procedures. Journal of Speech and Hearing Disorders, 38, 295—303. Prins, D., Mandelkorn, T., & Cerf, F. A. (1980). Principal and differential effects of Haloperidol and placebo treatment upon speech disfluencies in stutterers. Journal of Speech and Hearing Research, 23, 614—629. Quarrington, B. (1977). How do the various theories of stuttering facilitate our therapeutic approach? Journal of Communication Disorders, 10, 77—83. Resick, P. A., Wendiggensen, P., Ames, S., & Meyer, V. (1978). Systematic slowed speech: A new treatment for stuttering. Behav ior Research and Therapy, 16, 161—167. Rieber, R. W. & Wollok, J. R. (1977). The historical roots of the theory and therapy of stuttering. Journal of Communication Disorders, 10, 3—24. Rojahn, J. & Pesta, I. (1977). Die Sprechpause als Stotter-Inkompatible Reaktion: Therapeutische Abgrenzung und Einsatzmöglichkeiten bei Stotternden. Zeitschrift für Klinische Psychologie, 6, 281—302. Ryan, B. & Van Kirk, B. (1978). Monterey-FluencyProgram. Palo Alto, Cal.: Monterey Learning Systems (German Edition 1982: Monterey Sprachtrainingsprogramm. Palo Alto, Cal.: Monterey Learning Systems). Schwartz, M. (1976). Stuttering solv ed. Philadelphia: Lippincott. Shames, G. H. & Egolf, D. B. (1976). Operant conditioning and the management of stuttering. Englewood Cliffs, N. J.: Prentice-Hall. Sheehan, J. G. (1970). Role-Therapy. In J. G. Sheehan (Ed.), Stuttering. Research and therapy. 260—311. New York: Harper & Row. Toups, F. (1979). Empirische Untersuchungen zur Streßwirkung audiov isueller Selbstkonfrontation auf Stotternde. Frankfurt: Lang. Van Riper, C. (1973). The treatment of stuttering. Englewood-Cliffs: Prentice-Hall. Wendlandt, W. (1980). Verhaltenstherapie des Stotterns. Weinheim: Beltz. Wendlandt, W. (1984 ). Zum Beispiel Stottern. Stolperdrähte, Sackgassen und Lichtblicke im Therapiealltag. München: Pfeiffer. Widlak, H. (1977). Modifikation des Stotterns durch negativ e Praxis. Phil. Diss. Münster: Westfälische Wilhelms-Universität. Wingate; M. E. (1979). The loci of stuttering: grammer or prosody? Journal of Communication Disorders, 12, 283—290.
Peter Fiedler, Heidelberg (Germany)
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87. 1. 2. 3. 4. 5.
Language Changes in Old Age Organization of Semantic Information Language Comprehension Production of Discourse Language in Normal Aging, Aphasia, and Alzheimer’s Disease References
Old age is characterized by changes in many aspects of cognition, including memory, problem solving, and reasoning (Salthouse 1982). Until recently, however, it was believed that language was immune from the effects of aging found in other areas of cognition. For instance, less than 20 years ago, Riegel made the claim that “language functions remain highly stable and do not reveal any dramatic or ‚interesting’ changes in development” (Riegel 1973, 4 79) in old age. The thesis of this chapter is that such claims are only partly correct. Some aspects of language indeed remain stable and some change. In particular, despite the apparent preservation of semantic knowledge in old age, both comprehension and production of language show age-related changes consistent with the position that performance factors set limits on older adults’ ability to understand and produce language. The chapter is divided into four sections. Research dealing with the representation of semantic knowledge in old age is reviewed in the first section. The second and third take up issues related to comprehension and production of language, respectively. The fourth and last section compares language in normal aging to that in aphasia and in Alzheimer’s disease.
1.
Organization of Semantic Information
Within the framework of network models of memory (Anderson 1983), both semantic and episodic information are represented by nodes, which stand for concepts or propositions, and these nodes are connected by associative pathways. When a concept is encountered, its node is activated, and activation also spreads along associative pathways to related nodes, increasing their availability for further processing. These activation processes, both automatic and attentional, have been implicated in virtually all aspects of natural language understanding and production,
including perception of words in spoken or written form (McClelland/Rumelhart 1981), determining the syntactic structure of sentences (Tanenhaus/Dell/Carlson 1987), deriving the meaning of single sentences and entire discourses (Kintsch 1988), and producing discourse (Dell 1986). Activation of pragmatic or general world knowledge embodied in schemata is necessary for making inferences, for establishing the topic of a discourse, and for determining the antecedents of pronouns. Hence, differences across age in either the way knowledge is represented in memory or in the way that activation proceeds could result in both comprehension and production impairments. Evidence about possible age differences in the representation or activation of conceptual knowledge comes from a variety of sources, including word-finding difficulties, responses in word association tasks, representation of schemata, semantic priming in lexical decision and word naming, particularization of word meanings in discourse, and judgments of similarity or relatedness of concepts. 1.1. Word-Finding Difficulties There is little evidence for a decline in vocabulary size as people grow older (e. g. Salthouse 1982). Older adults do nevertheless have more word-finding difficulties than young adults. These are shown in reduced verbal fluency in tasks in which people are given a fixed amount of time to generate as many words as they can that meet specific criteria, such as beginning with a particular letter or being members of particular categories (Howard 1980; McCrae/Arenberg/Costa 1987; Schaie/ Parham 1977). Older adults are more prone than young adults to tip-of-the-tongue experiences in which familiar words are temporarily unretrievable (Burke/MacKay/Worthley/Wade 1991; Cohen/Faulkner 1986). There is increased difficulty in naming to definition in old age (Bowles/Poon 1985; Maylor 1990; but see Rissenberg/Glanzer 1987 for a counterexample). Picture naming errors are generally found to increase in old age, though perhaps not until the eighth decade of life (Albert/Heller/Milberg 1988; Borod/Goodglass/Kaplan 1980; Van Gorp/Satz/Kiersch/ Henry 1986), but some investigators report no age difference on this task (Flicker/Ferris/ Crook/Bartus 1987; Mitchell 1989).
87. Language Changes in Old Age
In spontaneous speech, there is some evidence for increased frequency of pauses, which may signal word-finding problems, but the findings are not consistent across studies (cf. 3.3.). In retelling stories, older adults are more likely to use pronouns without mentioning their antecedents (Cohen 1979; Obler 1980; Pratt/Boyes/Robins/Manchester 1989; Ulatowska/Cannito/Hayashi/Fleming 1985) though this may signal a problem in remembering previously mentioned antecedents rather than a general deficit in word retrieval. There have also been reports of fewer proper nouns, increased frequency of general nouns, and less lexical variety of nouns in the speech of older adults (Ulatowska et al. 1985), though studies reporting type/token ratios or number of unique words do not usually find age declines in these measures of lexical variety (Bromley 1991; Cooper 1990; Kemper/Kynette/Rash et al. 1989; Kynette/Kemper 1986; Walker/Hardiman/Hedrick/Holbrook 1981; Walker/Roberts/Hedrick 1988). Reduced verbal fluency, increased frequency of tip-of-the-tongue experiences, problems in confrontation naming and naming to definition, and word finding problems in spontaneous speech could all be symptomatic of changes in either the completeness or the organization of conceptual knowledge. That is, if semantic representations in old age contain fewer features or if the associations between concepts and their attributes have a different distribution of strengths than they do in younger individuals, then changes such as these would be expected. These changes, however, would also be consistent with problems in accessing the orthographic or phonological realizations of words even in the presence of an intact semantic system. There are a number of reasons for believing that the latter alternative provides a better account of the data. (1) Older adults produce fewer phonological features (first letters, number of syllables) of targets than young adults when in a tipof-the-tongue state (Burke/MacKay/Worthley/Wade 1991); this is more consistent with a transmission deficit in old age which reduces the availability of phonological information rather than a change in the structure of the semantic concepts themselves. (2) Phonemic cues are equally helpful as hints to young and older adults in confrontation naming tasks (Nicholas/Obler/Albert/Goodglass 1985) and orthographically similar primes are actually
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more helpful to the old than to the young in naming to definition (Bowles/Poon 1985). (3) An increase with age in the proportion of semantically related errors could indicate either a disruption (loss or disorganization) of information within specific semantic domains (if the errors are near synonyms or responses in the same category as the correct word) or of word finding problems (if the errors are circumlocutions such as cutting the wood for sawing). If anything, however, there is a drop in the proportion of semantically related errors and an increase in the proportion of circumlocutions (Albert/Heller/Milberg 1988; Bowles/Obler/Albert 1987; Nicholas/Obler/ Albert/Goodglass 1985). Taken together, these results are more in keeping with lexical retrieval failures than with semantic deficits. 1.2. Word Associations In free association tasks, the instructions are to give the first word that comes to mind when a stimulus word is presented. According to semantic network models, presentation of the stimulus word activates the node standing for this concept. Activation also spreads automatically from this node to all concepts having attributes in common with it and, hence, sharing pathways with it. The first word to come to mind should be the one whose concept has the most shared properties or whose semantic distance is the smallest. In controlled association tasks, further restrictions are placed on the response to be given. For instance, the task may be to produce a superordinate of the word or a physical characteristic of an object or an action that can be performed with the object. Here, network models would assume that there is a compound stimulus consisting of the word and the type of response to be produced. Activation from this compound stimulus may converge automatically on an appropriate response. Alternatively, all properties of the stimulus concept may be activated and the concept associated with the pathway labelled with the appropriate relation may be selected as the response. The results of both free and controlled word association tasks argue for preservation of the semantic system in old age. (1) Young and older adults produce pretty much the same types of responses. For instance, both young and older adults typically produce paradigmatic rather than syntagmatic responses in free association tasks (Burke/Peters 1986; Lovelace/Cooley 1982). When asked to pro-
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duce particular types of responses to words naming objects — a characteristic action, a distinctive physical feature, or a general associate — the percentage of acceptable responses does not differ reliably across age (Nebes/Brady 1988). When people are asked to produce properties for nouns, the breakdown of attributes into those referring to physical features, functional features, specifiers (elaborations on functions that specify their objects), category names, and exemplars is very similar for young and old (Stine 1986; see also Lovelace/Cooley 1982). Moreover, strong correlations are found between the frequencies with which young and older adults produce particular associates when generating members of taxonomic categories (Howard 1980) or properties of stimulus terms (Howard 1979). (2) The variability of associative responses seems fairly constant across age. As noted by Burke/Peters (1986), response variability would be expected to increase if older adults have atypical associations or if features important to meaning were absent. Although it has been reported that normal older adults produce a greater number of different associates or more unique associates (Riegel/Riegel 1964 ), such differences are generally not observed when young and older adults are carefully equated on education or vocabulary (Bowles/Williams/Poon 1983; Burke/Peters 1986; Howard 1979, 1980; Lovelace/Cooley 1982). Overall, then, there is considerable stability in the types of responses that older adults make and in the production frequencies for particular associates. 1.3. Schemata Our memories of experiences are organized in knowledge structures. Schemata are believed to play a central role in language comprehension and memory, guiding expectations about what will come next in a discourse, facilitating perception of individual words, and aiding in integration of old and new information (Sanford/Garrod 1981; Sharkey 1986). If young and older adults did not share knowledge structures or if there were age differences in accessing or modifying these structures, comprehension and communication could be severely impaired. Fortunately, however, there appears to be considerable similarity of conceptual organization across age. When asked to generate a sequence of actions that are typically performed by most people
V. Pathologies and Disorders of Language Development
in carrying out some activity such as going to the doctor or writing a letter to a friend, young and older adults produce much the same actions (Hess 1985; Light/Anderson 1983). Correlations between age groups are also quite high when actions are rated for typicality or necessity for completion of an activity or likelihood of occurrence during an event sequence (Hess 1985; Light/Anderson 1983; List 1986). Young and older adults also agree on the order of actions in carrying out particular activities (Roman/Brownell/Potter/ Seibold 1987). 1.4. Lexical Decision and Word Naming Tasks It takes less time to decide whether a string of letters is a word or to name a target when it is preceded by a semantically related prime word or by an appropriate sentence context than when it is preceded by an unrelated prime (Meyer/Schvaneveldt 1971; Stanovich/ West 1983). Such semantic priming effects are generally interpreted as evidence for spreading activation in a network and, therefore, similar patterns of semantic priming in young and older adults would constitute evidence for the integrity of the semantic system. That is, differences across age in the sensitivity of priming to variations in the associative strength of primes and targets, or to different prime-target semantic relationships, would suggest a semantic deficit. In addition, differences in the time course of activation could have consequences for the integration of information in a discourse. The available evidence from semantic priming studies, however, points to the absence of such a deficit. The extent of priming is generally evaluated by comparing latencies when the target is preceded by a related prime to latencies when the target is preceded by an unrelated prime or by a neutral prime. Comparable priming effects have been obtained in young and old when the target is a cohyponym of the prime (Howard/McAndrews/ Lasaga 1981), when the target names a descriptive property of the prime (Howard et al. 1981), when the target is an associate of the prime (Balota/Duchek 1988), and when the prime is a superordinate of the target (Balota/Duchek 1988; Burke/White/Diaz 1987). Both young and older adults also show facilitation in lexical decision and naming tasks when sentence rather than single word primes are used (Burke/Harrold 1988; Burke/ Yee 1984 ; Cohen/Faulkner 1983; Madden
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1986, 1988, 1989; Nebes/Boller/Holland 1986). In lexical decision (the task most often used to assess age-related differences in priming) the results reveal similarity in the extent of priming and no evidence for reduced benefits or costs when latencies following related and unrelated primes are compared to latencies following neutral primes (Bowles/Poon 1985; Burke/Yee 198 4 ; Chiarello/Church/Hoyer 1985; Howard 1983; Howard/McAndrews/ Lasaga 1981; Howard/Shaw/Heisey 1986; Madden 1986, 1988, 1989). Benefits are believed to reflect a mix of automatic and attentional processes, while costs are thought to arise solely from attentional processes; these results, then, argue against age differences in either automatic or attentional components of activation. Indeed, a recent metaanalysis (Laver/Burke 1990) found generally larger semantic priming effects in the old than in the young. As noted above, age differences in rate of activation could have consequences for both comprehension and production of language. If activation spreads more slowly in the old, less semantic priming should be obtained at very short prime-target asynchronies. This does not, however, appear to be the case (Balota/Duchek 1988; Burke/White/Diaz 1987; Madden 1989; Stern/Prather/Swinney/ Zurif 1991; but see Howard et al. 1986, for a different outcome). Some caution is nevertheless needed in evaluating studies of semantic priming in young and older adults. MacKay/Burke (1990) point out that older adults have more practice with semantically associated words, increasing the strength of their connections relative to younger adults, and that because of the many interconnections between nodes in a semantic network, there may be a summation of priming that masks age deficits in this domain. Moreover, because older adults have longer reaction times in semantic priming experiments, there is more time for activation to spread from prime to target. The evidence reviewed here thus does not constitute definitive proof of age constancy in the magnitude or rate of semantic activation. There is also reason to believe that intact semantic priming is at best weak evidence for preserved semantic structure because patients with aphasia or Alzheimer’s disease who perform poorly on overt semantic judgment tasks nevertheless show priming (Chertkow/ Bub/Seidenberg 1989; Warrington/Shallice 1984).
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1.5. Particularization of Word Meanings in Sentences The results of controlled association studies and judgments of similarity or relatedness (cf. 1.6.) suggest that young and older adults share beliefs about the properties and functions of objects. Different aspects of a word’s meaning are not equally salient in all contexts. Although some core or central properties may always be activated regardless of context, particular linguistic contexts emphasize or highlight different aspects of meaning, with unemphasized properties being inhibited (Tabossi/ Johnson-Laird 1980). If semantic structures were degraded in old age or if activation or inhibition processes were impaired, it would not be surprising to find that older adults were less precise in particularizing word meanings in discourse contexts. Hasher/ Zacks (1988) have recently argued that inhibitory processes are less efficient in old age and would therefore predict less effective or slower particularization of word meanings. The available evidence, however, gives no support for this conclusion. Young and older adults both show inhibition of properties of objects that are inappropriate in particular sentence contexts (Burke/Harrold 1988), activation of instruments implied by verbs (Burke/Yee 1984 ), and instantiation of general terms with specific category exemplars (Light/Valencia-Laver/Zavis 1991). 1.6. Judgments of Similarity Another approach to studying possible age differences in the structure of conceptual knowledge involves the use of tasks which require judgments about similarity between pairs of objects. For instance, people may be asked to judge whether two words mean approximately the same thing (Hertzog/Raskind/Cannon 1986; Madden 1985), to decide whether a word names a category member or whether two words belong to the same category (Hertzog et al. 1986; Mueller/Kausler/ Faherty 1980), or just to decide whether two words are related, without the precise nature of the relation being specified (Byrd 1984 ; Nebes/Brady 1988). Although older adults are slower than younger adults to make semantic judgments, their error rates are no higher, suggesting the availability of information about the relationships queried or, when the judgment is about simple relatedness, the availability of information that an association exists. When category instances
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varying in production frequency or typicality are used, the extent to which typicality affects response latency is the same across age, suggesting that category structure is similar across age (Byrd 1984 ; Hertzog et al. 1986; Mueller et al. 1980). Judgments of relatedness do not require that a basis for similarity be explicitly retrieved and judgments of the category membership or synonymity of two words do not require the production of these words. Older adults perform more poorly on tests in which particular relationships are explicitly queried. For instance, performance on the WAIS Similarities subtest, which requires the statement of how two things are related, declines with age (see Salthouse 1982 for a review). Riegel (1959) found that young and older adults equated on ability to select synonyms on a mutiple choice test had problems in choosing antonyms, in selecting salient properties, in choosing two coordinates for a target when a superordinate was not actually stated, and in solving verbal analogies which required computation of similarity relationships. These tasks are more specific in the knowledge they tap than tasks that involve production of properties or judgments of similarity or category membership; they require the abstraction and, in some cases, the verbalization of relationships between two objects. One hypothesis is that older adults are impaired in these processes, but that semantic structure is indeed intact. However, age differences are not observed when people are asked to select items that belong to a particular taxonomic category (Flicker/Ferris/Crook/Bartus 1986) or to explain why they categorized objects in particular ways (Smiley/Brown 1979). 1.7. Summary Little evidence has surfaced for age-related changes in semantic organization. Although older adults have word finding difficulties, the simplest explanation for these is that lexical access is impaired. There is great consistency in the type of word associations produced by young and older adults and little indication that word associations are more variable or idiosyncratic in the old. The representation of schematic information is similar in young and old. Semantic priming appears to be preserved in old age and, in fact, there is evidence that older adults may show greater priming than young adults. Young and older adults are equally likely to particularize word meanings in sentences. Older
adults are as accurate as young adults in deciding whether two concepts are related or whether they share particular aspects of meaning. Although the old do show declines on tasks which require the explicit statement or selection of the way in which words are related, it is not clear whether this result should be taken as signalling an alteration in semantic structures. The same result may be indicative of problems in accessing particular knowledge or even of shifts in the criteria for similarity without implicating a semantic deficit.
2.
Language Comprehension
Much of the research on language comprehension in old age has been carried out within a processing resources framework. There are two very good reasons for this. First, working memory plays a central role in most models of sentence and discourse comprehension. Limitations in working memory capacity (the ability to store and manipulate information over short periods of time) affect comprehension of complex sentences (Bock 1982) and integrative processes responsible for establishing discourse coherence (Kintsch/van Dijk 1978; Sanford/Garrod 1981). Second, older adults are slower to carry out cognitive operations than young adults and also demonstrate reduced working memory capacity (Light/Anderson 1985; Salthouse 1990). Hence, increasing presentation rate or working memory load should have more deleterious effects on comprehension in the old. Much (but not all) of the available evidence from studies of speech perception, sentence comprehension, and integration of information within a discourse is consistent with this view. 2.1. Speech Perception Evaluating the contribution of working memory or cognitive slowing to age-related impairments in comprehension is complicated by the fact that older adults also have impaired speech perception. Perception of words and sentences may be impaired to an extent greater than would be predicted from puretone audiometry (Jerger/Hayes 1977). Speech discrimination (assessed in terms of the proportion of words or sentences correctly identified at a given loudness) may be worse for sentences than for words in old age (Jerger/ Hayes 1977). Also, age differences in speech perception are intensified when speech is pre-
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sented under adverse listening conditions such as when speech is presented in noise or timecompressed by periodic deletions of small segments (Bergman 1980; Wingfield/Poon/Lombardi/Lowe 1985). Age-related decrements in speech perception may be due to changes in peripheral portions of the auditory nervous system or to more central changes, such as reduced speed in integration of information, or both. Several findings implicate central processes. Although the performance of the elderly is more affected by speeded presentation than that of the young, the presence of semantic, syntactic, or prosodic information in the material to be perceived is more beneficial to the old than to the young (Wingfield et al. 1985; Wingfield/Lahar/Stine 1989). Age differences in perception of words and sentences in noise are also reduced by the availability of appropriate sentential context (Cohen/Faulkner 1983; Hutchinson 1989; Obler/Nicholas/Albert/Woodward 1985). Similarly, in a wordonset gating paradigm (in which increasing amounts of word onset information are presented until the target can be identified), age differences in correctly identifying the first phoneme of the target at very short gates are reduced when sentence context is more constraining (Wingfield/Aberdeen/Stine 1991). These results argue for a central locus of impaired speech perception in the elderly. They also suggest that the interaction of topdown processes with sensory information is important in old age. Finally, we note that tests of word and sentence perception are typically tests of short-term memory which require subjects to repeat the items they have heard out loud; age-related declines are generally found in memory span, so that a greater decline in memory for sentences than for single words is unsurprising. 2.2. Sentence Comprehension Sensitivity to the syntactic constraints of language has been studied in a number of ways differing in the explicitness of the measures used. For instance, Wingfield/Poon/Lombardi/Lowe (1985) asked young and older adults to repeat 5- and 8-word strings that were normal sentences, syntactically correct but semantically anomalous strings, or random sequences presented at rates varying from 275 to 4 25 words per minute. The old showed relatively poorer performance than the young at fast rates, as first semantic and then syntactic redundancy were eliminated in
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the syntactically correct and random strings. When asked to segment either spoken or written prose for immediate recall, both young and old show respect for syntactic boundaries (Stine 1990; Wingfield/Lahar/Stine 1989). There is nonetheless some evidence that older adults allocate less time at sentence boundaries, suggesting that they do not engage in as much processing that integrates larger conceptual units as young adults; this would be consistent with a working memory deficit in old age (Stine 1990). Studies which directly manipulate variables expected to be sensitive to working memory limitations show mixed results. Age differences are sometimes found on the Token Test on which a series of commands of increasing syntactic and semantic complexity are given for manipulating small pieces of plastic which vary in size, shape, and color (e. g. Bergman 1980; Emery 1985; Lesser 1976), and Lesser (1976) has shown that scores on the Token Test correlate negatively with measures of short-term memory; however, age differences on this test are not universally obtained (see Light 1988 for a review). Experimental studies of the effect of syntactic complexity on comprehension have generally found that increasing syntactic complexity differentially impairs the performance of older adults. Thus, age differences are greater for verbatim and gist repetition of left-branching or center-embedded sentences than for right-branching sentences (Bergman 1980; Kemper 1986; Norman/Kemper/Kynette et al. 1991). Although young and old are equally able to judge the well-formedness of simpler sentences and to correct errors in syntactically anomalous ones (Bayles/Tomoeda/Boone 1985), age differences are found in judgments of the grammaticality of syntactically well-formed strings if these involve complex constructions (Pye/ Cheung/Kemper in press). Sentences containing center-embedded or left-branching clauses impose greater memory loads than those consisting of simple or right-branching clauses because of the greater separation of subject and predicate terms that belong together. Hence, there are greater concomitant risks of forgetting parts of the sentences or having difficulty in generating a reasonable interpretation of the constituents. In some cases, age differences in sentence comprehension may arise from the need to engage in fairly extensive problem solving. Emery (1985) found that pre-middle-aged high school graduates obtained higher scores than elderly aged 75
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and over on a battery of sentence comprehension tests. It is not always clear whether it is syntactic complexity or exessive reasoning demands which produces the age difference. For instance, in John runs faster than George but slower than Humphrey, the subject must construct a three term series by figuring out that Humphrey is faster than George, and in What is the relationship of my grandfather’s son-in-law to me?, reasoning about kinship terms is required. In both cases, working memory demands are high. There are, nonetheless, variables which should produce age differences in comprehension, if these are due to reduced working memory capacity, but which in fact do not. Thus, increasing the propositional density of sentences of constant length does not differentially reduce gist recall in the old (Stine/ Wingfield/Poon 1986) although greater propositional density may have more deleterious effects on recall of longer passages in the old (Stine/Wingfield 1990). Further, sentence complexity (whether a sentence is positive or negative) does not consistently interact with age in a sentence verification task (Craik/ Morris/Gick 1990). Nor does varying the size of a concurrent memory load differentially affect young and old sentence verification latencies; this is contrary to predictions from hypotheses that working memory mediates sentence comprehension (Craik et al. 1990). Some studies have included measures of working memory as well as comprehension; these studies generally report that comprehension correlates positively with memory span (Feier/Gerstman 1980; Kemper/Kynette/Norman 1992; Norman/Kemper/Kynette et al. 1991). In Kemper et al. and Norman et al.’s studies, the data suggest that correlations between age and comprehension are reduced by controlling statistically for working memory capacity; however, the significance tests that would unambiguously demonstrate the role of working memory in producing differential age differences as a function of complexity are not given (cf. Salthouse 1985). Further, Stine/Wingfield (1987) reported that age differences on a working memory measure could not fully account for age differences in recall of word strings, so that variables other than working memory capacity must also contribute here. 2.3. Integration of Information in Discourse As noted earlier, working memory is generally believed to play a major role in discourse
V. Pathologies and Disorders of Language Development
comprehension. In Kintsch/van Dijk’s (1978) model, construction of a coherent representation of a discourse proceeds in cycles. At the end of each cycle, there is too much information in the short-term buffer to be carried forward; only the most important and most recent propositions are maintained in the buffer for subsequent processing together with new inputs. The structure that evolves from this process is based on argument repetition. When there are no propositions remaining in the buffer that share arguments, it becomes necessary to either produce a bridging inference based on general world knowledge or to search all recently processed propositions to determine whether any contain arguments overlapping with those currently in the buffer. The final product is a coherent network of propositions which is organized hierarchically, with the most important propositions (i. e., those with the most argument repetitions) at the highest level. These more important propositions are known to be better recalled, a phenomenon called ‚the levels effect’. Within this framework, there are many ways for discourse processing to be compromised in old age. Reduction of buffer size would reduce the number of propositions that could be processed simultaneously as well as the number of propositions that could be carried over from cycle to cycle. As a consequence, the necessity for both inference generation and memory search would be increased. Either or both of these processes may be impaired in old age (Anders/Fozard/Lillyquist 1972; Craik/Byrd 1982). As a result, the coherence of discourse representations should be lower in old age. This model permits a number of specific predictions with regard to aging. (1) Older adults should show reduced recall of lower level propositions because fewer of these can be carried forward from previous cycles if buffer size is reduced. This result is sometimes obtained, but not always (cf. Cohen 1988). A recent meta-analysis found no consistent age difference in the magnitude of the levels effect (Zelinski/Gilewski 1988). (2) Older adults should be more sensitive to distance effects. Increasing the number of irrelevant propositions intervening between propositions to be linked reduces the likelihood that these propositions will reside simultaneously in the buffer and therefore reduces the likelihood that they will be linked. Because the number of propositions that can be processed in one cycle depends on buffer size, thought to be reduced in old age, dis-
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tance effects should be magnified in the old. Light/Capps (1986) found that young and older adults did not differ in ability to assign referents to ambiguous pronouns when memory load was low (i. e., when there was no material intervening between a sentence containing a pronoun and a sentence containing its possible antecedents) but older adults were less accurate when there were two intervening sentences. This result, however, was not replicated in a study using long passages (12 sentences) and many potential antecedents (Light/Anderson 1985); in this case young adults were better at answering questions about pronouns, but there was no interaction of age with distance. (3) Topic change should have more deleterious consequences for discourse comprehension in the old than in the young. Van Dijk/Kintsch (1983) note that the importance of material is largely determined by the extent to which it is relevant to the current topic of a discourse. When the amount of material intervening between two sentences to be integrated is held constant, the likelihood that the initial information will be in working memory is smaller when there has been a topic change that backgrounds it. Under these conditions, successful integration depends on retrieval of recently processed propositions which may have been forgotten. Older adults are relatively less able than young adults to detect anomalies when relevant information is backgrounded, and the effect appears to be related to forgetting that relevant information (Light/Albertson 1988). (4 ) If ability to draw inferences based on general world knowledge were impaired in old age, integration of discourse would be expected to suffer. It has been hypothesized that this should occur because of reduced working memory capacity in the old (Cohen 1979; Craik/Byrd 1982). Under most circumstances, however, older adults have no difficulty in generating pragmatic inferences. When comprehension is assessed during or immediately after a sentence is read, young and older adults give no evidence of differing in ability to draw inferences about the instruments with which actions are performed (Burke/Yee 1984 ), the instance of a category implied by a sentence context (Light/Valencia-Laver/Zavis 1991), the properties of nouns highlighted by sentences (Burke/Harrold 1988), the antecedents of noun-phrase anaphors (Light/Albertson 1988; Zelinski 1988; but see Hasher/Zacks 1988, for the sug-
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gestion that activation of antecedents takes longer in older adults), or the antecedents of pronouns (Light 1992; Light/Capps 1986). Some studies do find age differences in ability to draw inferences, but these generally have not used on-line measures of comprehension and, therefore, confound processes occurring during comprehension with those dependent on storage and retrieval (Till/ Walsh 1980) or use tasks involving heavy memory loads, leaving open the possibility that forgetting of relevant information or inability to activate previous information underlies problems in generation of inferences (Cohen 1979; Light/Anderson 1985; Light/ Capps 1986; Hasher/Zacks 1988). Moreover, even with longer passages or delays between study and test, age differences in memory for inferences are not always found (cf. Light 1992). In the studies reviewed thus far, inferences depended on general world knowledge where the literal meaning of sentences was involved. It is possible that access to general world knowledge in understanding more figurative language might be impaired in older adults. Some theorists have suggested that understanding figurative language requires two stages of processing, one in which a literal reading of an utterance is constructed and rejected and a second in which a contextually appropriate reading is produced (Searle 1979). The second process is viewed as more effortful and producing heavier demands on memory and, in the case of comprehending proverbs and metaphors, as requiring the computation of similarity relationships (Miller 1979). Hence, older adults, who may have difficulty in abstracting the basis of similarity between two concepts, might have greater difficulty than young adults in understanding proverbs and metaphors, though possibly not in understanding more formulaic indirect requests. The evidence in part favors this prediction, but in part does not. Bayles/ Tomoeda/Boone (1985) found no age differences in ability to judge the literalness or directness of utterances or to identify the illocutionary intent of a speaker. On the other hand, interpretation of proverbs has been found less accurate in older adults (Albert/ Duffy/Naeser 1987). This outcome may depend on the nature of the comprehension test used. Albert et al. used both free interpretation and forced-choice versions of Gorham’s Proverb Interpretation Test. Light and Owens (cf.Light 1992) found evidence for age differ-
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ences in comprehension of novel metaphors on a cued recall test but not on a more indirect sentence verification paradigm. 2.4. Summary Some, but not all, predictions based on the hypothesis that working memory deficits underlie impaired language comprehension in the elderly receive empirical support. In general, the old are less accurate than the young in repeating sentences with complex syntactic structures and in answering questions based on them. Studies in which measures of working memory as well as sentence comprehension have been assessed suggest that age differences in working memory capacity explain age differences in comprehension but the data are by no means compelling. Specific predictions about age-related changes in integration of discourse are only partially confirmed. Older adults are more affected by topic change in building a coherent discourse representation, probably because they forget or do not carry forward for further processing information necessary to establish coherence. However, levels effects do not appear to vary with age. Nor are processes involved in online inference generation or comprehension of figurative language susceptible to aging effects. Moreover, older adults do not show greater sensitivity to propositional density effects in sentence comprehension, though a working-memory hypothesis predicts that they should. Making sense of these findings is complicated by the fact that the role of working memory in sentence and discourse comprehension is not entirely understood. One approach is to treat working memory as a single pool of resources which can be assessed in a straightforward manner by obtaining an appropriate measure of working memory (Salthouse 1990). Although there is reason to believe that the operations underlying language comprehension draw upon resources distinct from those involved in other aspects of cognition (Baddeley/Logie/Nimmo-Smith/Brereton 1985), studies taking an individual difference approach to the role of working memory in age-related language impairment have been conducted within this single-pool framework. An alternate approach is that of Baddeley (1986) who has hypothesized that working memory consists of a central executive, together with a set of slave systems which have specialized storage functions. Within this framework two components, an articulatory
loop and a phonological store, are important for language. A number of possible roles have been suggested for a phonological memory store — maintaining information until analysis of earlier portions of a sentence is completed, maintaining information for resolution of local syntactic ambiguities, keeping lexical items in the syntactic representation, maintaining a back-up record for use when postinterpretive processes are needed to resolve ambiguities, rehearsing difficult material for verbatim repetition (Caplan/Waters 1990; Martin 1990). Studies designed to tease apart these possibilities with respect to aging remain to be performed. Finally, patients suffering from focal brain damage whose shortterm memory impairments are far more severe than those presented by normal older adults sometimes show quite good comprehension. A systematic comparison of such patients with normal elderly adults should reveal commonalities and differences in the nature of comprehension deficits in these populations.
3.
Production of Discourse
Working memory is believed to play an important role in speech production (Bock 1982; Levelt 1989), and, as a consequence, agerelated differences in language production paralleling those observed in language comprehension would be expected. Evidence germane to this question comes from examination of the syntactic complexity and coherence of discourse as well as analysis of the frequency of speech errors and repairs across age. 3.1. Syntactic Complexity One clear prediction is that reduced workingmemory capacity in old age should give rise to shorter and less syntactically complex spoken and written discourse. The evidence on this point suggests that this may be true but is not altogether consistent. Obler (1980) reported two studies of written descriptions of the cookie-theft picture from the Boston Diagnostic Aphasia Examination that suggested that older adults use more elaborate language. However, in both a naturalistic study of diaries and a laboratory study in which written language samples about a significant life event were obtained, Kemper (1987; Kemper/Kynette/Rash et al. 1989) found reliable declines in syntactic complexity; reductions were observed in the frequency of several
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clause types, including relative clauses, subordinates, gerunds, and double and triple embeddings. Similarly, Bromley (1991) reported a decrease in the use of subordinating conjunctions in older adults’ self-descriptions. The data are also somewhat equivocal with respect to speech. Walker/Hardiman/Hedrick/Holbrook (1981) computed the number of words in a T-unit (a main clause and any subordinate clauses attached or embedded in it) and found reliably shorter productions for older adults. Although the young had somewhat more words per clause and clauses per T-unit, these measures showed no age effects. In a second study, Walker/Roberts/Hedrick (1988) reported reliable age differences for both words per clause and words per T-unit, though not for clauses per T-unit, suggesting age differences in length but not complexity of discourse. An absence of reliable effects of age has also been reported for number of complex sentences (Shewan/Henderson 1988). Cooper (1990) found no decline across age in number of words produced, prepositional phrases per 100 words, or subordinate clauses per 100 words on a picture description task. In a study comparing the discourse of middle-aged and older nuns, Ulatowska/Cannito/Hayashi/Fleming (1985) found no difference across age in the complexity of expressions used to refer to entities within the discourse. These studies suggest that there are few changes across age in either the length or complexity of spoken discourse. However, Kemper and her colleagues have conducted a series of studies using more sensitive measures of syntactic complexity which challenge this conclusion. Although Kemper has found no age difference in mean length of utterance, the spontaneous speech of older adults shows a reduction in a variety of complex syntactic structures, especially left-branching constructions which tax working memory, and many of their grammatical errors were associated with attempts to use such structures (Kemper/ Kynette/Rash et al. 1989; Kemper/Rash/Kynette/Norman 1990; Kynette/Kemper 1986). Kemper has also amassed considerable evidence that working memory limitations are responsible for decreased use of complex syntactic structures in old age. Backward digit span, a measure of working memory, is an excellent predictor of mean clauses per utterance and per cent of left-branching clauses; adding age, education, and vocabulary does not improve prediction (Kemper et al. 1989). Drops in digit span over a three year period
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are also associated with a reduction in the use of left branching clauses (Kemper/Kynette/ Norman 1992). Moreover, of 11 complexity metrics studied by Cheung/Kemper (1992), 8 showed age-related declines; these 8 also had strong correlations with digit span, whereas the the 3 metrics which did not show age drops were unrelated to digit span. Interestingly enough, one of the metrics which was insensitive to age was propositional density, a variable which has relatively little effect on age differences in discourse comprehension. Finally, there is some evidence that older adults trade syntactic complexity for structural complexity of narratives, perhaps because of working memory limitations (Kemper 1990; Kemper/Rash/Kynette/Norman 1990). 3.2. Discourse Coherence Kemper (1990; Kemper/Rash/Kynette/Norman 1990) found that older adults’ written diaries and oral stories are more structurally complex than those of young adults in that they include multiple episodes, embedded episodes, and codas which draw a moral lesson from the events being narrated. Though evaluated by external raters as higher in quality, more interesting, and technically better, older adults’ narratives were less cohesive. With increasing age of the diarist, there was a concomitant decrease in the use of the more common cohesive devices, namely anaphora and conjunctions, though not in the use of lexical cohesion (repetition or synonyms), also a common device, or the less frequent devices of cataphora, exophora, ellipsis, and substitution of a nominal (e. g. one), a verbal (e. g. do it), or a clausal (e. g. so) in place of an item in the same grammatical class. Decreased cohesiveness was associated with increased structural complexity. A similar pattern of results was obtained for story telling, with the use of anaphora, conjunctions, and ellipsis declining with age and increased narrative complexity. Ambiguous reference also increases with age across a variety of discourse types including story retelling, story generating, answering questions, describing stereotypical action sequences, and making diary entries (Cohen 1979; Kemper 1990; Kemper/Rash/Kynette/Norman 1990; Pratt/ Boyes/Robins/Manchester 1989; Ulatowska/ Hayashi/Cannito/Fleming 1986). Ambiguous reference may be an accommodation to forgetting of proper names when retelling stories (Pratt et al. 1989) and is associated with lower
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performance on a memory test (Ulatowska/ Cannito/Hayashi/Fleming 1985). In addition, there is evidence that working memory contributes to the incidence of referential errors. Together with the frequency of use of character names, memory span predicts referential errors in story retelling, with age of participant making no further significant contribution to prediction (Pratt et al. 1989). Digit symbol substitution, a measure of processing resources, is negatively related to ambiguous use of pronouns (Ulatowska et al. 1986), while backward digit span is positively related to the use of anaphora, ellipsis, lexical repetition, and conjunction as well as to the occurrence of left-branching clauses and greater structural complexity of narratives (Kemper et al. 1990). These findings suggest that working memory is needed to produce narrative structures, to construct syntactically complex sentences, and to establish text coherence. 3.3. Speech Errors and Disfluencies Pauses and other disfluencies in speech may signal the need for time to plan what comes next in an utterance, to prepare to revise what has been said, or to emphasize a particular point; they may also stem from word-finding difficulties. The two prominent classes of theories of speech errors and repairs, monitoring theories and spreading activation theories (Levelt 1989; MacKay 1987), both make predictions about aging. Monitoring theories postulate an editor which can catch an error either before or after it is produced. Speech errors which actually occur represent monitoring failures, perhaps due to attentional lapses. Working memory deficits should increase attentional lapses and therefore result in greater numbers of speech errors and fewer repairs in the elderly. Moreover, increased planning time in old age might be associated with longer pauses. Spreading activation theories which posit transmission deficits also predict word finding difficulties in the old (cf. 1.1.) as well as poorer error detection (MacKay/Burke 1990). In MacKay’s (1987) model of error detection, the production of a speech error sends priming to an uncommitted node in the network; if this node is activated, its contents become conscious. Inadequate transmission reduces the likelihood that an uncommitted node will become activated in the old and, hence, reduces the likelihood of error detection. A number of studies have examined the frequency with which different types of dis-
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fluencies occur across age. Yairi/Clifton (1972) found an increase with age in total number of disfluencies (interjections, partword repetitions, word repetitions, phrase repetitions, revisions of incomplete phrases, disrhythmic phonations, and tense pauses), but the pattern of speech errors was similar for high school seniors and older adults. Interpreting their study is complicated by the fact that their older sample included residents of a nursing home, raising the possibility that increased disfluency is associated with poorer health. Walker/Roberts/Hedrick (1988) found an increase in the proportion of older adults producing revisions and interjections (empty words or filled pauses) but not repetitions. Their study, however, is flawed because (a) the educational level attained by the older adults in their sample was considerably lower (9 years) than that of the young adults (14 years) and (b) no statistics are reported (see also Walker/Hardiman/Hedrick/Holbrook 1981). In other studies, including some which used the same set of measures as Yairi and Clifton, few reliable effects of age on rate of speech errors or repairs are reported (Cooper 1990; Duchin/Mysak 1987; Kemper 1992; Kemper et al. 1989, 1990; Kynette/Kemper 1986; Pratt et al. 1989; Shewan/ Henderson 1988) though Cooper (1990) has observed longer filled pauses in older adults. On balance, then, there is as yet little solid evidence for an increase in speech errors or a drop in repairs in old age. Nevertheless, Kemper (1992) has recently suggested that there is a shift in the nature of some kinds of disfluencies in adults aged 60—74 and 75—90. In a study of sentence fragments, old-old adults were more likely to produce filled pauses marking problems in noun retrieval. False starts which occur just before verbs index problems in processing syntax in complex sentences; because the old-old produce fewer complex sentences, they show fewer false starts than the young-old. 3.4. Summary Spontaneous speech in old age is marked by reduced syntactic complexity and decreased use of certain cohesive devices, just as would be predicted by the hypothesis that language changes in old age arise from reduced working memory capacity. Moreover, there is some evidence from correlational studies that these effects are indeed the consequence of individual differences in working memory. Yet the narratives of older adults are more structur-
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ally complex and are rated as better than those of younger adults. These findings are unanticipated, but may reflect trade-offs between syntactic complexity and local cohesiveness with structural complexity. To some extent, also, they may reflect an increased concern on the part of older adults for clarity in communication. Use of simpler sentences and provision of the point or moral of a narrative result in listener-friendly discourse. On the other hand, ambiguous reference is certainly not considerate of listeners. At this time, then, the role of pragmatic considerations in the speech of older adults remains unclear. Another area of uncertainty is whether speech errors and monitoring failures increase with age as would be predicted by both working-memory and transmission deficit hypotheses.
4.
Language in Normal Aging, Aphasia, and Alzheimer’s Disease
Differentiating language changes which occur in normal aging from those in aphasia and senile dementia of the Alzheimer’s type has both theoretical and clinical implications. In this section, language in normal aging is briefly compared to language in aphasia and in Alzheimer’s disease. 4.1. Aphasia and Normal Aging When young and old are compared on standard neuropsychological batteries used to assess language deficits following focal brain damage, systematic age differences favoring the young are sometimes, but not always, found (Bayles/Tomoeda/Boone 1985; Emery 1985); when age-related differences are found, they may be secondary to cohort differences in education or hearing problems (Borod/ Goodglass/Kaplan 1980; Goldstein/Shelly 1984 ) when these are not controlled. When age differences are found on neuropsychological tests of language, they do not consistently resemble any one pattern of aphasia. The one possible area of similarity is that of word finding and confrontation naming. Many aphasics have confrontation naming problems (Goodglass 1980), and some residual anomia is common in patients who have otherwise recovered from aphasia. The lexical retrieval difficulty of healthy older adults shares some properties with at least some cases of anomic aphasia, though it is far less severe. That is, in both normal aging and
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anomic aphasia there may be problems in retrieving the phonological forms of words coupled with an intact conceptual system (cf. Kay/Ellis 1987). There is also some reason to believe that word-finding problems in anomic aphasia are more severe for nouns than for verbs, a pattern different from that found in agrammatism (Zingeser/Berndt 1990). Older adults, too, may show this asymmetry between nouns and verbs, though the evidence is far from conclusive. For instance, error rates on the Boston Naming Test show larger age differences than those on the Action Naming Test (Nicholas/Obler/Albert/Goodglass 1985). The pattern of speech disfluencies also suggests that the elderly have more difficulty in retrieving nouns than verbs, perhaps because of shifts in the syntactic complexity of their utterances (Kemper 1992). Finally, in a diary study, Burke/MacKay/Worthley/ Wade (1992) found that older adults had more tip-of-the-tongue experiences for proper names and common objects than young adults, but in an induced tip-of-the-tongue experiment, only the age difference for proper names was reliable. In the diary study, there was some evidence that the young had proportionately more problems with abstract words (verbs and adjectives) than the old; however, the young were in a formal educational setting that encouraged greater use of abstract words and therefore afforded more opportunities for abstract word retrieval difficulties. The naming problem in aphasia also has properties different from that in normal aging. Patients with anomic aphasia and those with Wernicke’s aphasia both tend to produce more pronouns without antecedents, deictic terms, paraphasias, and repetitions than age-matched controls; Wernicke’s aphasics produce neologisms whereas normal controls do not (Glosser/Deser 1990; Nicholas/Obler/Albert/Helm-Estabrooks 1985). There are few studies that explicitly compare language in aphasia and normal aging. Bayles/Boone/Tomoeda et al. (1989) compared normal elderly to fluent (Wernicke’s, transcortical sensory, conduction, and anomic) and nonfluent (Broca’s and transcortical motor) aphasics considerably younger than them in mean age but matched with them in education and estimated intelligence. Their test battery assessed oral object description, disambiguation of sentences containing lexical, structural, or logical ambiguities, word fluency, receptive vocabulary, reading comprehension of words, sentences, and par-
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agraphs, expressive pantomime, and picture description (scored for number of idea units). Both aphasic groups scored lower on all tests than the normal elderly group. The only tests on which the differences between elderly and aphasic groups were not reliable were word reading comprehension and pantomime expression for the fluent aphasics and word reading comprehension for the nonfluent aphasics. Fluent aphasics produce fewer complex sentences in spontaneous speech; their spontaneous speech is not, however, rated as less coherent on either local or global levels (Glosser/Deser 1990). They also produce a greater number of sentence fragments and anacolutha (changes of syntactic construction or contaminations of two or more syntactic structures within an utterance) than do controls (Blanken/Dittmann/Haas/Wallesch 1987). Relative to controls, then, fluent aphasics show preserved macrostructure and impaired microstructure. 4.2. Alzheimer’s Disease and Normal Aging Language impairment is characteristic of Alzheimer’s disease. Performance on neuropsychological tests is generally poorer and outside the normal range on almost all measures of language function though phonology appears to be well preserved — at least initially (Appell/Kertesz/Fisman 1982; Bayles 1982; Bayles/Boone/Tomoeda et al. 1989; Cummings/Benson/Hill/Read 1985). Not all aspects of language, however, are affected to the same degree. Early in the course of the disease, there is a dissociation between lexicalsemantic impairment and syntax which is opposite to that shown by agrammatic aphasics. That is, early in Alzheimer’s disease syntax is unaffected relative to the semantic system, whereas in agrammatism the reverse is true. For instance, in spontaneous speech, grammatical errors are few though utterances may be devoid of meaning (Bayles 1982; Hier/ Hagenlocker/Shindler 1985). The relative frequency of different syntactic constructions is similar in Alzheimer’s patients and in agematched controls (Kempler/Curtiss/Jackson 1987). Detection and correction of grammatical anomalies in sentences is better for syntactic than for semantic errors (Bayles 1982). In writing to dictation, homophone spelling is more accurate in the context of syntactic cues (my nose) than semantic cues (mouth nose) (Kempler et al. 1987). This does not mean, however, that syntax is completely spared even early in Alzheimer’s disease in-
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asmuch as syntactic processing in comprehension is affected (Emery 1985; Tomoeda/ Bayles/Boone et al. 1990). An increase in sentence fragments in spontaneous speech has also been reported (Hier et al. 1985; Ulatowska/Allard/Donnell et al. 1988), though this is not invariably found (Blanken et al. 1987). Thus, the emphasis must be on relative, rather than absolute, sparing of syntax in Alzheimer’s disease. The semantic deficit in Alzheimer’s disease is manifested in numerous ways. Some of these suggest that the problem lies in word finding. Thus, performance is lower on tests of confrontation naming, naming to definition, and verbal fluency (Appell et al. 1982; Huff/Corkin/Growdon 1986; Martin/Fedio 1983; Rissenberg/Glanzer 1987). Also, spontaneous speech in Alzheimer’s disease is noteworthy for its circumlocutions, ambiguous pronoun reference, excessive use of empty deictic terms and indefinite anaphora, and repetitions (Hier et al. 1985; Nicholas/Obler/ Albert/Helm-Estabrooks 1985), all of which are consistent with word finding difficulties. Consonant with this conclusion, Nicholas/ Obler/Albert/Helm-Estabrooks (1985) found a positive correlation between naming accuracy and number of content elements produced in a picture description task and a negative correlation between naming accuracy and number of indefinite terms; however, correlations of naming accuracy with other measures related to word-finding problems (deictic terms, pronouns without antecedents, comments on the task) were not statistically reliable. The fact that phonological cues benefit patients in confrontation naming tasks points to an impairment in accessing the phonological representations of words as the mechanism underlying such word-finding problems (Neils/Brennan/Cole et al. 1988), though Henderson/Mack/Freed et al. (1990) argue that it is also compatible with a disruption in the semantic system. Other findings seem more in line with a disruption within the semantic system due to loss or disorganization of conceptual information. (1) Patients unable to name a picture are often unable to answer questions about the concept which it represents (Chertkow/ Bub/Seidenberg 1989; Huff/Corkin/Growdon 1986) and there is evidence for greater consistency in errors than would be expected by chance when the same pictures are named on two occasions (Henderson/Mack/Freed et al. 1990). (2) Errors in confrontation naming are
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most often semantically related to targets, though in more severely affected patients there is an increase in unrelated responses (Bayles/Tomoeda 1983; Huff et al. 1986; Martin/Fedio 1983). (3) The word associations of patients are more idiosyncratic and show a reduction in the proportion of paradigmatic responses (though syntagmatic responding appears not to be affected — further evidence of preserved syntax), suggesting that features are lost (Gewirth/Shindler/Hier 1984 ; Santo Pietro/Goldfarb 1985). However, Abeysinghe/ Bayles/Trosset (1990) found that patients who gave no response, unrelated responses, or stimulus repetition responses on a word association test were sometimes able to give meaningful definitions for these items; they caution against accepting word association data as evidence for loss of conceptual knowledge and argue that abnormal responding arises from a loss of associations rather than of conceptual information. (4 ) Knowledge of scripts is impaired in Alzheimer’s disease; patients generate more actions which are implausible (though possible within script boundaries) and are less accurate in ordering pairs of actions (Grafman/Thompson/Weingartner et al. 1991). (5) Patients suffering from Alzheimer’s disease are less accurate in generating actions, physical features, or associates of objects (Nebes/Brady 1988) and in judging how important an associate is to the meaning of a concept (Grober/Buschke/ Kawas/Fuld 1985) or how strongly associated two words are (Abeysinghe et al. 1990). These tasks require retrieval of specific relationships or explicit judgments of degree of association. On tasks which measure knowledge of semantic relationships more indirectly and do not require a deep analysis of the nature of the relationsship between words, the performance of Alzheimer’s patients appears pretty much normal. For instance, patients and normal elderly adults show the same pattern of response times to actions, physical features, and associates of objects when asked to judge whether they are related (Nebes/Brady 1988) and show equal sensitivity to the response dominance of attributes in a similar task (Nebes/Brady 1990). If anything, patients appear to show greater semantic priming effects in lexical decision and word naming tasks (cf. Nebes 1989). 4.3. Summary In normal aging, many aspects of language, including both word-finding and comprehension and production of complex grammatical
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structures, show subtle changes which are not always detectable by standardized neuropsychological instruments. Although there is as yet no research that suggests a disproportionate impairment in one particular facet of language rather than another, such as might be expected in an aphasia resulting from focal brain damage, there is some similarity between word-finding difficulties in normal aging and anomic aphasia. In early Alzheimer’s disease, however, there is severe impairment in most aspects of language accompanied by a dissociation between syntax and semantics. The available evidence does not permit a choice among alternative explanations of the semantic deficit in Alzheimer’s disease. It seems likely that loss of conceptual information and problems in realizing the phonological representations of words both play a role. Two important questions that remain to be answered are whether the changes observed in normal aging presage those found in Alzheimer’s disease (i. e., are similar but less severe) and which of the mechanisms discussed above (or others, see Nebes 1989) are responsible for the pattern of spared and impaired language function in Alzheimer’s disease. Author’s Note: Preparation of this chapter was supported by National Institute on Aging Grant R37 AG02452.
5.
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Leah L. Light, Claremont, California (USA)
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VI. Indexes 88. Editors and Contributors James H. Abbs University of Wisconsin Speech & Motor Control Laboratories Waisman Center Madison, Wisconsin USA William Badecker The Johns Hopkins University Department of Cognitive Science Baltimore, Maryland USA Joseph Bayer Universität Düsseldorf Seminar für Allgemeine Sprachwissenschaft Düsseldorf Germany
Università di Brescia Clinica Neurologica Brescia Italy Alfonso Caramazza The Johns Hopkins University Department of Cognitive Science Baltimore, Maryland USA Sandra Chapman The University of Texas Callier Center for Communication Disorders Dallas, Texas USA
Kathryn A. Bayles University of Arizona Department of Speech and Hearing Sciences Tucson, Arizona USA
Ria De Bleser Rheinisch-Westfälische Technische Hochschule Aachen Neurologische Klinik Aachen Germany
Gerhard Blanken Universität Freiburg/Br. Forschungsschwerpunkt Neuropsychologie/ Neurolinguistik Deutsches Seminar Freiburg/Br. Germany
Gérard Deloche Hôpital de la Salpêtrière Salle Racine, Service du Prof. PierrotDesseilligny Paris France
Hugh W. Buckingham Louisiana State University Interdepartmental Linguistics Program College of Arts and Sciences Baton Rouge, Louisiana USA
Roxanne DePaul University of Wisconsin Departments of Neurology and Neurophysiology Medical School Madison, Wisconsin USA
Brian Butterworth University College Department of Psychology London United Kingdom
Jürgen Dittmann Universität Freiburg/Br. Deutsches Seminar Freiburg/Br. Germany
Stefano F. Cappa
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Barbara Dodd The University of Queensland Department of Speech and Hearing St. Lucia, Queensland Australia Christian Eggers Rheinische Landes- und Hochschulklinik Klinik für Kinder- und Jugendpsychiatrie Essen Germany Susan Ellis Weismer University of Wisconsin Department of Communicative Disorders Madison, Wisconsin USA Pierre Feyereisen Université Catholique de Louvain Département de Psychologie Expérimentale Unité de Neuropsychologie Cognitive Louvain-la-Neuve Belgium Peter Fiedler Universität Heidelberg Psychologisches Institut Heidelberg Germany Marilyn Ford Griffith University C. I. T. Division of Science and Technology Nathan, Brisbane Queensland Australia Carol A. Fowler Haskins Laboratories New Haven, Connecticut USA Angela D. Friederici Freie Universität Berlin Institut für Psychologie Berlin Germany Trian Fundudis The Royal Free Hospital, School of Medicine London United Kingdom
88. Editors and Contributors
Merrill F. Garrett University of Arizona Faculty of Social and Behavioral Sciences Cognitive Science Tucson, Arizona USA Pierre Goulet Centre Hospitalier Côte-des-Neiges Centre de Recherche Montréal, Québec Canada Hannelore Grimm Universität Bielefeld Fakultät für Psychologie und Sportwissenschaft Abteilung für Psychologie Bielefeld Germany Berthold Gröne Kliniken Schmieder Neurologisches Rehabilitationskrankenhaus Allensbach Germany Murray Grossman University of Pennsylvania Medical Center Department of Neurology Philadelphia, Pennsylvania USA Jennifer M. Gurd The Radcliffe Infirmary Neuropsychology Unit Oxford United Kingdom Curt Hamre Texas Tech University Department of Speech and Hearing Sciences Lubbock, Texas USA Didier Hannequin Hôpital Charles-Nicolle Rouen France William Harn Texas Tech University Department of Speech and Hearing Sciences Lubbock, Texas USA
88. Editors and Contributors
David E. Hartman University of Wisconsin Department of Neurology Madison, Wisconsin USA Claus Heeschen Max-Planck-Institut für Psycholinguistik Nijmegen The Netherlands Erika Hoff-Ginsberg University of Wisconsin-Parkside Division of Behavioral Science Kenosha, Wisconsin USA Ralph E. Hoffman Yale University School of Medicine New Haven, Connecticut USA Audrey L. Holland University of Arizona Department of Speech and Hearing Sciences Tucson, Arizona USA Charles Hulme University of York Department of Psychology Heslington, York United Kingdom Janis Costello Ingham University of California Santa Barbara Department of Speech and Hearing Sciences Santa Barbara, California USA Yves Joanette Centre Hospitalier Côte-des-Neiges Centre de Recherche Montréal, Québec Canada Helge S. Johannsen Universität Ulm Phoniatrische Ambulanz Ulm Germany Helga Johannsen-Horbach Schule für Logopäden Freiburg/Br.
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Germany Judith R. Johnston University of British Columbia School of Audiology and Speech Sciences Vancouver, British Columbia Canada Alan G. Kamhi Memphis State University Memphis Speech and Hearing Center Memphis, Tennessee USA Marie-Louise Käsermann Psychiatrische Universitätsklinik Bern Switzerland Janice Kay University of Exeter Department of Psychology Exeter United Kingdom J. A. Scott Kelso Florida Atlantic University Center for Complex Systems Boca Raton, Florida USA Raymond D. Kent University of Wisconsin Madison Waisman Center Madison, Wisconsin USA Andrew Kertesz University of Western Ontario Department of Clinical Neurological Sciences St. Joseph’s Hospital London, Ontario Canada Marcel Kinsbourne Boston University Behavioral Neurology Unit Boston, Massachusetts USA Susan E. Kohn Braintree Hospital Department of Neurology Braintree, Massachusetts USA
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88. Editors and Contributors
Israel Kolvin The Royal Free Hospital, School of Medicine London United Kingdom
Fernando Lolas Universidad de Chile Facultad de Medicina Santiago de Chile Chile
M. Mary Konstantareas University of Toronto Clarke Institute of Psychiatry Toronto, Ontario Canada
Christy L. Ludlow National Institute on Deafness and Other Communication Disorders Voice and Speech Section Bethesda, Maryland USA
Karen L. Landahl University of Chicago Department of Linguistics Chicago, Illinois USA
Donald G. MacKay University of California Los Angeles Department of Psychology Los Angeles, California USA
Yvan Lebrun Vrije Universiteit Brussel Faculteit Geneeskunde Neurolinguistiek Brussel Belgium
Brendan A. Maher Harvard University Department of Psychology Cambridge, Massachusetts USA
André Roch Lecours Centre Hospitalier Côte-des-Neiges Centre de Recherche Montréal, Québec Canada
John C. Marshall The Radcliffe Infirmary Neuropsychology Unit Oxford United Kingdom
Laurence B. Leonard Purdue University Department of Audiology and Speech Sciences West Lafayette, Indiana USA
Harald Marx Universität Bielefeld Fakultät für Psychologie und Sportwissenschaft Abteilung für Psychologie Bielefeld Germany
Ruth Lesser University of Newcastle-upon-Tyne Department of Speech Newcastle-upon-Tyne United Kingdom Willem J. M. Levelt Max-Planck-Institut für Psycholinguistik Nijmegen The Netherlands Richard S. Lewis Pomona College Department of Psychology Claremont, California USA Leah L. Light Pitzer College Claremont, California USA
Lynn Mawhood University of London Institute of Psychiatry De Crespigny Park London United Kingdom Paula Menyuk Boston University School of Education Literacy and Language Institute Boston, Massachusetts USA Edward C. Merrill The University of Alabama Department of Psychology Tuscaloosa, Alabama USA
88. Editors and Contributors
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Anne E. Mills Universiteit Amsterdam Algemene Taalwetenschap Amsterdam The Netherlands
David P. Roeltgen Hahnemann University Department of Neurology Philadelphia, Pennsylvania USA
Kay Mogford-Bevan University of Newcastle-upon-Tyne Department of Speech Newcastle-upon-Tyne United Kingdom
John C. Rosenbek W. S. Middleton Memorial VA Medical Center Audiology and Speech Pathology Madison, Wisconsin USA
Dave Müller Suffolk College Ipswich, Suffolk United Kingdom Michel Paradis McGill University Department of Linguistics Montréal, Québec Canada Sally J. Peterson-Falzone University of California San Francisco Department of Growth and Development San Francisco, California USA
J. Douglas Saddy The University of Queensland Psychology Department Brisbane, Queensland Australia Paul Satz University of California Los Angeles The Neuropsychiatric Institute & Hospital Los Angeles, California USA Gerheid Scheerer-Neumann Am Gottesberg 59 Bielefeld Germany
Klaus Poeck Rheinisch-Westfälische Technische Hochschule Aachen Neurologische Klinik Aachen Germany
Paul W. Schönle Kliniken Schmieder Neurologisches Rehabilitationskrankenhaus Allensbach Germany
Steven Z. Rapcsak University of Arizona Department of Neurology Tucson, Arizona USA
Hartmut Schulze Universität Ulm Phoniatrische Ambulanz Ulm Germany
Friedel M. Reischies Freie Universität Berlin Psychiatrische Klinik und Poliklinik Berlin Germany
Barbara B. Shadden The University of Arkansas Speech and Hearing Clinic Fayetteville, Arkansas USA
Donald A. Robin The University of Iowa Department of Speech Pathology and Audiology Wendell Johnson Speech and Hearing Center Iowa City, Iowa USA
Helmut Skowronek Universität Bielefeld Fakultät für Psychologie und Sportwissenschaft Abteilung für Psychologie Bielefeld Germany
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Anne Smith Purdue University Department of Audiology and Speech Sciences West Lafayette, Indiana USA Margaret J. Snowling University of Newcastle-upon-Tyne Department of Psychology Newcastle-upon-Tyne United Kingdom Manfred Spitzer Universität Heidelberg Psychiatrische Klinik und Poliklinik Heidelberg Germany Joseph P. Stemberger University of Minnesota Department of Communication Disorders Minneapolis, Minnesota USA Yasufumi Tanaka Jichi Medical School Department of Neurology Tochigi Japan Christine M. Temple University of Essex Department of Psychology Colchester United Kingdom Cynthia K. Thompson Northwestern University Department of Communication Sciences and Disorders Evanston, Illinois USA Betty Tuller Florida Atlantic University Center for Complex Systems Boca Raton, Florida USA Hanna K. Ulatowska The University of Texas Callier Center for Communication Disorders Dallas, Texas USA Diana Van Lancker University of Southern California
88. Editors and Contributors
Department of Veterans Affairs Outpatient Clinic Los Angeles, California USA Mathias Vogel Städtisches Krankenhaus MünchenBogenhausen Neuropsychologische Abteilung München Germany Claus-W. Wallesch Neurologische Universitätsklinik Freiburg/Br. Germany Sabine Weinert Universität Bielefeld Fakultät für Psychologie und Sportwissenschaft Abteilung für Psychologie Bielefeld Germany Marilyn C. Welsh University of Northern Colorado Department of Psychology Greeley, Colorado USA Dorothea Weniger Universitätsspital Zürich Neuropsychologische Abteilung Zürich Switzerland Klaus Willmes Rheinisch-Westfälische Technische Hochschule Aachen Neurologische Klinik Aachen Germany Wolfram Ziegler Städtisches Krankenhaus MünchenBogenhausen Entwicklungsgruppe Klinische Neuropsychologie München Germany Gerald N. Zimmermann Joe Johnston Law Firm P. C. Iowa City, Iowa USA
89. Index of Names
925
89. Index of Names A Aaron, P. G. 727, 737 Abbeduto, L. 580, 689, 691 Abberton, E. 514, 668 Abbs, J. H. 42, 417, 428 f, 433 f, 440, 448, 455, 462 ff, 468, 471, 477 ff, 867 Aberdeen, J. S. 905 Abeysinghe, S. C. 913 Abidi, R. 279 Abrams, R. 541 Abramson, A. 421 Ackermann, H. 469 ff Ackermann, N. 176 Adair, G. 808 Adams, A. D. 459 Adams, A. J. 734 Adams, C. 601, 718 Adams, H. M. 791 Adams, J. G. 446 Adams, M. R. 868, 884, 895 Adams, R. D. 439, 474 Adams, S. 434, 446, 847 Adelman, H. S. 715 Ader, D. N. 527 Adland, M. C. 597 Adler, S. 291 Agarwal, G. C. 454 f Ahola, H. 759 Ahrens, S. 512 Aimard, G. 264 Aitchison, J. 85, 826 Ajuriaguerra, J. de 341, 631 Akinaso, F. N. 23 Akmajian, A. 170 Aksu-Koc, A. A. 564 Al-Bamerni, A. 39 ff Alajouanine, T. H. 100, 187, 218, 226, 314, 335, 444 f, 586, 650 ff, 654 Alarcon, M. 768 f, 907 Albert, M. 484 Albert, M. L. 103, 110, 114, 155, 207, 232 ff, 264, 274, 279 ff, 283, 330, 335 f, 355, 357, 379, 392, 394, 396, 399, 499 ff, 901, 905, 911 f Albert, M. S. 900 f Alberti, L. 551 Alberts, M. C. 398 Albertson, S. 907 Alegria, J. 23, 712, 718, 757 f, 779, 781 Alexander, F. 511 Alexander, G. E. 465 Alexander, M. P. 114, 129, 214, 253, 264, 267 f, 379, 396 Alexander, R. 836, 838, 849 Alexandra, H. 597
Alfano, M. 410 ff Ali-Cherif, A. 106 Allard, L. 306, 392, 912 Allard, T. 500 ff Allen, G. 439, 642, 644 Allen, R. 597 Allison, R. S. 106, 230 Allport, D. A. 239, 258, 298, 336, 355 Allsop, D. 389 Alnosha, M. 501 Alpert, M. 514 f Als, J. 684 Altmann, H. 17 Altorfer, A. 551, 553 Alvord, E. C. 395 Alzheimer, A. 273 Amelang, M. 877 Ames, S. 895, 897 Amici, R. 468 Ammon, M. 579, 580 Anders, T. R. 906 Andersen, E. S. 682, 684 f Anderson, J. A. 123, 900 Anderson, J. D. 373 Anderson, P. A. 902, 904, 907 Anderson, R. J. 685 Anderson, S. 184 f Andreasen, N. C. 216, 514 ff, 534, 543, 545, 550 ff, 801 Andreewsy, E. 174, 177 Andresen, H. 105 Andress, M. J. 886 Andrews, C. E. 669, 671 Andrews, G. 842, 847, 866, 893 ff Andrews, N. 730 Angelergues, R. 326, 335 Anglin, J. M. 563 Angst, J. 514 Ansel, B. M. 847 Anshen, F. 27 Anstett, M. 718 Anthony, J. C. 525 Antonitis, J. J. 553 Apel, K. 633 Appelbaum, M. I. 139 f, 144, 146 Appell, J. 110, 273 f, 341, 392, 912 Appenzeller, T. 389 Aragona, J. A. 597 Aram, D. M. 577, 590, 600, 636, 651 f, 768 f, 771, 775, 829 Aramany, M. A. 489 Arbib, M. A. 6 Archangeli, D. B. 246 Archer, L. A. 589 Archibald, Y. 321 Ardila, A. 326, 380, 400
Arenberg, D. 900 Arend, R. 596 Aristotle 24 Armengol, C. G. 411, 413 Armstrong, E. 307 Arndt, W. 486, 828 Aronoff, M. 26 f, 170, 185 Aronson, A. E. 425, 427, 430, 438, 448, 453 ff, 458 f, 463, 465, 468 ff, 481 ff, 492 f, 496, 540, 835, 843 f, 851 Aronson, H. 515 Arsenault, J. K. 357 Arseni, C. 127 Arter, J. A. 754, 763 Artes, R. 373 Arthur, G. 630 Arthur, S. A. 267, 270, 273 f Asarnow, R. F. 799 f Ashayeri, H. 149, 279 Ashby, R. P. 819 Ashforth, P. L. 693 Aslan, Y. 489 Aslin, R. N. 561 Asperger, H. 804, 807 Asperger, S. 789 Assal, G. 267, 544 Aten, J. L. 362, 364, 367, 455 Atschkova, M. 797 Attwood, A. 576 Audet, L. 601, 829 Auerbach, S. H. 264, 500 ff Aust, S. D. 410 Austin, J. L. 16 Avancini, G. 468 Axline, V. 762 Aysto, S. 373 Azrin, N. H. 895
B Baars, B. J. 57 ff, 78 f, 90 Bachelet, J.-F. 566 Bachman, D. L. 357, 379 Bachy-Languedock, N. 359 Backman, J. 719 Backus, O. 487 Baddeley, A. 389, 908 Baddeley, A. D. 244, 334 f, 340, 347, 736 Badecker, W. 138, 145, 165, 182, 184 f, 191, 198, 266, 269, 345, 360 Bader, L. 163 Baer, T. 436 Baer, D. 889 Bahls, F. H. 498 Bailet, L. 779 Bailey, P. 121 Bain, B. 640 ff
89. Index of Names
926
Bainton, D. 352 Bak, T. 107, 112, 114 Baker, C. 199, 204, 339, 345 Baker, E. 103, 333, 355, 567 Baker, L. 580, 601 f, 789, 813 Baker, M. 27, 464 Baker, T. 305, 307, 309 Baker, V. 553 Bakker, D. 763 Balkany, T. 692 Ball, E. W. 757 Ball, K. 534 Ball, M. 439 Ballard, J. L. 488 f Balota, D. A. 902 f Balow, B. 755 Baltaxe, C. A. 814 Balthazar, M. 737 Bamford, J. 214, 660 f, 663, 668 f Bandur, D. L. 354, 358, 364 Bankson, N. W. 847, 853 Bar-Shalom, E. 729 Barat, M. 129 Barbeau, A. 379 Barber, J. 296 Bard, B. 598, 697 Barker, A. T. 131 Barlow, A. 789 Barlow, D. H. 145, 880 Barlow, H. B. 115, 122, 132 Barlow, S. M. 433 f, 455 Barnes, J. 464 Barnes, M. A. 256 Barney, H. L. 862 Baron, J. 129, 749, 757, 782 Barr, A. N. 398 Barrera, R. D. 818 Barresi, B. 357 Barrett-Boyes, B. G. 692 Barron, R. 730 Barron, R. W. 757 Barron, S. A. 398 Barry, W. 39 Bartak, L. 598, 602, 701 Barter, D. 295 f Bartlett, S. 776, 781 Bartolucci, G. 552, 813 Barton, D. 561 Bartus, R. T. 900, 904 Bartus, S. 394 Bashir, A. S. 854 Basili, A. G. 102, 336, 338, 346 Bass, C. 897 Bass, E. 410 Bassano, D. 563 Basser, L. S. 124, 648 f, 654 Bassich, C. J. 399, 439, 462 f, 465, 637 Basso, A. 156, 264, 314, 359, 380 Bassou, L. 762 Bastian, H. C. 263, 499
Bates, E. 5, 26, 139, 148, 177, 296, 309, 559, 561 f, 581, 589, 598 f, 631, 693, 706, 873 f Bathien, N. 472 Batussek, D. 877 Baudelaire, C. 226 Bauer, K. 314 Bauer, L. L. 453, 471, 842 Bauer, R. H. 760 Bauer, R. M. 211, 292, 499 Baum, S. 198, 211 Baum, S. R. 438 Bauman, M. 810 Baumgärtel, F. 881 Baumgartner, J. M. 459 Bax, M. 601 Baxter, D. M. 252, 266, 270 Bay, E. 103, 445, 544 Bayer, J. 164, 166, 181, 184 Bayles, K. A. 111, 273 f, 341, 389 ff, 397 f, 400, 905, 907, 911 ff Bear, D. 103, 500 ff Beattie, G. W. 50, 245, 526 Beau, S. C. 807 Beauvois, M. F. 157, 231, 257, 265, 267, 344, 358 f, 747 Beck, A. R. 292 Beck, C. 497 Beck, D. 314 Beck, I. 778 f Becker, J. T. 390 f, 395 f Becker, P. 894 Beckett, S. 94 Bedell, S. E. 410 Bedrosian, J. L. 641, 644, 691 Beech, H. R. 895 Beeghly, M. 597 Beekman, L. A. 292 Beery, Q. C. 489 Beeson, P. M. 267 Behrens, S. J. 295, 438 f Behrens, S. 176, 182, 184, 210, 213 Behrmann, M. 252, 295 Beitchman, J. 574, 601 f Beiter, A. 609 Béland, R. 191, 204 ff, 246 Bell, D. S. 129 Bell, L. 778 f Bell, K. R. 843 f, 848 Bell, W. 231 Bell-Berti, F. 37 ff Bellugi, U. 127, 176 f, 318, 674 f, 693, 817 f Belsky, M. W. 489 Benda, C. E. 692 Bender, L. 768, 795 Benedict, H. 561 ff Benedikt, M. 262, 264 Bengtsson, M. 412 Benguerel, A. 37, 40
Benigni, L. 561, 581, 631 Benjamin, B. 642, 644 Benke, T. 125 Benson, D. F. 98, 104, 107 ff, 112 f, 115, 123, 128 f, 187, 218 f, 221, 264, 273 f, 327 f, 341, 346, 378, 380 f, 390, 393, 411, 499, 518, 654, 912 Benton, A. L. 103, 137 f, 149, 220 f, 291, 390, 444, 499, 507, 518 Berberich, J. P. 811, 814 f Berendes, J. 497 Beresford, R. 832 Berg, L. 390 Berg, P. A. 530 Berg, T. 59, 77 Bergego, C. 326 Berger, P. A. 399, 514 Bergman, M. 905 Bergman, P. 768 Bergmann, G. 895 Bergmann, J. 20 Beringer, K. 523, 799 Berk, R. A. 146 Berke, G. S. 437 Berker, A. H. 107 Berker, E. A. 107 Berko, J. 176 Berko Gleason, J. 163, 306 f
cf.Gleason, J. B. Berlin, C. I. 210, 664 Berman, K. F. 588 Berman, R. A. 564 Berndt, R. S. 102, 156 f, 162, 177 f, 193, 211, 296, 336 ff, 343, 346, 911 Berney, T. 789 Bernhardt, M. 647, 651 f, 654 Bernstein, B. 599 Bernstein, J. C. 375 Bernstein, L. 459, 577, 627 f, 775 Bernstein, N. S. 416 Bernthal, J. E. 847 Berry, M. 18 Berry, M. F. 839 Berry, T. 355 Berry, W. R. 474, 483 Bertalanffy, L. von 418 Bertelson, P. 23, 588, 718, 757, 779, 781 Bertenthal, B. I. 586 Berthier, M. L 281 Berwick, R. C. 162, 165, 334 Besner, D. 259, 327 Bessell, N. J. 214 Besson, J. A. O. 514 Best, C. T. 589 Best, S. 826 Bester, S. 298, 365 Bettelheim, B. 701, 805, 808 Betten, A. 23 Bettes, B. A. 597
89. Index of Names
Betz, D. 761 f Beukelman, D. R. 51, 292, 460, 474, 843 f, 848 Bever, T. 11, 47, 162 f, 166, 221 Beveridge, A. W. 550 Bevington, L. J. 375 Beyn, E. S. 356 Bez, M. 367 Bhirle, A. M. 293 Bialystok, E. 614, 773 f, 777 Bianchi, L. 123 Biber, D. 23 Biemiller, A. J. 770 f Bienkowski, M. 13 Bierwisch, M. 73, 75, 77, 79, 89, 164 Bigelow, A. 682 f Bigler, E. D. 410 ff Bihrle, A. M. 221, 385 f, 693 Biklen, D. 819 f Billmann, D. 634 Bilmes, J. 20 Bingley, T. 589 f Biniek, R. 149 Binks, M. G. 327 Binnie, C. A. 672 Biorn-Hansen, V. 372 f Bioulac, B. 129 Birch, H. G. 591 Birdwhistle, R. L. 320 Bishop, D. 384, 601, 660, 689, 735 Bishop, D. M. V. 586, 590, 669 Bishop, D. V. M. 256, 313, 718, 735 Bishop, J. 667 Bisiacchi, P. 149 Blachman, B. 757, 778 f, 782 Black, F. O. 589 Black, S. 156 Black, S. E. 125, 252 Blackburn, W. D. 819 Blackburn, W. 868 Blacker, K. H. 514, 517 Blackman, A. 819 Blackwell, J. 690, 700, 702 ff, 706 Bladon, A. 39 ff Bladon, R. A. 214 Blair, C. 433 Blakar, R. M. 549, 551 Blake, P. 789 Blalock, J. 718 Blank, M. 708 Blanken, G. 102, 105 f, 110 f, 147, 188, 190, 226 f, 912 Blanton, S. 829 Blashfield, R. 717 Blaskey 268 Blass, T. 518 Blatchley, M. 641, 645 Bleier, M. 569 Bleile, K. M. 448
927
Bless, D. 472, 845 Bleuler, E. 524 f, 543, 545 Bleuler, J. F. 534 Bliklen, D. A. 273 f Blinkhorn, S. F. 316 Block, S. von 550 Blomert, L. 148, 174, 297 Blomstrand, C. 375 Blonsky, R. 465 Bloodstein, O. 864 f, 869, 871, 878, 885, 897 Bloom, L. 283 f, 563 ff, 568, 579, 598, 692 Bloom, S. R. 534 Bloomer, H. H. 487 Bloomfield, L. 24, 634 Blossom-Stach, C. 26, 339 Bluemel, C. S. 895 Blum, H. M. 552 Blum, I. 779 Blum, L. 630 Blumer, D. P. 516 Blumstein, S. E. 8, 103, 113, 155, 163, 198, 206 f, 210 f, 214, 333, 343, 438, 446 Blunk, R. 108 Boanter, M. T. 217 Bobath, B. 839, 849 Bobath, K. 839, 849 Boberg, E. 882 Bobon, J. 547 Boccardi, E. 106, 127 Bock, J. K. 5, 13, 21, 24 f, 73 f, 81, 85, 88, 295, 904, 908 Boder, E. 716, 733 Bodner-Johnson, B. 670 Bogen, J. E. 219 ff Bogyo, L. C. 267 Bohannon, J. 629 Böhme, G. 897 Bolinger, D. 216 f Bolla-Wilson, K. 266, 270 Boller, F. 142, 220, 233 f, 273, 325, 333, 346, 385, 394 ff, 903 Boller, M. 233 f Bollier, B. 484 Bolton, N. 515 Bond, S. L. 305, 307 Bondurant, J. L. 699 Bonhoeffer, K. 469 Bonin, G. V. von 121 Bonvillian, J. D. 298, 697, 815, 818 f Book, W. F. 67 Boomer, D. 47, 59, 76 Boon, D. R. 470 Boone, D. R. 392, 844, 851, 905, 907, 911 f Booth, J. C. 446 Borenstein, P. 363, 365, 374 Borges, J. L. 95
Borod, J. C. 125, 295, 298, 900, 911 Boruta, M. J. 762 Bosch, G. 800 Boshes, B. 465 Bosman, A. 761 Botez, M. I. 127, 379 Bothelo, M. A. S. 328 Botte, M. C. 500 Botwinick, J. 390 Bouchard, R. 112 f Bouchat, M. P. 295 Bouhuys, A. L. 518 Bouillaud, M. J. B. 445 Bountress, N. 827 Bourgeois, M. S. 355, 362 Bousha, D. M. 597 Boves, L. 867 Bowerman, M. 563 f, 567 Bowers, D. 211, 213, 291 f, 383 Bowers, M. B. 518 Bowey, J. A. 729, 773 f, 779 Bowlby, M. 726 Bowler, S. 437 Bowles, N. L. 900 ff Bowling, J. H. 375 Boyce, S. 39 f Boyd, J. B. 486 Boyes, C. 901, 909 Boyle, R. S. 273 Boylls, C. C. 417 Brackin, S. 621, 776 f Bradford, A. 828 Bradford, L. J. 486 Bradley, D. C. 164, 173 f, 178 Bradley, L. 715, 718 f, 724 f, 730, 733, 755, 757 f, 760 f, 778 f, 782, 832 Bradshaw, C. M. 513 f, 517 Bradshaw, J. L. 60, 63, 128, 221 Bradvik, B. 220 Brady, C. B. 394, 902 f, 913 Braff, D. L. 529, 530 Braginsky, B. M. 553 Braginsky, D. D. 553 Brain, W. R. 101, 110 Branch Coslett, H. 211, 213
cf.Coslett, H. B. Branco-Lefevre, A. F. 650 Brandi, L. 580 Brandt, J. 399 f, 726 Branwhite, A. B. 755 Brasel, K. 674 Brashear, H. R. 500 Bratley, P. 94 Brault, J. 552 Braun, H. I. 140 Braunstein, P. 814 Brazelton, T. 684 Brazil, D. 18 Bredart, S. 566 Breg, W. R. 693 Breitner, J. C. S. 391
928
Brennan, M. 674 Brennan, M. M. 912 Brennan, R. L. 143 Brereton, N. 908 Breskin, S. 50 Breslau, L. D. 514 ff Bresnan, J. 11, 25, 27, 166 Bressi, S. 340 Bretherton, I. 561 f, 581, 598 f, 631, 706 Breuninger, H. 761 f Brewer, D. 867 Brick, J. F. 500 Brickner, R. 235 Bridges, A. 689 Brierly, A. 828 Briggs, D. 553 Brihaye, J. 226 Brindley, P. 366 Brinkman, C. 319 Brinton, B. 620, 776, 782 Britton, P. G. 515 Broadbent, D. E. 341 Broca, P. 93, 107, 120, 226, 445, 449, 607, 647 Brodmann, K. 121 Brodsky, K. 768 Brody, B. A. 332 Brody, G. H. 792 Broen, P. A. 859 Broman, H. J. 792 Bromley, D. B. 901, 909 Brookhouser, P. E. 664 Brooks, A. 642, 644 Brooks, P. 688 Brookshire, B. L. 859 Brookshire, R. H. 292 f, 296, 306, 386 Brouwers, E. Y. M. 763 Brouwers, P. 340 f, 390 f Browman, C. P. 5, 35, 42 ff, 85 Brown, A. 634 Brown, A. L. 904 Brown, B. 734 Brown, C. 422, 436, 868 Brown, F. R. 807 Brown, G. 637 Brown, G. D. A. 28, 61 Brown, J. 547, 668, 875 Brown, J. B. 788 f, 791 f Brown, J. R. 425, 427, 438, 448, 453 ff, 459, 463, 465, 468 ff, 481 ff, 496, 499, 835, 843 f Brown, J. W. 107, 109, 112, 187 f Brown, K. 550 Brown, R. 59, 85, 284, 564 ff, 568 Brown, R. G. 396 Brown, R. W. 817 Brown, S. 861, 871 f Brown, W. S. 125, 131 Brown, W. T. 808 Browne, E. 791 f
89. Index of Names
Brownell, H. H. 138, 145, 221, 293 f, 364, 384 ff, 902 Bruce, C. 354, 358 Bruck, M. 719 Bruckert, R. 367 Brumfitt, S. 363, 374 Brun, A. 274, 401 Brundage, S. B. 886 Bruner, J. S. 596, 667, 814 Brunn, J. L. 254 Brunner, E. 653 Brunner, R. J. 105, 127, 381 Brust, J. 98 Brutten, E. 867, 869 Brutten, G. J. 888 Bruun, B. 98 Bryan, A. 683 Bryan, T. 619, 778 Bryant, P. E. 715, 718 f, 724 f, 730, 733, 755, 757 f, 778 f, 782, 832 Bryden, M. P. 212 Bub, D. N. 130, 155 f, 182, 255 ff, 267, 270, 344, 394, 745, 903, 912 Bucci, W. 516 Buchkremer, G. 552 Buchsbaum, M. S. 131, 541 Buchwald, J. 810 Buck, M. 372 Buckingham, H. W. 51, 85, 99, 101, 108 f, 154, 184, 187 ff, 199, 201, 204, 298, 444, 448, 551 Buday, E. 776 Buddenhagen, R. G. 692 Budinger, T. F. 274, 391 Buffery, A. W. H. 356 Buge, A. 379 Bühler, K. 161 Bull, D. 561 Bullard-Bates, C. 647, 649, 653 Bunk, D. 799 ff Bunney, W. E. 518 Burchinal, M. R. 664 Burd, L. 806 Burdach, K. F. 128 Burgemeister, B. 630 Burgess, R. 597 Burke, D. 630 Burke, D. M. 900 ff, 907, 910 f Burke, G. 601, 829 Burlingham, D. 598, 680 Burns, M. S. 198, 201 ff Burns, S. 396 Burres, M. J. K. 391 Burton, A. 356 Burton, E. K. 438 Burzio, L. 183 Busch, C. R. 296 Busch, J. 809 Buschke, H. 913 Bussing, A. 326
Butcher, A. 39, 41, 416 Butler, J. 862 Butler, N. 598 f Butler, S. 219, 561 Butler, S. R. 715 Butterfield, E. C. 715, 771 Butterfill, A. 643 Butters, N. 332, 394, 396, 399 f Butterworth, B. 3, 26, 50, 74, 84 f, 89, 124, 155, 181, 184, 188 ff, 199, 239, 242, 244 f, 247, 249, 340, 526, 536, 539, 728, 748 Buttet, J. 267 Buttrick, S. 11 f Buxbaum, J. 374 f Buyssens, E. 445 Buzolich, M. J. 854 Bybee, J. L. 27, 58, 60, 185 Byers, R. K. 654 Byng, S. 139, 142, 147, 254, 359 f, 365, 367, 384, 728, 744, 749 Byrd, M. 903 f, 906 f Byrne, B. 729, 738 Byrne, M. 453 Byrne, M. C. 841 f, 853 Bzoch, K. R. 858
C Cacioppo, J. T. 433 Cain, A. C. 769 Caine, E. D. 399, 505, 507 Cairns, H. 729, 775 Calavrezo, C. 895 Calcano-Perez, J. A. 341 Calculator, S. N. 854 Calderon, M. 212, 333 Caldognetto, E. 76 f Calhoun, W. F. 539 Caligiuri, M. 362, 430, 433 f, 440, 446, 463, 465, 479 Calkins, S. 580 Callaway, E. 131 Callias, M. 809 Caltagirone, C. 109, 295, 315, 333, 346, 378, 384 Camarata, S. 619 Cambier, J. 585 Cameron, C. 297 Cameron, H. 374 Camhi, J. 549 f Campbell, D. 589 Campbell, E. 748 Campbell, J. I. B. 328, 330 Campbell, L. 896 Campbell, M. J. 389 Campbell, R. 265, 292, 340, 588, 626, 728 Campbell, R. J. 836 Campbell, S. 650, 653 Campbell, T. 581
89. Index of Names
Campos, J. J. 586 Cancelliere, A. 255 ff, 344, 745 Cancro, R. 543 Candy, J. M. 389 Cannito, M. P. 293, 306, 901, 909 f Cannon, C. J. 903 Canter, A. 552 Canter, D. 140 Canter, G. J. 163, 198, 201 ff, 217, 292, 296, 465 Canter, J. 427 Cantor, R. 488 Cantwell, D. 580, 601 f, 701, 789, 813 Caparulo, B. 580 Capitani, E. 156, 314, 380, 390 Caplan, H. L. 597 Caplan, D. 101, 128, 138, 155, 157, 163, 165 f, 176, 184, 191, 199, 204, 246, 310, 315, 338 ff, 345 f, 908 Caplan, L. 230, 232 Caplan, R. 799 f Cappa, S. F. 128 f, 378, 380 f, 385 Cappella, J. N. 50 Capps, J. L. 907 Caramazza, A. 102 f, 115, 138, 145, 155 ff, 162 ff, 173 f, 176 ff, 181 ff, 191 f, 198 f, 251 ff, 259, 266 f, 269 ff, 289, 292, 309, 329, 336 ff, 344 ff, 359 f, 446 Cardoso-Martins, C. 700 Carey, S. 176, 339, 648, 654 Carlisle, J. A. 882 Carlomagno, S. 359 Carlson, F. 854 Carlson, G. 900 Carlson, N. R. 255 Carmichael, H. 599 Carney, E. 826 Carney, P. 39 Caronna, J. J. 411 Carpenter, M. D. 540 Carpenter, R. 642 ff Carpenter, R. L. 692 Carper, J. M. 125 Carr, E. G. 816, 818 Carrel, R. E. 660 f Carroll, B. J. 514, 517 Carroll, J. B. 140, 688 Carrow, E. 459 Carskaddon, G. 697 Carson, K. 390 Carter, A. L. 559 Carter, B. 778 ff Carter, R. 60, 63 Carter, R. L. 647, 649 Caruso, A. 438, 867 Carvell, S. 342 f, 346 Cary, L. 23, 718, 779, 781
929
Case, H. W. 897 Casey, D. M. 486 Caspary, P. 399 Casseday, J. H. 499 Castro, J. 684 f Castro-Caldas, A. 321 Cataldo, S. 712, 718 Catts, H. W. 622, 637, 711, 714, 716, 718 f, 756, 774 ff, 779 f Caudrey, D. J. 514 Cavalotti, G. 128, 381 Caverni, E. 106 Caverni, L. 127 Cazden, C. 773 f Celada, M. T. 525 f, 530 Celesia, G. G. 395 Cénac, M. 547 Cerf, A. 866 f Cerf, F. A. 896 Cermak, L. S. 333, 411 Chafe, W. 23, 217 Chaika, E. 525, 534 ff, 539, 545, 548 f, 552 Chain, F. 157 Chalian, V. A. 486, 488 f Chall, J. 775 Chalmers, D. 660, 663, 665 Champaud, C. 563 Chan, A. 596 Chance, B. 836 f, 839 f Chandler, J. 399 Chao, W. 29 Chapman, J. 549 f Chapman, J. P. 531 Chapman, J. S. 589 Chapman, K. 581, 615, 617, 619, 641 f, 644 Chapman, L. J. 528, 531 Chapman, R. S. 563, 566 ff, 574, 579, 621, 690 Chapman, S. 306 Chapuis, C. 600 f Charcot, J. M. 161, 262 f, 469, 647 Chase, C. 610 Chase, R. A. 852 Chase, T. N. 274, 391, 398 Chatrian, G. E. 498 Chavany, J. A. 378 f Chawluk, J. B. 341 Chedru, F. 157, 500 Chen, J.-H. 61 Chenery, H. J. 273, 289, 437 Cherry, E. C. 894 Chertkow, H. 155, 344, 394, 903, 912 Cheskin, A. 667 Chesnick, M. 610, 613 f, 617, 776 Chess, S. 809, 811 Chetnik, M. 792 Cheung, H. 905, 909 Chi, M. 630
Chia, K. S. 497 Chiarello, C. 384, 903 Chiat, S. 367, 831 Chierchia, G. 170 Childers, D. G. 437 Chistovich, L. A. 38, 416, 418, 421 Chocholle, R. 500 Choi, S. 562 Chomsky, N. 16, 35, 48, 92 f, 154, 162 f, 165 f, 170 f, 215, 251, 315, 578, 595, 679, 825 Christensen, J. M. 373, 489 Christinaz, D. 354, 358 Christman, S. S. 199, 201 Christopoulou, C. 298 Chui, H. C. 390 f Church, K. L. 384, 903 Churchill, D. 815 f Chusid, J. 127 Cicchetti, D. V. 534, 549 f, 597 Cicone, M. 220 f, 290, 385 Cipolotti, L. 231 Clahsen, H. 579 Clancy, P. 562 Clark, C. 140 f Clark, C. R. 854 Clark, D. 631 f, 773 f Clark, E. V. 29, 284, 338, 562, 578 Clark, H. H. 2 f, 11 f, 20 ff, 29, 217, 284, 290, 296, 338 Clark, J. M. 328, 330 Clark, L. W. 264 Clark, W. E. Le G. 499 Clark, W. M. 840 f Clarke, C. 826 Clarke, J. 587 Clarke, L. K. 762 Clarke, P. 363, 374 Clarke, R. 125 Claros-Salinas, D. 326 Clarus, A. 647, 654 Clay, M. M. 712 Cleeland, C. 483 Clegg, M. 574, 601 Cleland, L. N. 770 Clerebaut, N. 295 f Cleton, P. 252, 254 Clifton, C. 10 Clifton, N. F.,Jr. 910 Cloitre, M. 11 Cluytens, M. 779 Coates, R. 114, 126 f Cobb, H. 176 f, 182, 184 f Cobb, S. 515 f, 518 Cobrinick, L. 768 f Cockerill, H. 832 Code, C. 100, 123, 125, 218 ff, 226, 372, 374, 592 Coelho, C. A. 298 Coffman, J. A. 534 Coggins, T. 642, 644, 690 ff
930
Coghill, S. R. 597 Cohen, A. 283 Cohen, B. D. 549 f Cohen, D. 580, 602 Cohen, D. J. 693, 817 Cohen, G. 900 ff, 905 ff, 909 Cohen, l. G. 465 Cohen, I. L. 693 Cohen, J. 143 Cohen, L. 329 Cohen, M. 588 Cohen, R. 292, 333, 540, 553 Cohen, R. A. 792 Cohen, R. M. 516 Cohn, R. 326 Colby, K. M. 354, 358 Cole, H. J. 553 Cole, J. O. 516 Cole, K. 642 f Cole, K. J. 417, 434, 462 f, 478 Cole, M. 220, 273, 912 Cole, R. A. 58, 62 Cole, R. M. 852 Coleman, C. L. 853 f Coleman, D. 887 Coleman, M. 808 ff Collett, S. 599 Collier, G. 24 Collignon, R. 328 Collins, M. J. 366 Coltheart, M. 104, 146 f, 157, 181 f, 244, 251, 254 ff, 259, 267, 327, 343, 359 f, 364 f, 712, 728, 744, 749 f, 758 f, 770 Comings, B. G. 507 f Comings, D. E. 507 f Compton, A. 825, 847 Condino, R. 577, 775 Condon, W. S. 816 Conger, R. 597 Connell, P. 642 f, 644, 854 Conners, C. K. 763 Connor, N. P. 399, 436, 438, 462 ff, 478 Conrad, B. 469, 474 Conrad, R. 661, 663, 667 f, 672 ff Constantinidis, J. 341 Content, A. 712, 718, 757 f Conti-Ramsden, G. C. 699 f, 704 Conture, E. 867, 881, 888 ff Conway, D. 599 Cook, A. M. 853 f Cook, E. F. 410 Cook, M. 48 f Cooke, F. 888 ff Cooley, S. 901 f Cools, A. R. 395 Cooper, J. 559 f, 641 f, 644 Cooper, J. A. 652, 879, 881 Cooper, E. B. 887 ff Cooper, F. S. 127 f, 416, 711
89. Index of Names
Cooper, G. 395 Cooper, P. V. 901, 909 f Cooper, R. L. 668 Cooper, T. S. 416 Cooper, W. E. 25, 58, 62, 69, 113, 207, 209 ff, 213, 446 Cooperman, O. 598 Copeland, R. 298, 366, 688, 859 Coppola, V. A. 887 Corballis, M. C. 587 Corker, K. 518 Corkin, S. 340 f, 394, 912 Cornblatt, B. A. 800 Cornett, O. 663 Correll, P. 177 Corsiglia, J. 588 Corvin, J. 519 Cosi, P. 76 f Coslett, H. B. 102, 111, 291 f, 384, 500
cf. Branch CoslettH. Cossu, G. 718, 778 Costa, P. T. 900 Costa, L. 315, 886 Costello, A. 631 Costello, J. M. 877, 886 ff Coster, W. 597 Cotard, J. 647 Coughlan, A. K. 258, 384 Coulthart, M. 18 Cowan, H. 37, 40 Cox, A. 598, 602 Cox, A. D. 597 Cox, C. 340 f, 390 f, 399 Cox, M. D. 881 Cox, N. J. 879 Cox, P. 836 Coyle, J. M. 318 Cozolino, L. J. 525, 553 Craig, H. 620 Craik, F. I. M. 333, 906 f Crain, S. 176 f, 729 Crais, E. 621 Cramer, B. 725, 778, 782 Cramon, D. von 326, 438 f, 441, 446, 453 ff, 482, 496 Crary, M. A. 149, 446 Crawley, S. B. 700 Creedon, M. P. 816, 818 f Crespo, M. 653 Creutzfeldt, O. 130 Crinon, Y. 234 Crisi, G. 381 Critchley, E. M. R. 220 Critchley, M. 187, 218, 225 f, 228, 378, 380, 394, 444, 524, 714 Crockett, D. J. 140 f, 507 Crockett, H. G. 220 Croisile, B. 267, 270 Cromer, R. 595, 632 f, 689 Crompton, A. 5, 76, 199 Cronbach, L. J. 143
Crook, T. 391 f, 394, 900, 904 Crookes, T. 601 Cross, H. 868 Cross, S. 367 Cross, T. G. 667, 697 f, 700, 702 ff, 708 Crossland, J. 718 Crossley, R. 819 f Crothers, B. 835 Crow, T. J. 534 Crowe, T. K. 589 Crumley, R. L. 460 Crystal, D. 559, 577, 579, 580, 669 Cudahy, E. 637 Culatta, B. 642, 644 Culatta, T. 845 Culbertson, J. L. 661 Culp, D. 887 Culp, P. M. 854 Cummings, J. L. 219 f, 273 f, 341 f, 378, 390, 393, 396 f, 401, 411, 506, 912 Cunningham, A. 778, 782 Cunningham, A. E. 725, 758 Cunningham, C. 603 Cunningham, C. E. 690 f, 700, 702 ff, 706 f Cunningham, D. J. 125 Curcio, F. 580, 814 Curlee, R. F. 877 Curry, F. 866 Curry, L. M. 399 ff Curtis, S. 667, 670 Curtis, T. A. 488 Curtiss, B. 627 Curtiss, S. 392, 586, 591, 596, 598, 602, 627 f, 912 Cutler, A. 8, 9, 29, 56, 61, 75 f, 81, 83 f, 86, 164, 188, 221, 291 Cutsforth, T. D. 683 Cutting, C. 217 Cutting, J. 516 Czopf, J. 219, 591
D D’Antona, R. 129 D’Antonio, L. L. 861 D’Erme, P. 315 Dabul, B. 484 Dahmen, W. 326 Dakin, D. J. 94 Dale, P. 642 f Dale, P. S. 560 Dalla Barba, G. 231 Dallago, M. 760 Dalston, R. M. 436 f, 861 Dalton, P. 895 Daly, K. 811 Dalzell, J. 664
89. Index of Names
Damasio, A. R. 106, 110, 112, 128 f, 156, 402 Damasio, H. 112, 128 f, 212, 291, 381 Damico, J. 644 Damon, S. G. 354 Daniel, B. 482 Daniele, A. 155, 394 Daniloff, J. K. 211, 291, 298 Daniloff, R. 36 ff, 211, 416 Danly, M. 213 Danziger, W. L. 390 Daoust, H. 386 Darby, J. K. 513 f Dardarananda, R. 210, 212 f Darkins, A. 342, 396 f Darley, F. L. 154, 293, 425, 427, 438, 444 f, 447 ff, 453 ff, 459, 463, 465, 468 ff, 478, 481 ff, 496, 540, 628, 828, 835, 843 ff Datiles, U. P. 896 Davenport, Y. B. 597 David, C. 511 David, R. 295 David, R. M. 138, 352, 366 Davidovicz, H. M. 848 Davidson, B. 719 Davidson, B. J. 734, 738, 762 Davidson, M. 728 Davies, A. D. M. 314 Davies, B. 689 Davies, D. 690 Davies, J. 526 Davies, J. M. 518 Davies, P. 365, 389 Davies, R. 598 f Davies, S. E. 738 Davis, B. 827 Davis, G. A. 293, 299, 362 Davis, H. 700, 702, 706 Davis, J. M. 665, 668 Davis, L. F. 458, 839 ff, 849 Davis, P. J. 439, 474 Davis-Dansky, E. 661 Davis-Jones, G. A. 103 Dawes, V. A. 840 Dawson, D. 273 f Dawson, D. F. L. 552 Dawson, J. A 497 Dawson, M. E. 800 Day, B. L. 466 Dayton, C. M. 148 De Bastiani, P. 264 De Bleser, R. 105 f, 108, 149, 164, 166, 181, 184, 213, 219 f, 226 De Boysson-Bardies, B. 559 De Decker, B. 549 ff De Filippo, C. L. 673 f De Groot, M. B. 761 De Gruijter, D. N. M. 146 De la Monte, S. 395
931
De Nil, L. F. 888 De Renzi, E. 105, 138, 142, 158, 314, 319, 332 f, 346, 380 f, 393, 444, 449 De Sanctis, S. 795 De Villiers, J. 564, 566 De Villiers, P. 564, 566 De Vreese, L. 231, 233, 279 Deal, J. L. 447 DeBois, A. 845 Debray-Ritzen, P. 600 f Deck, J. 690, 700, 702 ff, 706 Deck, J. W. 333 DeClerk, J. 416 Deese, J. 28 Degos, J. D. 384 DeGuzman, G. C. 420 Dehaene, S. 329 DeHirsch, K. 768 f, 772 Dejerine, J. 105, 128 f, 253, 262 f, 381, 742 Dejerine-Klumpke, A. 128 DeJong, R. N. 470 del Viso, S. 75 ff, 80 f, 85, 87 Delacato, C. 754, 763 DeLacoste, C. 305, 307, 309 DeLaney, J. F. 398 Delattre, P. 37 Delbanco, T. L. 410 DelColle, J. D. 419 Delis, D. 216 Delis, D. C. 385 Dell, G. S. 5, 13, 28, 57 ff, 62, 76 ff, 81, 85, 87, 89, 242, 323, 900 Dell, M. 335 f Della Sala, S. 390 Deloche, G. 292, 326 ff DeLong, G. R. 807, 810 DeLong, M. R. 465 Delwaide, P. J. 453 Demain, C. 366 Dembitzer, H. M. 389 Demers, R. 170 Demol, O. 229 DeMyer, M. K. 805 f, 809 f Denckla, M. B. 327, 588, 738, 775 Denes, G. 149, 231, 233 f, 333, 500 f Dennis, M. 142, 313, 590, 648, 650 ff, 657 Denny, M. 866 DePaul, R. 433 f, 440 Derouesné, J. 257, 265, 267, 344, 358 f, 747 Déry, D. 295 Desberg, P. 756 Descartes, R. 94 Deser, T. 911 f DeSetto, L. 734 DeSouza, L. J. 489 Despert, L. 795
DeStefano, C. C. 293 Deutsch, G. 219 Deutsch, S. E. 447 DeVault, S. 792 DeVellis, R. F. 805, 811 Dever, R. 689 Devick, M. 264 Devoti, M. 655 Devreux, F. 231, 234 f Dewick, H. C. 314 DeWolfe, A. S. 540 Deykin, E. Y. 809 f Di Chiro, B. 398 Di Sciullo, A.-M. 27 Diamond, I. T. 499 Diaz, D. L. 902 f DiBartolomeo, J. R. 661 Dibden, S. N. 762 Dick, J. P. R. 466 Dickson, S. 829 Diebel, R. 396 Dieckmann, C. 550 Dijkstra, T. 9, 13 Dila, C. 588 Diller, L. 176 Dimmick, K. C. 487 f Dimond, S. J. 763 Ding, B.-Q. 718, 779 Dingwall, W. O. 210, 384 Dinner, D. S. 130 f Dinnsen, D. A. 831 DiSimoni, F. 540, 628 Dittmann, J. 105 f, 110 f, 541, 549 f, 552 f, 912 Dixon, R. M. W. 171 Doane, J. A. 551 f Dobben, G. D. 398 Dobie, R. A. 664 Dobrich, W. 577 Dobrovolsky, M. 170 Dobscha, S. 541 Dobslav, G. 683 Dodd, B. 667 f, 671 ff, 681, 688, 825 ff, 831 f Dogil, G. 189 Dollaghan, C. 643 f, 782 Donahue, M. 619, 775, 778 Donaldsen, G. W. 770 Donaldson, R. C. 487 f Dongelmans, J. 760 Donnell, A. 392, 912 Donovan, P. T. 463 Doody, K. 511 f Dordain, G. 384 Dordain, M. 184, 337, 384 Dore, J. 559, 562 Dorman, M. 866 Dorval, B. 569 Dosza, M. 893, 896 Douane, J. 802 Dougan, D. R. 716 Douglas, J. 598 f Douglass, L. 865
932
Dowden, P. A. 460 Downey, D. 779 f Downie, A. W. 463 Downing, J. 761, 774 Downs, J. A. 489 Doyel, A. 304 f, 307 ff Doyle, P. J. 355, 362 Draffan, J. 526 Drake, W. E. 588 Dratman, M. L. 805 Dreifuss, F. E. 768 Dressler, W. U. 57, 305 f Drevets, W. C. 390 Dreyfus, H. L. 124 Dromi, E. 561 Dronkers, N. F. 221 Dronsek, C. 164, 166 Drosdowski, G. 24 Duara, R. 274, 389, 391, 810 Dubois, J. 281, 335 Duchan, J. F. 577, 580, 689, 812 Duché, D. J. 795 Duchek, J. M. 902 f Duchen, L. W. 401 Duchin, S. W. 910 Duckworth, M. 439, 871 f Dudley, J. G. 470 Duffy, F. D. 373, 375 Duffy, F. H. 534, 907 Duffy, J. R. 291, 314 f, 446 Duffy, R. J. 291, 298, 314 f, 328 Duguay, M. J. 487 Dukette, D. 602 Dummer, L. 756, 761 Duncan, G. W. 129 Duncan, S. 551 Dunlea, A. 682, 684 Dunlop, D. B. 734 f Dunlop, P. 734 f Dunn, C. 641 f, 644, 827, 860 Dunn, J. 569 Dunn, L. 628 Dunn, L. 628 Dunn, L. M. 397 Dunn, L. N. 313 Dunton, S. 776, 782 Dupré, E. 234 Durand, C. 559 Durand, M. 444 f Durkin, D. 770 Dusser de Barenne, J. G. 121 Dworkin, J. 845 Dziatolowski, M. 396
E Earnest, M. P. 498 Easton, T. A. 417 Ebert, M. H. 399, 507 Eckerman, C. O. 569 Edell, W. S. 800 Edelman, G. 366
89. Index of Names
Edelstein, B. A. 882 Edgington, E. S. 147 Edler, M. 754 Edmundson, A. 139, 142, 147, 586, 718 Edwards, H. T. 702 ff, 707 Edwards, J. 435 Edwards, J. H. 598 f Edwards, M. 453 Edwards, R. M. 810 Efron, D. 320 Efron, R. 322 Egeland, B. 597 Eggers, C. 795 ff Eggert, G. 187, 189 Eglof, D. B. 894 Eheart, B. 700, 704, 706 Ehri, L. C. 712, 715, 718, 757 f, 774, 778 f, 781 Ehrich, V. 23 Eichler, W. 712 Eidelberg, D. 588 Eilers, R. 561 Einstein, A. 310, 315 Eisenberg, H. M. 219, 652 Eisenberg, L. 768 Eisenson, J. 98, 137, 187 f, 218, 384, 575, 626, 839, 872 Ekelman, B. 636 Ekelman, B. L. 577, 590, 600, 651 f, 775 Ekman, P. 295, 320 El-Awar, M. 396 El-Yousef, M. K. 518 Elbert, M. 831 Elder, L. 712, 718, 750 f Elghozi, D. 585 Eliason, M. 848 Elies, W. 497 Elkisch, P. 768 Elkonin, D. B. 757 Ellgring, J. H. 514, 517 f Elliot, D. E. 768 f Elliott, L. L. 610, 628 f Ellis Weismer, S. 631 ff, 775, 783
cf. Weismer, S. E. Ellis, A. W. 66 f, 69 ff, 123, 154, 199, 201, 203, 220, 242, 244, 252 f, 262, 265 f, 310, 344, 358, 360, 713 f, 719 f, 746, 911 Ellis, L. 439 Ellis, N. 712, 718 Ellis, N. R. 688 Elman, J. L. 9, 58, 245 Elson, A. 788, 791 f Elstner, W. 681 Elwood, D. L. 529 Emanuel, F. W. 439 Emery, O. B. 514 ff, 905, 911 f Emery, P. 298, 355 Emmonds, J. 170 Emmorey, K. D. 176 f, 210,
212 f, 800 Emrich, L. J. 486 Enderby, P. 149, 352, 365, 453, 459, 825 Endicott, J. E. 526, 805 Engel, D. 333, 540 Englund, E. 274 Entus, A. K. 589 Enzle, M. E. 24 Eppel, P. T. 813 Epstein, F. H. 410 Erber, N. P. 667, 672 Erickson, C. B. 860 Erickson, J. G. 689 Erin, J. N. 685 Erlenmeyer-Kimling, L. 800 Erskine, B. 634 Ervin-Tripp, S. 569 Escalona, S. 768 Escobar, M. D. 541 Escourolle, R. 379 Eslinger, P. J. 106, 110, 390 Espir, L. 218 Espir, M. L. E. 127 Estaban, A. 465 Estrem, T. 859 Estridge, N. M. 220 Evans, D. 689, 692 Evans, J. 620 Evans, M. 779 Evarts, E. 115, 455, 477 Evett, L. J. 252 Evrard, P. 651 ff Ewing-Cobbs, L. 652 Exline, R. V. 50 Exner, S. 263 Eyberg, S. M. 597 Eymard, L. 634 Eysenck, H. J. 315
F Faglioni, P. 393 Faber, R. 514 f, 540 f Faber-Langendoen, K. 273, 390 Faglioni, P. 314, 319, 380, 499 Faherty, A. 903 Fahn, S. 396 f Fair, C. 127 Faktorovich, N. 280 Falconer, M. 234 Falk, F. 514 Fann, W. E. 514 Fanshell, D. 18 Fant, G. 36 Farah, M. J. 156 Farber, D. S. 482 Faria, H. I. 549 Farmer, A. 842 Farnetani, E. 41 Farwell, C. B. 560 Farwell, R. M. 673
89. Index of Names
Fauconnier, G. 12 Faulkner, D. 900, 902, 905 Fawcus, M. 366, 374, 688 Fawcus, R. 688 Fay, D. 83, 86, 89, 161, 188, 563 Fay, W. 578, 811 f Fazio, B. 580 Feagans, L. 775 Fedio, P. 130 f, 274, 340 f, 391, 399, 912 f Feenan, K. 519 Feher, E. 26, 339, 401 Fehrenbach, R. A. 399, 541, 552 Feier, C. D. 906 Feldman, H. 675 Feingold, I. 763 Feldman, L. S. 342 Feldstein, S. 518 Felicetti, T. 809 Fellbaum, C. 154 Felton, R. 780 Fenelon, B. 734 f Ferenczi 510 Ferguson, C. A. 560, 826 Ferguson, S. 268 Fergusson, D. 599 Fernald, G. 760 Ferrari, C. 380 Ferreira, F. 10, 25 Ferreri, T. 184, 244 Ferrier, L. J. 619, 849, 853 Ferris, S. H. 391 f, 394, 900, 904 Ferro, J. M. 127, 321, 328, 653 f Ferry, P. C. 652 Ferster, C. B. 814 Fery, P. 252, 254 Fey, M. 560, 577, 580 f, 620 Fey, S. 618 Feyereisen, P. 289, 291 f, 295 f Fibiger, S. 866 Fiedler, P. 876, 893 ff Fiedorowicz, C. A. M. 760 Fife, D. 836 Figueira, M. L. 549 Fillenbaum, S. 280 Filley, C. M. 390 Fillmore, C. J. 217, 516 Finch, C. E. 389 Fincham, R. W. 103, 499 Fine, L. 486 Fine, J. 552 Finkelnburg, F. 314, 318, 328 Finkelstein, S. 108, 411, 447 Fischer, F. 778 ff Fischer, G. H. 144 Fischer, H. R. 549 Fischer, M. A. 691 Fischer, R. 267 Fischer, R. S. 114 Fischer, S. 818 Fischler, I. 393 Fish, B. 799, 805 Fisher, H. B. 465, 488 Fisher, J. H. 742
933
Fisher, J. M. 399 Fishman, M. 110 Fiske, D. W. 551 Fisman, M. 273 f, 341, 392, 912 Fitch, J. L. 367 Fitch-West, J. 356 f Fitz-Gibbon, C. T. 364 Fitzgerald, M. D. 566 Fitzpatrick, P. M. 298, 357 Flament, J. 226 Flechsig, P. 121 Fleming, S. G. 306, 901, 909 f Fletcher, J. M. 652, 716 Fletcher, L. 674 Fletcher, P. 578, 580, 582, 613, 669, 825 f, 828 Fletcher, S. G. 486, 489 Flicker, C. 394, 900, 904 Flicker, D. J. A. 514 Flood, J. 779 Flor-Henry, P. 534 Florès, C. 284 Florian, V. A. 671 Florin, I. 553 Flowers, C. R. 211, 291 f, 384 Flowers, K. A. 462 Flude, B. M. 252 f Fodor, J. A. 16, 23, 47, 153, 158, 162, 315, 388, 719 Fodor, J. D. 153 Foix, C. 234, 378 f Foldi, N. S. 220 f, 290, 293 Folger, M. 609 Folkins, J. 448, 844, 861 Folstein, M. F. 391 f, 399 f Folstein, S. 809 f Folstein, S. E. 391 f, 399 f Foltz, G. 719 Fomin, S. V. 417 Fontenelle, S. 768 f Foorman, B. 781 Foppa, K. 19, 553 Ford, B. L. 49 f Ford, M. 11, 48 ff, 82 Fornarolo, G. 719 Forner, L. L. 861 Forness, S. 716 f Forno, L. S. 395 Forrest-Pressley, D. 779 Forrest, K. 434, 446 Forrester, M. A. 569 Fors, S. 700, 704, 706 Forsell, C. 811 Fossler, H. 867 Foster, N. L. 274, 391 Foster, S. H. 568, 576, 642 Fourcin, J. 668 Fowler, A. E. 692 Fowler, C. A. 35, 38 f, 42, 60, 416 ff, 421, 738 Fowler, S. 735, 762 Fox, B. 757, 777 ff, 782 Fox, D. R. 859 Fox, J. 340
Fox, P. T. 131, 360 Foy, J. G. 799 f Fozard, J. L. 906 Fradis, A. 219 Fraiberg, S. 680 f, 684 f Fraknoi, J. 805 Frame, C. 530 Francis, H. 779 Frank, S. M. 505 f Frankel, M. 506 Franklin, M. B. 559, 562 Franklin, E. 154, 242 ff, 249, 292, 358, 364 f, 708 Fransella, F. 895 Fraser, C. 564 Fraser, W. I. 537, 539, 552 Frattali, C. M. 376 Frauenfelder, U. 9, 11, 13, 174, 244 Frazier, L. 8 ff Frederick, G. 130 Frederick Wetzel, W. 26 Frederix, M. 294 Freed, D. 394, 634, 912 Freedman, B. J. 550 Freedman, M. 379, 396 Freedman, N. 516 Freedman-Stern, R. 304 ff Freeman, B. J. 805, 809 Freeman, D. 37 Freeman, F. 866 Freeman, F. J. 446, 888 f Freeman, R. B. 589 Freeman, R. D. 680 Freeston, I. L. 131 Fregmen, A. 563 French, L. A. 563 f Freud, A. 598 Freud, S. 57, 90, 115, 121, 238, 242, 500, 523, 546, 646 f, 654 Freund, C. S. 500 Freund, H. 882 Freund, H. J. 319, 463 Fricchione, G. L. 413 Fried-Oken, M. 616 Friederici, A. D. 164, 174 ff, 179 Friedland, R. P. 274, 391 Friedman, E. 808 Friedman, J. 342 Friedman, M. 712, 756 Friedman, R. 792 Friedman, R. B. 199, 201, 203, 253, 267 f, 344 Friedrich, F. J. 253 Friel-Patti, S. C. 699, 704 Friel, J. 714 ff Friesen, W. 320 Fristoe, M. 291 Fritelli, G. 298 Frith, U. 712, 718, 727, 729, 746, 749, 756, 768 ff, 772, 807, 813
934
Fritsch, G. T. 120 Froeschels, F. 851 Frome Loeb, D. 615 Fromkin, V. A. 67, 70, 75 f, 78 f, 81, 84, 154, 164, 209 f, 229, 232, 322 f, 536, 591 Frommer, J. 515, 549 f Frost, D. 693 Frost, J. 715, 718, 755, 757 Frost, J. D. Jr. 507 Frost, J. L. 500 Frost, S. D. 486 Frostig, M. 754 Fry, D. 246 Fucci, D. 439 Fuchs, D. 755 Fuchsgruber, K. 894 Fujii, T. 499 Fujiki, M. 620, 776, 782 Fujimura, O. 434, 471 Fujita, F. 437 Fukatsu, R. 499 Fukusako, Y. 198, 201, 204 ff Fuld, P. 913 Fundudis, T. 788 ff Funkenstein, H. 379 Funnell, E. 155 ff, 182, 239, 257 f, 298, 344, 355, 728 Furman, L. 689 Furr, M. 828 Furth, H. 582 Furukawa, T. 271 Fuson, K. C. 325 Fust, R. S. 488 Fuster, J. M. 123
G Gabrieli, J. D. E. 396 Gaddes, W. H. 507 Gaddie, A. 220 Gagnon, J. 384 Gaines, N. D. 886 Gainotti, G. 109 f, 154 f, 295, 315, 333, 346, 384, 394 Gairdner 236 Galaburda, A. M. 121, 125, 379, 588, 598 Galin, D. 131 Galkin, T. W. 653 Gall, F. J. 120, 311 f, 315 Gallagher, T. 578 Gallivan, G. J. 497 Galton, F. 327 Gambetti, P. 395 Gamzu, E. 588 f Gandour, J. 206, 210, 212 f, 440, 560 Gans, C. 433 Ganz, E. 274, 391 Garcia-Albea, J. 75 ff, 80 f, 85, 87 Gardiner, M. F. 589
89. Index of Names
Gardner, H. 138, 145, 220 f, 290, 293 f, 312, 330, 335 f, 346, 355, 364, 384 ff, 635 Garfield, J. L. 13 Garman, M. 580, 669 Garmezy, N. 602 Garnham, A. 28, 61 Garnica, O. 561 Garrett, M. F. 4, 24, 47, 54, 59, 78 ff, 83 ff, 153, 158, 161 f, 164, 173 f, 178 f, 184, 189 ff, 232, 322 f, 360, 380, 541 Garrod, S. C. 902, 904 Garron, D. C. 340, 396 Garside, R. 788 Garvey, C. 569 Garvey, M. 600 Garwood, J. 292 Gascon, G. G. 501 Gascon, M. 589 Gates, J. E. 217 Gates, R. R. 674 Gautier, J. C. 110 Gavin, W. J. 561 Gawle, C. A. 446 Gay, T. 416 f Gazdar, G. 166 Gazner, P. 517 Gazzaniga, M. 98, 219 Geen, T. R. 433 Geers, A. 668 Geffen, G. 590 Gel’fand, I. M. 417 Gelb, I. J. 66 Gelfer, C. 39 f Gelman, R. 563 Gensior 211 Gentil, M. 418 Gentner, D. 43, 562 f Gentry, B. 634 Georgian, D. A. 488 Gerber, S. E. 661 Gerber, M. 779, 832 Gerdeman, B. 273 German, D. 616, 775 Gerratt, B. R. 437 Gerrig, R. J. 2, 12, 21 Gersten, M. 597 Gerstman, L. J. 50, 211, 906 Geschwind, N. 100, 103 f, 109, 112 ff, 121 ff, 125, 128 f, 193, 219, 228, 318 f, 335, 346, 356, 396, 500, 587 f, 598, 654 Gewirth, L. R. 913 Geyer, H. 342 Ghiotto, M. 566 Gholson, B. 633 f Gibbs, R. W., Jr. 21, 217 f, 221 Gibson, A. J. 515 Gibson, E. J. 712, 758 Gibson, J. J. 420 Gick, M. L. 906 Gigley, S. 176
Gilbert, H. R. 437 Gilbert, L. E. 661 Gilewski, M. J. 906 Gill, J. 48 f Gillberg, C. 807 ff Gillingham, A. 755 f, 760 Gillis, R. E. 488 f Gilman, S. 468, 470 Gimenez-Roldan, S. 465 Gittelmann, R. 763 Giustolisi, L. 155 Gjerde, P. F. 553 Glaister, J. 518 Glanville, B. B. 589 Glanzer, M. 900, 912 Glasner, P. J. 791 Glassmann, R. B. 124 Glaze, D. 507 Gleason, J. B. 103, 176, 332
cf.Berko Gleason, J. Gleber, J. 306, 308, 385 Gleitman, H. 697 Gleitman, L. R. 567, 681 ff, 697, 712, 756 Glenn, C. G. 155 Glennen, S. L. 854 Gligorijevic, B. 27, 185 Globus, M. 396 Gloning, I. 125, 281 Gloning, K. 125, 281 Glosser, G. 273, 295, 911 f Glucksberg, S. 296 Glushko, R. J. 758 Goad, H. 560 Godden, A. L. 886 Göddenhenrich, S. 147 f Godfrey, H. P. 517 Godfrey, J. 726 Goetz, L. 816 Goksen, I. 815 Goldberg, E. 232 f Goldberg, G. 113 Goldberg, R. L. 516 Goldberg, T. E. 768 f Goldblum, M.-C. 174, 176 f, 255, 279, 499 Golden, C. J. 399 Goldenberg, T. 644 Golder, H. K. 394 Goldfarb, N. 701 Goldfarb, R. 913 Goldfarb, W. 598, 701, 814 Goldfield, B. A. 561 f Goldfine, P. E. 808 Goldgar, D. E. 664 Goldin-Meadow, S. 563, 675 Golding, J. 599 Goldman, M. 482, 843 Goldman, P. S. 653 Goldman, S. 729 Goldman-Eisler, F. 47 ff, 245, 518 Goldman-Rakic, P. S. 123, 125
89. Index of Names
Goldsmith, H. 866 f Goldsmith, M. M. 486 Goldstein, D. M. 516 Goldstein, G. 354, 911 Goldstein, H. 355, 362, 598 f Goldstein, K. 107, 109, 112 f, 127, 161, 235, 244, 279 f, 314, 335, 372, 379 Goldstein, L. 5, 35, 42 ff Goldstein, M. A. 487 Goldstein, M. J. 551 ff, 802 Goldstein, M. N. 499 f Goldstein, R. 588 f Gole, G. A. 762 Golinkoff, R. M. 566 f Göllecz, V. 681 Gollomp, S. 342 Golper, L. 51 Goltz, F. 120 Gonon, M.-A. H. 367 Gonyea, E. F. 318 Gonzalez, E. G. 327 Gonzales, G. P. 217 Gonzales Rothi, L. J. 113, 321, 381
cf. Rothi, L. J. G. Gonze, J. C. 516 Goodenough, C. 163, 294 Goodenough-Trépanier, C. 386 Goodglass, H. 59, 100, 102 ff, 107, 109 f, 113 ff, 127, 138, 142, 154, 163, 165, 176, 187, 197, 207, 210, 212, 238, 264, 296, 298, 306 f, 332 f, 337, 339, 341, 356, 396, 446, 449, 900 f, 911 Goodkin, R. 354 Goodman, D. 417 Goodman, E. 518 Goodman, J. 754, 769 Goodman, N. J. 354 Goodman, R. A. 344 Goodman-Schulman, A. R. 266 f, 330 Goodwin, C. 30 Goody, J. 23 Goosens, M. 295 f Gopher, D. 70 Gopnik, A. 561 f Gordon, B. 156, 174, 390 Gordon, D. 12 Gordon, H. 219 Gordon, H. W. 279 Gordon, N. 600 Gordon, W. P. 399 f Gorham, D. R. 216 Gorniak, G. C. 433 Gosenfeld, L. F. 378 Goshorn, E. L. 474, 483 Goswami, U. 711, 715, 724 f, 730, 758 Götesham, K. 895 Gotlib, I. 598 Gottesman, I. 399
935
Gottlieb, G. L. 454 f Gottschaldt 314 Gottschalk, L. 511 Gottsleben, R. H. 688 Gottwald, S. R. 879, 888 ff Gough, P. B. 716, 718 f Goulandris, N. 726, 736 Gould, H. 862 Goulet, P. 384 ff Goyen, J. D. 734 f Gräbe, K. 434, 471 Gracco, V. L. 42, 417, 440, 462 f, 477 f, 867 Grady, C. L. 274, 389, 391, 810 Graetz, P. 149 Graff Radford, N. R. 381, 402 Grafman, J. 220, 325, 913 Graham, J. 498 Graham, P. J. 597, 601 Granholm, E. 399 f Granie, M. 762 Grant, S. R. 384 Grashey, H. 263 Grau, H. 395 Graves, R. 219 Gray-Silva, S. 657 Graziani, L. J. 768 Greden, J. F. 514, 517 Green, A. 597 Green, D. 282 ff Green, D. S. 661 Green, E. 112, 163, 176, 335 Green, G. 299, 363 Green, J. 402 Green, J. D. 819 Green, K. W. 674 Green, L. 700, 702, 706 Green, M. 601 Green, W. B. 674 Greenberg, S. 394 Greenblatt, S. H. 130 Greene, J. O. 50 Greenfield, P. 620, 633 Greenfield, P. M. 16 Greenstein, J. 737 Greenwood, R. 498 Gregory, H. 866 Gregory, H. H. 876, 888 ff Gregory, S. 667, 674 f Grewel, F. 326 ff, 427 Grice, H. P. 1, 3, 12, 17, 551 Griffith, F. A. 484 Griffith, V. E. 365 Griffiths, A. J. 670 Griffiths, C. 600 Griffiths, R. 518 Grimm, H. 580, 612 f, 697 ff, 702 ff, 707 f, 798, 801 Grinker, R. R. 799 Grober, E. 913 Grodzinsky, Y. 164 f, 279, 292 Grosjean, F. 284 Grossberg, S. 530 Grossfield, M. L. 264
Grossman, H. J. 688 Grossman, M. 176, 295, 329, 339, 341 ff, 346, 385 Grove, W. 515 Growdon, J. H. 394 f, 912 Grudin, J. T. 67 ff Gruendel, J. M. 569 Grundy, K. 825, 828 f Grunwell, P. 561, 827, 859 Grusche, A. 553 Guidotti, M. 378, 381 Guignard, F. 631 Guilford, J. P. 143 Guitar, B. 888, 893 ff, 897 Günther, K. B. 712 Gurd, J. M. 214, 313 f Gurfinkel, V. S. 417 Gustafson, L. 274, 401 Guthrie, D. 799, 805 Guthrie, J. T. 715, 758 Gutierrez-Mahoney, C. de 127 Gutman, A. J. 703, 705 Guttman, L. 140 Guttmann, E. 654 Gutzmann, A. 894 f Gutzmann, H. 895 Guyard, H. 367
H Haag, E. 100 Haak, N. J. 149 Haas, G. 110, 128, 357 Haas, J.-C. 105 f, 110 f, 912 Haas, K. 761 Habermann, G. 493 Habib, M. 106 Hackethal, R. 756, 761 Haden, P. 58 Hadley, P. 642 f Haegerstrom-Portnoy, G. 734 Hafitz, J. 565 Hagberg, B. 274 Hagen, C. 366 Hagen, J. W. 760 Hagenlocker, K. 341, 392, 912 Hagerman, E. L. 455, 836 f Hagerman, R. J. 808 Hagestedt, H. 797 Hagfors, C. 373 Hagiwara, H. 271 Hagnell, O. 388 Hagoort, P. 149, 177 f Hague, F. 392 Haken, H. 419 Hakes, D. 773 f Hakim, A. M. 395 Halfond, M. M. 879, 888 ff Halgren, E. 130 Hall, E. H. 515 Hall, H. R. 354 Hall, J. 719, 736
89. Index of Names
936
Hall, J. A. 514 Hall, L. J. 836 Hall, P. 601, 775 Hall, P. K. 827 Hallahan, P. 761 Halle, M. 35, 185, 825 Hallett, M. 462, 464 f Hallgren, B. 742, 768 Halliday, M. 826, 829 Halliday, M. A. K. 18, 304, 307, 550 Halls, J. W. 325 Halpern, L. 280 Halpern, W. I. 792 Halpin, T. J. 836 Ham, R. 832, 882 Hamayan, E. 827 Hambleton, R. K. 146 Hambly, G. 828 Hamby, S. 385 Hamm, A. 125, 587 Hammarberg, R. 36 ff, 416 Hammer, M. A. 628 f Hammill, D. D. 754 Hammond, J. 792 Hammond, K. M. 396 Hampson, E. 156 Hamre, C. 871, 875 Hamsher, K. 310, 313 Hanby, S. 296 Haney, J. 789 Hanley, J. 865 Hanley, J. R. 254, 314 Hannell, G. 762 Hannen, M. 610 Hannequin, D. 384 f Hänni, R. 551 Hanninen, R. 201, 205 Hansch, E. C. 390, 396 f Hanson, D. G. 437, 465 Hanson, V. L. 671, 673 Hanson, W. R. 333, 376, 396, 463, 483 Hansotia, P. 400 f Hanzlik, J. R. 700 Hardcastle, W. 435, 439, 826 Hardcastle, W. J. 446 Hardiman, C. J. 901, 909 f Harding, C. G. 567 Hardwick, J. 69 Hardy, J. C. 835 f, 839 ff, 848 ff Hardyck, C. 591 Hargrave, S. 760 Hargreaves, W. A. 514, 517 Hargrove, P. 643 Harita, Y. 861 Harley, T. A. 57, 77, 83, 85, 87, 90 Harlock, W. 114, 126 f Harn, W. 875 Harney, J. H. 211 Harnish, R. 170 Haroldson, S. 886, 888
Harris, J. 540, 550 Harris, J. C. 768 Harris, K. 37, 39 f Harris, K. S. 418, 435, 445 f Harris, M. 895 Harris, P. R. 131 Harris, S. L. 701, 703 Harris, T. L. 713, 775 Harris-Vanderheiden, D. 853 f Harrison, T. 131 Harrold, R. M. 902 f, 907 Harrow, M. 551 Hart, D. S. 527 Hart, H. 601 Hart, J. 156 f Hart, S. 392 f Hartje, W. 212, 291, 314, 326 Hartl, M. 712 Hartley, X. Y. 692 Hartman, C. H. 518 Hartman, J. 363 Hartman, M. D. 394 Hartmann, D. E. 428 f Hartmann, E. 435, 438 f, 482 Harvey, P. D. 549 f, 552, 802 Harvey, W. 94 Hasan, R. 304, 307, 550 Hasegawa, A. 489 Hasegawa, K. 130, 265, 271 Hasher, L. 400, 903, 907 Hasner, A. 862 Hasquin, J. 226 Hasselbring, T. S. 761 Hatano, G. 327 Hatfield, F. M. 266 ff, 296, 343, 353, 357, 359, 361, 364 f Hathaway, S. N. 57 Haub, G. 125 Hauser, S. L. 810 Hawes, A. 127 Hawk, A. M. 487 Hawkins, P. R. 47 Hawley, J. L. 843, 850 Haxby, J. V. 274, 389, 391 Hay, D. 599 Hayashi, M. M. 306, 901, 909 f Hayden, D. 484 Hayden, M. R. 398 Hayden, P. 868 Hayden, T. L. 788 Hayes, D. 904 Hazan, K. 292 Hazan, V. 668 Hazenberg, G. J. 402 Head, H. 104, 107, 109 f, 122, 129, 137, 238 f, 444 Healy, A. F. 58, 60 Healy, J. M. 768 f, 771 Heaton, R. K. 390 Hebrich, K. E. 422 Hécaen, H. 262, 264, 281, 315, 326, 335 f, 499, 647 ff Hedde, J.-P. 516
Hedgepeth, E. M. 514 Hedges, T. A. 454 Hedley-Whyte, E. T. 395 Hedley-Whyte, R. 230 Hedrick, D. L. 901, 909 f Heerlein, A. 512 Heeschen, C. 19, 22, 29, 100, 149, 161, 164, 174, 290 Heeschen, V. 23 Hefter, H. 463 Hegler, C. 280 Hegley, D. C. 528 Hegmann, J. 868 Heike, G. 322 Heilbronner, K. 263 Heilman, K. M. 103, 163, 176, 211, 213, 264 ff, 273 f, 291, 318, 321, 333, 338, 344, 383, 500 Heisey, J. G. 903 Heit, G. 130 Helfrich, H. 514 Heller 795 Heller, H. S. 900 f Helm, N. 234, 484 Helm, N. A. 114, 207 Helm-Estabrooks, N. 110, 127 ff, 298, 355 ff, 379, 392, 882, 911 f Helme, R. D. 455 Helmick, J. W. 373 Helps, R. 895 Hemphill, R. E. 500 Henderson, A. 48 ff Henderson, L. 255 Henderson, V. L. 909 f Henderson, V. W. 389 ff, 394, 912 Hendrickson, D. E. 316 Henke, W. 37 Henneaux, J. 445 Henry, R. 900 Henschen, S. E. 263, 325 f Herberman, M. A. 487 Hermann, K. 496 Hermelin, B. 668, 673, 816 Hern, C. L. 760 Herriman, M. 295, 298, 773 f Herrmann, M. 374 Hersen, M. 145, 880 Hersh, S. P. 810 Hertzog, C. 903 f Hess, C. W. 131 Hess, T. M. 902 Hesselink, J. 588 Hessler, G. 775 Heuyer, G. 795 Hewer, R. L. 149 Hewes, G. H. 817 Hewett, A. E. 760 Heyman, A. 273 f, 391 Hicks, D. M. 437
89. Index of Names
Hier, D. B. 220 f, 232, 341, 392, 810, 912 f Hildebrandt, N. 157, 166, 271 Hildreth, G. H. 761 Hildyard, A. 23 Hill, A. L. 692 Hill, D. 890 Hill, M. A. 273 f, 341, 390, 912 Hillert, D. 158 Hillier, N. E. 220 Hillinger, M. 718 Hillis, A. E. 155, 182, 184, 251 ff, 259, 266, 269, 271, 344 f Hillman, R. E. 437 Hillyard, S. A. 131 Hilt, D. C. 401 Hiltbrunner, B. 114 Hinchcliffe, M. K. 515 Hines, T. M. 397 Hingtgen, J. N. 805 f, 815 f Hinkle, W. G. 486 Hinshelwood, J. 713, 742 Hinton, G. 239, 259 Hinton, G. E. 123, 421 Hinton, V. 486 Hirano, A. 389 Hirano, M. 433, 499 Hirayama, K. 130, 265, 271 Hirose, H. 416, 435, 446, 453, 471 Hirsh-Pasek, K. 566, 715, 728 Hirson, A. 367 Hirst, W. 293, 410, 411 Hiscock, M. 590, 649 f Hitch, G. 736 Hitch, G. J. 326 Hitchcock, A. 93 Hitzig, E. 120 Hixon, T. J. 437, 458, 460, 482, 836, 842 f, 845, 850 Hodapp, R. 576 Hodge, M. 441 Hodges, R. E. 713, 775 Hodson, B. 847 Hoefnagel-Hohle, M. 591 Hoeman, H. W. 669, 671 Hoenkamp, E. 5, 12, 25 Hoff-Ginsberg, E. 568, 581, 691, 697 f, 702 Hoffman, R. E. 95, 515, 534 ff, 541, 549 ff, 798, 801 Hoffmann, G. M. 516 Hogaboam, T. 729 Hogan, R. 569 Hogben, G. L. 539 Hohenegger, M. K. 647, 649 Hohn, W. 757 Høien, T. 712 Hoit, J. D. 437, 446 Holbrook, A. 901, 909 f Holland, A. 307, 373, 394, 401 f, 903
937
Holland, A. L. 112, 138, 297, 354, 362 f, 365, 411 Hollien, H. 514, 517 Holligan, C. 736, 738 Holm, V. A. 664 Holmberg, C. 643 Holmberg, E. B. 437 Holmberg, S. 412 Holmes, D. W. 674 Holmes, G. 431, 468 f Holmes, J. 744 Holmes, V. M. 48 f, 82 Holroyd, T. 420 Holt, K. 643 Holtzhauer, F. J. 836 Holtzman, J. 221 Holtzman, J. D. 410 f Holyoak, K. 634 Holzmann, P. S. 799 Homatidis, S. 701 f, 809, 816 Hömberg, V. 463 Honda, K. 418 Hood, J. 602 Hood, L. 563 ff, 568, 598 Hoodin, R. B. 437 Hoole, P. 435, 438 f, 441, 482 Hooley, J. M. 598 Hooper, M. W. 389 Hoops, H. R. 840, 842 Hoops, R. 373 Hoosain, R. 70, 220 Hoover, T. M. 525 f, 528 Hopf, A. 398 Hopper, P. 217 Horek, F. B. 589 Horiguchi, S. 418 Hörmann, H. 12 Horn, D. 642, 644 Horn, L. C. 394 Horn, P. 177 Horne, D. 754 Horner, J. 51, 231, 234, 273 f, 447, 463 Hornsby, B. 730, 755 f, 759, 761 Horowitz, E. 872 Horowitz, L. M. 220 Horsborough, K. M. 667, 708 Horsburgh, G. 894 Horstink, M. W. I. 395 Horwitz, S. J. 768 f, 771 Hoskins, B. 633 Hotopf, W. H. N. 58 Hough, M. S. 293, 306, 446 Houillier, S. 326 Houlihan, J. P. 378 House, A. 862 Howard, D. 146, 154 f, 181, 184, 242 ff, 249, 257, 296, 340, 352 ff, 357 f, 360 f, 364 f, 536, 539 Howard, D. V. 900, 902 f Howell, E. A. 734 Howell, J. 125 Howell, P. 726
Howes, D. 112 Howes, D. H. 335 Howie, P. M. 842, 864, 893 ff, 897 Howlin, P. 580, 601 f, 701 Hoyer, W. J. 903 Hoyle, H. 631 Hoyt, B. D. 422 Hubbell, R. 636 Hubel, D. 122 Huber, H. P. 143 f Huber, S. J. 396 f Huber, W. 20, 100 f, 103 ff, 107, 109 f, 112, 114, 139 ff, 147 ff, 292, 306, 308, 321, 322, 385, 449 Hudson, J. 562 Huff, F. J. 390 f, 394, 912 f Hug, L. 848 Hughes, C. 778 f Hughes, D. 642 ff Hughes, M. 599 Hughes, R. 831 Hughlings Jackson, J. 226 ff, 232, 236
cf. Jackson, J. H. Huijbers, P. 85 Hulicka, I. M. 487 Hulme, C. 728, 730, 734 ff, 738, 753, 755 f, 759 ff Hulstijn, W. 867 f, 876 Hummer, P. 751 Humphrey, M. 789, 795, 804 Humphreys, M. 719, 736 Humphreys, G. W. 157, 252 ff Hündgen, R. 100 Hunker, C. 433, 472 Hunsley, Y. 868 Hunt, K. W. 540 Hunt, R. D. 399 Hunter, D. 818 Hunter, L. 439, 445 Huntley, R. 643 Huntley, R. A. 381 Hupet, M. 294 Hurford, J. R. 83 Hurlbut, B. I. 819 Hurrell, J. 462 Hurst, C. R. 507 Hurwitz, L. 230 Hurwitz, L. J. 106 Hutchinson, E. C. 333 Hutchinson, J. 440 Hutchinson, K. M. 905 Huttenlocher, J. 562 f, 566, 630, 768 f Huttenlocher, P. R. 768 f Hutton, J. E. 489 Hutton, J. T. 115, 125, 284 Hyde, M. 103, 176, 332 Hylkema, H. 66, 69 Hyman, B. 402 Hyman, L. M. 825 Hynd, G. W. 768, 770, 772
938
I Ianco-Worral, A. 779 Igoa, J. 75 ff, 80 f, 85, 87 Illes, J. 396, 399 f Illmer, R. 830 Inata, B. A. 819 Inbody, S. B. 401 Ince, L. P. 354 Ingham, J. C. 888, 890 Ingham, R. J. 886, 888 ff, 894 f Inglis, S. 699 f Ingram, D. 560 f, 581, 590, 611, 629 ff, 688, 817, 826, 847 Ingram, J. 800 Ingram, J. C. 537, 539 Ingram, J. C. L. 289, 437, 552 Ingram, T. S. 829 Ingram, T. T. S. 586, 836 Ingvar, D. H. 220, 274 Inhelder, B. 582, 631 Inoue, N. 112 Iran-Nejad, A. 669 Irigaray, L. 274, 341 Iritani, S. 396 Irle, E. 124 Irwin, J. V. 483 f Irwin, O. C. 454, 842 Isaacs, E. A. 22 Isaacs, E. B. 590 Ishiai, S. 271 Isserlin, M. 162 Isshiki, N. 861 Itoh, K. 471 Itoh, M. 198, 201, 204 ff, 436, 446 Iwata, M. 265, 271 f Iwata, W. 130 Izdebski, K. 433, 460
J Jabès, E. 96 Jackendoff, R. 158, 170 Jackson, C. 912 Jackson, C. 392 Jackson, J. H. 93, 100, 103 ff, 123, 132, 213, 218 f, 240, 262, 311, 314, 444, 872
cf.Hughlings Jackson, J. Jackson, N. E. 715, 770 f Jackson, P. L. 672 Jackson, R. K. 805 f Jacobsen, C. C. 123 Jacobsen, E. 851 Jacoby, C. G. 810 Jaeggi, A. 631 Jaffe, J. 50, 125, 220 Jaffe, M. B. 849 Jakimik, J. 58, 62 Jakobson, R. 59, 109, 162, 190, 279, 420 Jalinous, R. 131
89. Index of Names
James, J. E. 894 James, S. 778 f, 781 f Jan, J. E. 680 Jancey, C. 735 Jancovic, J. 463 f, 507 Janowsky, D. S. 518 Jansson, B. 412 Jarecki, J. 306 Jarvella, R. J. 21 Jaynes, J. 220 Jeannerod, H. 654 Jeeves, M. A. 748 Jefferson, G. 19 f, 28, 551 Jehle, P. 897 Jenkins, E. C. 808 Jenkins, J. J. 140, 353, 365 Jenkins, J. R. 754, 763 Jenkins, S. 601 Jensen, W. R. 818 Jerger, J. 500, 904 Jerger, S. 500 Jernigan, T. L. 588 Jerusalem, M. 878 Jespersen, O. 216 Jewer, D. D. 486 Jiménez-Pabón, E. 353, 365 Joanette, Y. 112, 193 f, 199, 201 ff, 384 ff, 470 Job, R. 155, 182 Johannsen, H. S. 495, 497, 876, 881 Johannsen-Horbach, H. 298, 484 Johns, D. F. 444 Johnson, A. 828 Johnson, B. H. 488 Johnson, C. 771 Johnson, D. 718 Johnson, G. F. 887 Johnson, L. J. 886, 888 Johnson, M. L. 598, 697 Johnson, W. 864, 871, 877, 880, 885 Johnson-Laird, P. N. 4, 12, 154, 315, 903 Johnston, C. 599 Johnston, J. R. 579 ff, 606, 612, 621 f, 629, 631 f, 634 ff, 641, 645, 775, 782 Johnston, R. B 589 Johnston, R. S. 736, 738, 750 Jolivet, R. 267 Jones, A. 688 Jones, A. C. 375 Jones, C. D. 788, 791 f Jones, E. G. 123 Jones, E. V. 360, 367 Jones, J. 802 Jones, J. E. 549 Jones, J. L. 13 Jones, K. L. 693 Jones, L. V. 104, 107, 109 f, 137, 139 f, 144, 146
Jones, O. H. M. 691 Jones, W. 435 Jongen, E. 229 Jongeward, R. H. 760 Jongman, A. 8 Jordan, M. I. 421 Jorgensen, E. O. 411 Jorm, A. F. 715, 734, 736 f, 778 Joseph, A. 598 Josiassen, R. C. 399 ff Joyce, J. 96 Juarez, L. 296 Junefelt, K. 680, 685 Junn, E. 634 Jusczyk, P. W. 561 Justin, C. 601 f Jüttemann, G. 880
K Kaas, J. H. 122 Kabe, S. 127 Kaga, K. 292 Kahn, J. 581 Kail, R. V. 760 Kaiser, A. P. 641, 643, 691, 697 Kaiser, G. 232, 330 Kaisse, E. 185 Kajaste, S. 410 f, 413 Kallman, C. 622, 627 Kalotkin, M. 866 Kamalashile, J. 838 f Kamhi, A. G. 579 f, 612, 621 f, 629, 631 ff, 637, 711, 714, 716, 756, 774 ff, 780 ff Kanner, L. 768, 795, 804, 806 ff, 811 ff Kanshepolsky, J. 500 Kant, I. 314 Kao, H. S. 70 Kaplan, B. 596 Kaplan, E. 59, 100, 103 f, 109 f, 115, 138, 142, 187, 216, 238, 264, 273, 295, 320, 339, 341, 356, 396, 449, 900, 911 Kaplan, J. 220 f Karagan, N. 792 Karis, D. 70 Karle, H. 735, 762 Karmiloff-Smith, A. 565, 567, 614, 773 f Karnell, M. P. 486 ff, 861 Kartsounis, L. D. 252 Kasari, C. 692 Kasbohm, M. 755 Käsermann, M. L. 550 f, 553, 799 Kastein, S. 851 Kaston, N. 643 f, 782 Kaszniak, A. W. 273 f, 389, 392, 394, 396, 400 Katz, J. 830 f Katz, J. J. 153
89. Index of Names
Katz, N. 567 Katz, R. 739, 779 f Katz, R. B. 102 Katz, W. 441 Katz, W. F. 200, 206 Kauders, O. 281 Kauffman, J. M. 761 Kausler, D. H. 903 Kavale, K. 588, 715 ff Kavanagh, K. T. 486 Kavrie, S. 273 Kawahata, N. 130, 271 Kawamura, M. 130, 265, 271 Kawano, M. 861 Kawas, C. 913 Kay, B. A. 416, 418 Kay, D. A. 563 Kay, J. 139, 142, 147 f, 154, 253 ff, 911 Kay-Raining Bird, E. 690 Kayton, L. 530 Kazdin, A. E. 145 Kazniak, A. W. 340 Kean, M.-L. 58, 148, 164, 174, 179, 181, 297 Kearns, K. P. 145, 366, 374, 481 ff, 854 Keating, P. 36 ff, 40 f Keenan, E. L. 25 Keenan, E. O. 569 Keil, F. 88 Kekelis, L. S. 682, 684 f Kellar, P. 383 Keller, E. 112, 193, 202 ff, 207, 435 Keller, L. 184 Kelley, J. 390 Kelley, J. J. 500 Kelly, C. A. 668 Kelly, J. 430 Kelly, M. 88 Kelly, M. P. 402 Kelly, P. 896 Kelso, J. A. S. 6, 416 ff, 42 ff Kelter, S. 20, 333, 540 Kemp, J. 579 Kemp-Fincham, S. I. 859 Kempen, G. 5, 7, 12, 25, 85 Kemper, S. 901, 905 f, 908 ff Kemper, T. 274 Kemper, T. L. 810 Kempler, D. 219 ff, 292, 392, 657, 912 Kendell, R. E. 537, 539, 552 Kendon, A. 50 Kendrick, D. C. 515 Kennedy, J. L. 399 Kent, J. F. 439 f, 449, 843, 846 Kent, R. D. 40, 198, 213, 418, 429, 439 ff, 446, 448 f, 453 ff, 463, 468 f, 471 f, 484, 841 ff, 846 f, 859 ff Kenyon, E. 864
939
Kephart, N. C. 754 Kerbeshian, J. 806 Kernan, K. T. 689 Kerner, E. 488 f Kerr, J. 742 Kerr, M. M. 760 Kerschensteiner, M. 105, 107, 109, 306, 314, 317, 320, 653 Kerstholt, M. 757 f Kertesz, A. 51, 98 f, 103 f, 109 f, 112 ff, 124 ff, 137 f, 142, 156, 182, 187, 189, 198, 255 ff, 264, 267, 270, 273 f, 310, 315, 341, 344, 379, 392, 447, 745, 912 Keßler, B. 894 Kessler, J. W. 768 f, 771 Keyser, A. 19, 107 Keyserlingk, D. Graf von 105, 108, 213 Khoshbin, S. 462 Kidd, K. K. 879 Kidd, M. 389 Kiernan, C. 692, 818 Kiersch, M. E. 900 Kilborn, K. 175 Kim, R. 482 Kimelman, M. D. Z. 291 Kimura, D. 16, 125, 127, 195, 321 f King, C. M. 669 King, K. 537, 539, 552 Kinsbourne, M. 103, 219, 252 f, 315, 335, 586, 588 ff, 649 f Kinsella, G. 373, 375 Kintsch, W. 900, 904, 906 f Kinzel, P. 283 Kiparsky, P. 185, 246 Kipfmueller, L. J. 486 Kirchner, D. M. 297 Kiritani, S. 453, 471 Kirkwood, C. R. 830 Kirkwood, M. E. 830 Kirov, K. 535, 798 Kirshner, H. S. 264, 270, 298, 402 Kirstein, L. 534, 549 ff Kitajima, K. 437 Kitamura, K. 271 f Kitchell, M. M. 768 f, 772 Kitchen, D. 775 Klatt, D. H. 8, 36, 246 Klauer, K.-J. 146 f Klawans, H. L. 396 Klee, A. 411 Klee, T. 566 Klee, T. M. 661 Kleffner, F. R. 588 f Kleiman, G. M. 736 Klein, A. 96 Klein, D. F. 763 Klein, E. 166, 569 Klein, J. D. 610, 830
Klein, K. 220 f Klein, S. K. 660, 664 Klein, W. 24 Klein-Konigsberg, E. 783 Kleinschmidt, M. 827 Kleist, K. 99 f, 107, 161, 379, 748 Klich, R. J. 446 Kliegl, R. 719, 734, 738, 762 Klima, E. S. 127, 318, 674, 817 Klinowski, J. 389 Klonoff, H. 140 f Klopp, K. 702 ff Klos, T. 514, 517 f Klouda, G. 848 Kluin, K. 470 Knapp, M. 123 Knell, E. 507 f Knesevich, J. W. 273, 391 Knight, C. 435 Knight, R. 514, 517 Knoll, R. L. 6, 418 Knopman, D. S. 127 f, 219 Knott, J. 865 Knowles, J. C. 488 f Knox, C. 726 Koch, U. 298, 511 Koegel, R. 815 Koemeda-Lutz, M. 292 Koenig, L. 622, 774, 776 f, 781 Koenig, W. 70 Koff, E. 295, 588 Koh, S. D. 529 f Kohn, B. 590 Kohn, S. E. 5, 58, 103, 112, 189, 194, 197 ff, 207, 345, 357 Koivuselka-Sallinen, P. 201, 205 Kolb, H. P. 166 Kolers, P. A. 328 Koliatsos, V. E. 465 Kolinsky, R. 757 Kolk, H. 19, 22, 29, 107, 162, 174, 290, 337 f, 346 Koller, J. J. 102, 336, 338, 346 Kolvin, I. 788 ff, 795, 800, 804, 806 König, U. 759 Konno, K. 127 Konstantareas, M. M. 701 f, 805, 809 f, 813 f, 816 ff Kooistra, C. A. 267, 270 Kopelman, M. D. 341 Kopp, H. G. 446 Korngold, B. 613, 776 Kornhuber, H. H. 105, 127, 381 Kornyey, E. 127 Kosc, L. 326 Koss, E. 274 Kosslyn, S. 581 Kossow, H.-J. 756, 759 f Koster, C. 148, 297 Kostic, A. 27, 185 Kotila, M. 410 f, 413
940
Kowal, S. H. 50 Kozhevnikov, V. A. 38, 416, 418, 421 Kraat, A. W. 354 Kracke, I. 632, 706 Kraepelin, E. 523 Krakow, J. 569 Krakow, R. 37, 39 f, 42 Kramer, E. 495 Kramer, J. 216 Kramer, R. 795 Krashen, S. 590 f Kratochwill, T. R. 145, 792 Kraus, J. F. 836 Krause, G. S. 410 Krause, R. 895 Krauss, R. M. 22, 296 Krauth, J. 143 Krech, H. 895 Kreindler, A. 219 Kreitler, H. 551 Kreitler, S. 551 Krekjarto, M. von 512 Kremin, H. 227, 255 Kretschmer, R. 699, 708 Kretschmer, R. E. 661, 670 f Krieg, W. J. S. 128 Kriegsmann, E. 641, 644, 699 f Krippendorff, K. 143 Kroll, R. 867 Kruger, S. D. 507 Krystal, H. 511 Kudrjawzewa, W. 797 Kuehn, D. P. 416, 459, 859 Kuenzel, H. 39 Küfferle, B. 552 Kugler, B. T. 514 Kugler, P. 44 Kuhl, D. E. 129, 398 Kuhl, P. 886 Kuiken, D. 24 Kulikowski, J. J. 735 Kumin, O. L. 320 Kuny, S. 514 Kunz, T. 381 Kunze, L. H. 664 Kupersmith, M. 396 Kupietz, S. S. 792 Kurlan, R. 504, 506 f Kurland, L. T. 389 Kusske, J. A. 395 Kussmaul, A. 499, 742 Kutas, M. 131 Kuypers, H. G. J. M. 123 Kwapil, T. R. 528 Kwiatkowski, J. 826, 847 Kynette, D. 901, 905 f, 908 ff
L La Barge, E. 391 LaBerge, D. 718
89. Index of Names
Labov, W. 18 Lacan, J. 546 Lackner, J. R. 7, 29 Lacoste-Utamsing, C. de 211 Lacy Costello, A. de 252, 379 f Ladd, D. R. 8 f Ladefoged, P. 199 f Ladusaw, W. A. 153 Laffal, J. 536 Laguna, J. F. 267 Lahar, C. J. 905 Lahey, E. 610 Lahey, M. 563, 565, 575, 577, 579 ff, 692, 775 Lahiri, A. 8 f Laiacona, M. 156 Laine, M. 385 Laine, T. 437 Laine, T. N. 264, 270 Lakoff, G. 17 Lakoff, R. T. 552 Lalljee, M. G. 48 f LaLonde, F. 391 Lambert, D. L. 760 Lambert, W. E. 280 Lamoureux, M. 386 Lancashire, M. 515 Lance, J. W. 453 Landahl, K. L. 487 f, 862 Landau, B. 681 ff Landau, W. M. 588 f Landau, W. M. 363 Landis, T. 219 Landon, M. 389 Lang, A. 506 Lang, A. E. 396 Lang, B. R. 486 Lang, C. 137 f, 143 Langacker, R. 873 Lange, H. W. 398 f, 463 Langer, K. G. 397 Lanin-Kettering, I. 551 Lanke, J. 388 Lansdell, H. 657 Lanto, A. 220 Lanyon, R. I. 894 f LaPointe, L. L. 139, 234, 364, 445, 447 ff, 463, 474, 481, 483 f, 848, 850 ff Lapointe, S. 81, 165, 184 Larbaud, V. 226 Large, B. 718 LaRiviere, C. 487 Larsen, R. E. 852 Larsen, S. C. 754 Lasaga, M. I. 902 f Lashley, K. S. 68, 120, 313, 418, 649 f, 657 Laskin, R. L. 861 Lasky, E. Z. 702 ff Lassen, N. A. 220 Latham, C. 643
Latham, N. 264 Laubstein, A. S. 63 Lauciello, F. R. 489 Laughlin, S. 357 Laurent, B. 267, 270 Laver, G. D. 903 Laver, J. 59, 76 Lavy, S. 395 Lawler, R. W. 328 Lawson, J. S. 549 f Lawson, L. 663 Layton, T. L. 690, 692, 819 Le Witt, P. A. 396 Le May, A. 295 Le Savoureux, X. 234 Le Carré, J. 94 Lea, J. 706 Leahy, J. 827 f, 831 f Leaper, C. 800 Lebel, M. 264 Leborgne 226 Lebrun, Y. 107, 226, 228 f, 231 ff, 330, 444 f Lechtenberg, R. 468 Leckman, J. F. 507 Lecky, B. 498 Leclercq, C. 328 Lecours, A. R. 58, 110, 112, 127 f, 187 ff, 193, 203, 283, 386, 444, 448, 534 ff, 544 ff, 552, 798 Ledoux, J. 293 Lee, L. 574, 578 Lee, R. 633 f, 775 ff, 781 f Leeper, H. A. 446 Lees, A. J. 395, 397 Leff, J. 514 f, 551 f Lehiste, I. 36, 209 Lehman, W. L. 487 Lehmkuhl, G. 317 ff, 321 Leibovitz, S. F. 818 Leidner, D. 37 Leifer, J. 691 Leiguarda, R. 281 Leiman, J. M. 13 Leischner, A. 100, 105 ff, 110 f, 114, 262, 264, 281 Leith, W. R. 454, 840 Leleux, C. 235, 330 Lelli, S. 465 LeMay, M. 588, 810 Lemme, M. L. 446, 459 Lempert, H. 589 f Lencher, O. 779, 832 Lenin, W. I. 226 Lenneberg, E. H. 6, 284, 586 f, 590 f, 596, 598, 647 ff, 654, 656 f, 666 Lennox, C. 809 Lenz, G. 552 Lenz, M. 760 Leodolter, R. 549, 551, 553
89. Index of Names
Leon, M. J. de 391 f Leonard, L. B. 293, 576, 580 f, 559 f, 609 f, 615, 617, 619 f, 626 f, 629 f, 635 f, 640 ff, 702, 704, 827 f Leonard, R. J. 488 f Leonhard, K. 327 Leopold, W. 283, 826 Lepage, Y. 386 LeResche, L. 525 Lerner, G. H. 30 Lerner, R. M. 880 Lesk, D. 127 Lesser, R. 148, 256, 265 f, 269, 271, 354, 358, 362 f, 365, 448, 905 Lesser, R. P. 130 f Lettich, E. 130 Levelt, W. J. M. 3 ff, 7, 13, 16, 19 f, 24 f, 29 f, 59, 75, 79, 82, 84, 86, 88 f, 163, 175, 179, 193, 242, 245 f, 908, 910 Levenson, R. A. 589 Leventhal, D. D. 530 Leventhal, H. 212 LeVere, N. D. 657 LeVere, T. E. 657 Levin, A. 762 Levin, B. E. 396 f Levin, H. 49 f, 712 Levin, H. S. 219, 652 Levin, S. 514 Levine, D. N. 127 Levine, H. L. 219, 588 Levinson, S. C. 18, 20 f, 361 Levis-Matichek, G. 550 Levitsky, W. 125 Levitt, A. G. 58, 60 Levitzky, W. 587 f Levy, C. 614 Levy, J. 219 Levy-Valensi, J. 546 Lewinson, M. 519 Lewis, B. 622, 636, 829 Lewis, D. A. 389 Lewis, J. 211 Lewis, J. M. 802 Lewis, M. 61, 602, 691 Lewis, R. B. 754 f Lewisohn, P. L. 529 Lewkowicz, N. K. 757 Ley, R. G. 212 Leybourne, P. C. 791 f Lezak, D. 311 Lhermitte, F. 58, 99, 110, 127, 157, 181, 187 f, 226, 231, 315, 335, 356, 448, 544, 586, 650 ff, 654
cf. L’Hermitte, F. L’Hermitte, F. 281 Li, E. C. 296 Libben, G. 285 Liberman, A. M. 8, 127 f, 416, 711, 718, 759
941
Liberman, D. 781 Liberman, I. Y. 671, 673, 736 ff, 759, 778 ff Liberman, R. P. 553 Libet, J. M. 519 Lichtheim, L. 100, 107, 109, 112, 131, 238 ff, 249, 262, 264, 379, 499 Lie, A. 757 Liebergott, J. 610, 613 f, 617, 776, 778, 875 Lieberman, A. 396 Lieberman, P. 16, 47, 342, 862 Liebmann, A. 574, 893 Liepmann, H. 227, 235, 318, 444, 447, 500 Lieven, E. V. M. 562 Lifrak, M. D. 385 Lifter, K. 565 Light, L. L. 902 ff, 907 Lightbown, P. 564 f, 598 Liles, B. 579, 621, 775 f, 781 Liles, B. Z. 314, 328 Lillo-Martin, D. 675 Lillyquist, T. D. 906 Lim, E. K. 497 Limber, J. 565 Lincoln, N. B. 352, 375 Lincourt, J. M. 550 Lindamood, L. P. 886 Lindblom, B. 36, 416 f, 421 Lindeboom, J. 402 Lindeneg, O. 411 Linder, B. 736 Linder, M. 714 Lindgren, A. G. H. 401 Lindner, K. 580 Lindsay, D. D. 463 Linebarger, M. C. 165, 177, 338, 346, 360 Linebaugh, C. W. 102, 220, 455, 460, 471 Linell, S. 365, 374 Lingoes, J. C. 141 Linville, R. 418, 868 Lishman, W. A. 516 Lisker, L. 421 Liss, J. M. 198, 446 Lissauer, H. 501 List, H. 560 List, J. A. 902 Litowitz, B. 550 Little, W. J. 835 Llabre, M. M. 396 f Lloyd, G. G. 516 Lloyd, H. 788 f, 791 f Lloyd, L. L. 291, 688 Lo Verso, F. 267 Lock, A. 817 Locke, J. L. 333 Locke, S. 184 Lockhart, R. S. 333 Loebell, H. 24 f, 73
Löfqvist, A. 36, 39, 43 f, 418, 421, 436 Loftus, N. 867 Logan, G. D. 330 Logemann, J. A. 460, 465, 488, 859 Logie, R. 340, 908 Logue, P. 231 Logue, V. 335 Lokker, R. 590 Lolas, F. 510 ff Lomas, J. 298, 365, 375 Lombardi, L. 21, 905 Long, J. 69 Long, J. S. 815 Longuet-Higgins, F. R. S. 329 Loonen, M. C. B. 228, 591, 652, 654 Looney, P. 609, 612 Lord, F. M. 143 f, 147 Lorenz, M. 515 f, 518, 535 Lorge, I. 630, 814 Lotter, V. 811 Lotz, W. 844 Lounsbury, F. G. 46 Lovaas, O. I. 811, 814 ff Love, R. J. 453, 455, 836 f Lovegrove, W. 735 Lovelace, E. A. 901 f Loveland, K. A. 683 Lovell, K. 631 Lovett, M. W. 730, 757 Low, J. M. 463 Low, L. Y. 757 Lowe, A. 626, 631 Lowe, D. 905 Lowe, J. B. 692 Lowel, S. H. 514 Lowell, E. L. 667, 670 Lubit, E. C. 852 Lubker, J. 36, 417 f Lucariello, J. 562 Lucas, S. A. 680 Lucchelli, F. 158 Luce, P. A. 8 Lucius-Hoene, G. 295 Luckau, J. 575 Lüders, H. 130 f Ludlow, C. L. 127, 399, 436, 438 f, 462 ff, 505, 507, 637, 646 Ludwig, O. 24 Lukatela, G. 27, 176, 185 Lund, N. 577 Lundberg, I. 712, 715, 718 f, 725, 755, 757, 778, 782 Lunzer, E. 631 Luria, A. R. 100, 104, 107, 110, 115, 129, 194, 235, 263, 274, 283 f, 319, 353, 356 f, 359, 380, 447, 649 f, 653, 657, 829 Luschei, E. S. 843, 846 f Lutz, J. 801
942
Luzzatti, C. 149, 314, 402 Lyle, J. G. 734 f Lyle, O. 399 Lylyk, P. 281 Lynch, J. L. 859 Lyon, G. 651 ff Lyons, J. 217 Lytton, H. 599
M Maassen, B. 88 f Macaluso-Haynes, S. 304 ff Macaruso, P. 729 Macaulay, R. 598 Mace, F. C. 553 Mace, W. 420 MacGillivray, I. 599 MacGregor, C. 712, 720, 728 Machemer, P. 759 f Machetanz, J. 441 Mack, J. E. 815 Mack, L. 291, 394 Mack, W. 394, 912 MacKain, K. 589 MacKay, D. G. 53, 55, 57 f, 60, 67 ff, 76, 78, 89, 900 f, 903, 910 f MacKay, D. M. 122 MacKay, I. R. A. 75 Macken, M. A. 681, 826 MacKenzie, R. A. 114, 128 Maclay, H. 47 Maclean, M. 718, 778 f MacLean, R. 715, 737, 778 MacMahon, B. 809 f Macnamara, J. 567 MacNeilage, P. F. 68, 200 ff, 206, 322, 416, 421 Macready, G. B. 148 MacWhinney, B. 5, 26 f, 58, 60, 185, 309, 578, 634, 873 f Madden, D. J. 902 f Magaro, P. H. 553 Magen. H. S. 36 Mägiste, E. 284 f Magno-Caldognetto, E. 41 Magnusson, E. 609, 826 Mahendra, B. 401 Maher, B. A. 515, 524 ff, 534 Mahl, G. F. 513, 518 Mahler, M. S. 768, 795, 804 Mahlmann, J. 394 Mahoney, G. 691, 700, 704, 706 Mahowald, M. W. 125 Mahy, J. 328 Majenson, T. 373 Majid, A. A. 486 Makkai, J. E. 217 Malaprop, Mrs. 248 Malatesha, R. N. 716 Maletta, G. J. 395 Malinsky, A. E. 149
89. Index of Names
Malone, M. 373 Malone, R. 373 Malony, H. N. 553 Mamelak, A. 528 Mammucari, A. 106, 295 Mancall, E. L. 399 ff Manchester, J. 901, 909 Mandelkorn, T. 896 Manelis, L. 220 Manis, F. 727, 758 Manktelow, R. T. 486 Mann, M. B. 487 Mann, V. A. 718, 737, 778 Mann, W. 497 Mannhaupt, G. 715, 757 f Mannuzza, S. 553 Manschreck, T. C. 515, 525 ff Manschreck, R. 866 Manuel, S. 37 Marcé, M. 262 Marcel, A. J. 255, 257 f, 344 Marcel, T. 746 Marchal, A. 37 f Marchant, R. 701 Marcie, P. 262, 264 Marcus, M. P. 334 Marek, A. 292 Margar-Bacal, F. 861 Marge, M. 575 Margolin, D. I. 255, 265 f, 269, 312, 394 Margules-Lavergne, M. 127 Mariano, G. 321 Marie, P. 103, 105, 128, 314, 361, 378 f, 648 Marin, O. S. M. 155, 157, 163, 166, 255 f, 258, 267, 274, 338, 343, 392, 500 f Mark, L. S. 736, 738 Markham, C. H. 398 Markides, A. 667 Marks, S. 693 Marquardt, T. P. 291, 296, 440, 484 Marr, D. 251 Marsden, C. D. 381, 396, 461 f, 507 Marsh, G. 712, 756 Marsh, H. W. 715 Marsh, J. T. 131 Marshall, J. C. 96, 103 f, 115, 154, 163, 181, 242 ff, 251, 254 f, 257 ff, 267, 311, 313, 343 f, 718, 728, 743, 745 ff, 750, 770 Marshall, R. C. 206, 363, 366 f, 440 Marslen-Wilson, W. 7 ff, 13, 176 f, 182, 184, 245 Martilla, R. J. 391 Martin, A. 340 f, 390 f, 912 f Martin, A. D. 145, 363 Martin, D. C. 394
Martin, F. 735 Martin, H. 691 Martin, J. R. 549 ff, 802 Martin, L. J. 465 Martin, N. 86, 190, 340, 343, 346 Martin, N. D. T. 693 Martin, R. 441, 886, 888 Martin, R. C. 26, 333, 338, 747, 908 Martin, W. R. W. 398 Martindale, C. 506 Martinet, A. 188 Martinkosky, S. 486 Martins, I. P. 321, 654 Martins, O. J. 489 Martone, M. 399 f Marttila, R. J. 264, 270 Marty, M. 514 f Marty, P. 510 Martyn, P. 366 Marx, H. 714 f Marx, R. 782 Masdeu, J. C. 379 Mason, J. C. 768 Mason, J. M. 712, 770 Masson, V. 367 Mastergeorge, A. 641, 644 Masters, G. N. 144 f Masterson, J. 254, 728, 744, 749, 775 Masullo, C. 109 Matas, L. 596 Mateer, C. A. 127, 130, 386 Matey, C. 708 Mather, V. G. 513 ff Mathews, C. 307 Mathieson, G. 395 Matison, R. 396 f Matthei, B. 176 Matthei, E. H. 174 Matthews, R. 715, 737, 778 Mattinger, M. 600 f Mattingly, I. G. 8, 773 f Mattison, R. 601 Mattson, P. 717 Mauer, D. 634, 637, 775, 777, 780 Mauer, H. 691 Mauldin, M. 459 Maurer, H. 700 Mavlov, L. 502 Mawhood, L. 600 ff Maxfield, K. E. 682, 685 Maxwell, S. 775 May, K. 797 May, E. B. 305, 307 Mayendorf, E. 121, 127 Mayer, K. 164, 229 Mayeux, R. 391, 396 f Mayfield, J. 597 Maylor, E. A. 900 Mazaux, J. M. 129
89. Index of Names
Mazurski, P. 357 Mazzocchi, F. 127 Mazzucchi, A. 107, 165, 337, 344 f McAdam, D. 865 McAndrews, M. P. 902 f McBride, K. E. 104 f, 107, 109 f, 112, 137, 279, 310 McBurney, P. H. 401 f McCabe, A. 701 f McCabe, K. D. 810 McCabe, P. 98, 114, 127, 264, 270, 315 McCall, G. N. 852, 867 McCarley, R. W. 534 McCarthy, R. A. 156 ff, 178, 255 f, 311, 340, 344 ff, 358, 380, 745 McCauley, C. 688, 690 McCauley, R. J. 138, 574 McClean, M. 866 f McClelland, J. L. 9, 26 f, 121, 123, 245, 252, 257, 347, 713, 758, 900 McCloskey, L. 569 McCloskey, M. 138, 145, 329 f McClure, P. H. 768, 770, 772 McConell, K. 830 McConkey, R. 691 McConnell-Ginet, S. 170 McCrae, R. R. 900 McCulloch, W. S. 121 McDonald, A. 820 McDonald, E. T. 836 f, 839 f, 853 McDonald, F. I. 847 McDonald, S. 386 McDowell, F. H. 397 McGarr, N. S. 436 McGee, R. 600 ff, 716, 719 McGhie, A. 549 f McGinnis, A. R. 685 McGlone, J. 125 McGregor, C. J. 756 McGregor, K. 642, 644 f McGuirk, E. 352 McHenry, M. A. 437 McHugh, P. R. 391 f McInally, K. 365 McKean, K. 526 McKenna, P. 154 McKenna, R. A. 129 McKenzie, D. 716, 719 McKeown, T. 598 f McKinstry, R. E. 489 McLaughlin, B. 526 McLaughlin, T. F. 760 McLean, W. T. 654 McLoughlin, P. 155 McMiken, B. 460 McMullen, P. A. 156 McNay, A. 795, 804 McNeil, M. R. 105, 198, 291, 434, 439, 445 ff, 581, 847
943
McNeill, D. 24, 59, 85, 295 McNicol, D. 537, 539 McNinch, G. 779 McNutt, J. 827 McPherson, H. 816 McPherson, P. M. 808 McQuarter, R. 641, 643 McReynolds, L. J. 145 McReynolds, L. V. 837 f, 841, 853 f McTear, M. 569 McWilliams, B. J. 858, 860 f Mead, J. 482, 843 Meadow, K. P. 673 ff Meadows, J. C. 381 Meeks, L. M. 273 Mehegan, C. C. 768 Mehler, J. 174 Mehringer, E. J. 487 Meichenbaum, D. H. 754 Meier, E. 292 Meikle, M. 352 Mein, R. 692 Meininger, V. 157 Melamed, E. 395 f Melin, L. 895 Meline, N. 777 Meline, T. 621, 776 f Mellits, E. D. 589 Mellits, D. 622, 627 Meltzoff, A. N. 562 Mendelsohn, M. 210 Mendelsohn, S. 281 Mendez, M. 342, 396 f Mendlewicz, J. 516 Menn, L. 5, 107, 148, 164 f, 337, 559 ff, 692 Mentz, L. 660 f, 663, 669 Menyuk, P. 559 ff, 607, 609, 611 ff, 616 f, 622, 697, 773 f, 776, 778 f, 781, 875 Meringer, R. 76, 164, 229 Merory, J. 264 Merrill, E. C. 690 Merrit, D. 621 Mervis, C. B. 700 Merwin, G. E. 497 Merzenich, M. M. 122 Meselam, L. 559 Mesher, R. A. 498 Meshoulham, U. 734 Mesibov, G. 816 Messick, C. 631, 642, 644 Messick, S. 140 Mesulam, M. M. 120, 211 Metter, E. J. 129, 333, 376, 396, 398, 463, 483 Metz, D. E. 439 Meudell, P. R. 333 Meulenbroek, R. G. J. 66, 69 Meyer, A. S. 5, 86 Meuse, S. 296 Meyer, D. E. 902
Meyer, M. M. 156 Meyer, V. 895, 897 Meyer-Osterkamp, S. 553 Meyers, R. 314 Meyers, R. H. 398 Meyers, S. C. 886, 888 f Meyerson, M. D. 488 Meynert, T. 127 Mezey, G. 602 Mezger, G. 106 Miceli, G. 107, 109, 154, 164 f, 178, 181, 183, 185, 199, 266, 269, 271, 333, 337, 344 f, 384 Michaux, L. 795 Michel, D. 221 Michel, F. 367 Michelow, D. 385 Miezejeski, C. M. 692 Migault, P. 546 Miklowitz, D. J. 551 f Milani, N. 655 Milavetz, J. J. 528 Milberg, W. 155, 394, 900 f Mildworf, B. 396 Miles, T. R. 715, 717, 730, 755 f, 759, 761 Millay, K. 726 Miller, C. 74 Miller, C. A. 25 Miller, C. L. 365 Miller, D. 199, 201, 203 Miller, E. 392, 397 Miller, G. A. 4, 154, 518 f, 529 f, 531, 550, 907 Miller, J. 409 ff Miller, J. G. 551 Miller, J. P. 566, 574, 576, 579 f Miller, P. D. 761 Miller, R. 559, 562, 681 Miller, S. 530 Miller, W. K. 540 Mills, A. E. 667, 680 ff, 685 Mills, B. 699 f Mills, J. R. 770 f Mills, K. R. 131 Mills, M. 597 Milner, B. 333, 588, 590, 648, 655 Milroy, A. L. 363, 365 Minear, W. L. 835 Miner, L. E. 681 Minifie, F. 40 Minkowski, M. 279 ff Minsley, G. E. 486 Miron, M. S. 162 Mishkin, M. 123, 125, 389 Mishler, E. G. 802 Mitchell, D. B. 900 Mitchell, S. J. 465 Mitchum, C. C. 211, 343 Mittenecker, E. 525 Mittler, P. 599 Mitto, H. 482
944
Miyake, Y. 327 Mizutani, T. 395 Mlcoch, A. G. 448 Mochizuki, H. 130, 271 Moely, B. E. 760 Moes, E. J. 411, 413 Mogford, K. 666 f, 672, 674 f Mohide, A. 376 Mohr, J. P. 108, 127, 129, 447 Molfese, D. L. 589 Molino, M. 526 Moll, K. L. 37, 39, 416, 418 Molloy, R. 221 Molsa, P. K. 391 Monakow, C. von 124 Monoi, H. 198, 201, 204 ff Monroe, P. A. 498 Monsel, Y. 296 Monsell, S. 6, 341 Montanelli, D. 670 Montessori, M. 760 Montgomery, A. A. 672 Montgomery, K. 399 Moog, J. 668 Moon, J. 844, 845 Moore, B. D. 219 Moore, D. J. 489 Moore, G. P. 437 Moore, M. E. 579 Moosy, H. 401 f Mora, G. 792 Morais, J. 23, 590, 712, 718, 757 f, 779, 781 Morasch, H. 481 ff, 496 More, S. T. 553 Moreau, T. 591 Morehead, D. 631 Moreines, J. 333 Morey, R. 24 f, 73 Morgan, A. 379 Morgan, B. R. 826 Morgan, D. 634 Morgan, P. 713 Morgan, W. J. 437 Morgan, W. P. 742 Morgenstern, C. 94 Mori, E. 499, 501 Morice, R. D. 537, 539, 552, 800 Morley, E. 598 Morr, K. E. 437, 861 Morris, H. 845 Morris, H. L. 858, 860 f Morris, J. C. 273, 390 f, 402 Morris, R. 716 f, 719 Morris, R. G. 340 f, 906 Morris, S. E. 839, 849 f Morrison, F. J. 758 Morrison, J. H. 389 Morrissey, P. 433 Morrow, D. G. 12 Morstyn, R. 534 Mortimer, J. A. 390, 395 ff Morton, J. 4, 6, 95, 102, 154,
89. Index of Names
174, 242, 245, 256, 259, 266, 344, 744, 749 Morucci, J. P. 762 Moscovitch, M. 252, 384 Moseley, M. J. 699 f, 703 f, 707 Moser, E. 712 Moser, M. 252 Moses, I. C. A. 515 Moses, J. A. 385, 399 Moses, P. J. 514 Moss, T. 789 Mossige, S. 551 Mota, M. 279 Motley, M. 57 ff, 78 Motomura, N. 499 Motta, M. 233 Mounin, G. 99, 181 Mountcastle, V. B. 122 Mowrey, R. A. 75 Moy, A. C. 390 f Mross, E. F. 308 Mueller, E. 569 Mueller, J. H. 903 f Mueller, R. A. G. 21 Mugford, J. 374 Mühlemann, T. 19 Mulac, A. 578 Mulder-Hajonides van der Meu- len, W. R. 518 Mulford, R. C. 681 ff, 685 Mulhall, D. J. 363, 373 Müller, D. J. 372 ff Muller, F. 478 Müller, L. 512 Mulley, G. P. 352, 375 Mulligan, M. 434, 446, 847 Mulvena, A. 660, 663 Mundy, P. 692, 704 f Mungas, S. 530 Munhall, K. G. 35, 43 f, 67, 418, 420, 422, 447 Munk, H. 120 Murata, S. 271 ff Murawski, B. J. 413 Murdoch, B. E. 273, 289, 437, 827 Murphy, D. L. 516 Murphy, J. F. 760 Murray-Branch, J. 641 f, 644 Murray, D. C. 518 Murray, N. M. 131 Murray, T. 430 Murray, T. J. 896 Murry, T. 446 M’Uzan, M. de 511 Myers, D. 154 Myers, F. L. 865, 888 ff Myers, P. S. 220 Myerson, R. 163, 176 Myklebust, B. M. 454 f Mysak, E. D. 910 Mysak, E. 836, 849 f, 852
N Nachmani, G. 549 f NacNeilage, P. 440 Nadeau, S. E. 107, 129 Nadler, R. D. 434 Naeser, M. A. 110, 125, 127 ff, 220, 357, 379, 438, 500 ff, 588, 907 Nagafuchi, M. 590 Nagata, K. 130, 271 Nair, R. 574, 601 Nakles, K. O. 355 Nasrallah, H. A. 534 Nass, R. D. 98 Nathan, D. 698 Nathan, R. G. 715 Nation, J. 577, 600, 775 Naunton, R. F. 463 f Naus, M. J. 760 Nauta, W. J. H. 123 Naville, F. 396 Navon, D. 221 Nayak, N. 217 f, 221 Neale, J. M. 550, 802 Nebes, R. D. 219, 341, 390 f, 394, 902 f, 913 Needleman, H. 664 Needleman, R. M. 768 f Neff, W. D. 499 Neils, A. 829 Neils, J. 273, 912 Neilson, P. D. 429, 433, 455, 847 Neisser, U. 755 Nelson, H. E. 311 Nelson, K. E. 581, 561 ff, 569, 598, 697, 815, 818 Nelson, L. 633 f, 776 f, 781 f Nelson, R. 459 Neophytides, A. N. 398 f Neri, M. 233 Nesdale, A. R. 718 f Nespoulous, J.-L. 181, 184, 191, 194, 199, 201 ff, 337, 444 Netley, C. 586 Netsell, R. 418, 429, 448, 453, 455, 465, 468 f, 471 f, 480 ff, 841 ff, 852 Netsu, R. 291 Nettleton, J. 358 Nettleton, N. C. 128, 221 Neufeld, R. W. J. 529 Nevert, M. 544 Neville, H. J. 131 Nevlund, G. N. 514 Newcombe, F. 154, 242 ff, 251 f, 254 f, 257 ff, 267, 344, 384, 743, 745, 750 Newhoff, M. 559, 776 Newman, D. R. 760 Newman, P. J. 514 Newman, S. 701 Newman, S. P. 735, 762
89. Index of Names
Newman, S. S. 513 ff Newport, E. L. 697 Ng, B. K. 497 Niaz, L. 525 Niccum, N. 127 f Nichelli, P. 332, 346 Nichols, I. A. 666 Nicholas, L. E. 292 f, 296, 306, 386 Nicholas, M. 295, 392, 901, 905, 911 f Nicol, J. 11 Nicolich, L. 631 Nie, H.-Y. 718, 779 Nielsen, G. 50 Nielsen, J. M. 104, 263, 499, 592 Niemeier-Wind, K. 698 Niemeyer, W. 714 Niemi, J. 201, 205, 385 Nienhuys, T. G. 667, 708 Nigro, G. 634 Nilipour, R. 149, 279 Nilsonne, A. 514 f, 519 Nilsson, J. 465 Nimmo-Smith, I. 908 Nippold, M. 618, 634, 776, 871 Nittrouer, S. 418 Nober, E. H. 848 Nocentini, U. 394 Nolan, B. 401 Nolan, J. 789, 792 Nolan, K. A. 266, 270 Noll, J. D. 291, 448 Nooteboom, S. G. 29, 76 Norman, A. 792 Norman, S. 905 f, 909 Norris, M. 800 Norrsell, N. 219 North, A. J. 304 ff Noth, J. 399 Nöth, W. 550 f Novak, M. 609 Novelly, R. A. 385 Novick, M. R. 143 f, 146 f Novoa, O. P. 380 Nozoe, I. 433 Nudelman, H. B. 422 Nuechterlein, K. H. 552 f, 800 Nunberg, G. 12 Nunn, R. G. 895 Nutt, J. G. 464 Nye, C. 576, 588, 642, 715
O O’Brien, D. 866 O’Connell, A. 311 O’Connell, B. 589 O’Connell, D. C. 47, 50 O’Connor, N. 692, 816 O’Dwyer, N. J. 429, 433, 455 O’Gara, M. M. 859 O’Gorman, A. M. 651 f, 655 O’Grady, L. 675
945
O’Grady, W. 170 O’Kelly-Collard, M. 702 f O’Neill, B. P. 430 Oakley, A. E. 389 Ober, B. A. 274, 394 Obeso, J. A. 507 Obler, L. K. 110, 148, 164, 274, 279 ff, 283, 306 f, 392, 901 f, 905, 908, 911 f Obrebowski, A. 836, 840 f Ochs, E. 23 Odell, K. 439, 445 Oerlemans, M. 832 Ogden, J. A. 590 Ogle, J. W. 262, 264 Öhman, S. 36, 38 ff Ohtomo, R. 130, 271 Ojemann, G. 130, 281, 585, 591 Oller, D. K. 559, 561, 667 f Olness, G. 641, 645 Olofsson, A. 715, 719, 725, 778 Olsen, J. F. 782, 791 Olsen-Fulero, L. 697 f Olson, D. 581 Olson, D. R. 23 Olson, M. R. 685 Olson, R. 718 f, 730, 734, 738, 758 f, 762 Olswang, L. 640 ff Oltmanns, T. F. 515, 530, 550 Ombredane, A. 281, 444 f Ong, W. J. 23 Onslow, M. 886, 889 Oranen, M. 373 Orchard-Lisle, V. 155 Orgass, B. 142, 314, 318 Ornstein, P. A. 760 Ornstein, R. 131 Orsini, D. L. 655 f Orth, U. 441 Orton, S. T. 713, 742, 755, 865, 868 Ortony, A. 669 Osborn, E. 544 f, 547 Osgood, C. E. 47, 162, 220 Öst, L. 895 Ostergaard, A. L. 333, 337 Ostrau, R. 754 Ostrin, R. K. 336, 346 Ostry, D. J. 67, 418, 435, 845 Otomo, K. 667 Ouhalla, J. 166 Ounsted, C. 789, 795, 800, 804 Oviatt, S. L. 562 Owings, N. O. 692 Owrid, H. L. 664 Oxman, J. 817 f Oxman, T. E. 512 Ozanne, A. 827
P Paccia, J. M. 580, 814 Paccia-Cooper, J. 25, 211
Pachalska, M. 374 Pacini, L. 468 Packard, J. J. 212 Paden, E. 609 Paine, R. S. 835 Paivio, A. 49, 760 Pakstis, A. J. 507 Palermo, D. 589 Pallie, W. 587 Palmer, J. M. 373 Palmer, M. F. 839, 842 Paltan-Oritz, J. D. 402 Palumbo, C. L. 127, 220, 438 Panagos, J. 612 Pandya, D. N. 123 Panizza, M. 465 Pantaleoni, C. 655 Panzeri, M. 184, 244 Papagno, C. 105, 110, 113, 226, 378, 380 f, 385 Papalelondi, H. 590 Papandropoulou, I. 777, 779 Papanicolaou, A. C. 219 Pappadis, T. 222 Paquier, P. 96, 139, 148 f, 271, 279, 281 f, 285, 653 Paradise, J. L. 664 Parasnis, I. 673 Parham, I. A. 900 Parisi, D. 103 Parke, K. L. 685 Parker, D. 439 Parker, E. B. 791 Parker, S. W. 768 Parkes, C. 158 Parkin, A. J. 409 ff Parkins, R. A. 588 Parkison, R. C. 354, 358 Parks, S. L. 805 Parlato, V. 359 Parlow, S. 591 Parnas, J. 801 Parr, S. 365 Partz, M.-P. de 182, 359 Parush, A. 845 Pascher, W. 493, 495 Pashek, G. V. 112 Pate, D. S. 190, 346 Patel, P. 574 Patterson, K. E. 104, 154, 181 f, 199, 242, 252 ff, 265, 267 f, 343 f, 347, 358, 360, 364 f, 747, 770 Patterson, R. 553 Paul, R. 580, 602, 612, 693, 805, 820 Paull, A. 375 Pauls, D. L. 507 Paulsen, O. G. 551 Paulson, G. W. 396 f, 464 Pavlidis, G. T. 734, 762 Pawley, A. 216 f Payne, R. W. 527
89. Index of Names
946
Pearce, J. 391 Pearl, R. 619, 778 Pearson, C. 788, 791 f Pease, D. M. 295 Peltzer, L. 343 Penagos, B. 400 Pence, C. 792 Penfield, W. 127, 130, 281, 590, 648 f, 655 Penn, C. 295, 299, 549 Penn, R. D. 454 f Penney, J. P. 398 Pennington, B. F. 713, 748, 768 ff Perani, D. 381 Perdue, S. 799 Perecman, E. 279, 383, 547 Perelló, J. 493 Perenin, M. T. 654 Perez-Pereira, M. 684 f Perfetti, C. A. 711 f, 714, 716, 719, 729, 770, 774 f, 778 f, 782 Perkell, J. S. 39, 437 Perkins, W. H. 877, 895, 897 Perlman, R. 698 Perlman-Lorch, M. 295 Perloff, B. F. 811, 814 f Perrault, C. R. 534 Perron, C. 184, 337 Perrot, M. 546 Perry, B. 776 Peselow, E. 519 Pesenti, M. 327 Pessin, M. S. 108, 447 Pesta, I. 895 Peterham, B. 354, 366 Peters, A. D. 886 Peters, A. M. 564, 569, 578 Peters, H. 867 f Peters, H. F. M. 876 Peters, L. 901 f Peters, T. J. 888 Petersen, B. P. 818 Petersen, D. 469 f Petersen, O. 715, 718 Petersen, S. E. 131, 360 Peterson, G. 36 Peterson, G. A. 690, 701 ff, 707 Peterson, G. E. 862 Peterson, J. J. 332, 335, 341 Peterson, L. R. 332, 335, 341 Peterson, L. N. 298 Peterson, M. 602 Peterson, O. 755, 757 Peterson-Falzone, S. J. 486, 858, 860 ff Petrauskas, R. 716 Petrides, M. 333 Petrinovitch, L. F. 591 Petrosino, L. 439 Petry, S. 390 Pettersen, R. B. 551
Petty, S. H. 212 f Pfaffenberger, U. 549, 552 Pfeiffer, R. A. 125 Pfohl, B. 515 f Phelan, J. G. 540 Phelps, W. M. 835 Philipps, A. 768 Philips, B. J. 859 ff Phillip, R. 825 Phillips, C. G. 115, 122, 132 Phillips, F. 734 Phipps, J. B. 104, 115, 142, 198 Piaget, J. 284, 631, 679, 817 Piattelli-Palmarini, M. 679 Piazza, D. M. 590 Pichard, L. 298 Pick, A. 99, 103, 161, 188, 263, 273 f, 280 Pick, J. 867 Pickard, L. 365, 375 Pickering, M. 367 Pieczuro, A. 319, 444, 449 Piehler, M. 307 Pieniadz, J. M. 588 Pierce, S. 813 Pierce, R. S. 292 f, 306 Piercy, M. 589, 626 f Pierrehumbert, J. 34 Piersel, W. C. 792 Pillon, A. 182 Pillon, B. 356 f Pinard, G. 515 Pinker, S. 27, 347, 578, 629 Pinkerton, G. 599 Pinsky, S. 865 Pioger, D. 444 Pirozzolo, F. J. 390, 395 ff, 401, 734, 762 Pirsig, W. 497 Pisoni, D. B. 8, 57, 201, 630 Pitres, A. 263, 280 f, 283 f Pizzamiglio, L. 103, 106 Plank, D. M. 486 Platt, L. F. 824, 842, 847 Plaut, D. C. 259 Pleh, C. 305 f Podoll, K. 399 Podraza, B. L. 154 Poeck, K. 100 f, 103 ff, 114, 139 ff, 148, 213, 219 f, 226, 306, 314, 317, 318 ff, 402, 449, 653 Pogacar, S. 402 Poisson, M. 379 Poizner, H. 127, 318 Polinsky, R. J. 465, 505, 507 Polk, M. 125 Pollak, H. 518 Pollnow, H. 795 Pollock, J. Y. 166 Polyak, S. 128 Poncet, M. 106, 207 Poon, L. W. 900 ff, 905 f
Pope, B. 518 Porch, B. E. 138, 354 Poremba, M. 469 f Porot, A. 544 Porter, R. 866 Porter, S. 827 Portnoy, R. A. 453, 471 Poser, W. E. 469, 474 Posner, M. I. 131, 253, 360, 400 Post, R. M. 518 Posteraro, L. 344 f Potegal, M. 399 Potter, H. H. 221, 385 f, 902 Potter, M. C. 21 Potter, R. E. 354 Pötzl, O. 280 f Poulous, M. G. 882 Pound, A. 597 Powell, J. 854 Powell, T. P. 123 Powelson, J. A. 221, 386 Power, D. J. 669 Power, M. J. 49 f Power, R. J. D. 329 Powers, G. R. 860 Powers, M. 609, 829 Prather, P. 903 Pratt, M. W. 901, 909 f Pratt, R. T. 335 Preisler, G. 684 Prelock, P. 612, 631 Prescott, T. E. 446, 540 Presnell, L. 668 Price-Williams, D. 691 Price, D. L. 401 Price, T. R. 108 Prince, A. 347 Pring, T. R. 146, 352, 364 Prins, D. 888, 890, 896 Prinz, P. 619 Prior, M. 576, 599 Prizant, B. M. 578, 580, 601, 685, 812 f, 829 Pruszewicz, A. 836, 840 f Prutting, C. A. 297, 578, 667, 669 f, 691 Pruzanksy, S. 858 Pruzek, R. M. 734 Ptacek, P. 373 Puckering, C. 597 Pugh, A. K. 762 Pulgram, E. 66, 70 Pullum, G. 166 Purdy, P. D. 211 Purpura, D. P. 810 Pustrom, E. 791 f Putman, A. 843 Putnam, A. H. B. 458, 460 Putterman, A. H. 552 Pye, C. 560, 905 Pylyshyn, Z. W. 23, 515 Pysh, F. 599
89. Index of Names
Q Quadfasel, F. 104, 113 f, 193, 219, 228 Quarrington, B. 897 Quatember, R. 125 Quick, C. A. 497 Quigley, S. P. 661, 669 ff, 674 Quin, P. T. 842 Quinious, R. 367 Quinn, M. 628 Quinn, P. 866 Quinteros, B. 367 Quinton, D. 598
R Rabbitt, P. 69 Rack, J. 727 f, 738, 748, 832 Rad, M. von 510 f Radtke, R. 231 Rafal, R. D. 155, 253 Ragain, R. D. 690 Ragin, A. B. 515 Raher, J. 518 Raichle, M. E. 131 Raison, A.-M. 182 Ramer, A. 559, 562, 598 Ramig, L. 430 Ramig, P. R. 895 Ramsing, S. 375 Rancurel, E. 379 Ransby, M. J. 730, 757 Ranschburg, P. 713 f Rapcsak, S. Z. 265, 267 f, 269 ff, 273 f Rapin, I. 576, 660, 664 Rapp, B. C. 155, 192, 251, 254, 259 Rapport, R. L. 281 Rasch, G. 144 Rash, S. 901, 908 f Rashotte, C. 737 Raskind, C. L. 903 Rasmussen, K. 887 Rasmussen, T. 590, 648, 655 Ratajczak, H. 145 Ratcliff, G. 103, 588 Ratner, N. B. 886, 888 Rausch, M. A. 540 Raveh, A. 141 Raven, J. C. 311, 314 Rayner, K. 734 Razzano, C. 106 Read, C. 718, 758, 761, 779 Read, D. E. 386 Read, S. 221, 273 f, 341, 390, 411, 912 Reader, M. 763 Reagan, R. 11 f Rebelsky, G. F. 666 Recasens, D. 41
947
Reckermann, U. 759 Record, R. G. 598 f Redeker, G. 22 Redshaw, J. 599 Reed, C. 433 Reed, C. G. 886 Reed, E. S. 448 Reed, G. F. 788 Reed, M. 726 Reed, T. 399 Rees, J. 598 Rees, N. 626 f, 629 ff Regenstein, Q. R. 413 Rehm, L. P. 517 Reich, A. R. 437 Reich, P. 413 Reich, P. A. 58, 62, 78 f, 85, 87, 89 Reichle, T. 295 Reichler, R. J. 805, 811 Reichstein, M. B. 514, 516, 540 Reinarz, S. J. 588 Reinmuth, O. M. 401 Reinvang, I. 148 Reisberg, B. 391 f Reischies, F. M. 515 ff Reitsma, P. 760 Rekart, D. M. 154 Remez, R. E. 35, 416, 418 Remits, A. 292, 315 Renfordt, E. 519 Rentschler, G. J. 487 Repp, B. 34 Rescorla, L. 562, 574 Resick, P. A. 895, 897 Rétif, J. 232 Rett, A. 807 Reuter, E. 690, 700, 702 ff, 706 Reuter, P. E. 759 Reuter-Lorenz, P. A. 254 Reyes 306 Reynell, J. 681 Reynolds, A. 49 Reynolds, J. 827 Reznick, J. S. 561 f Rhoads, J. 514 Ribot, T. 280 Rice, B. 375 Rice, M. 563, 642 f Richard, J. 341 Richardson, J. T. E. 258 Richardson, R. T. 465 Richman, L. C. 768 f, 772 Richman, N. 574, 597 f, 601 Richter, R. 98 Ricks, D. M. 812 Riddoch, M. J. 157, 252 ff Rieber, R. W. 893 Riedel, K. 103 Riege, W. H. 333, 376, 398 Riegel, K. F. 900, 902, 904 Riegel, R. M. 902 Rigrodsky, S. 230 f
Riley, G. D. 880 f, 888 ff Riley, J. 880 f, 888 ff Rilke, R. M. 96 Rimbaud, A. 93 f Rimland, B. 808 f Rinne, U. K. 391 Riordan, C. J. 417 Ripley, K. 642 f Risberg, J. 274, 401 Rissenberg, M. 900, 912 Risser, A. 137 f, 142, 144, 149 Rittenhouse, R. 669 Ritvo, E. R. 805, 809 Riva, D. 655 Rivera, V. 459 Rivoria, P. 396 Rizzo, M. 129 Robbins, L. D. 497 Robenalt, K. 691 Roberts, F. J. 515 Roberts, J. E. 664 Roberts, L. 127, 130, 281, 590, 648 f, 655 Roberts, P. M. 901, 909 f Roberts, R. J. 588 Robertson, G. 516 Robertson, I. 354 Robertson, M. M. 506 Robin, D. A. 212, 447, 843, 846 ff Robins, E. 805 Robins, S. 901, 909 Robinson, E. 777 Robinson, J. 862 Robinson, P. 832 Robinson, R. 829, 831 Robinson, R. G. 108, 266, 270, 372 Robinson, R. J. 598 Robinson, R. O. 592 Robinson, S. 268 Robinson, W. 599, 777 Robson, C. 688 Rochester, S. R. 47 ff, 540, 549 ff, 802 Rochford, G. 95 Rochun, J. 602 Rocissano, L. 568 Rodgers, B. 716 Rodnick, E. H. 551, 802 Roeltgen, D. P. 264 ff, 272 ff, 344 Roemer, R. A. 131, 399 Roessmann, U. 395 Roger, A. 335 f Rogers, H. 273 f Rogers, S. 768 ff Rogers-Warren, A. 641, 643 Rogow, S. M. 683 Rojahn, J. 895 Rollin, W. J. 374 Rom, A. 580 Roman, M. 221, 294, 385, 902
948
Romani, C. 155, 181, 185, 259, 266, 269, 344 Romeo, D. J. 699 Rommetveit, R. 551 f Rondal, J. A. 566, 580, 690 ff, 694, 702 f, 705 Rondot, P. 472 Rorabaugh, A. 219 Rorsman, B. 388 Rosati, G. 264 Rose, D. F. 651 f, 768 f Rose, F. 218 Rose, F. C. 411 Rosen, G. D. 588 Rosen, J. 726 Rosen, J. J. 124, 396 f Rosen, M. S. 488 Rosenbaum, B. 552 Rosenbaum, F. 464 Rosenbaum, M. 373 Rosenbek, J. C. 108, 213, 439 f, 445 ff, 474, 478, 481 ff, 843, 846 ff, 850 ff Rosenberg, J. 127, 463 Rosenberg, S. 50 Rosenberg, S. 580, 688, 691 f Rosenberg, S. D. 512, 549 f Rosenberger, P. B. 810 Rosenbloom, L. 660 Rosendahl, P. 642 f, 644 Rosenfield, D. B. 422 Rosenschein, S. 401 f Rosenstein, H. 486 Rosenstein, J. 668 Rosenthal, V. 174, 176 f Rosenthal, W. 575 Rosman, N. P. 810 Rosner, B. A. 830 Rosner, J. 757, 778, 780 Ross, A. 544 Ross, E. D. 211, 383 Ross, J. 598 Ross, J. R. 17, 29 Ross, R. 586, 598 Ross, W. 760 Rosselli, D. 400 Rosselli, M. 326, 400. Rossiter, D. 365 Rosvold, H. E. 653 Roth, F. 631 f Roth, F. 775 Rothermel, R. D. 768 f Rothi, L. J. G. 265 ff, 270, 273, 291, 321, 333
cf. GonzalesRothi, L. J. Rothwell, J. C. 466, 507 Rouillon, F. 189 Rourke, B. 601, 716 Rousseau, J. 231, 234 f Routh, D. 757, 777 ff, 782, 832 Rovner, B. 390 Rowan, L. 615, 619 Rowland, C. 680, 684
89. Index of Names
Rowley, D. T. 125, 298 Roy, E. A. 322 f, 481 Roy, J.-Y. 515 Rozin, P. 712, 756 Rubens, A. B. 113, 125, 127, 219, 229, 265, 267 ff, 273 f, 379, 499 Rubin, E. H. 390 Rubin, H. 739 Rubin, K. 877 Rubin, P. 35, 416, 418 Rubio, S. 229, 233 Rubow, R. 479 Rucklos, M. E. 529 Rudel, R. 714, 738, 775 Rudert, H. 497 Rue, S. 886 Ruesch, H. 510 Rufo, D. 588 f Rugg, M. 736 Rühmke, H. C. 549 Ruiz, M. 295 Rumelhart, D. E. 121, 123, 252, 257, 347, 421, 900 Rumsey, J. M. 588, 810 Runyan, C. M. 886 f Runyan, S. E. 887 Rupp, J. 49, 551 Russell, J. 859 Russell, W. R. 127, 499 Rustin, L. 888 ff Rutherford, B. 454, 840 ff Ruthven, L. 354 Ruttenberg, B. A. 805 Rutter, M. 580, 597 ff, 701, 714, 716, 792, 806, 809 f, 813 Rutter, D. R. 517, 526, 549, 553, 802 Ruyter, L. 779 Ryalls, J. H. 198, 200 f, 213 f, 295, 446 Ryan, B. P. 886 ff, 897 Ryan, B. V. K. 887 Ryan, E. 773 f, 777 Rydell, P. J. 812 Ryding, E. 220
S Sabatino, D. A. 755 Sabo, H. 693 Sabourin, L. 384 f Sabsay, S. 691 Sacco, P. R. 439 Saccuzo, D. P. 530 Sachs, J. 565 f, 598, 697 Sacks, H. 17 ff, 551 Saddy, J. D. 157 f, 172, 177 Sadock, J. M. 17 Sadowska, M. 309 Safar, P. 410 Safer, M. A. 212
Saffran, E. M. 86, 102, 111, 157, 163, 165 f, 177, 190, 255 f, 258 f, 267, 274, 338, 340, 343, 346, 392, 500 f Sag, I. 166 Sagar, H. J. 396 Sagart, L. 559 Saillant, B. 157 Sailor, W. 816 Saint-Cyr, J. A. 396 Salas-Provance, M. 859 Salasoo, A. 211, 343 Salazar, A. 463 Salend, S. J. 886 Salfield, D. M. 788 Salmon, D. P. 394 Salomon, E. 161 Salonen, L. 356 Salthouse, T. A. 66 ff, 900, 904, 906, 908 Saltzman, E. L. 6, 35, 44, 416, 418, 420, 422 Samarin, W. J. 547 Samuels, I. 332 Samuels, S. J. 712, 718 Sander, E. K. 559 Sanders, S. 789 Sands, E. 354, 365 Sands, E. S. 446 Sandson, J. 232 f, 402 Sandyk, R. 516 Sanford, A. J. 902, 904 Sanides, F. 120 f, 125 Sansone, F. 489 Santo Pietro, M. J. 230 f, 913 Santos, M. E. 321 Sanynl, M. A. 664 Sarason, J. G. 518 Sarno, M. T. 138, 354, 364 f, 652 Sartori, G. 155, 182 Sasanuma, S. 198, 201, 204 ff, 436, 446 Sastry, M. 397 Satz, P. 591, 647, 649, 653, 655 ff, 714 ff, 719, 900 Saussure, F. de 24 Savage, K. 259, 750 Savage, R. D. 515 Savage-Rumbaugh, E. S. 16 Savic, S. 830 Savich, P. 631 f, 775 Sawada, T. 112 Sawashima, M. 453, 471 Sawyer, D. J. 761 Sax, D. S. 399, 499 Sayers, B. M. 894 Scanlon, D. M. 715, 757, 782 Scarborough, H. 577 Schaaf, H. G. 489 Schaefer, E. F. 21 ff, 290 Schaefer, S. 453 Schaeffer, B. 811, 814 f, 817 Schafer, R. 515
89. Index of Names
Schaie, K. W. 900 Schatzberg, A. F. 516 Scheerer-Neumann, G. 712, 717, 755, 758 ff Scheerer, E. 23 Schegloff, E. A. 17 ff, 27, 29, 551 Scheibler, D. 511 Scheltens, P. 402 Schenkein, J. 20 Scherer, K. R. 6, 514, 518 Scherer, N. J. 692 Schery, T. 629 Schiavetti, N. 439 Schiefelbusch, R. L. 688 Schienberg, S. 447 Schiff, N. B. 379, 598, 830 Schinsky, L. 487 Schirmer, B. R. 670 Schlageter, N. L. 389 Schlanger, B. B. 211, 688 Schlanger, P. 211 Schlatter, T. 551 Schlee, J. 714 Schlenk, K.-J. 20 Schlesinger, H. S. 674 f Schlesinger, I. M. 140 Schliesser, H. F. 840, 842 Schlöndorff, G. 497 Schmidt, A. 131 Schmidt, P. 546 Schmidt, R. C. 418 Schmidt-Knaebel, S. 549 ff, 553 Schnada, H. 552 Schneider, D. 228 Schneider, E. 395, 845 Schneider, K. 523 Schneider, L. 633 Schneider-Rosen, K. 597 Schnitzer, M. L. 164 Schnurr, P. P. 512 Schochet Jr., S. S. 500 Schodorf, J. K. 702 ff, 707 Schoene, W. C. 379 Schöfer, G. 511 f Scholes, R. 163, 176, 333, 338 Scholl, M. E. 610, 629 Scholl, M. H. 701 Scholtz, O. B. 397 Scholz, J. P. 419 Schonauer, K. 552 Schönemann, P. H. 140 Schöner, G. S. 419 Schönle, P. W. 434, 441, 468 f, 471 f, 474 Schopler, E. 792, 804 ff, 811, 816 Schouten, H. J. A. 143 Schrader, J. 471 Schreuder, R. 11 f, 244, 756 ff Schriefers, H. 4, 13, 86 f, 242, 245 Schrier, R. 155 Schroder, K. F. 398
949
Schuell, H. 137, 140, 353, 364 f Schuler, A. L. 578, 811 ff, 816 Schulmann, X. 234 Schulsinger, F. 801 Schulsinger, H. 801 Schulte-Mönting, J. 107 Schultz, A. R. 853 Schultz, M. 875 Schultz-Coulon, H.-J. 493 Schulz, G. S. 462 f Schulze, G. 513, 518 Schulze, H. 279, 281, 876 f, 879 ff Schulze, K. 754 Schumacher, E. 791 f Schunk, D. H. 3, 20 Schvaneveldt, R. W. 902 Schwalbe, J. 280 Schwartz, I. L. 792 Schwartz, J. 50, 212 Schwartz, K. 463 Schwartz, M. 459 Schwartz, M. F. 138, 155, 157, 163, 165 f, 177, 189, 255 f, 258, 267, 274, 313, 336 ff, 343, 346, 360, 392, 894 Schwartz, M. S. 220, 274 Schwartz, R. 551, 560, 581, 609, 615, 617, 631 f, 641 f, 644 Schwartz, S. 541 Schwartz, S. E. 690 Schweickert, J. 292 Scoresby Jackson, R. 280 Scott, C. 360 Scott, C. M. 139, 142, 147, 563 Scott, E. P. 680 Scott, S. 736 Scovel, T. 591 Seaman, D. 576, 642 Searle, J. R. 16 f, 907 Sears, R. L. 895 Secada, W. G. 325 Sedory, S. E. 463 f Seeman, M. V. 540, 553 Seemüller, E. 105, 127 Segalowitz, S. J. 589, 592 Segarra, J. 104, 113 f, 193, 219, 228 Segui, J. 9, 13, 174 Seibold, M. S. 902 Seidenberg, M. S. 13, 256, 347, 358, 394, 713, 719, 758, 903, 912 Seider, R. A. 879 Seifert, M. 758 Seilo, M. T. 487 f Selby, G. 129, 395 Selemon, L. D. 123 Selfridge, J. A. 529 f, 550 Seligman, M. E. P. 563 Selkirk, E. 27 Sell, M. 642 f Sell, S. 830
Sells, P. 166, 170 Selnes, O. A. 127 f, 219, 390 Seltz, O. 24 Seltzer, B. 390 f Semel, E. 776 Semenza, C. 158, 184, 231, 244, 500 f Semzova, M. E. 680 Senft, G. 28 Serdaru, M. 129 Sergent, J. 147 Serkerke, H. J. 518 Seron, X. 174, 177, 182, 292, 294, 296, 315, 326 ff, 651 Seth, G. 867 f Seuren, P. M. 12 Sevush, S. 264 ff, 270, 274 Sewell, W. 789 Seymour, P. H. K. 712, 718, 720, 728, 746, 748, 750 f, 756 Shadden, B. B. 410 Shafer, S. 98 Shaffer, L. H. 68 f Shaiman, S. 42 f, 417, 477 Shakespeare, W. 95 Shalcross, R. 685 Shallice, T. 138, 145 ff, 155 f, 182, 238 f, 253 ff, 265 f, 270, 289, 310, 311, 335 f, 344, 346, 743, 745, 747, 750, 903 Shamblin, L. 459 Shames, G. H. 877, 894 Shands, H. 510 Shane, H. C. 849, 853 f Shanks, J. C. 488 f Shankweiler, D. 127 f, 176 f, 416, 445 f, 671, 673, 711, 718, 729, 736, 738, 759, 778 ff Shapira, J. 390 Shapiro, B. E. 213 Shapiro, J. 454 Sharbrough, F. W. 500 Share, D. L. 715 f, 719, 737, 778 Share, J. B. 692 Sharifi, H. 690, 692 Sharkey, N. E. 902 Sharkey, R. W. 553 Sharp, J. P. 458, 460 Shattuck-Hufnagel, S. 5, 53, 55 f, 58, 60, 75 ff, 190 f, 204 f, 246 Shatz, M. 567 ff, 581, 697 f Shaughanessy, A. 844 Shaw, C. 886 Shaw, J. 730 Shaw, P. 185 Shaw, R. E. 420 Shaw, R. J. 903 Shawker, T. H. 435 Shea, P. 738 Shea, S. L. 561 Sheard, C. 439, 474 Shedd, D. 488
89. Index of Names
950
Sheehan, J. G. 896 Shelburne, S. A. 131 Shelly, C. 911 Shelton, R. L. 486, 828, 858, 860 f Shenaut, G. K. 394 Sheppard, A. 114, 125 f, 128 Sheppard, J. 836 f Sheppard, J. L. 715 Sheppard, M. J. 715 Sherematta, W. A. 112 f Sheridan, J. 156 Sheridan, M. 589 Sheridan, M. R. 462 Sheridan, R. B. 248 Sherman, G. F. 588 Sherman, J. C. 292 Sherman, T. 704 f, 799 f Sherrod, K. B. 690 f, 700 ff, 707 Sherwin, I. 390 f Shewan, C. M. 163, 297, 354, 358, 364, 374, 446, 484, 909 f Shewell, C. 182 Shillock, R. C. 28 Shillock, R. S. 61 Shimamura, A. P. 394 Shimkunas, A. M. 553 Shimshon, R. 95 Shin, T. 433 Shindler, A. G. 232, 341, 392, 912 f Shindo, M. 292 Shine, R. E. 887 Shinn, P. 206 Shinoda, Y. 115 Shipley, E. F. 567 Shipley-Brown, F. 210 Shipp, T. 433, 488 Shishido, F. 130 Shoemaker, D. 867, 869 Shokhor-Trotskaya, M. K. 356 Shopen, T. 29 Short, A. 816 Short, E. 775 Shoulson, I. 399 Shprintzen, R. 845, 852 Shriberg, L. 609, 612, 826, 847 Shrum, W. 886 Shulman, M. 776, 781 Shumway-Cook, A. 589 Shurcliff, A. 758 Shuttleworth, E. C. 396 f, 402 Shye, S. 140 f Siddall, M. 631 Sidman, M. 354 Sidtis, J. J. 212, 219, 221 Siegel, L. 603, 736, 768 f Siegel, L. S. 702, 704, 707 Siegel, R. 750 Siegman, A. W. 49, 518 Siemens, H. 759 Sieroff, E. 252 f Sifneos, P. 511
Sigman, M. 692, 704 f Signoret, J.-L. 356 f Sih, C. C. 886 Sihvonen, R. 373 Silber, R. 560 f Silberberg, M. C. 755, 768 f, 771 Silberberg, N. E. 755, 768 f, 771 Silva, P. A. 598 ff, 602, 660, 663 Silverberg, R. 279 Silveri, M. C. 154 f, 164, 178, 181, 185, 271, 295, 344, 394 Silverman, G. 526 Silverman, I. 49 f Silverman, J. 384 Silverman, M. 354, 365 Silverman, W. 693 Silvers, G. 69 Sim, V. M. 518 Simmons, J. 814 f Simmons, N. 514 Simmons, N. N. 474, 481 ff Simon, D. 778, 780 Simon, H. A. 220 Simpson, H. 598 Simpson, T. L. 293 Sinclair, H. 777, 779 Singer, H. 782 Singer, H. S. 504, 507 Singer, M. 802 Singh, N. N. 760 Sison, C. E. 354 Sjogren, H. 391, 401 Sjogren, T. 401 Ska, B. 199, 204 f Skarakis, E. A. 669 Skarakis, S. 620 Skarakis-Doyle, E. 641, 644 Skarbek, A. 48 ff Skelly, M. 357, 373, 487 ff Skenes, L. L. 138 Skinhoj, E. 220 Skinner, B. F. 95, 595 Skjelfjord, V. 756 Sklar, M. 142 Skolnick, M. 845, 852 Skovengaard, J. 529 Skowronek, H. 715 Skuse, D. 596 Skydsgaard, H. B. 742 Slade, A. 596 Slaghuis, W. 735 Slauson, T. J. 394 Slaymaker, F. L. 47 Sledge, W. 95, 534 ff, 798 Slobin, D. I. 58, 60, 388, 564, 633 Sloman, L. 816, 818 Smiley, P. 562 Smiley, S. S. 904 Smirnov, B. 280 Smit, I. 651 Smith, A. 107, 123, 220, 433, 609, 864 ff
Smith, B. A. 734 Smith, C. 777 Smith, C. M. 393 Smith, C. S. 567 Smith, D. W. 693 Smith, E. 395, 397 Smith, G. A. 514 Smith, H. 539 Smith, J. 48 f, 689 Smith, J. C. 131 Smith, K. L. 58, 198 f, 201, 203 ff, 207, 357 Smith, L. 295, 297, 582 Smith, M. 39, 226 Smith, M. E. 130 Smith, M. L. 333 Smith, N. 667, 826 Smith, N. V. 688 Smith, S. 394, 400 Smith, S. D. 748 Smith, S. T. 273 Smith, T. 815 Smith, W. 845 Smolak, L. 697 Smyth, M. M. 66, 69 Snow, C. E. 568 f, 591, 690, 698 Snowling, M. J. 717 ff, 725 ff, 736, 739, 753, 748, 756, 768 ff, 772, 832 Snyder, C. R. 400 Snyder, L. 562, 581, 598 f, 614, 706, 779 f Snyder, W. B. 273 Soares, C. 284 Sokol, S. M. 330 Solin 281 Solomons, L. M. 95 Solvberg, H. A. 551 Soma, Y. 271 f Sommers, R. 827, 829, 831 Sommers, R. K. 445, 447 Somodi, L. 843, 846 f Sonies, B. C. 435 Sonne, H. 552 Sooudi, I. 486 Sorby, W. A. 866 Sorensen, J. M. 209 Sorgato, P. 319 Souques, A. 231, 234 Sourander, P. 391 Southard, D. 417 Southwood, H. 894 Spalding, L. M. K. 327 Spanier, G. B. 880 Spanton, S. 391 Sparks, R. 484, 499 Spearman, C. 311 f Spector, D. J. 487 Speedie, L. 211, 266, 270, 291, 384 Speers, R. W. 791 f Speidel, G. E. 685 Spekman, N. 775
89. Index of Names
Spence, M. A. 809 Spencer, A. 27, 827, 831 Sperber, D. 12, 17 Sperber, R. D. 688, 690 Sperry, R. W. 219, 315 Spieker, S. 589 Spieß, P. von 516 Spiker, D. 700 Spinnler, H. 314, 390, 499 Spitzer, M. 528 Spitzer, R. L. 526, 805 Sprainger, N. 832 Spreen, O. 103, 137 f, 142, 144, 149, 499, 507 Spriestersbach, D. C. 845 Spring, B. 553 Spurzheim, J. C. 120 Spyer, G. 763 Square, P. A. 322, 445, 447 Square-Storer, P. 481, 484 Squire, L. R. 330, 389 Sroufe, L. A. 596 f Ssucharewa, G. 796 St. John, M. 26 St. James-Roberts, I. 586 St. Louis, K. O. 882 Stachowiak, F.-J. 105, 109, 306, 354 Stackhouse, J. 728, 748, 832 Stafford, C. 739 Stafford, J. A. 391 Stahl, S. A. 761 Stampe, D. 825 Standke, R. 514 Standop, R. 876, 893 ff Stanley, G. 734 Stanovich, K. E. 713, 715, 717 ff, 725, 729, 774, 778 f, 781 f, 902 Starch, S. A. 375 Stark, R. 775 Stark, R. E. 558, 575, 577, 589, 608 f, 622, 627 f, 635 Starkstein, S. E. 108, 281, 372 Starkweather, C. 865, 868, 888 ff Starkweather, C. W. 876 f, 879, 884 Starkweather, J. A. 514, 517 Starosta-Rubinstein, S. 398 Stassen, H. H. 514 Steel, A. McP. 735 Steele, R. D. 298 Steer, M. 840 Stefanik, K. 896 Steger, J. A. 734 Steiger, J. H. 140 Stein, C. 729, 775 Stein, D. G. 124 Stein, G. 95 f Stein, J. F. 735, 762 Stein, S. 293 Steinkamp, M. W. 669 Stemberger, J. P. 24, 26 f, 53,
951
56 ff, 75 ff, 80, 85, 87, 154, 185, 246 Stengel, E. 281, 500 Stephenson-Opsal, D. 888 Sterling, W. 233 Stern, C. 562, 903 Stern, D. 589 Stern, W. 562 Stern, Y. 391 Sternberg, R. J. 634, 688 Sternberg, S. 6, 418 Sterzi, R. 381 Stetson, R. H. 420 Stevens, K. 862 Stevens, K. N. 8 Stevens, T. J. 398 Stevenson, J. 574, 597 f, 601 Stevenson, M. B. 700 Stewart, I. 660, 663 Stewart, M. A. 810 Stiassny, D. 333 Stiassny-Eder, D. 220 Stickgold, R. 528 Stillman, B. W. 755 f, 760 Stine, E. A. L. 902, 905 f Stitzer, M. 518 Stockert, F. G. von 797 Stockert, Th. von 113, 163, 499 f Stockman, D. 11 Stoddart, F. J. 518 Stoel-Gammon, C. 559 f, 609, 667, 688, 691 Stoessl, A. J. 398 Stokes, T. F. 889 Stokoe, W. 674 Stone, G. O. 713 Stone, M. 434 f Stopek, S. 515, 534, 549 ff, 801 Storandt, M. 390 Storch, E. 500 Strachen, A. M. 551 Straf, M. 85 Strand, E. A. 446 Strang, J. 601 Strauss, E. 591, 649, 655 ff Sträussler, E. 280 Strawson, C. 749 Streiner, D. 813 Strober, M. 551 Stroud, A. 700, 702, 706 Strub, R. L. 330, 335 f, 346 Strube, E. 585 Stuart, M. 712 Studdert-Kennedy, M. 127 f, 416, 421, 589, 711 Sturm, W. 326 Stuss, D. T. 113, 221, 380, 518 Stutte, H. 794, 797 Stutts, N. 819 Sudhalter, V. 693 Sugarman-Bell, S. 567 Sugishita, M. 127, 271 f Sulkava, R. 391
Sullivan, E. V. 375, 396 Sulzer-Azaroff, B. 818 Sundberg, J. 417 Sunderland, T. 268 Sussman, H. 440 Sutherland, G. R. 693 Svendsen, P. 811 Swanson, L. 615 Swartz, L. 551 f Swartz, S. 551 f Swash, M. 393, 459 Sweet, E. 127 Sweet, J. J. 514 Swift, L. H. 553 Swinney, D. A. 11, 221, 291, 903 Swisher, L. 574, 646, 668 Syder, F. H. 216 f Symonds, C. P. 411 Syrdal-Lasky, A. 726 Szabady, E. 513, 517 Szasz, T. S. 553 Szentagothai, J. 122 Szeszulski, P. 727
T Taborielli, A. 264 Tabossi, P. 903 Taft, L. 8 Taft, M. 758 Tager-Flusberg, H. 565, 569, 580, 777, 813 Taimi, E. G. 455, 836 f Tallal, P. 212, 575, 586, 588 f, 598, 602, 608 f, 622, 625 ff, 635, 775, 782, 831 Tamaru, F. 499 Tan, C. T. 281 Tanabe, H. 112 Tanaka, Y. 271 ff, 292, 501 Tanenhaus, M. K. 13, 256, 900 Tanguay, P. E. 799, 810 Tannen, D. 20, 23 Tanner, S. 895 Tannock, R. 700 f, 704, 706 Tanokushi, F. 861 Tanridag, O. 264, 270 Taraban, R. 26 Tarlow, S. 333, 399 Tarone, E. 283 Tassinary, L. G. 433 Tatsumi, I. 446 Taylor, A. E. 396 Taylor, G. 511 f Taylor, H. G. 400 f Taylor, H. J. 714 ff Taylor, I. 48 f Taylor, L. 588, 715 Taylor, M. A. 541 Taylor, M. L. 446 Taylor, N. 779 Taylor, P. J. 516
89. Index of Names
952
Taylor, W. L. 526 Teele, D. W. 610, 830 Teetson, M. 447 Tegart, L. 482 Teigen, J. 553 Temple, C. M. 728, 745 ff, 750 f Templin, M. 559, 563, 574, 628 Teng, E. L. 390 f Terbeek, D. 217 Terrell, B. 581, 631 f, 641, 644 Terrence, C. F. 398 Terry, R. D. 389 Tetreault, L. 515 Teuber, H.-L. 314, 590, 648, 651 f, 654 Teyler, T. J. 131 Thal, D. 644, 693 Thal, L. J. 390 Thiersch, C. 166 Thomas, A. P. 295 Thomas, D. 93 Thomas, P. 537, 539, 552 Thompson, C. K. 354, 837 f, 841, 854 Thompson, J. 563 Thompson, K. 913 Thompson, M. M. 692 Thomson, M. 714, 755, 761 Thorner, G. 398 Thorpe, K. 599 Thorpe, P. 51 Throckmorton, M. 791 Thurston, J. R. 549 ff Thurstone, L. L. 311 ff Thurston, S. 49 Till, R. E. 907 Tinker, M. 734 Tissot, R. J. 99, 181 Tizard, B. 598 f Tizard, J. 598 Tobin, H. 668 Tolhurst, D. J. 735 Toma, S. 472 Tomblin, J. 601, 628 ff, 636, 775 Tomiyasu, U. 411 Tomoeda, C. K. 111, 392 ff, 905, 907, 911 ff Tompkins, C. A. 51, 211, 291 f, 384, 386 Tonelli, L. 76 f Toner, M. A. 439 Tonkonogy, J. 127 Tonkovich, J. D. 484 Tordoff, V. 736 Torgesen, J. K. 718 f, 724, 737, 756, 779, 781 Tornéus, M. 757, 782 Toro, F. R. 391 Torrey, E. F. 810 Torrey, J. 770 Toshi, A. 279 Tough, J. 568 Toups, F. 896
Towbin, K. E. 507 Towne, R. L. 446 Townsend, D. L. 488 Toyokura, Y. 271 f Tramer, M. 788 Tranel, D. 212 Travis, L. 544 f, 547, 865, 868 Treiman, R. 57, 59 f, 63, 246, 715, 728, 730, 757 ff, 782 Treisman, A. 251 Treitel 574 Tremaine, R. V. 283 Trénel, X. 234 Tress, W. 515, 549, 552 Triden, K. A. 888 Trillet, M. 267, 270 Tronick, E. 684 Trosset, M. W. 392, 394, 913 Trost, J. E. 198, 202, 205 ff, 860 Trost-Cardamone, J. E. 859, 861 Truswell, L. 566 Tsai, L. 810 Tsai, S. Y. 274, 393 Tseng, C.-H. 198, 446 Tsetlin, M. L. 417 Tsuang, M. T. 552 Tsukagoshi, H. 271 Tsvetkova, L. S. 362, 380 Tucker, D. 233 Tucker, D. M. 268 Tucker, G. J. 512, 549 Tucker, H. M. 493 Tuller, B. 42, 44, 177, 417 f, 420 ff, 446 Tuller, B. H. 7 Tunmer, W. E. 716, 718 f, 773 f, 779 Tupper, A. 352 Turkewitz, G. 591 Turner, B. H. 123 Turner, G. 434, 693 Turock, D. L. 418 Turvey, M. T. 27, 35, 44, 185, 416 ff, 420, 472 Tweedy, R. J. 397 Tweney, R. D. 669 Twentyman, C. T. 597 Tyler, L. K. 9 f, 158, 176, 182, 184 f, 245 Tyler, S. A. 216 Tyson, J. 488 f Tzara, T. 95 Tzorztis, C. 103, 335 f
U Udwin, O. 693 Uhl, G. R. 401 Uhly, B. 333 Ulatowska, H. K. 304 ff, 320, 392, 901, 909 f, 912 Ulliana, L. 888 Ulrich, G. 499
Ungerer, J. 704 f Urwin, C. 684 Ushijima, T. 416, 446, 471, 866
V Vagges, K. 41, 76 f Vaid, J. 589 Valdimarsdottir, A. 551 Valdois, S. 194, 201 ff, 207 Valencia-Laver, D. 903, 907 Valenstein, E. 103, 321 Vallar, G. 340, 380 f, 385 Valsiner, J. 145 Valtin, R. 711 f, 714, 718 van Belle, W. 549 f van Bijsterfeld, D. 551 Van Bogaert, L. 234 Van Bon, W. H. J. 756 ff Van Bosch, K. 759 Van Buren, J. 130 van Campe, J. 549 f Van de Craen, P. 549, 551 van de Sandt-Koenderman, M. 651, 653 Van Demark, D. R. 860 van den Bercken, J. H. L. 395 Van den Berg, J. W. 491 van der Kaa, M. 315 Van der Kaa, M. A. 292, 296 van der Kamp, L. J. P. 146 van der Linden, M. 315 Van der Loos, H. 122 Van der Spuy, H. 603, 702, 704, 707 Van der Wissel, A. 716 van Dijk, T. A. 18, 308, 904, 906 f van Dongen, H. R. 228, 591, 651 ff van Dongen, K. J. 591, 651 f Van Eeckhout, P. 356 f van Galen, G. P. 66, 68 ff Van Gorp, W. 900 van Grunsven, M. 19, 107, 162, 337 f, 346 van Harskamp, F. 228 van Hesch, J. 651 Van Hoek, K. 675 Van Horn, G. 127 Van Hout, A. 651 ff Van Lancker, D. 93, 210, 212, 216 ff, 267, 291 f, 657 Van Leeuwen, H. M. P. 763 Van Kirk, B. 897 Van Kleeck, A. 773 f, 781 f van Mier, H. 148, 297 van Nes, F. L. 68 ff van Orden, G. C. 241, 713, 748 Van Riper, C. 483 f, 864 f, 878, 894 ff Van Wagenen, L. 818 Van Wagtendonk, B. 739
89. Index of Names
Van Wijk, C. 7 Vance, K. T. 393 Vandehaar, C. 860 Vanderheiden, G. C. 853 f Vanderlinden, M. 292 Vanier, M. 199, 204, 339, 345, 546, 548 Vanier-Clément, M. V. 534 ff, 552, 798 Vargha-Khadem, F. 590, 651 f, 655 Varley, D. 862 Varney, N. R. 291, 588 Vasconcellos, M. J. 762 Vatikiotis-Bateson, E. 42, 416 ff Vaughn, C. 551 f Vaughn 367 Vellutino, F. R. 588, 714 f, 717, 719, 734, 757, 774 f, 782 Venezky, R. L. 256, 712 Ventry, I. M. 598, 664, 830 Venus, C. A. 292 Vergo, T. 489 Verity, M. A. 401 f Vernea, J. J. 264 Vernon, M. 598 Vetter, H. 513, 534 Veyrac, G.-J. 279, 281 Victor, M. 459 Vignolo, L. A. 105 f, 127 ff, 138, 142, 264, 310, 314, 319, 378, 380 f, 444, 449, 499 Vihman, M. M. 559, 561, 563, 681, 875 Villa, G. 154, 164, 178, 199, 266, 269, 295, 315, 344 f, 378 Villard, P. 181 Villaroya, O. 748 Villegas i Bessora, M. 552 f Vincent, R. 409 ff Viney, L. 511 Visch-Brink, E. G. 651, 653 Vlay, S. C. 413 Vogel, F. S. 389 Vogel, M. 439, 455, 469 ff, 481 ff, 496 Vogel, S. 775 Voigt, L. 797 Volkmar, G. R. 817 Volpe, B. T. 212, 219, 221, 397, 410 f Vonsattel, J. P. 398 Vorberg, D. 4, 13, 242, 245 Vosse, T. 5 Vrtunski, P. 220 Vygotsky, L. 773 f
W Wachs, T. D. 596 Wada, J. 125, 587, 655 ff Wade, D. T. 149, 367
953
Wade, E. 900 f, 911 Wadsworth, J. F. 735, 762 Waggener, J. D. 500 Wagner, R. K. 718, 724, 737, 756, 779, 781 f Wahrborg, P. 363, 365, 373 f Wainer, H. 140 Wales, R. 386 Walker, J. A. 253 Walker, L. C. 465 Walker, M. 158 Walker, V. G. 901, 909 f Walkup, J. T. 504, 507 Wall, J. 122 Wall, M. J. 865, 888 ff Wall, S. 715, 719, 725, 778 Wallach, G. 775 Wallach, L. 757 Wallach, M. A. 757 Waller, M. R. 293 Wallesch, C.-W. 100, 104 ff, 110 ff, 226, 298, 374, 381, 399, 484, 912 Walsh, D. A. 907 Walsh, M. J. 219 Walter, D. O. 589 Walters, W. C. 129 Wanamaker, W. M. 395 Wapner, W. 384 f Ward, C. D. 314 Ward, P. H. 437 Warden, B. S. 465 Warnke, A. 713 Warren-Leubecker, A. 629 Warren, D. H. 679 f, 685 Warren, D. W. 437, 486, 845, 861 Warren, H. 57 Warren, P. 9 f Warren, R. K. 5, 76, 88 Warren, S. 641, 643 Warrington, E. K. 129, 154 ff, 178, 252 ff, 266, 270, 311, 315, 335 f, 340, 344 ff, 358, 379 f, 384, 394, 743, 745, 747, 750, 903 Wason, P. C. 315 Wasserman, G. 597 Wasterlain, C. G. 129 Watabe, S. 499 Watamori, T. S. 373 Waters, G. S. 256, 340, 908 Watkins, L. B. 291 Watson, L. R. 817 Watson, P. J. 437 Watson, R. T. 291, 321, 333, 338 Watson O’Reilly, A. 567 Watt, J. 579 Watt, M. 362, 365 Watters, G. V. 651 f, 655 Watts, D. 599 Watts, M. 354 Waugh, P. 292
Waxier, N. E. 802 Webb, M. E. 553 Webb, W. G. 402, 453 Weber, C. 864, 867 f Weber, J. A. 668 Webster, C. D. 815 ff Webster, W. G. 868, 882 Wechsler, A. F. 401 f Wechsler, D. 311, 397 Wechsler, E. 352 Wediggensen, P. 895, 897 Weekes, B. 259, 750 Wegener-Sleeswijk, B. 682, 686 Wegner, M. L. 306 Weigl, E. 164, 712 Weiher, E. 39, 41, 416 Weikers, N. J. 500 Weinberg, A. 162, 165, 334 Weinberg, B. 486 Weiner, F. 847 Weiner, H. 543 Weiner, P. 574 Weiner, W. J. 396 f Weinert, S. 580, 702, 706 Weingartner, H. 396, 399, 516, 913 Weinheimer, S. 22 Weinraub, M. 697 Weinreich, U. 217 Weinrich, M. 298, 355 Weinstein, E. A. 384 Weinstein, S. 314 Weintraub, S. 138, 294, 396, 802 Weintraub, W. 515 Weir, W. F. 328 Weisenburg, T. 104 f, 107, 109 f, 112, 137, 279, 310 Weisiger, B. E. 439 Weismer, S. E. 606, 641 f, 644
cf.Ellis Weismer, S. Weismer, G. 434, 437, 441, 446, 465, 472, 831, 847 Weiss, A. 615 Weiss, D. A. 851 Weiss, D. G. 364, 366 f Weiß, R. 514 Weiss Boyel, A. 305 ff Weissberg, R. 86 Weissler, M. C. 486 Weisstein, C. C. 515, 525 f, 528 Weitzman, R. S. 488 Welch, V. 756 Wells, C. E. 402 Wells, F. L. 67, 69 Wells, G. 568 Wells, S. E. 395 Welsh, C. 541, 552 Welsh, M. C. 768 ff Welsh, V. 712 Welt, C. 477 Wenar, C. 805 Wendlandt, W. 884, 895 ff Wenig, P. 434, 471
89. Index of Names
954
Weniger, D. 100 f, 103 ff, 109 f, 114, 139 ff, 143, 210 ff, 291 Wepman, J. M. 104, 107, 109 f, 137, 353, 361, 372 Wergeland, H. 791 Werner, H. 596 Werner, O. 550 Wernicke, C. 100, 103 f, 107, 109, 112, 115, 120, 123, 128, 161, 187, 189, 238, 240, 242, 245, 262 f, 516, 607, 647 Wertheimer, M. 310 Wertz, R. T. 298, 364, 366 f, 445, 449, 478 Wessels, J. 176 West, J. 668 West, K. L. 551 f, 802 West, L. J. 69 West, R. F. 719, 902 Westby, C. 782 Wetzel, W. F. 339 Wexler, N. S. 400 Weylman, S. T. 221, 293 f, 385 Wheeler, R. L. 488 Whitaker, H. 101, 188, 193, 219, 229, 236, 274, 501 Whitaker, H. A. 101, 130, 164, 188, 236, 281, 392, 590 f, 648 f, 650 f, 653, 657 White, B. C. 410 White, C. A. M. 367 White, H. 902 f White, N. 590 White, R. 400 Whitehouse, D. 768 Whitehouse, P. J. 401 Whitman, E. N. 514 Wickelgren, W. 634 Widlak, H. 894 Wiener, M. 295 Wiesel, T. 122 Wiig, E. 374, 776 Wilbur, R. 670 Wilcox, J. 668 Wilcox, M. 609 Wilcox, M. J. 362 Wilcox, M. J. 293, 299 Wilcox, S. 698 Wilkes-Gibbs, D. 3, 22, 296 Wilkins, A. 384 Wilkins, R. 788 ff Wilkinson, W. E. 391 Wilks, V. 273 Willanger, R. 411 Willbold, B. 484 Willbrand, M. 827 Willeford, J. 831 Williams, D. 902 Williams, D. E. 888 ff Williams, D. R. R. 367 Williams, E. 27 Williams, J. 756, 782 Williams, J. C. P. 692
Williams, M. 599 Williams, R. J. 421 Williams, R. L. 760 Williams, R. S. 402, 810 Williams, S. 600 ff Williams, S. E. 296 Williamson, D. A. 789 Willis, T. 641, 644 Willmes, K. 103 ff, 110 f, 114, 139 ff, 143 ff, 212, 291, 319, 321, 364, 449 Wilsher, C. R. 763 Wilson, B. C. 848 Wilson, B. 146, 252 f Wilson, D. 12, 17 Wilson, D. H. 219 Wilson, K. 736 Wilson, K. J. 843, 850 Wilson, R. S. 396 Wilson, V. 791 f Wimmer, H. 712, 751 Windsor, J. 206, 440 Wing, A. M. 69 Wing, C. 642, 644 Wing, L. 576, 804, 806 f, 811 Wingate, M. E. 871 ff, 877, 895 Wingfield, A. 5, 905 f Winner, E. 220 Winnitz, H. 827 f Winstein, C. J. 478 Winters, L. C. 50 Wise, B. 718, 730, 758 f Wise, S. P. 115 Wisniewski, A. M. 399 Wisniewski, K. E. 692 Witelson, S. F. 125, 587, 608 Witzel, M. A. 861 Woggon, B. 514 Wolchik, S. A. 701, 703 Wolf, M. 616 Wolf-Schein, E. G. 693 Wolfe, J. 399 f Wolff, S. 789 Wolfe, V. E. 455, 471 Wollok, J. R. 893 Wolozin, B. L. 389 Wong, B. 782 Wood, D. J. 670 Wood, F. 780 Wood, H. A. 670 Wood, J. 866 Wood, S. 700, 704, 706 Wood, V. A. 149 Woodall, S. 641, 644 Woodcock, R. W. 854 Woodhouse, L. 373 Woods, B. T. 590, 648, 651 f, 654 Woods, R. T. 354 Woodward, S. 905 Woolsey, T. 122 Workinger, M. S. 454 Workman, S. H. 685 Worsham, N. 818
Worthley, J. S. 900 f, 911 Wright, B. D. 144 f Wright, C. E. 6 Wright, H. L. 788 ff Wright, P. 830 Wrobel, J. 549, 551 Wulbert, M. 699 f Wulfeck, B. 139, 148, 177, 296 Wunderlich, D. 17 Wundt, W. 161 Wykes, T. 515, 552 Wynne, L. 802 Wyrsch, J. 549
Y Yaghmai, F. 588 Yairi, E. 879, 887, 910 Yamada, J. 628 Yamada, T. 381 Yamadori, A. 155, 271 ff, 498 f, 501 Yaqub, B. A. 501 Yarnell, P. R. 411, 498 Yates, A. J. 402 Yee, P. L. 902 f, 907 Yeni-Komshian, G. H. 500 f Yirmiya, N. 692 Yoder, D. 837 f, 841 Yoder, P. J. 691, 697, 819 Yokota, T. 271 Yonas, A. 758 Yorkston, K. M. 51, 292, 460, 474, 843 f, 848 Yoshioka, H. 43, 418, 421 Young, A. B. 398 Young, A. W. 123, 220, 242, 244, 252 f, 310, 358 Young, G. 589 Young, M. 842, 847 Young, R. R. 453 Younger, R. 827 Yudkovitch, E. 701 Yudovich, F. 829 Yule, W. 603, 693, 716 Yules, R. B. 852
Z Zacks, R. T. 400, 903, 907 Zager, R. P. 768 Zahn-Waxler, C. 597 Zaidel, D. 315 Zaidel, E. 123, 220, 315, 750 Zajdeman, H. 701 f Zambolin, A. 381 Zangwill, O. L. 280, 310, 315, 327 Zavis, D. 903, 907 Zbrodoff, N. J. 330 Zegers, F. E. 716 Zeigler, M. 643 Zeki, S. M. 115, 122, 132
89. Index of Names
Zelinski, E. M. 906 f Zelmanovicz, J. 281 Zettin, M. 158 Zeumer, H. 108 Zgoralewicz, B. 836, 840 f Zhang, Y.-F. 718, 779 Ziegler, W. 435, 438 f, 441, 446, 453 ff, 469, 481 ff, 496 Zielinski, W. 715 Zifcak, M. 778 Zigler, E. 576
955
Zilboorg 510 Zimerman, S. 739 Zimmermann, G. 422, 436 Zimmermann, G. 865, 867 f Zimmerman, H. M. 389 Zimmermann, R. 489 Zinelli, P. 344 f Zingeser, L. B. 178, 296, 911 Zolman, J. E. 715 Zouboff, A. 226 Zuberbier, E. 514, 516 ff
Zubin, J. 553 Zue, V. W. 8 Zurif, E. B. 103, 138, 145, 163 f, 173 f, 176, 178, 210, 291 f, 294, 296, 309, 338, 355, 364, 384, 386, 446, 729, 775, 903 Zwicky, A. M. 12, 188 Zwirner, E. 514 Zwitserlood, P. 9, 13 Zyski, B. J. 438
90. Subject Index The organization of the handbook allows readers to find their topics of interest by way of the volume’s list of contents as well as the list of contents preceding each article. Accordingly, the subject index could be confined to include only the most important additional terms. In compound terms the adjective is listed first (e. g. ‘amnestic aphasia’). Specifying attributes follow the reference noun (e. g. ‘aging, normal’). E xplanatory supplements to terms are given in parentheses after the term (e. g. ‘muteness (in autism)’). Recurring terms have received only one page reference per article.
A Aachen Aphasia Test (AAT 114, 139 acoustic signal 416 acoustic-phonetic analysis 8 activation threshold hypothesis (of multilingualism) 282 acute aphasia 114, 149 adaptation theory 19, 162 adaptive spelling program 761 adjacency pair 20, 551 aerodynamic parameters 437 affect-laden words 511 affective intent 210 afferent motor aphasia 356 aging, normal 911 agnosic alexia 253 agrammatic (aphasics) 29, 99, 336, 912 agrammatic comprehension 158 agrammatic speaker 360 agrammatic speech 160 agrammatism 25, 173, 181, 651 agrammatism (and multilingual- ism) 279 agraphia 130, 343 agraphia (for letters) 327 agraphia with alexia 264 akinesia 462 alexia 129, 343 alexia (for letters) 327 alexia without agraphia 253
alliteration 191, 231 allograph 66 allophone 199 alphabetic stage (of reading development) 746 Alzheimer’s disease 154, 273, 326, 340, 900 Alzheimer’s disease, neuropsychology of — 389 Alzheimer’s disease, neuropathology of — 389 Alzheimer patients 219 American Sign Language (A. S. L.) 298, 662 American Association on Men- tal Retardation 688 American Psychiatric Associa- tion 704 Amerind 298 amnesic patients 340 amnestic aphasia 402 Amsterdam Nijmegen Everyday Language Test (ANELT) 148 amyothrophic lateral sclerosis 459 analogical reasoning 634 analogy 265 analogy approach 199 anaphoric reference 94 anarthria 444, 496 Anglo-American 715 animal 16 anomia 235, 289, 651 anomic aphasia 110, 332 anoxic encephalopathy 409
antagonistic muscles, co-activa- tion of — 866 anterior aphasia 104 aphasia 911 aphasia syndromes 198 aphasic agraphia 264 aphasics (and schizophrenics) 540 aphasiological studies, history of — 238 aphemia 379, 444 aphonia 458 apraxia 289 apraxia of phonation 206 apraxia of speech 198, 428, 478, 875 aprosodia 383 Arabic 76 Arabic digits 325 area, cortical 121 arithmetical abilities 325 articulations, compensatory 860 articulatory buffer 6 articulatory encoding 37 articulatory gesture 34, 416 articulatory loop 908 articulatory program 6 Asperger’s syndrome 789, 804 asphyxia, perinatal 591 association area 122 associational processes, disturbances of — 524 associational intrusion 531 associative intrusions 525
89. Index of Names
956
associative thread 527 assonance 191, 231 asymbolia 314 at-risk children (for childhood schizophrenia) 801 ataxic dysarthria 428, 468, 478 attention deficit 601, 780 attentional disorders 253 atypical child 794 atypical development 804 audiological treatment 661 auditory perceptual problem 726 auditory processing 626 auditory-verbal STM impair- ment 335 autism 574 autistic children 701, 771 automatic speech 93, 218 automatism 100 auxiliaries 175, 177
B babbling 558, 666, 680, 812, 875 basal ganglia 120, 381 basal ganglia disease 466 behavior modification (of read- ing disabled children) 759 behavioral therapy 354 Behaviour Observation Scale for Autism (BOS) 805 Behaviour Rating Instrument for Autistic and Atypical Children (BRIAAC) 805 bilingual (aphasia) 96, 278 Bilingual Aphasia Test (BAT) 149, 286 bilingualism, neuropsychology of — 278 biofeedback 479, 894 biofeedback, aerodynamic 482 bipolar affective psychosis 513 blend (error) 89, 161, 188, 230 blindness 680 Bliss symbols 298, 355, 819 bloodflow studies 219 body postures, abnormal 840 body reactions, abnormal 840 Boston Diagnostic Aphasia Examination (BDAE) 138, 341, 396, 540, 908 Boston Naming Test (BNT) 138, 739, 911 bottom-up information process- ing 629 bradykinesia 462 Brain Function Therapy 356 breathing patterns 458 brief visual displays 735 British Abilities Scales Test of Word Definitions 739
British Sign Language (B. S. L.) 662 Broca’s aphasia 107, 126, 402, 607 Broca’s aphasic 19, 22, 193, 198, 210, 305, 329, 332 Broca’s area 123, 239 Brown’s four factors 871 bulbar palsy, progressive 459
C Caldwell Inventory of Home Stimulation 699 callosal agenesis 748 callosal-sectioned patients 219 canonical babbling 558 cardiac arrest survivors (linguis- tic deficits in -) 414 CAT (computerized axial tomography) 602, 809 cerebellar ataxia, hereditary 469 cerebral organology 311 cerebral palsy 574 checkoff monitor 190 child, young stuttering — 889 childhood aphasia 647 Childhood Autism Rating Scale (CARS) 805 childhood laterality 590 childhood onset schizophrenia 806 childhood schizophrenia 794, 804 children, subgroups of speech disordered — 827 Chinese 70, 161, 212, 711 Chinese reader 749 chromosomal abnormality 692 clause 26 cliché 93, 216 click paradigm 540 clinicoanatomical correlation 125 closed class element 81 closed class vocabulary 164, 169 closed class word 536 Cloze technique 526 cluttering 233 CNS lesion 607 coarticulation 200 Code-Müller psychosocial scale of adjustment 374 cognitive deficits (in aphasia) 311 cognitive deficits (in schizophre- nia) 541 cognitive development 581, 596 Cognitive Grammar theory 872 cognitive load (and speech er- rors) 57 Cognitive Neuropsychological Therapies 358 cognitivists 581 coherence 307
cohesion 307, 550 cohesive weakness 552 cohort theory 8 Columbia Mental Maturity Scale (CMM) 630 communication skills 373 communication system, alterna- tive 853 communication system, augmentative 853 communication system, non- speech 853 communicative competence 567 communicative intention 1, 72 compensatory technique 848 competency problem 388 Competition Model 872 completion phenomenon 229 comprehension disorders 195, 290 computer simulation 239 conceptual impairment 310 conceptual processing, ‘top- down’ — 769 conceptual system 72, 289 conceptualizer 1 concreteness 266 conduction aphasia 112 conduction aphasics 193, 198, 332 conductive hearing loss 663 conduite d’approche 99, 112, 193 conduite d’écart 112, 193 confrontation naming 192 connectionism 121 connectionist model (of speech production) 421 connectionist models of writing 263 construct validity 140 contamination 188 content network approach 484 content validity 146 content word 199 contextual facilitation 296 contextual influence 290 contiguity disorder 162 conventional expression 216 conversation 290 conversational analysis 18 Conversational Coaching Sys- tem 362 conversational discourse 305 coordination dynamics (in speech) 417 coproduction theories (of coarticulation) 38 coprolalia 219, 504 cortex 120 cortical dysarthria 444 counselling therapy 363
89. Index of Names
craniofacial malformations, congenital 858 Creutzfeldt-Jakob disease 402 cricoarytaenoidankylosis 497 critical period (for language acquisition) 591 cross-modal syntactic priming 175 cued speech 662 CYCLE 628 cytoarchitectonics (cortical) 121
D deaf children 708 deep agraphia 267, 359 deep dyslexia 129, 244, 251, 359 deep structure 25 degenerative dementia 235 degrees of freedom (in speech) 416 dementia 313 dementia infantilis 794 dementia praecocissima 794 dementia severity 390 depressed patients 530 depression 513, 597 deprivation 183, 591, 596 derivational errors 266 derivational morphology 176 determiner 176 developmental deep dyslexia 750 developmental dyslexia 588, 768 developmental dysphasia 574 developmental dyspraxia 827 developmental morphemic dyslexics 728 developmental phonological dyslexia 728, 747 developmental reading disorders 742 Developmental Sentence Analy- sis 578 developmental spelling impair- ment 268 developmental stuttering 234 developmental surface dyslexia 728, 744 deviant language 579 diadochokinesis 846 diaschisis 124 digit span 736, 909 direct instruction (of reading disabled children) 755 direct-route reading 255 f disconnexion syndrome 239 discourse 303 discourse analysis 18 discourse coherence 909 discourse feature 703 discourse processing 11 discrimination learning task 634 discrimination task 627
957
disfluency 910 disintegrative speech 797 dissociation (in task perform- ance) 146 dissociations 239 dominant hemisphere distur- bance (in schizophrenia) 534 Down syndrome 586, 688, 699 dream 523 DSM-III (Diagnostic and Statis- tical Manual) 575, 805 dual route models of reading 744 dual task paradigm 589 Dutch 19, 76, 337, 759 dynamic aphasia 359 dysarthria 651 dysarthrophonia 496 dyskinetic dysarthria 839 dyslexia 713 dysphasia 806 dysprosody 469
E early infantile autism (EIA) 804 echo-answer 229 echolalia 100, 193, 580, 812 echopraxia 234 educational retardation 600 educational model 713 efferent motor aphasia 356 elective mutism 574, 788 electro-cortical stimulation (and multilingualism) 281 Electroencephalography (EEG) 131, 809 electroglottography (EGG) 436 electromagnetic articulography (EMA) 434, 471 electromyography (EMG) 416, 433, 866 electropalatography 435 elementaristic strategy (of lan- guage processing) 705 ellipsis 29 emotion 291 emotional content 385 emotional meaning 511 emotional stress 553 English 9, 27, 36 f, 55, 70, 76, 79, 95 f, 163, 172, 182, 191, 210, 279, 282, 322, 328, 338, 360, 564, 580, 610, 662, 751, 759 environmental specificity 596 epileptic fits 231 equipotentiality hypothesis 647 ethnomethodology, sociolinguis- tic 361 Event-Related Potentials (ERP) 131
evoked potentials 219 expansion 641 expletives 216 expressive aphasia 104 eye dominance 734 eye movements 734 eye-voice-span 713
F face-to-face interaction 16 facet theory 140 family therapy 363, 374 feature spreading (and coarticulation) 37 feedback, negative (in stuttering) 886 fine-tuning 698 finger agnosia 328 finger-spelling 662 Finnish 70, 205, 711 flaccid dysarthria 430 Flemish 226 fluency facilitators (in stuttering) 889 fluency interruptors (in stutter- ing) 889 fluency training 894 fluent aphasia 104, 210 focused stimulation 642 formal thought disorder 540 formal verbal paraphasia 188 formulator 24 fragile X syndrome 586, 692, 808 French 24, 96, 204, 226, 328, 359 Freudian 96 Freudian error 55 Friedreich’s ataxia 469, 470 frontal lobe insult 333 frontosubcortical system 217 function word 161 Functional Communication Therapy 361 functor 199
G general intelligence test 688 generative transformational grammar 162 gentle onset (and stuttering) 894 German 17, 19 f, 23, 25, 29, 75 ff, 161, 177, 210, 227, 580, 613, 681, 703, 712, 751, 759 Gerstmann syndrome 326 f gestalt-like strategy (of language processing) 705 gestural behavior 320 gesture-to-picture matching tasks 291 global aphasia 105, 127
89. Index of Names
958
global aphasics 220, 333 Global Deterioration Scale 391 glue ear 660 Gottschald’s Hidden Figures Test 314 Government and Binding 165 grammatical awareness 779 grammatical development 564 grammatical deviance (in schizophrenic speech) 538 grammatical encoding 4 grammatical judgment screening test (for elementary school- aged children) 782 grammatical(ity) judgement 165, 177, 211, 338 grammatical morpheme 538 grammatical role 88 grammatical word 536 grapheme 66, 252 graphemic buffer 266, 344 graphemic buffer agraphia 269 graphic motor pattern 66 Greek 280
H hallucination 796 handedness 125, 656 haplology 55 head turning 589 hearing impairment 574 hearing-loss 660 Hebrew 164, 279, 580, 734 Helm Elicted Language Syntax Stimulation (HELPSS) pro- gramme 357 hemidecorticates 590 hemidecortication 313 hemiplegia 647 hemisphere (cerebral) 120 hemisphere equipotentiality 590 hemisphere structure 587 hemispherectomized adults 219 hemispheric asymmetries 210 hemispheric dominance 647 hesitation, pathological 51 heuristic strategy 163, 173 heuristic procedures in speech comprehension 292 hierarchical planning 632 high functioning (in autists) 575 Huntington’s disease 462 Huntington’s disease, neuropathology of — 398 Huntington’s disease, neuropsychology of — 398 hyperkinetic dysarthria 429 hypernasality 458, 483, 841 hypoglossal nerve 458 hypokinetic dysarthria 428 hypospontaneity (of speech) 651 hypothesis testing 633
I idea unit 50 ideomotor apraxia 320 idiom 216, 292 Illinois Test of Psycholinguistic Abilities (ITPA) 737 illocutionary intention 1 imageability 266 imitation 595, 641, 685 imitative language 580 impression-management (and schizophrenia) 553 incidental language teaching 641 incoherence (of discourse) 30, 524 incremental production 25 incrementality 74 f indirect requests 216 Indo-European 265 infantile autism 794 infantile cerebral injury 313 infantile personality 510 inflection 183 inflectional morphology 176 information processing difficul- ties 606 inner speech 335 insertion paradigm 177 interactive activation models 242 interarytaenoidfibrosis 497 interhemispheric speech organization 656 internal speech 6 intersegmental durations 446 intonation 209 intraarticulator kinematics 446 intrahemispheric speech organization 656 intraoral pressure 458 invariance hypothesis (of lateralization) 649 invariant lateralization hypothe- sis 587 invasive (in conversation) 553 irregular words 265 isolation of the speech area (syndrome) 104, 113, 193 Italian 76 f, 165, 177, 183, 610, 748 iteration 234
J Japanese 130, 204, 265, 271, 282 jargon aphasia 95, 187, 535 jargon, neologistic 99 jargon, phonemic 99 jargon, semantic 99, 232
K Kana 130, 271
Kanji 130, 271 Kanner’s syndrome 804 key-word technique 484 Kiddie Formal Thought Disor- der Scale (K-FTDS) 799 kinematic events 867 kinematics 434
L Landau-Kleffner’s syndrome 227 language acquisition device (LAD) 586 language competence 582 language delay 574, 597, 635 language disabled children 771 Language Enrichment Therapy programme 356 language experience approach (to reading disability) 761 language input 580, 698 language learning environment 829 language onset 681 Language Oriented Therapy (LOT) 354 language performance 582 language system model 872 language teaching strategy 702 language treatment 640 LARSP 669 laryngeal nerve 458 larynx 491 latent schizophrenia 794 later onset autism 807 lateral shift hypothesis 592 lateralization (and multilingual- ism) 281 lateralization (of higher mental functions) 98 learnability theory 629 learning of words 339 legasthenia 714 Leiter International Perform- ance Scales 630 lemma 4, 25, 75 letter shape map 252 letter-by-letter reading 253 lexeme 5 lexical access 872 lexical agraphia 267 lexical bias 59, 63, 78 lexical comprehension 154 lexical decision 173 lexical decision (in schizophre- nia) 528 lexical development 561, 609 lexical deviance (in schizophre- nia) 534 Lexical-Functional Grammar 25 lexical selection deficit 154 linguistic agraphias, anatomic relationships of — 269 linguistic competence 558
89. Index of Names
linguistic input 580 lip-reading 668 lobectomy 655 localization (cerebral) 120 logoclonia 235 logogen model 242 logogen system 744 logographic reading 746 long-term memory 737 loose thinking 683 low functioning (autists) 575 lower motor neuron dysarthria 457
M malapropism 55, 83, 188 maltreated children 597 mania 513 manic psychoses 801 manics 537, 552 markedness (phonological) 59 mass-spring system 418 maternal adjustment (to child language) 706 mathematical processing 325 Matthew-effects 720 maxillary reshaping prostheses 488 meaning postulates 154 medical model 574, 713 Melodic Intonation Therapy (MIT) 356, 484 mental lexicon 4 mental model 12 mental retardation 574, 586, 700, 806 mentally retarded children 771 message 3 f, 24, 72, 289 message, coherent 535 message, derived 11 metabolic disorder 692 metacognition 773 metacommunicative (commen- tary) 550, 553 metalanguage 773 metalinguistic awareness 774 metalinguistic problems 615 metalinguistic skills 773 metalinguistic task 778 metalinguistic training (of read- ing disabled children) 782 metaphor 292, 385, 813 metrical frame 5 microcomputer 354 micrographia 234 Mill Hill Synonyms Test 314 Mini-Mental State Examination 391 minimal aphasia 380 minimal attachment 10 minimal brain damage (MBD) 681 minimal dysphasia 378
959
Minnesota Test for the Differen- tial Diagnosis of Aphasia 353 mixed dysarthria 430 mixed transcortical aphasia 113 MLU (mean length of utter- ance) 566, 589, 610, 631, 689, 700 modeling 641 modularity (of mind) 16, 26, 315 module, cortical 122 monemic paraphasias 188 monitor(ing) 6, 161, 193, 242 monophasia 225 monosynaptic reflexes 455 morpheme-sized processing units 269 morphological category 55 morphological composition 182 morphological development 564, 610 morphological error 58 morphological paraphasias 181 morphology 161, 191, 246 morphosyntax (and schizophre- nia) 552 motherese 581, 697 motor aphasia 104 motor control (of speech) 417, 448 motor pathologies (in schizophrenia) 527 motor skills, intentional 44 motor speech problems 213 movement parameters (in motor speech disorders) 432 movements, involuntary 463 multi-infarct dementia 235 multidimensional scaling proce- dure 140 multilingual (aphasia) 96 multiple sclerosis 219 multisensory teaching (of read- ing disabled children) 760 muscle action potentials 433 muscle spindles 455 muteness (in autism) 811 mutism 378, 650, 801 myasthenia gravis 460 myoclonus, palatal 430, 469 myoelastic-aerodynamic theory (of voice production) 491 myopathy 460
N naming deficits 738 narrative discourse 305 narrative superstructure 305 nativists 595 nature-nurture debate 580 neglect dyslexia 252
neologism 94, 99, 184, 198, 544, 796, 911 neologistic jargon aphasia 231 neologistic oral reading 192 network, associative 528 network models of memory 900 network model (of speech production) 77 network system 85 neurodegenerative disease 154 neurodevelopmental treatment 849 neurological abnormality 589 neuropsychological test of lan- guage 911 neurosis 510 New Adult Reading Test 311 non-fluency 127, 652 non-nutritive sucking disinhibi- tion paradigm 589 non-word production 203 nonfluent (aphasia) 104, 210 nonpropositional speech 291 nonverbal behavior 289 nonverbal comprehension in aphasia 291 nonvocal rehabilitation tech- niques 298 nonword 78 nonword reading 727
O olivo-ponto-cerebellar degenera- tion 469 open class element 81 open class vocabulary 164, 169 open-class word 538 operant discrimination learning 759 ophthalmological intervention (in reading disability) 762 optic aphasia 102 optic aphasia for colours 359 oral apraxia 319, 444 oral-mandibular dystonia 463 organismic specificity 596 orofacial sensory input 478 orthographic lexicon 759 orthographic processes 66 orthographic skills 758 orthographic stage (of reading development) 746 orthographic system 265 Orton-Travis theory (of stutter- ing) 865 otitis media 609, 663 overextension 562, 683
P paired-associate learning 738 palatal lift prosthesis 460
89. Index of Names
960
paligraphia 234 palilalia 96, 233, 463 palipraxia 234 pantomime 314 pantomime agnosia 289 paragrammatic(al) (speech) 99, 160, 534 paragrammatism 181, 797 paragrammatism (and multilingualism) 279 parallel distributed processing 347 paraphasia 651 paraphasia, semantic 99 paraphasia, phonemic 99 parent-child-interaction 701 parental psychological disorders 880 parental report 724 parietal agraphia 264 Parkinson’s disease 96, 314, 342, 461, 478 Parkinson’s disease, neuropathology of — 395 Parkinson’s disease, neuropsychology of — 395 part of speech 54 particle 17 pause 46 pause-filler 216 pause lenght 526 Peabody Picture Vocabulary Test (PPVT) 313, 397, 628, 700 PEG (pneumoencephalogram)
809 perceptual bias 61 perceptual decoding skills, ‘bot- tomup’ — 769 performance problem 388 perseveration 100, 188, 231 pervasive developmental disor- der (PDD) 805 pharmacotherapy (in reading disability) 763 phase transition (among articulatory gestures) 420 Phoenician reader 749 phoneme to grapheme conver- sion 265 phoneme-grapheme-correspondence 756 phonemic approximations 202 phonemic buffer 199 phonemic clause 47 phonemic errors (in children) 842 phonemic paraphasias 182, 187, 197, 245 phonetic derivation 484 phonetic disintegration 444 phonetic feature 8 phonetic gesture 43 phonetic placement technique 483
phonetic transition (in stutter- ing) 875 phonetics 34 phonics approach (to reading disability) 756 phonologic buffer 345 phonological agraphia 266 phonological alexia 359 phonological awareness 724, 778 phonological blocking 154 phonological-core variable-difference model 719 phonological development 558, 609 phonological disorders, familial 829 phonological disorder (in speech disorderd children) 826 phonological distortion 198 phonological dyslexia 244, 257 phonological encoding 5, 245 phonological feature 34, 58 phonological information 416 phonological lexical representa- tion 245 phonological lexicon 199 phonological processing 718 phonological reading 255 phonological representation 194 phonological representation, underlying 246 phonological segment 416 phonological store 908 phonological unit 419 phonological universals 421 phonological word production, model of — 199 phonology (in stuttering) 872 phononeuroses 493 phonoponoses 493 phonotactic contraints 56 photoglottography (PGG) 436 Pick’s disease 154 Pick’s disease, neuropathology of — 401 Pick’s disease, neuropsychology of — 401 Pitres’ rule 280 pneumograph 437 Polish 711 poly-infarct dementia 231 polyneuropathies 460 poor reader 714, 756 poor speller 756 Positron Emission Tomography (PET) 131 posterior aphasia 104 pragmantax 17 pragmatic development 618 prelingual hearing loss 665 prelinguistic infant 560 prepositions 174
prescriptive teaching (of reading disabled children) 754 prespeech 558 primary auditory cortex 500 priming 88 priming effect 690 progressive lateralization hypothesis 587, 648 progressive aphasia 156 progressive supranuclear palsy 234 Progressive Matrices 311, 314 Promoting Aphasics’ Communicative Efficiency (PACE) 298, 362 pronominal reversal 813 proper noun 176 propositional 3 propositional speech 93 propositionality 872 prosodic decoding 9 prosodic development 814 prosodic specification 5 prosody 226, 291 prosody (in stuttering) 871 protostuttering 875 prototypicality 88 proverb 216 Proverb Interpretation Test 907 pseudo-psychopathic schizophre- nia 794 pseudobulbar dysarthria 453 psychiatric disorders (other than schizophrenia) 538 psychoanalysis 510 psychoanalytical 511 psycholinguistic models of language processing 352 Psycholinguistic Assessment of Language Processing in Aphasia(PALPA) 148 psychological reality 48 psychometrics 140 psychoneurotic (patients) 511 psychosis of childhood 804 psychosocial adjustment to aphasia 372 psychosocial sequelae 600 psychosomatic disease 510 psychotherapy (in reading dis- ablity) 762 punning 525 pure agraphia 264 pure alexia 129, 359 pure word-blindness 253 pure word deafness 128, 240 pyramidal tract 455
R random generator 189 rapid automatized naming task (RAN) 738, 780
89. Index of Names
reading development 778 reading difficulties 600 reading disability (in speech disordered children) 832 reading disorders 240 reading route 744 receptive aphasia 104 reciprocity 699 recurring utterances 213 reference 22 referential communication 550 reinforcement (and stuttering) 894 reinforcers, positive (in stutter- ing) 886 relaxation techniques 484 reliability (psychometric) 143 repair 7, 19, 27 repetition 525 repetition deficit 336 repetition method 626 reproduction conduction apha- sia 345 reproduction deficit 336 resource 282, 289 respiratory kinematics 437 respiratory system 457 responsiveness 700 retinocentric feature map 251 retro-lental fibroplasia (RLF) 681 Rett syndrome 807 RH-damaged patients 210 rhythmic-prosodic structure of speech 706 Ribot’s rule 280 right hemisphere 217 right hemisphere-damaged pa- tients 333 rigidity 463 Roman numerals 325 root morphemes 199 Russian 25, 164, 226, 279
S Scale of Social Participation in Play 631 scan-copier 77, 190 schizophasia 535 schizophrenia 602, 794 schizophrenia, diagnosis of — 522 schizophrenic discourse 549 schizophrenic language 95 schizophrenic syndrome of childhood 794 schizophrenic utterances 549 selection restriction (semantic 3 selective reinforcement 595 self-monitoring 895 semantactic development
961
cf. se-mantic development, cf. syn-tactic development semantic agraphia 268 semantic decomposition 153 semantic development 612 semantic dyslexia 255 semantic errors 182 semantic jargon aphasia 232 semantic paragraphia 154, 188, 267 semantic priming 155, 902 semantic priming (in Alzhei- mer’s disease patients) 393 semantic priming (in schizophre- nia) 528 semantic reading error 258 semantic role 73 sensori-motor intelligence 581 sensorimotor correction 478 sensorimotor integration 427 sensorimotor processes (in speech) 476 sensory aphasia 104 sensory deficits 194 sensory feedback (in speech) 476 sentence level 73 Sentence Level Auditory Comprehension (SLAC) pro- gramme 357 sequencing task 627 serial speech 216 serial memory 627 sex differences (in cerebral organization) 125 shift error 81 short-term memory 706, 736 short-term verbal memory 195 shyness, inordinate 788 sign language 662 sign language aphasia 318 similarity disorder 162 simultaneous communication training (in autism) 818 single case studies 165 single word-reading task 727 slang 216 slip of the tongue 189, 204, 536, 875 SLIPS task 60 social-interactive model of language acquisition 684 socialization style 706 socio-emotional behavioral disorders 601 somatoform disorder 510 sound blending test 737 sound categorization task 724 sound error 76 Spanish 75 ff, 85, 87, 279, 748 spasmodic dysphonia 462 spastic cerebral palsy 454
spastic dysarthria 428, 840 specific language impairment 574 speech act 17, 289, 361 speech automatism 227 speech error 25, 910 speech fluency 198 speech formulas 216 speech initiation reaction time 462 speech intelligibility 667, 847 speech perception 904 speech sound durations 446 speech sound sequencing 484 speech style 697 speech training approach (to autism) 814 speed-accuracy trade-off 70 spelling disorder (in speech disordered children) 832 stage theories of reading development 712 stereotyped form 216 stereotyped utterances 218 stimulation therapy 353 stranding exchange 80 stutter-specific constellations 880 stuttering 422 stuttering children 870 stuttering, development of — 879 stuttering, motor instability in — 866 stuttering, multifactorial models of — 865 stuttering, neurogenic 235 stuttering, psychogenic 880 subcortical dementia 342 subcortical structures 129 subglottic pressure 843 subsystems hypothesis (of multilingualism) 282 supplementary motor area 319 supplementary speech area 127 surface agraphia 359 surface dyslexia 104, 129, 251, 359 surface dyslexia, acquired syndrome of — 768 surface structure 4 Swedish 76, 725 syllabic structure 199 syllabification 5 syllable 53, 57, 76, 420 syllable constraints 191 syllable (in stuttering) 871 symbiotic psychosis 794, 804 symbolic play 622, 631 Symbolic Play Test 631 symbolic representation hypoth- esis 632 syndromes of aphasia 356 Syndromwandel 105 synergetics 419
962
synergy 43 syntactic categories, major 170 syntactic categories, minor 170 syntactic complexity 48 syntactic complexity (in stutter- ing) 871 syntactic contamination 161 syntactic development 565, 612 syntactic loss hypothesis 337 syntactic persistence 73 syntactic priming 73, 175 syntactic processing, autonomy of — 9 syntactic structure 539
T tactile aphasia 359 tardive dyskinesia 463 task demands 289 task-dynamic model (of speech production) 422 teaching deficit 755 telegraphic speech 564 telegraphic style 22 telescopage 188 Templin-Darley Screening Test of Speech Articulation 628 temporal coordination, interarticulatory 472 tense 23, 27 Test for Reception of Grammar 689 text comprehension 306 text production 305 Thai 210 thalamus 120, 381 thematic role 4, 24, 88 thought disorder 550 thought disturbance 522 tip-of-the-tongue case 82 tip-of-the-tongue experience 5, 59, 85, 900 Token Test 138, 335, 393, 540, Token Test for Children 628 tone 209 topicalization 296 Tourette’s disease 219
trajectories (of articulatory movement) 435 transcortical motor aphasia 113, 127, 235, 240, 379 transcortical sensory aphasia 113, 128, 193, 240 transitional probability (in speech) 47 translation, compulsive 279 translation, paradoxical 279 translation theories (of speech production) 35 traumatic mutism 788 Treatment of Aphasic Persevera- tion (TAP) 355 Turkish 564 turn(-taking) 19, 361, 551, 568, 685 twins 599, 809
U ultrasound imaging 435 underextension 562 unilateral upper motor neuron dysarthria 428
V verbal paraphasia 187 verbal repetition deficits 725 verb retrieval 178 verbalism 683 verbigeration 797 vibrotactile aids 673 video-endoscopy 435 Visual Action Therapy (VAT) 357 visual dyslexia 254 visual error 182, 254, 266 visual handicap 680 visual imagery 581 visual input lexicon 252 visual memory ability 734 visual-spatial code (in writing and typing) 70 voice onset time (VOT) 446 voice production 491 voice tremor 430
Voluntary Control of Involun- tary Utterances (VCIU) 355 VOT (voice onset time) 628
W WADA procedure 219 Wallonian 328 Wechsler Adult Intelligence Scale (WAIS) 311, 393 Wechsler Memory Scale 393 Wernicke’s aphasia 96, 109, 128, 187, 607 Wernicke’s aphasic 20, 29, 193, 198, 210, 305, 329, 332 Wernicke’s area 128, 239 Wernicke-Lichtheim diagram 100, 238 Western Aphasia Battery (WAB) 115, 138, 341 Williams syndrome 586, 692 WISC 669 word association 901 word awareness 779 word class 266 word exchange 79, 84 word fluency task 873 word length 201 word monitoring 174, 184 word naming task 902 word order 161 word priming 178 word repetition task 780 word spurt 562 word substitution 82 word-blindness, congenital 742 word-finding difficulties 900 word-form dyslexia 253 word-onset gating paradigm 905 word-salad 535 working memory 86, 190, 736, 904 writing disorders 241 written discourse 305
X X-ray microbeam (XRMB) 434
