Clinical Aphasiology: Future Directions

Clinical Aphasiology This book presents a collection of cutting edge work from leading researchers and clinicians arou...

Author: Ball Damico

231 downloads 1172 Views 2MB Size Report

This content was uploaded by our users and we assume good faith they have the permission to share this book. If you own the copyright to this book and it is wrongfully on our website, we offer a simple DMCA procedure to remove your content from our site. Start by pressing the button below!

Report copyright / DMCA form

DOWNLOAD PDF

Clinical Aphasiology

This book presents a collection of cutting edge work from leading researchers and clinicians around the world on a range of topics within Clinical Aphasiology. However, more than this, the volume is also a tribute to Chris Code, one of the foremost scholars in the ﬁeld. Professor Code has made a galvanizing impact on the ﬁeld: as a savant, a motivator and an impresario of trends which have resulted in several signiﬁcant developments in the ﬁeld. In the ﬁrst chapter of this book the editors outline the considerable contributions Chris Code has made to the area. The remaining contents have been divided into three main approaches to the study of aphasia, reﬂecting Professor Code’s own interests. First are the contributions that fall under the heading of Conceptual Considerations. These are mainly interdisciplinary in nature, spanning linguistics, phonetics, psychology and neurology, as well as social aspects of communication disorders. The second section of the book deals with Research Considerations, with chapters ranging from how the study of disrupted communication can inform models of normal language processing, through tone production and processing in speakers with aphasia, to anomia and progressive multifocal leukoencephalopathy. Each of these chapters explores diﬀerent aspects of research methodology, including quantitative and qualitative research. The ﬁnal section of the collection deals with Clinical Considerations; the chapters here cover counselling, computerized training, cultural and linguistic diversity in aphasia, right hemisphere disorders, and communication problems in the dementias. Clinical Aphasiology will be an invaluable tool for both students and practitioners in speech and language pathology, psychology, neurology, and related ﬁelds. Martin J. Ball is Hawthorne-Board of Regents’ Support Fund Endowed Professor, Head of the Department of Communicative Disorders, and Director of the Doris B. Hawthorne Center for Special Education and Communication Disorders at the University of Louisiana at Lafayette. Jack S. Damico holds the Doris B. Hawthorne Eminent Scholar Professorship in Communicative Disorders at the University of Louisiana at Lafayette and is a Fellow of the American Speech-Language-Hearing Association.

Clinical Aphasiology Future directions

Edited by Martin J. Ball and Jack S. Damico

A Festschrift for Chris Code

First published 2007 by Psychology Press 27 Church Road, Hove, East Sussex BN3 2FA Simultaneously published in the USA and Canada by Psychology Press 270 Madison Avenue, New York, NY 10016 Psychology Press is an imprint of the Taylor & Francis Group, an Informa business This edition published in the Taylor & Francis e-Library, 2007. “To purchase your own copy of this or any of Taylor & Francis or Routledge’s collection of thousands of eBooks please go to www.eBookstore.tandf.co.uk.” © 2007 Psychology Press All rights reserved. No part of this book may be reprinted or reproduced or utilized in any form or by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying and recording, or in any information storage or retrieval system, without permission in writing from the publishers. This publication has been produced with paper manufactured to strict environmental standards and with pulp derived from sustainable forests. British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Library of Congress Cataloging in Publication Data Clinical aphasiology : future directions / edited by Martin J. Ball and Jack S. Damico. p.; cm. Includes bibliographical references and index. ISBN-13: 978–1–84169–670–6 (hardcover) ISBN-10: 1–84169–670–6 (hardcover) 1. Aphasia. 2. Speech disorders. 3. Language disorders. I. Ball, Martin J. (Martin John) II. Damico, Jack Samual. III. Code, Christopher, 1942– [DNLM: 1. Aphasia—Festschrift. WL 340.5 C6386 2007] RC425.C55 2007 616.85′52—dc22 2006032956 ISBN 0-203-96255-9 Master e-book ISBN ISBN: 978–1–84169–670–6

Contents

Professor Chris Code’s publications and presentations Tabula gratulatoria Contributors Preface 1 Chris Code’s contribution to aphasiology

x xx xxiii xxvi 1

MARTIN J. BALL AND JACK S. DAMICO

PART I

Conceptual considerations 2 Investigations in speech and language and related disorders: Crossing the boundaries between disciplines—a tribute to Chris Code

15

17

MANFRED HERRMANN AND THORSTEN FEHR

3 Independent evidence for the uniﬁcation of explanatory paradigms in the neurosciences

28

HUGH W. BUCKINGHAM AND SARAH S. CHRISTMAN

4 The social and neuropsychological underpinnings of communication disorders after severe traumatic brain injury

42

SKYE McDONALD

5 Social validation of recovery in aphasia

72

LEONARD L. LaPOINTE AND KERRY L. LENIUS

6 Interactional aphasia: Principles and practices oriented to social intervention JACK S. DAMICO, MARTIN J. BALL, NINA N. SIMMONS-MACKIE AND NICOLE MÜLLER

92

vi

Contents

PART II

Research considerations 7 From the study of language dysfunction and handicap to a better understanding of linguistic processing in normality

105

107

JEAN-LUC NESPOULOUS AND JACQUES VIRBEL

8 Production and perception of word tones in patients with brain damage

125

INGER MOEN

9 Subcortical aphasia: Historical perspective and contemporary thinking

136

BRUCE E. MURDOCH

10 Mechanisms of lexical selection and the anomias

156

TOBIAS BORMANN, GERHARD BLANKEN AND CLAUS-W. WALLESCH

11 Repetitive verbal behaviours in PML: An exploratory study of conversation

168

NICOLE MÜLLER, ALANA KOZLOWSKI AND PATTIE DOODY

12 Multiparty interactions in aphasia

181

ALISON FERGUSON

13 Stroke stories: Conveying emotive experiences in aphasia

195

ELIZABETH ARMSTRONG AND HANNA K. ULATOWSKA

PART III

Clinical considerations

211

14 Counseling families and adults with speech and language disorders: The view from a wellness perspective

213

AUDREY L. HOLLAND

15 Cultural dimensions of aphasia: Adding diversity and ﬂexibility to the equation

222

CLAIRE PENN

16 Assessment of aphasia in a multi-lingual world SUSAN EDWARDS AND ROELIEN BASTIAANSE

245

Contents 17 Computerized aphasia treatment outcomes research: The past and a proposal

vii 259

RICHARD C. KATZ AND ROBERT T. WERTZ

18 Traumatic brain injury rehabilitation: Advanced communication training perspectives

270

LEANNE TOGHER

19 The future of our knowledge about communication impairments following a right-hemisphere lesion

284

YVES JOANETTE, MAUD CHAMPAGNE-LAVAU, KARIMA KAHLAOUI AND BERNADETTE SKA

20 Progressive language and speech disorders in dementia

299

MARIA PA˛ CHALSKA

Author index Subject index

325 339

Gabrielle Code

Professor Chris Code’s publications and presentations

Books Müller, D., Munro, S., & Code, C. (1981). Language assessment for remediation. Beckenham, UK: Croom Helm. Code, C., & Müller, D. (Eds.) (1983). Aphasia therapy. London: Edward Arnold. (Translated and published in Italian as Terapia dell’Afasia. Roma: Marrapese Editore, 1984.) Code, C., & Ball, M. (Eds.) (1984). Experimental clinical phonetics. London: Croom Helm. Code, C. (1987). Language, aphasia and the right hemisphere. Chichester, UK: John Wiley. (Translated and published in Japanese, Central Foreign Books, Tokyo, 1990.) Code, C. (Ed.) (1989). The characteristics of aphasia.Brain damage, behaviour and cognition series. Hove, UK: Lawrence Erlbaum Associates Ltd. (Previously published by Taylor & Francis, London.) Code, C., & Müller, D. (Eds.) (1989). Aphasia therapy (2nd ed). London: Cole & Whurr. Code, C., & Müller, D. J. (1992). The Code-Müller protocols: Assessing perceptions of psychosocial adjustment to brain damage. Kibworth: Far Communications. Code, C., & Müller, D. J. (Eds.) (1995). The treatment of aphasia: From theory to practice. London: Whurr. Code, C., & Müller, D. J. (Eds.) (1996). Forums in clinical aphasiology. London: Whurr. Code, C., Wallesch, C.-W., Lecours, A.-R., & Joanette, Y. (Eds.) (1996). Classic cases in neuropsychology. Hove, UK: Lawrence Erlbaum Associates Ltd. Ball, M. J., & Code, C. (Eds.) (1997). Instrumental clinical phonetics. London: Whurr. McDonald, S., Togher, L., & Code, C. (Eds.) (1999). Traumatic brain injury and communication disorders. Hove, UK: Psychology Press. Code, C., Wallesch, C.-W., Lecours, A.-R., & Joanette, Y. (Eds.) (2003). Classic cases in neuropsychology: Volume II. Hove, UK: Lawrence Erlbaum Associates Ltd. O’Halloran, R., Worrall, L., Code, C., Toﬀolo, D., & Hickson, L. (2004). The inpatient functional communication interview. Bicester, UK: Speechmark Publications. Code, C. (Ed.) (2006). The representation of language in the brain. Hove, UK: Psychology Press. Tesak, J., & Code, C. (in press). Milestones in the history of aphasia: Theories and protagonists. Hove, UK: Psychology Press.

Chris Code’s publications

xi

Chapters in books Code, C. (1983). Hemispheric specialization retraining in aphasia: Possibilities and problems. In C. Code & D. Müller (Eds.), Aphasia therapy. London: Edward Arnold. Code, C., & Müller, D. (1983). Perspectives in aphasia therapy. In C. Code & D. Müller (Eds.), Aphasia therapy. London: Edward Arnold. Müller, D., & Code, C. (1983). Interpersonal perceptions of psychosocial adjustment in aphasia. In C. Code & D. Müller (Eds.), Aphasia therapy. London: Edward Arnold. Code, C. (1984). Delayed auditory feedback. In C. Code & M. Ball (Eds.), Experimental clinical phonetics. Beckenham, UK: Croom Helm. Code, C., (1984). Dichotic listening. In C. Code & M. Ball (Eds.), Experimental clinical phonetics. Beckenham, UK: Croom Helm. Code, C., & Ball, M. (1988). Apraxia of speech: The case for a cognitive phonetics. In M. Ball (Ed.), Theoretical linguistics and disordered language. Beckenham, UK: Croom Helm. Code, C. (1989). From symptoms to syndromes to models: The nature of aphasia. In C. Code (Ed.), The characteristics of aphasia. Hove, UK: Lawrence Erlbaum Associates Ltd. Code, C. (1989). Speech automatisms and recurring utterances. In C. Code (Ed.), The characteristics of aphasia. Hove, UK: Lawrence Erlbaum Associates Ltd. (Previously published by Taylor & Francis, London.) Code, C., & Müller, D. J. (1989). The future history of aphasia therapy. In C. Code & D. Müller (Eds.), Aphasia therapy (2nd ed). London: Cole & Whurr. Code, C. (1994). The role of the right hemisphere in the treatment of aphasia. In R. Chapey (Ed.), Language intervention strategies in adult aphasia. Baltimore, MD: Williams & Wilkins. Code, C., & Müller, D. (1995). Cognitive and neuropsychological approaches. In C. Code & D. J. Müller (Eds.), The treatment of aphasia: From theory to practice. London: Whurr. Code, C., & Müller, D. (1995). Eﬃcacy & eﬀectiveness. In C. Code & D. J. Müller (Eds.), The treatment of aphasia: From theory to practice. London: Whurr. Code, C., & Müller, D. (1995). Pragmatic, linguistic and functional perspectives. In C. Code & D. J. Müller (Eds.), The treatment of aphasia: From theory to practice. London: Whurr. Code, C., & Müller, D. (1995). Psychosocial perspectives. In C. Code & D. J. Müller (Eds.), The treatment of aphasia: From theory to practice. London: Whurr. Code, C. (1996). Aphasia therapy. In J. G. Beaumont & J. Sergent (Eds.), Blackwell dictionary of neuropsychology. Oxford, UK: Blackwell. Code, C. (1996). Auditory techniques. In C. Code & M. Ball (Eds.), Instrumental clinical phonetics (2nd ed). London: Whurr. Code, C. (1996). Classic cases: Ancient and modern milestones in the development of neuropsychological science. In C. Code, C.-W. Wallesch, Y. Joanette, & A.-R. Lecours (Eds.), Classic cases in neuropsychology. Hove, UK: Lawrence Erlbaum Associates Ltd. Code, C. (1996). Speech from the isolated right hemisphere? Left hemispherectomy cases E.C. and N.F. In C. Code, C.-W. Wallesch, Y. Joanette, & A.-R. Lecours (Eds.), Classic cases in neuropsychology. Hove, UK: Lawrence Erlbaum Associates Ltd.

xii

Chris Code’s publications

Code, C., & Müller, D. (1996). Assessing for treatment. In C. Code & D. J. Müller (Eds.), Forums in clinical aphasiology. London: Whurr. Code, C., & Müller, D. (1996). Computers in clinical aphasiology. In C. Code & D. J. Müller (Eds.), Forums in clinical aphasiology. London: Whurr. Code, C., & Müller, D. (1996). Issues in clinical aphasiology. In C. Code & D. J. Müller (Eds.), Forums in clinical aphasiology. London: Whurr. Code, C., & Müller, D. (1996). Psychosocial issues. In C. Code & D. J. Müller (Eds.), Forums in clinical aphasiology. London: Whurr. Code, C. (1997). A metamodel for recovery from aphasia. In J. Ponsford, P. Snow, & V. Anderson (Eds.), International perspectives in traumatic brain injury. Melbourne: Australian Academic Press. Code, C. (1997). Aphasia recovery, therapy and psychosocial adjustment. In A. Baum, C. McManus, S. Newman, J. Weinman, & R. West (Eds.), The Cambridge handbook of psychology, health & medicine. Cambridge, UK: Cambridge University Press. Code, C. (1997). Experimental audioperceptual techniques. In M. J. Ball & C. Code (Eds.), Instrumental clinical phonetics. London: Whurr. McDonald, S., Togher, L., & Code, C. (1999). The nature of traumatic brain injury: An overview. In S. McDonald, L. Togher, & C. Code (Eds.), Traumatic brain injury and communication disorders. Hove, UK: Psychology Press. Togher, L., Code, C., & McDonald, S. (1999). Communication problems following traumatic brain injury. In S. McDonald, L. Togher, & C. Code (Eds.), Traumatic brain injury and communication disorders. Hove, UK: Psychology Press. Togher, L., Hand, L., & Code, C. (1999). Exchange of information in the talk of people with traumatic brain injury. In S. McDonald, L. Togher, & C. Code (Eds.), Traumatic brain injury and communication disorders. Hove, UK: Psychology Press. Herrmann, M., Müller, D. J., Ebert, A. D., & Code, C. (2000). Erwartungshaltungen an psychosoziale Anpassung nach Hirnschadigungen. In W. Fries & C. Wendel (Eds.), Ambulante Komplex-Behandlung von Hirnverletzten Patienten. München: W. Zuckschwerdt Verlag. McCooey, R., Toﬀolo, D., & Code, C. (2000). Assessing and treating functional communication in the acute hospital. In L. Worrall & C. Fratalli (Eds.), Functional communication. New York: Thieme Science. Code, C., & Hogan, A. (2001). Engaging the client in a helping relationship. In A. Hogan (Ed.), Hearing rehabilitation for deafened adults. London: Whurr. Code, C., Eales, C., Pearl, G., Conan, M., Cowin, K., & Hickin, J. (2003). Supported s-help groups for aphasic people: Development and research. In I. Papathanasiou & R. de Bleser (Eds.), The science of aphasia: From therapy to theory. London: Elsevier. Code, C., & Herrmann, M. (2003). The relevance of emotional and psychosocial factors in aphasia to rehabilitation. In W. H. Williams & J. J. Evans (Eds.), Biopsychosocial approaches to neurorehabilitation: Assessment and management of neuropsychiatric mood and behavioural disorders. Hove, UK: Psychology Press. Code, C., & Joanette, Y., (2003). Neural plasticity in the control of language in the adult brain: The role of the separated right hemispheres in cases PS, VP and JW. In C. Code, C.-W. Wallesch, Y. Joanette, & A.-R. Lecours (Eds.), Classic cases in neuropsychology: Volume II. Hove, UK: Lawrence Erlbaum Associates Ltd. Code, C., & Müller, D. (2003). Psychosocial and quality of life issues in treatment. In R. Kent (Ed.), The MIT encyclopaedia of communication disorders. Cambridge, MA: MIT Press.

Chris Code’s publications

xiii

Kaczmarek, B., Code, C., & Wallesch, C.-W. (2003). ‘Z’. In C. Code, C.-W. Wallesch, Y. Joanette, & A.-R. Lecours (Eds.), Classic cases in neuropsychology: Volume II. Hove, UK: Lawrence Erlbaum Associates Ltd. Code, C. (2004). Syllables in the brain. In R. Hartsuiker, R. Bastiaanse, & A. Postma (Eds.), Phonological processing and monitoring. Hove, UK: Psychology Press. Code, C., Müller, N., Tree, J. T., & Ball, M. J. (2006). Syntactic impairments can emerge later: Progressive agrammatic agraphia and syntactic comprehension impairment. In C. Code (Ed.), The representation of language in the brain. Hove, UK: Psychology Press. Code, C., & Wallesch, C.-W. (2006). The form of representation of language in the brain and the inﬂuence of John C. Marshall. In C. Code (Ed.), The representation of language in the brain. Hove, UK: Psychology Press. Code, C. (in press). Aphasia recovery, therapy and psychosocial adjustment. In A. Baum, C. McManus, S. Newman, J. Weinman, & R. West (Eds.), The Cambridge handbook of psychology, health & medicine (2nd ed). Cambridge, UK: Cambridge University Press. Code, C. (in press). The operculum syndrome: Foix-Chavany-Marie Syndrome. In M. McNeil (Ed.), Clinical management of sensorimotor speech disorders (2nd ed). New York: Thieme Publishers.

Papers in peer-reviewed journals Code, C. (1979). Genuine and artiﬁcial stammering: An EMG comparison. British Journal of Communication Disorders, 14, 5–16. Code, C. (1980). Delayed auditory feedback and auditory-feedback masking with stammerers and normal speakers. Australian Journal of Human Communication Disorders, 8, 40–48. Code, C., & Müller, D. (1980). Is the Edinburgh Masker really successful? British Journal of Disorders of Communication, 15, 141–142. Code, C. (1981). Dichotic listening with the communicatively impaired: Results from trials with a short British-English dichotic word test. Journal of Phonetics, 9, 375–383. Code, C. (1982). Neurolinguistic analysis of recurrent utterances in aphasia. Cortex, 18, 141–152. Code, C. (1982). On the origins of recurrent utterances in aphasia. Cortex, 18, 161–164. Code, C., & Ball, M. (1982). Fricative production in Broca’s aphasia. Journal of Phonetics, 10, 325–331. Müller, D., Code, C., & Mugford, J. (1982). Predicting psychosocial adjustment in aphasia. British Journal of Disorders of Communication, 17, 23–29. Code, C. (1983). On “Neurolinguistic analysis of recurrent utterances in aphasia”: Reply to De Bleser & Poeck. Cortex, 19, 261–264. Code, C. (1986). Catastrophic reaction and anosognosia in anterior–posterior and left–right models of the cerebral control of emotion. Psychological Research, 48, 53–55. Code, C., & Gaunt, C. (1986). Treating aphasia and apraxia with a combined speech and gesture approach: A single case study. British Journal of Disorders of Communication, 21, 11–20.

xiv

Chris Code’s publications

Code, C., & Brown, J. W. (1987). Aphasia from the wrong (right) hemisphere: Questions for crossed aphasia. Aphasiology, 1, 401–402. Code, C., & Lodge, B. (1987). Language in dementia of recent referral. Age and Ageing, 16, 366–372. Code, C., & Rowley, D. (1987). Age, sex, handedness and aphasia type. Aphasiology, 1, 339–345. Code, C. (1991). The computerized Boston: Aphasia assessment database with diagnostic features. Computer Users in Speech and Hearing, 7, 314–322. Code, C. (1994). Speech automatism production in aphasia. Journal of Neurolinguistics, 8, 135–148. Code, C., Rowley, D. T., & Kertesz, A. (1994). Predicting recovery from aphasia with connectionist networks: Preliminary comparisons with multiple regression. Cortex, 30, 527–532. Ball, M. J., Code, C., Rahilly, J., & Hazlett, D. (1994). Non-segmental aspects of disordered speech: Developments in transcription. Clinical Linguistics and Phonetics, 8, 67–83. Code, C. (1995). Asymmetries in ear movements and eyebrow raising in men and women and right and left handers. Perceptual and Motor Skills, 80, 1147–1154. Code, C., & Ball, M. J. (1995). Syllabiﬁcation in aphasic recurring utterances: Contributions of sonority theory. Journal of Neurolinguistics, 8, 257–265. Code, C. (1996). Aphasia therapy. British Journal of Clinical Psychology, 35, 157–159. Code, C., Khanbha, F., Isman, K., & Mattiazzo, V. (1996). Perceptions of emotional and psychosocial state in laryngectomised patients, their signiﬁcant others and clinicians at three months post-surgery. Asia Paciﬁc Journal of Speech, Language and Hearing, 1, 91–104. Harasty, J., Halliday, G., Code, C., & Brooks, W. (1996). Anatomical evidence for a visual and auditory semantic network in a case of focal dementia. Brain, 119, 181–190. Hemsley, G., & Code, C. (1996). Interactions between recovery in aphasia, emotional and psychosocial factors in subjects with aphasia, their signiﬁcant others and speech pathologists. Disability and Rehabilitation, 18, 567–584. Herrmann, M., Code, C. (1996). Weighting of items on the Code-Müller protocols: The eﬀects of clinical experience of aphasia therapy. Disability and Rehabilitation, 18, 509–514. Code, C. (1997). Can the right hemisphere speak? Brain and Language, 57, 38–59. Herrmann, M., Hogan, A., Müller, D., & Code, C. (1997). Psychosoziale Anpassungsleistungen und Therapieziele bei Sprach- und Kommunikationsstorungen – Untersuchungen mit den Code-Müller Protokollen. Neurolinguistik, 11, 1–21. Togher, L., Hand, L., & Code, C. (1997). Analyzing discourse in the traumatic brain injury population: Telephone interactions with diﬀerent communication partners. Brain Injury, 11, 169–189. Togher, L., Hand, L., & Code, C. (1997). Disability following head injury: A new perspective on the relationship between communication impairment and disempowerment. Disability and Rehabilitation, 18, 559–566. Togher, L., Hand, L., & Code, C. (1997). Measuring service encounters with the traumatically brain injured population. Aphasiology, 11, 491–504. Code, C. (1998). Models, theories and heuristics in apraxia of speech. Clinical Linguistics and Phonetics, 12, 47–66.

Chris Code’s publications

xv

Cowell, S. F., & Code, C. (1998). Thinking nuclear medicine: PET activation. Journal of Nuclear Medicine Technology, 26, 17–22. Nespoulous, J.-L., Code, C., Virbel, J., & Lecours, A.-R. (1998). Hypotheses on the dissociation between “referential” and “modalizing” verbal behaviour in aphasia. Applied Psycholinguistics, 19, 311–331. Code, C. (1999). Re-assembling the brain: Are cell assemblies the brain’s language for recovery of function? (Commentary) Behavioural and Brain Sciences, 22, 282. Code, C., Hemsley, G., & Herrmann, M. (1999). Emotional reactions to aphasia. (Special Issue on Psychosocial Issues in Aphasia) Seminars in Speech and Language, 20, 19–31. Code, C., Müller, D. J., & Herrmann, M. (1999). Perceptions of psychosocial adjustment to aphasia: Studies with the CMP. (Special Issue on Psychosocial Issues in Aphasia) Seminars in Speech and Language, 20, 51–63. Code, C., Müller, D., Herrmann, M., & Hogan, A. (1999). Perceptions of psychosocial adjustment to acquired communication disorders: Studies with the Code-Müller protocols. International Journal of Communication Disorders, 34, 193–207. Harasty, J., Halliday, G. M., Kril, J. J., & Code, C. (1999). Speciﬁc temperoparietal gyral atrophy reﬂects the pattern of language dissolution in Alzheimer’s disease. Brain, 122, 675–686. Hogan, A., Code, C., Taylor, A., & Wilson, D. (1999). Employment and economic outcomes for deafened adults with cochlear implants. Australian Journal of Rehabilitation Counselling, 5, 1–8. McCabe, P., Sheard, S., & Code, C. (1999). What do speech pathologists know about HIV? Advances in Speech Language Pathology, 1, 9–18. Code, C. (2000). Not fractionating, converging. Brain and Language: Millennium Issue, 71, 44–45. Cowell, S. F., Egan, G. F., Code, C., Harasty, J., & Watson, J. D. G. (2000). The functional neuroanatomy of simple calculation and number repetition: A parametric PET activation study. NeuroImage, 12, 565–573. Katz, R., Hallowell, B., Code, C., Armstrong, E., Roberts, P., Pound, C., et al. (2000). A multi-national comparison of aphasia management practices. International Journal of Language and Communication Disorders, 35, 303–314. Roger, P., Code, C., & Sheard, C. (2000). Assessment and management of aphasia in a linguistically diverse society. Asia-Paciﬁc Journal of Speech and Language, 5, 21–34. Code, C. (2001). Multifactorial processes in recovery from aphasia: Developing the foundations for a multilevelled framework. Brain and Language, 77, 25–44. McCabe, P., Sheard, C., & Code, C. (2002). Acquired communication impairment in people with HIV. Journal of Medical Speech-Language Pathology, 10, 183–199. Simmons-Mackie, N., Code, C., Armstrong, E., Stiegler, L., & Elman, R. (2002). What is aphasia? Results of an international survey. Aphasiology, 16, 837–848. Code, C. (2003). The quantity of life for people with chronic aphasia. Neuropsychological Rehabilitation, 13, 365–378. Code, C. (2003). Vocalisation and the development of hand preference (Commentary). Behavioural and Brain Sciences, 26 (2), 215–216. Code, C., & Heron, C. (2003). Services for aphasia, other acquired adult neurogenic communication and swallowing disorders in the United Kingdom, 2000. Disability and Rehabilitation, 21, 1231–1237. Code, C., & Herrmann, M. (2003). The relevance of emotional and psychosocial factors in aphasia to rehabilitation. Neuropsychological Rehabilitation, 13, 109–132.

xvi

Chris Code’s publications

Roberts, P., Code, C., & McNeil, M. (2003). Describing participants in aphasia research. Part 1: Audit of current practice. Aphasiology, 17, 911–932. Ball, M. J., Code, C., Tree, J., Dawe, K., & Kay, J. (2004). Phonetic and phonological analysis of progressive speech degeneration: A case study. Clinical Linguistics and Phonetics, 18, 447–462. Chung, K. K. H., Code, C., & Ball, M. J. (2004). Speech automatisms and recurring utterances from aphasic Cantonese speakers. Multilingual Communication Disorders, 2, 32–42. Togher, L., McDonald, S., Code, C., & Grant, S. (2004). Training communication partners of people with TBI: A randomised controlled trial. Aphasiology, 18, 313–335. Code, C. (2005). First in, last out: The evolution of lexical aphasic speech automatisms to agrammatism and the evolution of language. Interaction Studies, 6 (2), 311–334. Code, C., Lincoln, M., & Dredge, R. (2005). Asymmetries in mouth opening during word generation in male stuttering and non-stuttering participants. Laterality, 10 (5), 471–486. Code, C., Müller, N., Tree, J. T., & Ball, M. J. (2006). Syntactic impairments can emerge later: Progressive agrammatic agraphia and syntactic comprehension impairment. Aphasiology, 20, 1035–1058. Code, C., & Wallesch, C-W. (2006). The form of representation of language in the brain and the inﬂuence of John C. Marshall. Aphasiology, 20, 819–822. Power, E., & Code, C. (2006). Waving not drowning: Utilising gesture in the treatment of aphasia (Commentary). Advances in Speech-Language Pathology, 8, 115–119. McCooey-O’Halloran, R., Worrall, L., Code, C., & Hickson, L. (in press). Development of a measure of communication activity for the acute hospital setting Part II: Item analysis, selection and reliability. Journal of Medical Speech-Language Pathology. McCabe, P., Sheard, C., & Code, C. (submitted). Longitudinal communication impairment in the AIDS dementia complex (ADC): A case report. Journal of Communication Disorders. McCabe, P., Sheard, C., & Code, C. (submitted). Pragmatic skills in people with HIV/ AIDS. Disability and Rehabilitation. Packman, A., Code, C., & Onslow, M. (submitted). On the cause of stuttering: Integrating brain and behavioral research. Journal of Neurolinguistics.

Invited presentations Code, C. (1990). Modelling lexical speech automatisms. Invited Paper for Symposium on Repetitive Verbal Behaviour, European Cognitive Neuropsychology Workshop, Bressanone, Italy (January). Code, C. (1990). The right hemisphere and interhemispheric inhibition in aphasia. Invited Paper for the Third National Aphasiology Symposium, Gdansk University, Poland, October. Code, C. (October–November 1990). The role of the right hemisphere in the recovery and treatment of aphasia: A critical appraisal. ‘Lecture tour’ of the USA: University of Texas at Dallas; VA Center Dallas; Arizona State University at Tempe; University of Northern Arizona; VA Center Martinez, California. Code, C. (1990). The role of the right hemisphere in the recovery and treatment of

Chris Code’s publications

xvii

aphasia: A critical appraisal. Invited Guest Speaker at Annual Congress of the American Speech and Hearing Associated, Seattle (November). Code, C. (1991). Developments in the Code-Müller protocols: The British studies. Invited Guest Speaker to the Linguistics Society, University of Freiburg, Germany (July). Code, C. (1991). Problems in predicting clinical recovery from aphasia. Invited paper presented at the British Aphasiology Society Conference, University of Sheﬃeld (September). Code, C., & Müller, D. J. (1992). Measuring perceptions to psychosocial adjustment in aphasia. Workshop presented to British Aphasiology Society Meeting, University of Sheﬃeld (June). Code, C. (1992). Psychosocial and emotional reactions to brain damage. Invited Seminar, School of Behavioural Studies, Macquarie University, Sydney (August). Code, C. (1992). Emotional and psychosocial reactions to aphasia. Invited Workshop, Lotte Stewart Hospital, Sydney (September). Code, C. (1993). Examining perceptions to psychosocial adjustment in aphasia. Invited Seminar, University of Queensland (May). Code, C. (1993). Recovery from aphasia. Invited Workshop, University of Queensland (May). Code, C. (1993). Linguistic aspects of speech automatisms in aphasia. Invited Seminar Department of Linguistics, University of Sydney (August). Code, C. (1993). Speech automatisms in aphasia. Invited Seminar, Speech Pathology Department, Prince Alfred’s Hospital Sydney (September). Code, C. (1993). Psychosocial adjustment and emotional reaction to aphasia. Invited Keynote Presentation. First Aphasiology Symposium of Australia, Sydney (October). Code, (1994). The role of the right hemisphere in recovery and treatment of aphasia. Invited Workshop, Flinders University, Adelaide (April). Code, C. (1994). Emotional and psychosocial reactions to aphasia. Invited Workshop, University of Melbourne (September). Code, C. (1994). The linguistics of aphasic speech automatisms. Invited Keynote Presentation at the Fourth Annual Symposium of the International Clinical Linguistics & Phonetics Association, New Orleans (November). Code, C. (1994). Invited discussant. 1st Australian Symposium on the Neuropsychology of Asian Language Processing. University of New South Wales, Sydney (December). Code, C. (1995). Sprache und Gehirn. Invited Workshops. Summer School, University of Freiburg, Germany (August). Code, C. (1995). Aphasic speech automatisms. Invited presentation in the Jacques Lordat Laboratory, University of Toulouse (October). Code, C. (1995). The role of the right hemisphere in recovery and treatment. Invited 4 Hour Workshop: German Neuropsychological Society Conference, Würtzburg, Germany (October). Code, C. (1995). A metamodel of recovery from aphasia. Invited Keynote Paper, German Aphasiology Society Annual Conference, Magdeburg (November). Code, C. (1997). The lateral shift hypothesis: The role of the right hemisphere in the recovery and treatment of aphasia. Invited Workshop, Annual Conference of the Australian Society for the Study of Brain Impairment, Brisbane (November). Code, C. (1997). Speech production from the right hemisphere. Invited Plenary

xviii

Chris Code’s publications

Presentation, Annual Conference of the Australian Society for the Study of Brain Impairment, Brisbane (November). Code, C. (1998). Psychosocial adjustment to aphasia. Invited Workshop to College of St Mark and St John, Plymouth. Code, C. (1998). Psychosocial adjustment to aphasia. Invited Presentation to University of Southwestern Louisiana, Lafayette. Code, C. (1998). Recovery from aphasia. Invited presentation at Louisiana State University, Baton Rouge. Code, C. (1998). The role of the right hemisphere in speech production. Invited Seminar, School of Psychology, University of Cardiﬀ. Code, C. (1999). The neural and cognitive representation of syllables and apraxia of speech. Invited Workshop Presentation, Max Planck Institute, University of Nijmegen, Holland. Code, C. (1999). What’s right about speech? Invited Keynote Presentation, Annual Conference of the German Neuropsychological Society, Köln, Germany. Code, C. (2000). Self help for aphasia. Invited presentation, Aphasia, a day of talks, discussions and workshops in memory of Felicity Osborne, July 14, Birkbeck College, London. Code, C. (2000). Calculation and number repetition: PET evidence. Invited Seminar, Cognitive Neuroscience, Birkbeck College, London (July). Code, C. (2000). Brain plasticity and speech control by the right hemisphere: Converging evidence from aphasia, brain imaging, split-brain and hemispherectomy. Keynote Address to the Spanish Neurological Society Conference, Marbella, Spain, October 28. Code, C. (2001). Invited discussant for recovery symposium. European Cognitive Neuropsychology Workshop, Bressanone, Italy (January). Code, C. (2001). Calculation and the brain: PET studies. Invited presentation, Exeter Neuroscience Network (November). Code, C. (2002). Calculation and the brain: Past and prospective PET studies. Invited presentation, University of Bremen. Code, C. (2002). The psychosocial impact of aphasia. Invited presentation, Department of Neuroscience, University of Bremen. Code, C. (2003). Numbers in the brain. Hanse Institute for Advanced Study, Invited Fellowship Lecture, Delmenhorst, Germany (December). Code, C., Ball, M., Tree, J., Dawe, K., Kay, J., & Edwards, M. (2003). Progressive cortical anarthria with apraxias. Invited Visiting Professorship Lecture, University of Louisiana at Lafayette (March). Code, C., Tree, J., Dawe, K., Kay, J., Ball, M., & Edwards, M. (2003). Progressive cortical anarthria with apraxias. Invited Presentation, ‘Vocalise to Localise’ Symposium, University of Grenoble (January). Code, C. (2004). The psychosocial impact of aphasia. Invited Keynote Presentation International Aphasia Rehabilitation Conference, Milos, Greece (August). Code, C. (2004). Disordered communicative interaction: Current and future approaches to analysis and treatment. Invited Discussant, Stirling University Management Centre, Stirling, October 26. Code, C. (2004). Mechanisms of aphasic speech automatism production. Invited Keynote Presentation, Argentinian Aphasia Symposium, November 21–24, Buenos Aires (funded by British Council). Code, C. (2004). Psychosocial life and aphasia. Invited Keynote Presentation,

Chris Code’s publications

xix

Argentinian Aphasia Symposium, November 21–24, Buenos Aires (funded by British Council). Code, C. (2004). Speech production from the left and right hemispheres following brain damage. Invited Keynote Presentation, Argentinian Aphasia Symposium, November 21–24, Buenos Aires (funded by British Council). Code, C. (2005). The recovery of aphasia. Invited Keynote Presentation, Third Congress of Croatian Speech and Language Pathologists, September 28–October 1, Dubrovnik, Croatia. Code, C. (2005). The evolution of aphasic speech automatisms to agrammatism and the evolution of human language. Invited Presentation, Macquarie University, Sydney, October 31. Code, C. (2005). Big writing. Invited Presentation, School of Communication Sciences and Disorders, November 6. Code, C. (2006). Presenting the past and passing the future of clinical aphasia. Invited Keynote Presentation, International Aphasia Rehabilitation Conference, Sheﬃeld, (June). Code, C. (2006). Unfolding the past of aphasia rehabilitation. Invited Keynote Presentation, Nordic Conference on Aphasia: New Knowledge – New Directions, September 14–16, Oslo, Norway. Code, C. (2007). Invited Keynote Speaker, 7th International Scientiﬁc Meeting of Faculty of Logopedics, Zagreb, Croatia, July 14–16.

Other public output Unrefereed articles/software Code, C. (1980). The shifting brain. Therapy, 6. Code, C. (1985). Investigating the eﬃcacy of treatment for aphasia with a simple ABA single-case design. Bulletin of the College of Speech Therapists, 394, February. Code, C. (1986). Hearing therapy and the training of speech therapists. Hearing Therapy, 8, October. Code, C., Purser, H., & Rowley, D. (1986). Developing an aphasiology archive. Speech Therapy in Practice, 2. Code, C., Heer, M., & Schoﬁeld, M. (1989). The computerized Boston. Far Communications Ltd. (Software Program) Code, C. (1990). Secrets of the brain’s right hemisphere. Therapy Weekly, 16, April 26. Code, C. (1990). An expert prognosis. Therapy Weekly, 16, June 7. Code, C. (1990). Aphasia assessment: The computer meets the Boston. Speech Therapy In Practice. Code, C. (1994). Towards a post-graduate profession. Bulletin of the College of Speech and Language Therapists, January. Code, C. (1999). Meeting expectations. Speech and Language Therapy and Communication in Practice. Code, C. (1999). Proﬁles of ADA self-help groups. Speaking Up, December. London: ADA. Code, C., & Heron, C. (2001). Aphasia services in the United Kingdom. Therapy Weekly.

Tabula gratulatoria

Apart from the contributors, the following requested to have their names listed as well-wishers. Evelyn Abberton Elise Baker Susan Balandin Kirrie Ballard Marcelo Berthier Maria Black Bronagh Blaney Richard Body Marian Brady Jason Brown Shelagh Brumﬁtt Sally Byng Stefano Cappa Shula Chiat Kevin Chung Carl Coelho Francesca Cooper Patrick Coppens Alison Crutchley Lucy Dipper Gerry Docherty Patrick Doyle Joe Duﬀy Martin Edwards Pam Enderby Paul Fletcher Elaine Funnell Jack Gandour Hilary Gardner

University College London, England University of Sydney, Australia University of Sydney, Australia University of Sydney, Australia Hospital Universario Malaga, Spain University College London, England University of Ulster, Northern Ireland University of Sheﬃeld, England Glasgow Caledonian University, Scotland New York University School of Medicine, USA University of Sheﬃeld, England Connect UK Clinica Neurologica dell’Università di Brescia, Italy City University London, England University of Hong Kong, PR China University of Connecticut, Storrs, USA University of Wales Institute, Cardiﬀ, Wales Plattsburgh State University of New York, USA University of Huddersﬁeld, England City University London, England University of Newcastle, England VA Pittsburgh and University of Pittsburgh, USA Mayo Clinic, Rochester, MN, USA University of Birmingham, England University of Sheﬃeld, England University College Cork, Ireland Royal Holloway College London, England Purdue University, USA University of Sheﬃeld, England

Tabula gratulatoria Mike Garman Fiona Gibbon Jackie Guendouzi Jennifer Gurd Brooke Hallowell Linda Hand Jenny Harasty Bill Hardcastle Diane Hazlett Ruth Herbert Anne Hesketh Nigel Hewlett Argye Hillis John Hodges Anthony Hogan Jennifer Horner David Howard Sara Howard Walter Huber Debbie James Janice Kay Kevin Kearns Belinda Kenny Thomas Klee Annu Klippi Herman J. Kolk Matti Laine Margaret Leahy Guylaine Le Dorze Kerrie Lee Eeva Leinonen Carolyn Letts Michelle Lincoln Marjorie Lorch Felice Loverso Jane Maxim Lise Menn

xxi

University of Reading, England Queen Margaret University College, Edinburgh, Scotland University of South Alabama, USA Oxford University, England Ohio University, Athens, USA University of Sydney, Australia University of New South Wales, Australia Queen Margaret University College, Edinburgh, Scotland University of Ulster, Northern Ireland University of Sheﬃeld, England University of Manchester, England Queen Margaret University College, Edinburgh, Scotland Johns Hopkins University, Baltimore, USA University of Cambridge, Addenbrooke’s Hospital, UK University of Sydney, Australia Medical University of South Carolina, Charleston, USA University of Newcastle, England University of Sheﬃeld, England University of Aachen, Germany Flinders University, Adelaide, Australia University of Exeter, England MGH Institute of Health Professions, Boston, USA University of Sydney, Australia University of Newcastle, England University of Helsinki, Finland Nijmegen University, The Netherlands Åbo Akademi University, Finland Trinity College Dublin, Ireland Université de Montréal, Canada University of Sydney, Australia University of Hertfordshire, England; Oulu University, Finland University of Newcastle, England University of Sydney, Australia University College London, England Casa Colina Centers for Rehabilitation, Pomona, CA, USA University College London, England University of Colorado at Boulder, USA

xxii

Tabula gratulatoria

Jane Marshall John Marshall Robert Marshall Nadine Martin Tricia McCabe Sharynne McLeod Malcolm McNeill Mike McTear Kate Morton Dave Müller Siân Munro Penelope Myers Marilyn Newhoﬀ Lyndsey Nickels Mark Onslow Aileen Patterson Mick Perkins Lisa Perkins Brian Petheram Emma Power Friedmann Pulvermüller Alison Purcell Vicki Reed Katherine Ross Dave Rowley Avraham Schweiger Lewis Shapiro Christine Sheard Mark Tatham Jeremy Tree David Trembath Heather Van der Lely Jan Van Doorn Brendan Weekes Bill Wells Klaus Willmes Richard Wise Linda Worrall Wolfram Ziegler

City University London, England University of Oxford, England University of Kentucky, USA Temple University, USA University of Sydney, Australia Charles Sturt University, Australia University of Pittsburgh, USA University of Ulster, Northern Ireland University of Essex, England Suﬀolk University College, England University of Wales Institute Cardiﬀ, Wales Mayo Clinic, Rochester, MN, USA San Diego State University, San Diego, USA Macquarie University, Australia University of Sydney, Australia University of Ulster, Northern Ireland University of Sheﬃeld, England Jersey Health Authority, Channel Islands, UK Frenchay Hospital, Bristol, England University of Sydney, Australia University of Konstanz, Germany University of Sydney, Australia James Madison University, Virginia, USA Carl T. Hayden VA Medical Center, Phoenix, and Arizona State University, Tempe, USA De Montfort University, England Academic College of Tel Aviv-Yaﬀo, Israel San Diego State University, San Diego, USA University of Sydney, Australia University of Essex, England University of Exeter, England University of Sydney, Australia University College London, England Umeå University, Sweden; University of Sydney, Australia University of Sussex, England University of Sheﬃeld, England University of Aachen, Germany Imperial College, London, England University of Queensland, Australia Städtisches Klinikum München, Germany

Contributors

Elizabeth Armstrong Department of Linguistics, Macquarie University, Sydney. Martin J. Ball Department of Communicative Disorders, University of Louisiana at Lafayette, USA. Roelien Bastiaanse Center for Language and Cognition, University of Groningen, The Netherlands. Gerhard Blanken Department of Psycholinguistics, University of Erfurt, Germany. Tobias Bormann Department of Psycholinguistics, University of Erfurt, Germany. Hugh W. Buckingham

Louisiana State University, Baton Rouge, USA.

Maud Champagne-Lavau Faculté de médecine, Université de Montréal and Centre de recherche, Hôpital Sacré-Coeur de Montréal, Canada. Sarah S. Christman The University of Oklahoma, Health Sciences Center, Oklahoma City, USA. Jack S. Damico Department of Communicative Disorders, University of Louisiana at Lafayette, USA. Pattie Doody Department of Communicative Disorders, University of Louisiana at Lafayette, USA. Susan Edwards School of Psychology and Clinical Language Sciences, University of Reading, UK. Thorsten Fehr Institute for Cognitive Neuroscience and Center for Advanced Imaging (CAI), Bremen University, Germany. Alison Ferguson Australia.

Speech Pathology Program, University of Newcastle,

xxiv

Contributors

Manfred Herrmann Institute for Cognitive Neuroscience and Center for Advanced Imaging (CAI), Bremen University, Germany. Audrey L. Holland Tucson, USA.

Regents’ Professor Emerita, University of Arizona,

Yves Joanette Centre de recherche, Institut universitaire de gériatrie de Montréal and Faculté de médecine, Université de Montréal, Canada. Karima Kahlaoui Centre de recherche, Institut universitaire de gériatrie de Montréal, Canada. Richard C. Katz Veterans Aﬀairs Medical Center, Phoenix, Arizona and Arizona State University, Tempe, USA. Alana Kozlowski Department of Communicative Disorders, University of Louisiana at Lafayette, and Communication Disorders and Deaf Education, Lamar University, Texas, USA. Leonard L. LaPointe Regional Rehabilitation Center, Florida State University, Tallahassee, USA. Kerry L. Lenius Regional Rehabilitation Center, Florida State University, Tallahassee, USA. Skye McDonald School of Psychology, University of New South Wales, Sydney, Australia. Inger Moen Department of Linguistics and Scandinavian Studies, University of Oslo, Norway. Nicole Müller Department of Communicative Disorders, University of Louisiana at Lafayette, USA. Bruce E. Murdoch School of Health and Rehabilitation Sciences, The University of Queensland, Australia. Jean-Luc Nespoulous Laboratoire Jacques-Lordat, University of ToulouseLe Mirail, France. Maria Pa˛chalska Department of Developmental Psychology and Neurolinguistics, Institute of Psychology, Marie Curie-Sklodowska University, Lublin, Poland. Claire Penn School of Human and Community Development, University of the Witwatersrand, Johannesburg, South Africa. Nina N. Simmons-Mackie Department of Communication Sciences and Disorders, Southeastern Louisiana University, Hammond, USA. Bernadette Ska Centre de recherche, Institut universitaire de gériatrie de Montréal and Faculté de médecine, Université de Montréal, Canada.

Contributors

xxv

Leanne Togher School of Communication Sciences and Disorders, University of Sydney, Australia. Hanna K. Ulatowska School of Behavioral and Brain Sciences, University of Texas, Dallas, USA. Jacques Virbel Institut de Recherche en Informatique de Toulouse, University Paul Sabatier, Toulouse, France. Claus-W. Wallesch Department of University Magdeburg, Germany.

Neurology,

Otto-von-Guericke-

Robert T. Wertz Formerly Veterans’ Administration Medical Center, Nashville, USA.

Preface

This book is a collection of the cutting edge work of many leading researchers and clinicians exploring topics within clinical aphasiology. However, it is more than this; it is also a tribute to our friend and colleague, Chris Code. Chris has been a prime mover in many areas of aphasiology over the years, and we discuss his contribution to the ﬁeld in some detail in the ﬁrst chapter of this book. The remaining contents we have divided into three main approaches to the study of aphasia, reﬂecting Chris’s own interests. First, we have ﬁve contributions that fall under the heading of Conceptual considerations. These are mainly interdisciplinary in nature, thus reﬂecting Chris’s expertise and interests that span linguistics, phonetics, psychology and neurology, as well as social aspects of communication disorders. The second section of the book deals with Research considerations, with seven chapters ranging from how the study of disrupted communication can inform models of normal language processing, through tone production and processing in speakers with aphasia, to anomia and progressive multifocal leukoencephalopathy. Each of these chapters explores diﬀerent aspects of research methodology, reﬂecting Chris’s interests in quantitative research (e.g., his work on perceptual psychoacoustics), and qualitative research (e.g., discourse analysis). The ﬁnal section of the collection deals with Clinical considerations, and the seven chapters here cover counselling, computerized training, cultural and linguistic diversity in aphasia, right hemisphere disorders, and communication problems in the dementias. Again, this part of the collection reﬂects Chris’s long-term interests in the clinical aspects of aphasiology, as well as the research aspects. The authorship of the chapters in this volume reﬂects Chris’s strong international ties. We have contributions from the United Kingdom, the United States, Australia, Germany, France, Norway, South Africa, The Netherlands, Canada and Poland. The names in the Tabula Gratulatoria reﬂect an even wider range of countries. We would like to thank Ben Rutter for compiling the indexes. This collection honours Chris’s contribution to the ﬁeld, and marks his 65th birthday. However, this is not to suggest that he is about to give up his

Preface

xxvii

research into neurological disorders – arguably one of the most fascinating areas within communication disorders. Indeed, we look forward to many more years of interesting and important work emerging from the depths of the Devonshire countryside, with the support of his ‘partner in greatness’ Christine. Martin J. Ball Jack S. Damico Lafayette, Louisiana, August 2006

1

Chris Code’s contribution to aphasiology Martin J. Ball and Jack S. Damico

Introduction Chris Code is one of the foremost scholars in aphasiology today, and has advanced the ﬁeld in many ways. Over a professional career that has spanned nearly 30 years, he has authored or co-authored more than 120 publications and has served as a faculty member or research Fellow in eight institutions of higher learning in the United Kingdom, Australia, and Europe. Importantly, he was the Founding Editor of Aphasiology: An International and Interdisciplinary Journal in 1987 and he has continued to serve as Editor in Chief of that journal. When looking back over the career of a colleague like Chris, there are many achievements that may be highlighted. For example, he has eﬀectively trained scores of students around the world, and he has employed his considerable talents as an editor, editorial board member and reviewer for no less than 16 journals and book series. The measure of Chris Code as a professional, however, must encompass several other areas as well. First, he has produced an impressive list of research and clinical publications that have inﬂuenced several ﬁelds, but especially clinical aphasiology. His enthusiasm for his work comes through in these publications as he has advanced our understanding of the areas of aphasia, phonetics, the role of the right hemisphere in speech and language, psychosocial adjustments to brain damage, patient rights issues, and traumatic brain injury. Indeed, a survey of his publications shows contributions in at least 18 distinct research areas in the human communication sciences and disorders. Second, he has been an enthusiastic collaborator with a network of colleagues that spans the United Kingdom, North American, Europe, and Australia. Starting with his earliest collaborations with Müller and Ball in the early 1980s until his most recent articles and book projects, Chris Code has worked closely with no fewer than 60 professionals in his research activities. In these collaborations, he has functioned both as a colleague of equal standing and as a mentor for younger colleagues. Finally, Chris Code has had a galvanizing impact on the ﬁeld of clinical aphasiology as a savant, a motivator, and an impresario of trends that have resulted in several rather signiﬁcant developments in the discipline. Despite all his other

2

Ball and Damico

accomplishments, this last area may be his most important contribution of all. In this chapter we brieﬂy discuss several areas of achievement that mark Chris Code’s career. We survey the areas within aphasiology that have been his special concern as indicated by his publications, and we discuss his rather considerable inﬂuence as an instigator and/or supporter of various developments in clinical aphasiology. Regarding his research and clinical publications, we approach his work under the following broad headings: psychosocial and emotional reaction to brain damage and communication impairment; linguistics and phonetics of aphasia and related disorders; right hemisphere language and speech; and international aspects of aphasiology. The focus on his inﬂuence will encompass his role as Editor in Chief of Aphasiology: An International and Interdisciplinary Journal and how he has employed this journal to advance the discipline.

Research accomplishments Psychosocial adjustment to brain damage Beginning with some of his earliest research, Chris Code has been interested in documenting and describing the social and emotional changes that often accompany aphasia (Müller & Code, 1983; Müller, Code, & Mugford, 1982) and this focus has been an enduring theme in his published work (e.g., Code, 1997a; Code, Hemsley, & Herrmann, 1999; Code & Herrmann, 2003; Code & Müller, 1989, 1995a, 1996). Taking a more expanded view than was common at the time, Code and colleagues stressed an eﬀective hybrid model of aﬀective issues in aphasia by advocating that emotional issues and experience must always be viewed on an individual basis and within social contexts (e.g., Code, 1986, 1997b; Code & Müller, 1995a; Hemsley & Code, 1996; Müller & Code, 1983). In a series of research studies, he and colleagues have been able to show how the emotional state can have a signiﬁcant impact on motivation, physical functioning, and cognitive and linguistic processing and that these changes may signiﬁcantly impact recovery from aphasia (e.g., Code, 1997b, 2001; Code & Herrmann, 2003; Code & Müller, 1992; Code, Müller, & Herrmann, 1999; Hemsley & Code, 1996). Perhaps his most signiﬁcant achievement regarding psychosocial adjustment has been the development and application of the Code-Müller Protocols. These protocols have developed over time (Code & Müller, 1992; Herrmann & Code, 1996; Müller & Code, 1983; Müller, Code, & Mugford, 1982) and are intended to examine perceptions of psychosocial well-being. By employing these protocols, Code and others have been able to study depression, motivation, and other emotional responses to both the impact of aphasia and how recovery may proceed (e.g., Code, 1986, 1997b; Code & Herrmann, 2003; Code & Müller, 1989). This work has also helped determine how various levels of optimism about recovery across the various players in the rehabilitative

Chris Code’s contribution to aphasiology

3

context (i.e., individual with aphasia, signiﬁcant others linked to these individuals, therapist) may contribute to the complex interaction between perception of potential, psychosocial factors, and recovery in aphasia (e.g., Code, Müller, & Herrmann, 1999; Hemsley & Code, 1996). With additional applications of the protocols using a multiple-attribute utility technique to assign weightings that eﬀectively rank individual priorities of psychosocial adjustment (Herrmann & Code, 1996), it has been shown that diﬀerent individuals perceive very diﬀerent priorities during recovery and these may have an important impact on expectations and treatment variables (e.g., Hemsley & Code, 1996; Müller, Code, & Mugford, 1982). In addition to his own work with the Code-Müller Protocols, this procedure has been widely employed in other research and clinical venues (see Code, Müller, & Herrmann, 1999; Code, Müller, Herrmann, & Hogan, 1999), and has been inﬂuential in the movement toward consideration of quality of life issues (Code, 2003; Code & Müller, 2003; Worrall & Holland, 2003), the Life Participation Approach to Aphasia (Chapey et al., 2001), and various social models of aphasia (Lyon & Shadden, 2001; Shadden, 2005; SimmonsMackie, 2001). Linguistic investigations: Speech automatisms Another of Chris Code’s main interests has been the study of lexical and nonlexical speech automatisms, also known as real-word and nonmeaningful recurrent utterances (Chung, Code, & Ball, 2004; Code, 1982a, 1982b, 1987, 1989a, 1994a; Code & Ball, 1994). Chris’s work in the 1980s included the ﬁrst important studies of this area since Alajouanine (1956) and, with colleagues, he has assembled a database of both lexical and nonlexical speech automatisms in English, German, and Cantonese. However, his work in this area is not restricted to simply “butterﬂy collecting” (important as it is to acquire ample exemplars of a phenomenon, it is also important to investigate it). The main thrust of this analysis has been ﬁrst, in the area of linguistic analyses of the speech automatisms he and colleagues have collected, and second, on the origins of speech automatisms. One of the ﬁrst analyses Code conducted on the English data (Code, 1982a) was a phoneme frequency analysis. This was applied to both the real-word and non-meaningful recurrent utterances with interestingly diﬀerent results. With the real-word tokens, there was a high correlation between the sounds used and the sounds of normal conversational English. Looked at more closely (in terms of place and manner of articulation, and voicing) some diﬀerences emerged. These were in respect of manner of articulation with plosives occurring more often in the real-word recurrent utterances than in normal speech (up from 29% to 40%; Code, 1982a, 1989a). Explanations for these ﬁndings may be found in terms of sonority theory and we return to this below. Signiﬁcantly fewer English sounds occurred in the non-meaningful recurrent utterances collected from the English subjects as compared to the

4

Ball and Damico

real-word examples (21 of 44 phonemes as opposed to 40 from 44). There was also a greater consonant to vowel ratio (47% to 53% compared to normal English 62.5% to 37.5%, and in the real-word recurrent utterances 56% to 46%). A place, manner, and voicing analysis again showed that the manner category was the one that deviated most from normal speech, with plosives accounting for 62% of the consonants. In a later study (Code & Ball, 1994, 1995), the authors looked for explanations for the phonotactic patterns and inventory constraints in both the English non-meaningful recurrent utterances, and German data collected by Blanken, Wallesch, and Papagno (1990). The high proportion of plosives partly reﬂects motorically easier sounds to produce; but also ﬁts into the requirements of the perceptually driven sonority sequencing principle (SSP; Ball, Müller, & Rutter, forthcoming), where (in syllable initial position at least) plosive–vowel sequences are preferred. Interestingly, the SSP also predicts that in syllable ﬁnal position (where a coda consonant occurs) the consonant will be ranked higher on the sonority hierarchy than are plosives. In the data reported in Code and Ball (1994) we do indeed ﬁnd in ﬁnal position a preference for fricatives and nasals over plosives, although open syllables were the dominant pattern (as predicted by universals of syllable structure). The authors use these results to speculate on the nature of sonority, and whether it is a hard-wired feature of phonological processing or simply an artefact of the speech production process. Code (1982a) also undertook a linguistic analysis of the real-word recurrent utterances. As an initial step he examined frequency of occurrence of the words used in the English data. He determined that the majority of the separate words used (proper names and expletives were excluded as not being represented in the normative data) were in the common category: 86% were words occurring 50 times per million or more in normal conversational English. Code then presents a syntactic analysis of the data. The majority of the real-word recurrent utterances were of the form pronoun + verb (often I + modal, e.g., I want to, I can’t, I can try). Expletives were the next most common form, followed by proper names, yes/no, and numbers. Repeated forms were also common, and a range of other syntactic patterns were seen. Chung, Code, and Ball (2004) extended the analysis to Cantonese speech automatisms (both real-word and non-meaningful). Results showed very similar patterns to those found with the English and German examples. As we noted earlier, Chris Code is also interested in the origin of speech automatisms, and Code (1982b) addresses this area. Various attempts to account for real-word forms have been proposed: for example, that the utterance is one the patient intended to produce at the very moment of the stroke, or that it was the last utterance actually produced before the stroke occurred. Alajouanine (1956) felt these two approaches could be combined into the notion that the utterance is the last thought being organized into an utterance before the stroke. However, Code argues convincingly that the origin of realword speech automatisms has more to do with post-onset factors than with

Chris Code’s contribution to aphasiology

5

pre-onset ones. For example, the use of family names, frustration expressed through expletives and pronoun + verb forms can all be accounted for as being the patient’s ﬁrst attempted utterances on regaining consciousness after a stroke. Code points out that the non-word examples are clearly not propositional speech, but even the real-word ones cannot be so described, as they are invariant and so stereotypical. He notes the view that there is righthemisphere involvement in the production of non-propositional speech, and concludes “that the right hemisphere is subserving the initial and continuing production of RUs [recurrent utterances], perhaps to diﬀerent degrees in the two linguistically distinct types” (Code, 1982b, p. 163). Phonetic investigations Chris Code has been especially interested in the application of instrumental phonetic techniques to the study of a variety of speech disorders, and his survey of psychoacoustic techniques with stuttering and aphasia can be found in his 1984a, 1984b, and 1997a work. In this section, however, we concentrate on two areas of his research: apraxia of speech and progressive speech deterioration. Apraxia of speech Chris Code’s interest in apraxia of speech was sparked by an early study with Martin Ball (Code & Ball, 1982; see also Code & Ball, 1988). In this study, the subject investigated was able to use voicing appropriately in English sonorant sounds (where contrastive voicing does not play a part), but produced target voiced obstruents mainly without vocal fold vibration. Interestingly, however, the subject was able to distinguish ﬁnal fortis and lenis obstruents through maintaining the pre-consonantal vowel length diﬀerence found in English; indeed, she compensated for the loss of voicing by enhancing the vowel length diﬀerences considerably. These ﬁndings led to a consideration of how traditional binary divisions of speech (phonetics versus phonology) might account for the apraxia of speech, and discussion of alternative models. Chris Code returned to apraxia of speech in a major review (Code, 1998). In this paper, Code examines a range of multilevel accounts of speech production and discusses where in these models aphasia, apraxia of speech, and dysarthria might ﬁt. Code concludes that as apraxia of speech is a disorder that has both phonetic and phonological implications, work in this area “has contributed signiﬁcantly to the rethinking of the relationship between phonology and phonetics . . . and highlighted the need for a phonetically derived phonology” (Code, 1998, p. 62). This last point is seen in recent models that posit some kind of phonetic planning component between the phonological organization, and the articulatory implementation levels. It also chimes well with recent approaches to theoretical phonology (such as Government Phonology, Gestural Phonology, and Usage-based Phonology: see

6

Ball and Damico

Ball et al., forthcoming) that emphasize phonetic and cognitive aspects of speech organization. Progressive speech deterioration Recently Chris Code has undertaken investigations of a rare case of progressive speech deterioration (Ball, Code, Tree, Dawe, & Kay, 2004; Code, Müller, Tree, & Ball, 2006). The authors present a range of instrumental analyses of the segmental and suprasegmental characteristics of the client, and it is interesting to note that whereas some of these showed simpliﬁcations (e.g., epenthetic vowels in consonant clusters), others showed complicating changes (such as adding /l/ after /u/ in open syllables, and /p/ or /b/ to /r/ initial words). A variety of phonological accounts were discussed that could throw light on the client’s speech patterns and their progressive deterioration over time. The authors conclude that the client’s speech patterns show that his relatively rare progressive speech degeneration “can be captured in terms of a cognitive model of representation, together with a gestural formalism that can show the loss of integration between the various motor systems of speech (and on occasion, total deletion of a gesture)” (Ball et al., 2004, p. 460). The eventual complete loss of intelligibility of the client some months after the data reported were collected shows that the gestural uncoupling and deletion had continued to devastating eﬀect. The important aspect of this study was that Code and his colleagues demonstrated that unusual cases such as the one reported here are amenable to investigation through phonetic description and phonological analysis, and that such studies may throw light on both the case and on theory building itself. The role of the right hemisphere As a result of his commitment to aphasia rehabilitation, Dr Code also has a longstanding interest in the contribution of the right hemisphere of the brain to language and speech processing. There are two likely reasons for this interest. First, as a trained neuropsychologist, Chris Code has not limited his theorizing or his research to the left hemisphere when discussing speech and language processing. His academic and clinical training enabled him to consider the rather substantial contributions that the right hemisphere has to various types of perceptual and cognitive processing and how it may also impact other meaning-making systems (Code, 1989b, 1996, 1997c). Second, because of his belief in the rehabilitative process and the need for defensible models, principles, and approaches to eﬀective rehabilitation (e.g., Code, 1994b, 1999, 2000, 2001; Code & Brown, 1987; Code & Müller, 1989, 1995b, 1995c), he and his colleagues have considered various viable rehabilitation models. In his 1987 text, Language, aphasia, and the right hemisphere, Dr Code eﬀectively discusses the arguments and the data for a fair consideration of

Chris Code’s contribution to aphasiology

7

the role of the right hemisphere in speech and language processing and in aphasia rehabilitation. For example, he presents detailed data from various disciplines that substantiate the role of the right hemisphere in cognitive processing, in some aspects of linguistic comprehension, in the more automatic, non-propositional aspects of speech production, and in some of the extra-linguistic aspects of communication. This text provided timely summaries of the research and served as an eﬀective review on the right hemisphere for a generation of students and professionals in speech-language pathology. This 1987 text also dealt extensively with the “lateral shift hypothesis” as it relates to recovery from aphasia. Taking its simplest variant (“following left brain damage there is a shift to the undamaged right hemisphere for language processing”, p. 110) and several other formulations, Chris discussed several ways that this hypothesis may be applied as a potential recovery mechanism for aphasia and how it relates to other mechanisms of recovery. He then presented a wide range of data from lesion case studies, cerebral blood ﬂow studies, experiments using sodium amytal, electroencephalography, and dichotic listening, and evidence from behavioural studies to assess the evidence for the lateral shift hypothesis. While there was some indication that the right hemisphere does play a role in recovery from aphasia, his ﬁndings did not strongly support this hypothesis. Instead, he found that the impact of the right hemisphere on recovery from aphasia was not uniformly demonstrated. While there appeared to be some variation depending on the individual with aphasia, the severity of aphasia, and time post-onset, the right hemisphere does not appear to be a fully equivalent backup system to the left hemisphere, and its impact does not produce eﬀective change in either the quality or quantity of recovery of function. While some aphasic syndromes may be more involved with right hemisphere functioning than previously believed, “right hemisphere involvement in language processing following left hemisphere damage is probably dependent upon a complex interplay of a range of variables” (1987, p. 148). Since the publication of his 1987 book, Code has continued to contribute to the data regarding right hemisphere processing of speech and language. While still uncertain about the contribution of the right hemisphere to language rehabilitation (Code, 1994b; Code & Joanette, 2003), he has presented data suggesting that some preserved utterances (formulaic expressions) noted in severely impaired individuals with aphasia may be processed in the right hemisphere (Code, 1996, 1997c) and that the right hemisphere does play a role in the creation and functioning of some discourse elements (Code, 1996) and in other forms of symbolic processing in individuals with aphasia (Cowell, Egan, Code, Harasty, & Watson, 2000). As he continues to investigate hypotheses regarding language processing and aphasia (e.g., Code, 1997d, 1999, 2001; Code & Joanette, 2003; Harasty, Halliday, Kril, & Code, 1999; Nespoulous, Code, Virbel, & LeCours, 1998), it is expected that this right hemisphere focus will continue.

8

Ball and Damico

International issues As a professional who has worked at universities across the world, Chris Code has also emphasized an international perspective in his work and collaborations. This is evident in his focus on service delivery and research across linguistically diverse populations (e.g., Chung, Code, & Ball, 2004; Roger, Code, & Sheard, 2000) and his work compiling classic cases in neuropsychology across a number of languages and cultures (Code, Wallesch, Lecours, & Joanette, 1996, 2003). He has also collaborated with various colleagues across the world to compare knowledge of aphasia in the public domain (Simmons-Mackie, Code, Armstrong, Steigler, & Elman, 2002), and to investigate and compare aphasia management practices across national boundaries (Katz et al., 2000). In each of these studies there has been an opportunity to demonstrate that although there are some diﬀerences regarding institutional and cultural variables, there is also a foundational similarity among those professionals who work in clinical aphasiology throughout the world. To some extent these studies are beneﬁcial in that they emphasize the similarities rather than the diﬀerences in our discipline despite ethnocentric beliefs and practices.

Inﬂuence as accomplishment In this initial chapter we have attempted to provide a sampling of the many research contributions that Chris Code has made over his 30 years to the area of clinical aphasiology. We have cited studies and provided numbers as objective evidence of his achievements. However, his impressive publication record represents only a fraction of his accomplishment in the ﬁeld. For even if Chris Code had not published extensively himself, his inﬂuence would still be profound. Inﬂuence is an interesting phenomenon. One cannot always anticipate how much inﬂuence an individual might have in any given ﬁeld. Often, those with large numbers of publications or other quantiﬁable indices may have little or no impact on a given ﬁeld, while an individual with one powerful idea or a galvanizing personality may act as a catalyst for signiﬁcant change. That is because inﬂuence is not so much an indication of one’s productivity but, rather, a measure of one’s impact on others. When viewed from this perspective, Chris Code has had an exceptional career. When he proposed and then served as the instigator and prime motivator for the journal Aphasiology: An International and Interdisciplinary Journal, he provided the ﬁrst real opportunity to create an international forum for clinical aphasiology and this forum may be his most enduring accomplishment. In the mid-1980s there were venues for the publication of papers in aphasia and the powerful clinical forum created by Bruce Porch, Clinical Aphasiology Conference, was already in its 15th year. However, the published articles in clinical aphasiology were spread across numerous journals and were often

Chris Code’s contribution to aphasiology

9

hard to locate and the Proceedings of the Clinical Aphasiology Conference were privately published with a limited circulation. Within this context, Chris Code saw an opportunity to establish a journal speciﬁcally directed toward aphasiology and its treatment. Importantly, he did not squander this opportunity. Rather, he tirelessly worked and networked, travelled and corresponded, encouraged and cajoled professionals in the ﬁeld – both established researchers and neophytes – to extend their ideas, marshal their data, and prepare manuscripts for his journal. Due to his eﬀorts, Aphasiology: An International and Interdisciplinary Journal has developed from a twiceyearly publication to a monthly publication, and is currently recognized as the leading journal in the ﬁeld of clinical aphasiology. Over its 20 years of publication, Aphasiology has published 184 issues containing more than 1050 papers and articles. In a recent keynote at the International Aphasia Rehabilitation Conference in Sheﬃeld England, Code provided some interesting data on the content of Aphasiology over its 19 year history (Code, 2006). According to his ﬁgures, the journal has published 821 articles that were of direct clinical relevance and 270 of those were reports of treatment studies. These ﬁgures do indicate that Aphasiology is the primary venue for aphasia research – especially as it relates to clinical issues. Indeed, even the annual Proceedings of the Clinical Aphasiology Conference is now published in this journal. Impressive as the journal as been in capturing the majority of clinical research in aphasia and in providing a powerful centralized venue for the discipline, it was the way Chris Code has used the journal that has been most inﬂuential. With an eye toward a more international perspective, he has used his position as Editor in Chief to encourage more interaction and communication between professionals around the world. He has sought out and encouraged clinical aphasiologists on six continents to publish in the journal, and through the invited Forums section that highlights particular themes discussed by invited participants, he has fostered collaborative interactions across these diﬀerent countries and across related professional disciplines. This has resulted in greater awareness of the researchers and the theoretical, research, and clinical issues that are of particular concern in various locales. Due to his eﬀorts in Aphasiology and the progressive development of Internet technologies, clinical aphasiology is truly a shared international discipline. Perhaps Chris Code’s greatest accomplishment as Editor in Chief, however, relates to his encouragement and support of various topics, themes, or types of research. Using the Forum format, he has encouraged important research, discussion, and advocacy regarding a number of important clinically related areas. Service delivery issues in aphasia, psychosocial and social issues like sense of self after aphasia, quality of life issues, family therapy, and a focus on types of therapies are areas that Dr Code has eﬀectively inﬂuenced through the journal. Additionally, Aphasiology has been the journal most supportive of qualitative research studies. Through his encouragement and care when advocating for this non-experimental research paradigm, Aphasiology is the

10

Ball and Damico

leading journal in the human communication sciences in disorders regarding this powerful research tradition. Consequently, the discipline is richer and has greater understanding of the complexity of language, aphasia, and social action as a result. When Dr Code’s inﬂuence on the discipline of aphasia is measured with Aphasiology as one of his instruments of support, advocacy, and change, Chris Code is accomplished indeed. In his book Crowds and Power (1984), the author Elias Canetti discussed the importance of social, political, and intellectual movements and how they were created. He stated that for such movements to occur, there is the need to have eﬀective “crowd crystals”. That is, individuals or small groups of individuals that serve as a seed crystal does in chemistry, to precipitate crowds into action and belief. When looking over Chris Code’s research career and his great inﬂuence on the ﬁeld of clinical aphasiology through his encouragement and advocacy as the Editor in Chief of Aphasiology, we must see him as a “crowd crystal”, a precipitator of the highest order. It is for his eﬀorts and his extensive accomplishments that we dedicate this volume to him.

References Alajouanine, T. (1956). Verbal realization in aphasia. Brain, 79, 1–28. Ball, M. J., Code, C., Tree, J., Dawe, K., & Kay, J. (2004). Phonetic and phonological analysis of progressive speech degeneration: A case study. Clinical Linguistics and Phonetics, 18, 447–462. Ball, M. J., Müller, N., & Rutter, B. (forthcoming). Phonology for communication disorders. Mahwah, NJ: Lawrence Erlbaum Associates, Inc. Blanken, G., Wallesch, C. W., & Papagno, C. (1990). Dissociations of language functions in aphasics with speech automatisms (recurring utterances). Cortex, 26, 41–63. Canetti, E. (1984). Crowds and power. New York: Farrar, Straus & Giroux. Chapey, R., Duchan, J., Elman, R., Garcia, L., Kagan, A., Lyon, J., et al. (1994). Life participation approach to aphasia: A statement of values for the future. In R. Chapey (Ed.), Language intervention strategies in aphasia and related neurogenic communication disorders (4th ed., pp. 235–246). Philadelphia: Lippincott, Williams & Wilkins. Chung, K., Code, C., & Ball, M. J. (2004). Speech automatisms and recurring utterances from aphasic Cantonese speakers. Journal of Multilingual Communication Disorders, 2, 32–42. Code, C. (1982a). Neurolinguistic analysis of recurrent utterances in aphasia. Cortex, 18, 141–152. Code, C. (1982b). On the origins of recurrent utterances in aphasia. Cortex, 18, 161–164. Code, C. (1984a). Delayed auditory feedback. In C. Code & M. J. Ball (Eds.), Experimental clinical phonetics. London: Croom Helm. Code, C. (1984b). Dichotic listening. In C. Code & M. J. Ball (Eds.), Experimental clinical phonetics. London: Croom Helm. Code, C. (1986). Catastrophic reaction and anosognosia in anterior–posterior and

Chris Code’s contribution to aphasiology

11

left–right models of the cerebral control of emotion. Psychological Research, 48, 53–55. Code, C. (1987). Language, aphasia and the right hemisphere. Chichester, UK: John Wiley. Code, C. (1989a). The characteristics of aphasia. Hove, UK: Lawrence Erlbaum Associates Ltd. Code, C. (1989b). Speech automatisms and recurring utterances. In C. Code (Ed.), The characteristics of aphasia. Hove, UK: Lawrence Erlbaum Associates Ltd. (Previously published by Taylor & Francis, London.) Code, C. (1994a). Speech automatism production in aphasia. Journal of Neurolinguistics, 8, 135–148. Code, C. (1994b). The role of the right hemisphere in the treatment of aphasia. In R. Chapey (Ed.), Language intervention strategies in adult aphasia. Baltimore, MD: Williams & Wilkins. Code, C. (1996). Speech from the isolated right hemisphere? Left hemispherectomy cases E.C. and N.F. In C. Code, C.-W. Wallesch, Y. Joanette, & A.-R. Lecours (Eds.), Classic cases in neuropsychology. Hove, UK: Lawrence Erlbaum Associates Ltd. Code, C. (1997a). Experimental audioperceptual techniques. In M. J. Ball & C. Code (Eds.), Instrumental clinical phonetics (pp. 228–261). London: Whurr. Code, C. (1997b). Aphasia recovery, therapy and psychosocial adjustment. In A. Baum, C. McManus, S. Newman, J. Weinman, & R. West (Eds.), The Cambridge handbook of psychology, health & medicine. Cambridge, UK: Cambridge University Press. Code, C. (1997c). Can the right hemisphere speak? Brain and Language, 57, 38–59. Code, C. (1997d). A metamodel for recovery from aphasia. In J. Ponsford, P. Snow, & V. Anderson (Eds.), International perspectives in traumatic brain injury. Melbourne: Australian Academic Press. Code, C. (1998). Models, theories and heuristics in apraxia of speech. Clinical Linguistics and Phonetics, 12, 47–66. Code, C. (1999). Re-assembling the brain: Are cell assemblies the brain’s language for recovery of function? (Commentary) Behavioural and Brain Sciences, 22, 282. Code, C. (2000). Converging not fractionating. Brain and Language: Millennium Issue, 71, 44–45. Code, C. (2001). Multifactorial processes in recovery from aphasia: Developing the foundations for a multilevelled framework. Brain and Language, 77, 25–44. Code, C. (2003). The quantity of life for people with chronic aphasia. Neuropsychological Rehabilitation, 13, 365–378. Code, C. (2006). Back to the future: A recent history of aphasia rehabilitation. A keynote speech at the 12th International Aphasia Rehabilitation Conference, Shefﬁeld, UK, June. Code, C., & Ball, M. J. (1982). Fricative production in Broca’s aphasia: A spectrographic analysis. Journal of Phonetics, 10, 325–331. Code, C., & Ball, M. J. (1988). Apraxia of speech: The case for a cognitive phonetics. In M. J. Ball (Ed.), Theoretical linguistics and disordered language (pp. 152–167). London: Croom Helm. Code, C., & Ball, M. J. (1994). Syllabiﬁcation in aphasic recurring utterances: Contributions of sonority theory. Journal of Neurolinguistics, 8, 257–265. Code, C., & Ball, M. J. (1995). The status of sonority theory: Evidence from syllabiﬁcation in aphasic recurring utterances. In K. Elenius & P. Branderud (Eds.),

12

Ball and Damico

Proceedings ICPhS 95 Stockholm (Vol. 4, pp. 480–483). Stockholm: KTH & Stockholm University. Code, C., & Brown, J. W. (1987). Aphasia from the wrong (right) hemisphere: Questions for crossed aphasia. Aphasiology, 1, 401–402. Code, C., Hemsley, G., & Herrmann, M. (1999). Emotional reactions to aphasia. Seminars in Speech and Language, 20, 19–31. Code, C., & Herrmann, M. (2003). The relevance of emotional and psychosocial factors in aphasia to rehabilitation. Neuropsychological Rehabilitation, 13, 109–132. Code, C., & Joanette, Y. (2003). Neural plasticity in the control of language in the adult brain: The role of the separated right hemispheres in cases PS, VP and JW. In C. Code, C.-W. Wallesch, Y. Joanette, & A.-R. Lecours (Eds.), Classic cases in neuropsychology: Volume II. Hove, UK: Lawrence Erlbaum Associates Ltd. Code, C., & Müller, D. (Eds.) (1989). Aphasia therapy (2nd ed.). London: Cole & Whurr. Code, C., & Müller, D. J. (1992). The Code-Müller protocols: Assessing perceptions of psychosocial adjustment to brain damage. Kibworth: Far Communications. Code, C., & Müller, D. (1995a). Psychosocial perspectives. In C. Code & D. J. Müller (Eds.), The treatment of aphasia: From theory to practice. London: Whurr. Code, C., & Müller, D. (1995b). Cognitive and neuropsychological approaches. In C. Code & D. J. Müller (Eds.), The treatment of aphasia: From theory to practice. London: Whurr. Code, C., & Müller, D. (1995c). Eﬃcacy and eﬀectiveness. In C. Code & D. J. Muller (Eds.), The treatment of aphasia: From theory to practice. London: Whurr. Code, C., & Müller, D. (1996). Psychosocial issues. In C. Code & D. J. Müller (Eds.), Forums in clinical aphasiology. London: Whurr. Code, C., & Müller, D. (2003). Psychosocial and quality of life issues in treatment. In R. Kent (Ed.), The MIT encyclopaedia of communication disorders. Cambridge, MA: MIT Press. Code, C., Müller, D. J., & Herrmann, M. (1999). Perceptions of psychosocial adjustment to aphasia: Studies with the CMP. Seminars in Speech and Language, 20, 51–63. Code, C., Müller, D., Herrmann, M., & Hogan, A. (1999). Perceptions of psychosocial adjustment to acquired commnication disorders: Studies with the Code-Müller protocols. International Journal of Communication Disorders, 34, 193–207. Code, C., Müller, N., Tree, J. T., & Ball, M. J. (2006). Syntactic impairments can emerge later: Progressive agrammatic agraphia and syntactic comprehension impairment. Aphasiology, 20, 1035–1058. Code, C., Wallesch, C.-W., Lecours, A.-R., & Joanette, Y. (Eds.) (1996). Classic cases in neuropsychology. Hove, UK: Lawrence Erlbaum Associates Ltd. Code, C., Wallesch, C.-W., Lecours, A.-R., & Joanette, Y. (Eds.) (2003). Classic cases in neuropsychology: Volume II. Hove, UK: Lawrence Erlbaum Associates Ltd. Cowell, S. F., Egan, G. F., Code, C., Harasty, J., & Watson, J. D. G. (2000). The functional neuroanatomy of simple calculation and number repetition: A parametric PET activation study. NeuroImage, 12, 565–573. Harasty, J., Halliday, G. M., Kril, J. J., & Code, C. (1999). Speciﬁc temporoparietal gyral atrophy reﬂects the pattern of language dissolution in Alzheimer’s disease. Brain, 122, 675–686. Hemsley, G., & Code, C. (1996). Interactions between recovery in aphasia, emotional and psychosocial factors in subjects with aphasia, their signiﬁcant others and speech pathologists. Disability and Rehabilitation, 18, 567–584.

Chris Code’s contribution to aphasiology

13

Herrmann, M., & Code, C. (1996). Weighting of items on the Code-Müller protocols: The eﬀects of clinical experience of aphasia therapy. Disability and Rehabilitation, 18, 509–514. Katz, R., Hallowell, B., Code, C., Armstrong, E., Roberts, P. M., Pound, C., et al. (2000). A multi-national comparison of aphasia management practices. International Journal of Language and Communication Disorders, 35, 303–314. Lyon, J. G., & Shadden, B. (2001). Treating life consequences of aphasia’s chronicity. In R. Chapey (Ed.), Language intervention strategies in aphasia and related neurogenic communication disorders (4th ed., pp. 297–314). Baltimore, MD: Williams & Wilkins. Müller, D., & Code, C. (1983). Interpersonal perceptions of psychosocial adjustment in aphasia. In C. Code & D. Müller (Eds.), Aphasia therapy. London: Edward Arnold. Müller, D., Code, C., & Mugford, J. (1982). Predicting psychosocial adjustment in aphasia. British Journal of Disorders of Communication, 17, 23–29. Nespoulous, J.-L., Code, C., Virbel, J., & Lecours, A.-R. (1998). Hypotheses on the dissociation between “referential” and “modalizing” verbal behaviour in aphasia. Applied Psycholinguistics, 19, 311–331. Roger, P., Code, C., & Sheard, C. (2000). Assessment and management of aphasia in a linguistically diverse society. Asia-Paciﬁc Journal of Speech and Language, 5, 21–34. Shadden, B. B. (2005). Aphasia as identity theft: Theory and practice. Aphasiology, 19, 211–223. Simmons-Mackie, N. (2001). Social approaches to aphasia intervention. In R. Chapey (Ed.), Language intervention strategies in aphasia and related neurogenic communication disorders (4th ed., pp. 246–268). Baltimore, MD: Williams & Wilkins. Simmons-Mackie, N., Code, C., Armstrong, E., Stiegler, L., & Elman, R. (2002). What is aphasia? Results of an international survey. Aphasiology, 12, 837–848. Worrall, L. E., & Holland, A. (2003). Editorial: Quality of life in aphasia. Aphasiology, 17, 329–332.

Part I

Conceptual considerations

2

Investigations in speech and language and related disorders Crossing the boundaries between disciplines—a tribute to Chris Code Manfred Herrmann and Thorsten Fehr

Sydney University, 1997

Introduction Our research in speech and language started in the early 1980s and focused primarily on topics in the ﬁeld of aphasia rehabilitation. Nonverbal communication as a compensatory means of communication in severe aphasia, psychosocial alterations following aphasia and psychosocial adjustment to aphasia, the neuronal basis of depressive disorders in aphasic patients, and the investigation of speciﬁc goals of aphasia rehabilitation are just some of the topics that were originally inﬂuenced by Chris Code. Chris not only initiated part of our research but he also participated in several investigations. Even when we expanded the scope of our investigations into basic research (such as molecular neurobiology or the spatiotemporal analysis of neuronal correlates of number processing) Chris was with us – not only in a theoretical sense but also in person (i.e., spending sabbaticals in our labs or as a scientiﬁc fellow invited by the Hanse Institute for Advanced Studies). In this chapter, we try to delineate part of this cooperation between Chris and ourselves, which up to now has not only survived more than two decades but also bridged research on diﬀerent continents.

18

Herrmann and Fehr

Nonverbal communication in severe nonﬂuent aphasia About 25 years ago, our research group, formerly located at Freiburg University, started investigations in the ﬁeld of aphasia and related disorders. Our ﬁrst studies focused on the issue of communication and communication strategies in people with severe and chronic aphasia. We tried to analyze nonverbal communication as a compensatory behavioral strategy in severely nonﬂuent aphasia. Based on videotaped conversation sequences we investigated the use of nonverbal communication between aphasic patients and their communication partners. The data derived from that study show that aphasic patients used nonverbal channels of communication signiﬁcantly more often, and for a signiﬁcantly longer period of time, than their healthy partners. We concluded that severe aphasic patients use nonverbal communication strategies in natural conversation settings as a means of compensation for verbal deﬁcits, and that these spontaneously used communication strategies should extend the scope of speech therapy towards communication therapy (Herrmann, Reichle, Lucius-Hoene, Wallesch, & Johannsen-Horbach, 1988). In a follow-up study with 20 chronically nonﬂuent aphasic patients with moderate or severe language deﬁcits we could demonstrate that communicative and neurolinguistic deﬁcits did not correlate and that non- and paralinguistic communication accounted for the communicative eﬃciency in nonﬂuent aphasia (Herrmann, Koch, Johannsen-Horbach, & Wallesch, 1989). These preliminary data also gave a ﬁrst indication of communicative eﬃciency in nonﬂuent aphasia being strongly aﬀected by both the psychosocial status of the patient and his family and emotional disorders resulting from stroke. At that time (the early 1980s), there were only few aphasia therapists and speech pathologists who were engaged in investigating psychosocial changes and emotional disorders following stroke and aphasia. We, by chance, became acquainted with a young lecturer from the Leicester Polytechnic, UK, who presented a research instrument and some data on expectations concerning psychosocial adaptation in chronic aphasia. Chris Code was one of the authors of the Code-Müller Scale of Psychosocial Adjustment (SPA; Müller, Code, & Mugford, 1983; Müller & Code, 1983) nowadays known as the Code-Müller Protocols (CMP; Code & Müller, 1992). Since then, we have established a long-lasting friendship and fruitful scientiﬁc cooperation bridging continents and covering a variety of research topics in the ﬁeld of speech and language and related disorders.

Psychosocial alterations following aphasia In 1985 we started with a number of studies investigating psychosocial changes resulting from communicative impairment in chronic aphasic patients and their relatives. We found that aphasic patients and relatives suﬀer from a considerable amount of professional, social, familial, and psychological stress

Investigations in speech and language and related disorders

19

(Herrmann, Bartels, & Wallesch, 1993a; Herrmann, Johannsen-Horbach, & Wallesch, 1992; Herrmann & Wallesch, 1989; Johannsen-Horbach, Wenz, Fünfgeld, Herrmann, & Wallesch, 1993), which in turn seems to be a limiting factor in patients’ rehabilitation (Herrmann, 1997; Herrmann, JohannsenHorbach, & Wallesch, 1993b). In a longitudinal study with 58 stroke patients and their relatives we were able to demonstrate that aphasic patients and relatives experience signiﬁcantly more severe professional and social changes than subjects without aphasia and their families. Aphasia itself, however, seems to have no substantial eﬀect on adaptive or maladaptive coping strategies or activities of daily living (Herrmann, Bartels, Britz, & Wallesch, 1995b). In a small pilot study we investigated ten chronically aphasic patients and their relatives with respect to the emotional experience of psychosocial changes and the individually perceived stresses and burdens posed by diﬀerent stroke symptoms (Wenz & Herrmann, 1990). The most striking result from that study was that the respective speech therapists expected the patients to be most severely stressed by speech and language disorders, while the patients’ relatives thought that both aphasia and hemiparesis contribute equally to the patient’s stresses. The patients themselves, however, reported to be most severely aﬀected by motor symptoms (see Figure 2.1). Based on these ﬁndings we decided to dedicate part of our research on interpersonal perceptions of psychosocial adjustment to aphasia.

Figure 2.1 Stresses and burdens in chronic aphasic patients as perceived by the patients, their respective relatives and speech therapists (modiﬁed from Wenz & Herrmann, 1990).

20

Herrmann and Fehr

Psychosocial adjustment to aphasia: Applications of the Code-Müller protocols (CMP) The CMP (formerly known as the Scale of Psychosocial Adjustment, SPA) were introduced by Chris Code and colleagues in 1983 (Code & Müller, 1992; Müller & Code, 1983; Müller et al., 1983) and originally aimed to compare perceptions of psychosocial adjustment to aphasia from the separate perspectives of patients, relatives, and speech therapists. The CMP consisted of ten items on psychosocial expectations derived from an expert rating, which covered the following topics: (1) the ability to work, (2) receiving speech therapy, (3) independence of others, (4) meeting friends socially, (5) coping with depression, (6) following interests and hobbies, (7) speaking to strangers, (8) coping with frustration, (9) making new personal relationships, and (10) coping with embarrassment. In a ﬁrst study (Herrmann & Wallesch, 1989), we found that aphasic patients and relatives signiﬁcantly overestimated the patient’s ability to cope with psychosocial stresses when compared to the assessment of their respective speech therapists. This study replicated the original ﬁndings by Chris Code and colleagues, and the ﬁndings of our ﬁrst study were also corroborated by a series of future studies. In our view, these data showed that a considerable number of patients and relatives expected – even after years of limited progress – that the premorbid status might eventually be restored. This “unhealthy attitude” (Helmick, Watamori, & Palmer, 1976), on the other hand, could lead to signiﬁcant emotional and psychosocial crises on the part of the relatives and of the patients. Apart from the above described use of the CMP as an instrument that targeted the expectations of psychosocial adjustment to aphasia, we also introduced the CMP items as a scale reﬂecting particular objectives of aphasia rehabilitation (Herrmann & Wallesch, 1990). By means of the multi-attribute utility technique (MAUT; Edwards & Newman, 1982), we investigated the therapeutic staﬀ of a Neurological Rehabilitation Center (occupational therapists, physiotherapists, neuropsychologists, neurologists, and speech therapists) with respect to the relative importance of CMP items / topics as speciﬁc goals of aphasia rehabilitation. The data of this study indicated that the speciﬁc demands of diﬀerent therapeutic methods and approaches clearly inﬂuence the appraisal of abilities for psychosocial adaptation and aphasia rehabilitation. In 1995, when Chris came over from Sydney to Germany to spend part of his sabbatical in our lab at Freiburg University, we conducted a bigger study with 122 professionals engaged in aphasia therapy (Herrmann & Code, 1996). These aphasia therapists participated in a summer academy on “Language and Brain” that was held at Freiburg University and was organized by Gerhard Blanken. The participants were asked to rank and weight the relevance of the items of the CMP for assessing the expectations of psychosocial adjustment to aphasia as a general target of aphasia rehabilitation. The data show two major results: (1) for professionals working in aphasia

Investigations in speech and language and related disorders

21

rehabilitation independence from others and emotional adaptation emerge as the most important domains on the CMP (see Figure 2.2), and (2), the relevance of CMP items as potential targets in aphasia therapy changes with duration of clinical experience. In 1997, when the ﬁrst author of the present chapter spent part of his sabbatical at Sydney University, we worked up our studies on the CMP in two review papers (Code, Müller, Hogan, & Herrmann, 1999b; Code, Müller, & Herrmann, 1999c). During the last couple of years we have also started to use the CMP as teaching material in courses on neurological and neuropsychological rehabilitation. Within a special education program in clinical neuroscience, fourth year psychology students are expected to participate as visiting students in speech and language therapy, occupational therapy, physiotherapy, and neuropsychological therapy. Before starting the practical courses we always introduce the CMP (and the respective results derived from the ranking and weighting procedure) as a common starting point for discussing the relative importance of diﬀerent goals of aphasia rehabilitation. Interestingly, the relative weightings of the CMP items in naïve or untrained students do not diﬀer signiﬁcantly from the weightings given by experienced aphasia therapists (see Figure 2.2). Disagreement in the assessment of the relative

Figure 2.2 Distribution of relative item weightings of the Code-Müller Protocols (CMP; mean scores). Weightings are standardized to a mean weight of .10. Dark bars show the weightings of experienced aphasia therapists (N = 60) and bright bars indicate the weightings of 4th year psychology students (N = 78). Error bars represent ± 1 SEM, p values refer to t-tests (two-sided).

22

Herrmann and Fehr

importance of rehabilitation goals was only found with respect to the ability to work, following interests and hobbies, and coping with frustration. And only the ability to work (again) was judged a signiﬁcantly more important rehabilitation goal by untrained psychology students.

Emotional disorders in aphasia: Post-stroke depression and neuropathological correlates As already mentioned above, our experience with the use of nonverbal behavior as a compensatory means of communication in severe aphasia seemed to be highly inﬂuenced by both the psychosocial and the emotional status of the patients and relatives. We, therefore, also started to investigate depressive mood changes following brain lesions in aphasic and non-aphasic stroke patients. In a ﬁrst study conducted from 1987 to 1991 we investigated depressive alterations in acute and chronic aphasic patients with ﬁrst-ever single left-sided stroke lesions (Herrmann et al., 1993a). Patients with major depression were only found in the acute group, and only among those with nonﬂuent aphasias. Brain imaging data showed that it was not the volume of the lesion but only the lesion location that had a major impact on the type and severity of depressive symptoms. Superimposition of brain lesions of aphasic patients with major depressive disorders demonstrated a common subcortical lesion area involving putaminal and external pallidal structures, which we interpreted to account for the pathogenesis of post-stroke depression. We were able to replicate these ﬁndings in two broader studies (Herrmann, Bartels, Schumacher, & Wallesch, 1995a, and Beblo, Wallesch, & Herrmann, 1999), both of which supported the hypotheses that (1) brain lesions of the left hemisphere basal ganglia and surrounding white matter tend to play a decisive role in the development of major depression in the early stage after stroke, and (2) (functional) disruption of frontostriatal circuits seems to contribute to the underlying pathophysiology of post-stroke depression. These data, however, only account for the development of severe depressive disorder (major depression) in aphasic patients during the post-acute stage after stroke onset, but obviously do not contribute to the pathophysiology of depressive disorders emerging in the later course of stroke and aphasia. Based on data from our own studies (Herrmann et al., 1995b; Herrmann et al., 1992; as well as studies from other colleagues) we argued that during the course of aphasia rehabilitation there are diﬀerent stages during which the patients exhibit a speciﬁc vulnerability to developing depressive disorders. In a ﬁrst approach we classiﬁed these stages as “primary,” “secondary,” and “tertiary” (Herrmann & Wallesch, 1993). These terms, however, mainly reﬂect the time of occurrence of depression in aphasia rehabilitation and do not specify the underlying pathophysiology of diﬀerent types of depression. At that point of our studies in speech and language and related disorders, Chris again joined our group and helped us to characterize and diﬀerentiate the

Investigations in speech and language and related disorders

23

distinct sub-types of depressive disorders during long-term aphasia rehabilitation (Code, Hemsley, & Herrmann, 1999a; Code & Herrmann, 2003).

The neuronal basis of number representation and mental calculation During the sabbatical stay of the ﬁrst author of the present chapter at Sydney University in 1997, Chris Code was heavily engaged in disentangling the mystery of number processing and mental calculation by the use of positron emission tomography (Cowell & Code, 1998; Cowell, Egan, Code, Harasty, & Watson, 2000). While these very ﬁrst investigations on number processing were based on simple calculation tasks, we decided to use a more complex paradigm and advanced methods of spatiotemporal analysis of brain activity in future studies. From 2002 to 2004, Chris was invited to Bremen University for several research stays as a fellow of the Hanse Institute for Advanced Studies, and we decided to resume investigations on the neuronal basis of mental calculation. During the last couple of years, a huge volume of studies have been published, which investigated “mental calculation” or “number processing” by using diﬀerent study designs including diﬀerent operators, diﬀerent stimulation modalities, and diﬀerent complexities of mental calculation tasks. Our combined UK (Exeter)–Germany (Bremen) approach aimed at spatiotemporal analysis of neuronal correlates of diﬀerent stimulation modalities (auditory versus visual), task complexities (e.g., “simple tasks” with results in the number domain below 10 or “complex tasks” with results in the number domain between 10 and 100), and basic operations (+, −, ×, /) during mental calculation. Prior to fMRI and MEG examinations we started with a German pilot study on a behavioral data level (reaction times (RTs), error rates) followed by a parallel study with British students at Exeter University. Surprisingly, students from Bremen University presented faster RTs than the age-matched British group (see Figure 2.3), while error rates did not diﬀer signiﬁcantly between groups. So far, we do not have a strong explanation for how these diﬀerences originate, and how Chris might have contributed to this result. In both groups, participants showed longer RTs for complex tasks in comparison to simple tasks. The auditory presentation mode produced longer RTs than the visual presentation mode. In a further study combining functional magnetic resonance imaging (fMRI) and magnetencephalography (MEG), 11 German subjects were scanned with both methods while they performed the same tasks evaluated in the pilot study. Data derived from event-related fMRI showed a network of activated areas for complex tasks in contrast to simple tasks in prominently right frontal, parietal and central regions. A preliminary ﬁnding demonstrated diﬀerent task-related and task modality speciﬁc spatiotemporal characteristics of source space activity as revealed by seeded dipoles based on the fMRI regions of interest (ROI) and minimum-norm (L2) estimates (see Figure 2.4).

24

Herrmann and Fehr

Figure 2.3 Reaction times for complex mental calculation tasks (/: division; −: subtraction; ×: multiplication; +: addition) with auditory (left) and visual (right) stimulation modes for two age-matched groups of German (Bremen University; dark bars) and British (Exeter University; bright bars) students. Error bars represent ± 1 SEM, p values refer to t-tests (two-sided).

At the present point of analysis our data show that diﬀerent arithmetic operations should be analyzed independently of each other. Furthermore, the present data indicate that there is no empirical basis for the comparison of studies using diﬀerent presentation modalities.

Conclusions Most of the studies presented in this chapter were initiated or motivated by the research or research interests of Chris Code. These areas reﬂect a very broad range of scientiﬁc interest, with respect to both research topics and research methods. The bracket, however, that encloses these diversiﬁed activities is always the issue of speech and language and related disorders. Although our studies in the periphery of “aphasiology proper” always remained low-budget research, a great number of PhD students and postdocs participated in the series of investigations as described before. Furthermore, part of the research methods originally developed by Chris and colleagues were also taken into teaching modules in universities and further education in neurological and neuropsychological rehabilitation. So we are quite sure that our cooperation with Chris Code will continue for the next decades and that Chris will also accompany our next projects on the molecular basics of brain disorders (Herrmann & Ehrenreich, 2003) and neuroprotection (Ehrenreich et al., 2004).

Investigations in speech and language and related disorders

25

Figure 2.4 Left: data from mental calculation processes after auditory stimulation; right: data from mental calculation processes after visual task presentation (both columns represent the contrast “complex” vs. “simple” tasks). The upper row shows MEG signal space averaged responses and the corresponding global ﬁeld power (GFP) time courses with the respective maxima. The middle row shows minimum-norm (L2) estimates according to marked GFP maxima. The lower row shows fMRI contrasts and illustrates corresponding dipole positions seeded into a standard brain volume (Talairach Space).

References Beblo, Th., Wallesch, C. W., & Herrmann, M. (1999). The crucial role of frontostriatal circuits for depressive disorders in the post-acute stage after stroke. Neuropsychiatry, Neuropsychology, and Behavioral Neurology, 12, 234–246. Code, C., Hemsley, G., & Herrmann, M. (1999a). The emotional impact of aphasia. Seminars in Speech & Language, 20, 19–31.

26

Herrmann and Fehr

Code, C., & Herrmann, M. (2003). The relevance of emotional and psychosocial factors in aphasia to rehabilitation. Neuropsychological Rehabilitation, 13, 109–132. Code, C., & Müller, D. J. (1992). The Code-Muller protocols: Assessing perceptions of psychosocial adjustment to brain damage. Kibworth: Far Communications. Code, C., Müller, D. J., & Herrmann, M. (1999c). Perceptions of psychosocial adjustment to aphasia. Seminars in Speech & Language, 20, 51–62. Code, C., Müller, D. J., Hogan, A., & Herrmann, M. (1999b). Perceptions of psychosocial adjustment to acquired communication disorder: Applications of the Code-Müller protocols. International Journal of Language and Communication Disorders, 34, 193–207. Cowell, S. F., & Code, C. (1998). Thinking nuclear medicine – PET activation. Journal of Nuclear Medicine Technology, 26, 17–22. Cowell, S. F., Egan, G. F., Code, C., Harasty, J., & Watson, J. D. (2000). The functional neuroanatomy of simple calculation and number repetition: A parametric PET activation study. NeuroImage, 12, 565–573. Edwards, W., & Newman, J. R. (1982). Multiattribute evaluation. Beverly Hills, CA: Sage Publications. Ehrenreich, H., Aust, C., Krampe, H., Jahn, H., Jacob, S., Herrmann, M., et al. (2004). Erythropoietin: Novel approaches to neuroprotection in human brain disease. Metabolic Brain Disease, 19, 195–206. 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. Herrmann, M. (1997). Studying psychosocial problems in aphasia: Some conceptual and methodological considerations, Aphasiology, 11, 717–726. Herrmann, M., Bartels, C., Britz, A., & Wallesch, C. W. (1995b). The impact of aphasia on the patient and family in the ﬁrst year post-stroke. Topics in Stroke Rehabilitation, 2, 5–19. Herrmann, M., Bartels, C., Schumacher, M., & Wallesch, C. W. (1995a). Poststroke depression: Is there a patho-anatomical correlate for depression following the post-acute stage of stroke? Stroke, 26, 850–856. Herrmann, M., Bartels, C., & Wallesch, C. W. (1993a). Depression in acute and chronic aphasia: Symptoms, pathoanatomical–clinical correlations, and functional implications. Journal of Neurology, Neurosurgery, and Psychiatry, 56, 672–678. Herrmann, M., & Code, C. (1996). Weightings of items on the Code-Müller protocols: The eﬀects of clinical experience on aphasia therapy. Disability and Rehabilitation, 18, 509–514. Herrmann, M., & Ehrenreich, H. (2003). Brain derived proteins as markers of acute stroke: Their relation to pathophysiology, outcome prediction and neuroprotective drug monitoring. Restorative Neurology and Neuroscience, 21, 177–190. Herrmann, M., Johannsen-Horbach, H., & Wallesch, C. W. (1992). Psychosocial aspects of aphasia. In D. Lafond, Y. Joanette, J. Ponzio, R. Degiovani, & M. Taylor-Sarno (Eds.), Living with aphasia: Psychosocial issues (pp. 187–206). San Diego, CA: Singular. Herrmann, M., Johannsen-Horbach, H., & Wallesch, C. W. (1993b). Empathy and aphasia rehabilitation: Are there contradictory requirements of treatment and psychological support? Aphasiology, 7, 575–579

Investigations in speech and language and related disorders

27

Herrmann, M., Koch, U., Johannsen-Horbach, H., & Wallesch, C. W. (1989). Communicative skills in chronic and severe nonﬂuent aphasia. Brain and Language, 37, 339–352. Herrmann, M., Reichle, T., Lucius-Hoene, G., Wallesch, C. W., & JohannsenHorbach, H. (1988). Nonverbal communication as a compensative strategy for severely nonﬂuent aphasics: A quantitative approach. Brain and Language, 33, 41–54. Herrmann, M., & Wallesch, C. W. (1989). Psychosocial changes and psychosocial adjustment with chronic and severe nonﬂuent aphasia. Aphasiology, 3, 513–526. Herrmann, M., & Wallesch, C. W. (1990). Expectations of psychosocial adjustment in aphasia: A MAUT study with the Code-Müller scale of psychosocial adjustment. Aphasiology, 4, 527–538. Herrmann, M., & Wallesch, C. W. (1993). Depressive changes in stroke patients. Disability and Rehabilitation, 15, 55–66. Johannsen-Horbach, H., Wenz, C., Fünfgeld, M., Herrmann, M., & Wallesch, C. W. (1993). Psychosocial aspects in the treatment of adult aphasics and their families: A group approach. In A. Holland, & M. Forbes (Eds.), Aphasia therapy today: World perspectives (pp. 319–334). San Diego, CA: Singular. Müller, D. J., & Code, C. (1983). Interpersonal perceptions of psychosocial adjustment to aphasia. In C. Code, & D. J. Müller (Eds.), Aphasia therapy (pp. 101–112). London: Edward Arnold. Müller, D., Code, C., & Mugford, J. (1983). Predicting psychosocial adjustment in aphasia. British Journal of Disorders of Communication, 18, 23–29. Wenz, C., & Herrmann, M. (1990). Subjective perception and the emotional experience of psychosocial changes: A comparison between patients and their relatives. Psychotherapie, Psychosomatik, Medizinische Psychologie, 40, 488–495.

3

Independent evidence for the uniﬁcation of explanatory paradigms in the neurosciences Hugh W. Buckingham and Sarah S. Christman

Introduction In this chapter we propose to trace the recent history of a counterintuitive observation in the neurosciences that comprises descriptions of active processing whereby strong stimulus forces evoke weak or insigniﬁcant associations, and where weak forces evoke stronger associates. This phenomenon has been labeled “paradoxical,” since it is opposed to the normal situation whereby strong elements in a network associate with their most frequent associates, and weak elements in a network associate with less frequent associates. We chart the trajectory of the notion as it weaves its way from the Pavlovian physiology of conditioned reﬂexes and stimulus–response motorsensory reﬂexes of vegetative and alimentary levels to the neuropsychology of Sigmund Freud, Alexander Luria, and the connectionist modeling of late twentieth-century neuropsychological science. Our purpose is to highlight the fact that the threads of this paradoxical phase of stimulus–response balance, or rather imbalance, have been cast at three distinct levels of explanation in the neurosciences: Pavlovian physiology; Luria’s concomitant neuropsychology of language; and Trevor Harley’s connectionist modeling. We emphasize that the situation is one that argues for a uniﬁcation or alignment rather than any reduction of Luria’s neurolinguistics or Harley’s connectionism to Pavlov’s physiology. Independent ﬁndings of similar phenomena from distinct scientiﬁc methodologies in the neuropsychology of language serve to strengthen each paradigm, and rather than fractionating the neurosciences, there is a growing convergence, alignment, or uniﬁcation of information (Code, 2000). Scientiﬁc investigation is often driven by: (1) the (frequently unstated null hypothesis) search for evidence for one or another hypothesis or model previously proposed in the literature, (2) a straightforward and unbiased search for possible evidence for a deductive prediction, and (3) the search for further occurrence of inductively predicted correlations between events. Often, diﬀerent explanatory methodologies and paradigms will uncover a similar set of observations in nature, all of which are in “alignment” (Gotts & Plaut, 2004, p. 332) in some way or another. Compatible ﬁndings from distinct

Uniﬁcation of explanatory paradigms in the neurosciences

29

methodological inquiries are extremely important in accessing the contributions of the respective explanatory accounts. The position we adopt in this preliminary study is that the “uniﬁcation” of the sciences avoids the metaphysical trappings of a “reductionist” stand, which would have us believe that ultimately our understanding of the physical universe will itself reduce to the physical – whence the word “physics” is derived. That is, all sciences will eventually come to be explained in the terms of that science. Once we abandon the fear or lingering doubts that mental objects can be understood as objects in nature nevertheless (see Chomsky, 2000, 2002, on language as a natural object) and therefore studied as such, the eschewing of reductionism and the embracing of a uniﬁcation view of the sciences is a great deal easier to tolerate. Buckingham and Christman (2004a, p. 292) adopted this view in unifying the heterogeneous methodologies on the issue of perseveration written for a special journal volume collection of papers: neuropharmacological, connectionist, neuropsychological, linguistic and rehabilitative. We carefully resisted the ancient tendency to imply that ultimately all will reduce to the biochemistry of the synapse, only to wait around for physics to explain that. The topic for our chapter is an outgrowth of an essay by one of us (Buckingham, forthcoming) on Alexander Luria, which made reference to a special issue project of Chris Code in the journal Aphasiology, edited by the Polish neuropsychologist Bozydar Kaczmarek in 1995. Chris’s contributions as a scientist as well as an editor of books and journals have inﬂuenced us all in one or another way. The present chapter draws from connectionist modeling in a historical framework. Here, again, we note Chris’s research contributions in stochastic predictions of recovery from aphasia with connectionist networks (Code, Rowley, & Kertesz, 1994) and yet another special editorial project with Harley’s (1993) detailed overview and assessment for Aphasiology on connectionism. Chris, the scholar-researcher, has contributed both as principal editor of two recent volumes of classical cases in neuropsychology (Code, Lecours, Joanette, & Wallesch, 1996; Code, Wallesch, Joanette, & Lecours, 2003) for Psychology Press, and has chapters in these volumes as well. The marks of Chris’s editorial scholarship and scientiﬁc research are accordingly implicit through our contribution to his Festschrift.

Ivan Pavlov – physiology Ivan Pavlov (1962) originally worked out physical principles that he labeled as “laws of strength” or “rules of force.” He was a physiologist, and his explanatory idiom was the development of conditioned reﬂexes of sensory-motor nerve physiology. Most undergraduates in psychology have studied at least the rudiments of Pavlov’s investigations “of the dog, this friend of man since pre-historic times” (Pavlov, 1962, p. 87). His commitment to physiology was straightforward from the beginning. He wrote that he was trying to comprehend the totality of the dog’s nervous system, “purely physiologically without

30

Buckingham and Christman

using any psychological ideas or terms” (Pavlov, 1962, p. 87). He conditioned the alimentary functions of the dog through the “coupling,” as he writes, of various kinds of outside stimuli (whistles, metronomes, lights, bells, and the like) with presentations of food. As we all recall, he therefore could elicit many gustatory motor secretions of saliva with one or another of these sensory stimuli. Reﬂecting on his work in a paper delivered at the Sorbonne, Paris, in December 1925, he claimed in French that, “At the present time we have facts which warrant the assumption that the act of coupling is even an elementary physiological process” (Pavlov, 1962, p. 88). Unfortunately, there is no evidence at all that Pavlov was aware of the early suggestions of David Hartley (1746, 1749; Buckingham & Finger, 1997) to the same eﬀect. In his study of canine physiology, Pavlov found that the repeated administration of coupled sensory stimuli led simultaneously to the easy activation of speciﬁc (conditioned) motor responses and the thorough inhibition of competing responses. He believed that this natural phenomenon also characterized the activity underlying many of the aspects of consciousness that he studied, such as narcolepsy, hypnotic states, severe psychotic and neurotic states, the “oneiroid” phases of pre-sleep, and the deeper phases of slumber. For Pavlov, the continuum from wakefulness to complete sleep mirrored in an important sense a continuum from total consciousness to unconsciousness. He conceived of a multitude of diﬀerence “phases” along this continuum, each characterized by diﬀerent admixtures of activation and inhibition levels of associated conditioned couplings between elements. All phases were tied to the interplay, or stasis, of activation and inhibition, inhibition becoming stronger and stronger in phases that approached sleep. Phases were diﬀerentiated by Pavlov in terms of the behavioral consequences of the many shifts in the balance of strong and weak stimuli, their activations and inhibitions. The conditioned reﬂex was the sine qua non of Pavlovian physiology. For Pavlov, “The idea of reﬂex in physiology, the gift of Descartes’ genius, is, of course, a purely natural-science idea” (Pavlov, 1962, p. 87).

Pavlov’s paradoxical state Pavlov’s experiments indicated that not all states of full physiological (or mental) conditioning were instantly achieved; rather the course of the conditioning process moved behavioral responses through a series of behavioral phases. Of interest is the phase that Pavlov labeled “paradoxical.” For an illustration, we look at the work in Pavlov’s laboratory by one of his collaborators, Dr. Razenkov. The experimental paradigm provided a subject (e.g., a dog) with coupled presentations of whistles, metronome beats, and rhythmic mechanical stimulations of the skin, the ﬂashing of an electric bulb and the delivery of food. Razenkov brought about “the normal eﬀect of the positive conditioned stimuli” (Pavlov, 1962, p. 132) when the stimulus strength yielded 30 drops of salivation. At ﬁrst presentation, it turned out that the whistle evoked 5 drops of saliva, the metronome 3.5 drops, the tactile

Uniﬁcation of explanatory paradigms in the neurosciences

31

stimulations 3 drops, and the bulb ﬂashes 2 drops. Pavlov writes that “the stimuli ranged in strength, from the strong to the weak, thus: whistle, metronome beats, mechanical stimulation of the skin and ﬂashing of the bulb” (Pavlov, 1962, p. 133). Clearly, not all stimuli appeared equally strong, forceful, or eﬃcient at eliciting a desired response. This observation led to a crucial follow-up investigation with the same experimental subject. We ﬁrst note that in the above original set of stimuli, the tactile mechanical stimuli included 24 contacts within the 30 second introduction of the stimulus, and again it elicited 3 drops of saliva. The second experiment was one in which, along with the other positive stimuli of the ﬁrst experiment, a diﬀerentiated tactile stimulus of 12 per minute was applied during 30 seconds and followed without any interval by the positively conditioned tactile stimulus of 24 per minute, which was also continued for 30 seconds and then reinforced in the typical fashion. The next day the dog was subjected to another experiment where he was tested with the original set of stimuli from experiment 1. One English translation of this paper has Pavlov claiming that the small factor of introducing the 12 per minute tactile stimulus “produced an extraordinary eﬀect” (Green, 2006, p. 4). Pavlov, in another translation of this paper, writes, “The day after this experiment [the second one, HB/SC] and during the subsequent nine days all the conditioned reﬂexes disappeared and were manifested only very rarely and to a minimal extent. This period was followed by a very special period” (Pavlov, 1962, p. 133). Experiments in this special period, which lasted 14 days showed “extremely peculiar changes” (Green, 2006, p. 4). The peculiar and extraordinary eﬀects were that the mechanical stimulation now elicited 5.5 drops of salivation, the bulb ﬂashing 3 drops, the metronome beats 1 drop, and the whistle 0 to 0.3 drops. Crucial for our chapter is the following statement by Pavlov (1962, p. 133): The result, as you see, is quite the reverse of what formerly occurred normally: strong stimuli either failed to act or barely acted, while the weak stimuli produced an eﬀect even greater than normal. Following the example of N. Vvedensky, we named this state of the hemispheres the paradoxical phase. The 14-day paradoxical phase slowly shifted to a phase where all previous stimuli seemed to have returned to their original strength or force, since the whistle (4 drops) and the metronome (4.5 drops) again elicited strong responses. This phase of response strength overlap came to be called the phase of “equalization,” where strong and weak stimuli had an equal likelihood of eliciting the same response. We do not consider this phase in the present chapter, although it, too, comprises an intriguing alternative to normal stasis where strong evokes strong and weak evokes weak. The eﬀect of the second experiment was an inhibitory one, and it was this inhibition that brought about the counterintuitive switch in the rule of force. In any event,

32

Buckingham and Christman

for Pavlov, its outcome pointed to a physiology that eschewed all psychology. Our goal now is to show how the explanatory account of this paradoxical phase was lifted from the neuronal level to the neuropsychological level and from there, through Hebbian learning, to modern connectionist modeling.

Alexander Luria – neuropsychology Luria (e.g., 1962/1980, 1973) borrowed the so-called laws of strength/rules of force from Pavlov in his explanations of paraphasia within his neuropsychological model of language and its related accounts of linguistic breakdown secondary to neurological damage. Luria accounted for the normal and abnormal evocation of diﬀerent linguistic constituents such as phonemes and words within the physiological idiom of Pavlov’s nervous laws. Phonemic and lexical access were captured by the same laws. Luria’s neuropsychology at the very least pointed to a certain compatibility of the explanatory accounts of physiology and the burgeoning ﬁeld of the neuropsychology of language – often referred to as “neurolinguistics” by Luria. Luria, however, was not a reductionist and resisted at all costs a complete reduction of his explanatory paradigm to the domain of physiology. Homskaya (2001) charts Luria’s initial attraction to Sigmund Freud’s work at the psychological level, and his psychophysical accounts of human language and its breakdown in aphasia. Freud’s “software” approach to the functionality of language and cognition inﬂuenced Lev Vygotsky as well, and both Vygotsky and Luria developed theories of how society and culture were tightly interwoven with the complexities of human cognition. Later, as a medical student of neurology and subsequently a physician who worked with all aspects of the neuropsychology of brain and behavior, Luria consistently kept the physical and the psychological apart. His take on the mind– brain issue was that of Freud, and as a consequence, he was indebted to John Hughlings-Jackson, whose inﬂuence on Freud was marked throughout Freud’s (1891) book on aphasia. Luria’s philosophy, accordingly, took the form of a “psychophysical parallelism,” a kind of dualist “identity theory,” not unlike Hughlings-Jackson’s theory of “concomitance,” deﬁned as a togetherness of mind and brain running concurrently and bringing about a “coin-like” single eﬀect, where both are considered as the respective sides of that coin. Nevertheless, when it came to accounting for paraphasias, Luria continually gave credit to Pavlov for notions such as the paradoxical phase (e.g., Luria, 1973, pp. 44, 157, 317; and 1962/1980, pp. 513–518). Luria’s (1973, 1962/1980) neurolinguistic descriptions of lexical or phonemic paraphasias were couched in terms of selection errors, wherein target words or sounds were thought to be erroneously chosen from among their (inappropriately) highly activated competitors. In the normal case, highly activated competitors would naturally be those with strong associations (as per Pavlov’s law of strength) to intended targets. For example, if a speaker were trying to access the word “college,” he would have a statistically greater

Uniﬁcation of explanatory paradigms in the neurosciences

33

likelihood of activating (and then inhibiting) strong associates, such as “school” or “university,” than weakly related associates such as “kindergarten,” “hospital,” or “gymnasium.” The same principles were thought to apply to phonological as well as lexico-semantic processing. Luria believed that a certain amount of cortical tone and mobility were necessary for eﬃcient linguistic processing, and he suggested that these requisites became impaired as a consequence of neurological pathology. For Luria, physiological paradoxical and equalization states induced by brain damage were completely compatible with concomitant linguistic outcomes, such as semantic paraphasias, given his predisposition toward psychophysical parallelism. In his view, a system driven to the paradoxical activation of weak rather than strong associates for a stimulus would be statistically more likely to produce weakly related semantic paraphasias such as “kindergarten,” “hospital,” or “gymnasium” than strongly related associates (such as “school” or “university”) when attempting the target word “college” during a naming task. In an equalization state of processing, Luria predicted that strong and weak associates for a target would have a statistically equal chance of being activated, since a reduction of cortical tone would cause normal mechanisms of competitor inhibition to fail. This was thought to be the most likely neurolinguistic (and, indeed, connectionistic) characterization of severe anomia, where a likely outcome of the equalization phase would be no output at all. The paradoxical stage, on the other hand, would reveal statistically greater probabilities of weaker associates – a greater likelihood for error.

D. O. Hebbian learning The link between a neural associationism and modern connectionism revolves around the ideas of D. O. Hebb (1949). The notion that couplings are strengthened between neurons that act in synchrony is most often referred to as “Hebbian learning.” A large number of theoretical rules that mediate this learning in domains referred to as “neural” networks have been proposed in the last several decades. The notions go back to William James (1890) and to the summation idea that brain activity is governed by the sum of concurrent inputs to a given single neuron as long as there are (1) a high frequency of simultaneous synaptic connections, (2) intense ﬁrings, and (3) no other leaks of the ﬁrings into other neurons. All must converge on a single neuron unit. At this point, the Aristotelian notions of strength of associative force can be quantiﬁed into mathematical summation. Also needed are the mathematical transformations of inhibition and the formulae of change so that activated forces can return to their original values “at rest” (resting levels). These “neural” networks typically support three levels of linguistic processing: semantic/conceptual, lexical, and phonological. Others have been added, but for our purposes a three-level system will be all that is needed. In language, frequency of usage often determines the physiological resting values of neurolinguistic units in many models. Furthermore, just as the

34

Buckingham and Christman

setting of initial “weight” values may vary, the nature of the spread of neural activation through the system may also vary. Some view the spread of activation as going from level to level more or less instantaneously, while others incorporate a cascading spread, where subsequent levels may start their activation before all activations at the earlier levels are ﬁnished. Most systems have feedback between and among levels, and some are set up so that elements at their tactic levels may send inhibitory volleys to others at that level. Many models that are organized in the ways indicated above and that have cascading spread are referred to as models of interactive activation (Dell, 1986). The connectionist model we are drawing from, which unwittingly simulated the paradoxical phase, is one proposed by Trevor Harley and his colleague, Siobhan MacAndrew (1992).

Harley’s connectionist model of lexicalization This model was created to account for substitution errors among whole words. It can handle phonemic substitutions as well, but Harley and MacAndrew (1992) concentrated on lexical retrieval processes. Theirs was an interactive activation model, closely related to those constructed by Gary Dell (1986) and more recently by Dell, Schwartz, Martin, Saﬀran, and Gagnon (1997). There is a three-layer architecture containing 26 nodes at the semantic level, 70 nodes at the lexical level, and 21 nodes at the phoneme level. That is, there are 26 conceptual categories, 70 words, and 21 phonemes. As is the case with most of the connectionist models that have been constructed to date, the linguistic nodes have limited domains at each level. There are feedback connections between the phonological and lexical levels. Unlike many other models of this type, the authors built in semantic representations that would allow for a “richness” component to concepts with a high degree of imageability. At the lexical and phonological strata, inhibitory links were established, which highlight the eﬀects of intra-level “competition,” but which when operating normally serve to speed up processing by inhibiting inappropriate competitors – phonemes competing with phonemes and words competing with words. Inhibitory intra-level connections, when working, provide accounts of lexical priming in naming, while when inhibition falters, eﬀects such as the “phonological blocking” of tip-of-the-tongue (TOT) eﬀects are nicely illustrated. Clusters of plan-external competing phonologically related word forms can severely interfere with lexical access. Harley and MacAndrew (1992) tested four hypotheses with this model: that (1) altered decay rates would interfere with word ﬁnding; (2) loss of intra-level inhibition would interfere with word ﬁnding; (3) increased random “noise” would interfere with word ﬁnding; and (4) reduction in connection weights between the semantic level and the lexical level (i.e., reduced ﬂow of activation from the semantic to the lexical level) would interfere with word ﬁnding. As with many models of its type, this system can account for aspects of recovery in aphasia as well as the inﬂuence of frequency of usage and

Uniﬁcation of explanatory paradigms in the neurosciences

35

imageability eﬀects in paraphasic errors. The model computes the input summation formulae for activation spreading through the system, and it computes formulae for return rates for each cycle (“processing epoch”) to resting levels. Whether returning from higher activation levels or from lower levels due to inhibition, processing nodes must reset to their resting stages in normal fashion for the system to work normally for each cycle. Needless to say, slowed decay rates from recent activation and weakened weight connections between levels would lead to perseveration of words as well as of phonemes (Buckingham & Christman, 2004b). This model has parameters as well for processing lateral inhibition among nodes at the same level. Here, the authors manipulate intra-tactic inhibition at the lexical level only. As mentioned earlier, the focus of the Harley and MacAndrew (1992) study was on lexical access and substitution. Suﬃce it to say that the lexical level sends outputs to the phonological level and, for production, ﬁve-slot serially ordered phonological templates serving as output frames must be ﬁlled. The production level is left in a rather primitive form, allowing for no phonotactic constraints, and speciﬁcation of all input features is characterized simply as “on–oﬀ” binary units. Harley and MacAndrew motivate many of these shortcomings with arguments for simplicity. The simulations of connectionist models for pathology come from diﬀerent arrays of alterations of weights, decays, and the addition of inhibition by “noise” at diﬀerent locations in the system. Harley and MacAndrew (1992) “lesion” their system in varying ways in order to evaluate their impact (re: the above four hypotheses) on lexical access failure. All other parameters distinct from weight values are considered to be “control parameters.” These include post-activation decay, amounts of random “noise,” the eﬀect of lexical frequency, and the time the external semantic input is received by the semantic units. The investigators search for any errors the model may produce in response to some external semantic input. They are speciﬁcally testing for inductively based predictions from the aphasia literature on the origin of paraphasias – words in English, and words that could be but are not in English. Some of the non-words produced by the model bear a form transparency to the external semantic input (called the “target”), whereas others do not. Some call all non-word productions “neologisms” (e.g., Butterworth, 1979), while others reserve the term “neologism” for non-words whose form is opaque to any likely target word in the context of the utterance (Buckingham & Kertesz, 1976). An example of this model’s activity may be illustrative at this point. Suppose that an external semantic input (the so-called “jolt”) to the processing model is the word “cow.” In a normal cycle, that word would send a jolt of activation to, say, ﬁve semantic categories: animal, dairy related, fourlegged, adult, female. Those categories would converge onto the lexical item , which would in turn send activation to the phonemes /k/ and /aw/ (a diphthong counts as one phonemic unit). The normal output would be the CV word /kaw/. In Harley and MacAndrew’s study, the word “cow” is the

36

Buckingham and Christman

input target for each hypothesis-testing. For comparison, they plotted not only the activations of the target against the processing cycle time, but also those parameters for “calf” (semantically and phonologically related associate), for “dart” (unrelated), for the onset /k/ phoneme (of “cow” and of “calf ”) and for the onset phoneme /d/ of “dart.” The test of hypothesis 1 did not show much eﬀect in the Harley and MacAndrew (1992) study. With increases in the rate of decay alone, the response “cow” was signiﬁcantly favored. They then combined decay rate with a time delay of the external semantic input to the semantic level. They observed that doing this reduces the target activation to near zero, but it reduces all possible word competitors as well. In eﬀect, little if anything is produced – somewhat akin to the “equalization” phase of Pavlov, but we are not charting that phase abnormality in this chapter. This simulation is not without interest, however. The authors rather doubt that decay rate alteration alone is likely to be a good explanatory account of paraphasia. In any event, as they point out, connectionist theory would actually predict that decay rate lesions should only give rise to “smart” errors, whereby inter-level connectivity is still apparent. This would not be the case at least for jargon or complex neologisms, or for the error: “cow” → “dart.” Harley and MacAndrew next tested for loss of intra-level inhibitory connections, leaving vertical connections and decay rates unaltered mathematically (e.g., “unlesioned”). Even though logic seemed to predict that lowered levels of inhibition at the word level would serve to promote many similar competitors with the target, in this study, the target word was still signiﬁcantly more likely to be produced over all other possible candidates. Even when the authors added random noise under this condition, there was no noticeable increase in errors – and certainly no production of jargon neologisms. Research is still ongoing to try to ﬁnd accounts for lexical priming and TOT errors, but Harley and MacAndrew found no help in these domains when altering intra-level word inhibition, even with added noise to the system. Hypothesis 3 was then tested. Random initial noise was added to the system but it failed to evoke much eﬀect for severe paraphasia. Hypothesis 4 was tested last, with a method involving the weakening of the connection strengths between concept nodes and lexical nodes, resulting in weaker lexical activations from the semantic level. Previous studies (e.g., Miller & Ellis, 1987) had indicated that interferences in the normal connectivity between the semantic and lexical level set the stage for neologistic production, where underlying targets would be accordingly blocked in the production line, but where other processes would come to bear on the production of surrogate forms that would in turn eﬀectively mask the access block. Those “abstruse” neologisms (Lecours, 1982) would appear bizarre and opaque as to some underlying target. This account of neology was ﬁrst labeled “the anomia theory” by Brian Butterworth (1979). Harley and MacAndrew, however, observed that weakened weights alone between the semantic and the lexical level did not have much of a dilatory eﬀect on word

Uniﬁcation of explanatory paradigms in the neurosciences

37

ﬁnding. Continually weakening the connections over time still showed that the target was more likely to be activated, but eventually other semantic competitors would decrease even more rapidly, still being distinguished from the target, but waning in appearance so that semantic paraphasias fade away from the picture, leaving other types of lexical substitutions to be occasionally produced. These are then likely to be only form related and not semantically related. Also, since frequency and imageability result in higher resting levels of activation, they may play a role in word selection such that their potency may counterbalance the overall weakening of the semantic to lexical connections. With respect to the outcome of the test for hypothesis 4, Harley and MacAndrew (1992, p. 382) state that, “Although this gives a more satisfying distribution of lexical activations than the other accounts, it still fails to satisfy the criterion that, on some occasions, the activation of competitors should be above that of the target.” They then introduced some random variation into the weakening of the semantic–lexical connections. Accordingly, they could increase the severity of lesioning “by adding an amount of normally distributed random noise to each connection and increasing the standard deviation of that noise distribution” (Harley & MacAndrew, 1992, p. 382). In this way, without being aware of the long history of the “paradoxical phase,” they ended up simulating the extraordinary, very special, and counterintuitive phenomenon of Pavlov’s famous inhibitory phase. The other astounding outcome was that Harley and MacAndrew actually had to add increased inhibition with the random noise to the already weakened connections. Recall that Pavlov’s abnormal phases were largely due to increased inhibition in one way or another. Harley and MacAndrew (1992, p. 382) wrote: Random lesioning of alphasl [“alpha semantic lexical” – the name of their parameter that governed the rate of spread of activation between the semantic and lexical levels – HB/SC] aﬀects the target lexical unit such that the greater the severity of the lesioning, the lower the probability of the target unit being highly activated. Further, the greater the lesioning, the higher the probability of other lexical units being highly activated. In other words, the greater the severity of the lesioning, the more likely it is that weak associates will be activated where strong ones should be produced. Harley and MacAndrew (1992) thus describe precisely the paradoxical eﬀect captured by the diﬀerent scientiﬁc paradigms of Pavlov and Luria before them. Figure 3.1 (Harley & MacAndrew’s Figure 9, 1992, p. 382) shows that for input target “cow,” the weaker associate “calf” is more highly activated throughout increasing time in cycles, although activation levels begin to decrease after 10 time in cycles. The paradox continues nevertheless to the 40 time in cycles, where “cow” almost approaches “dart,” which is practically

38

Buckingham and Christman

Figure 3.1 The eﬀects of introducing some random variation (noise) into the weakened weight connections of the semantic to lexical levels. Normally distributed random noise was added to each connection. The severity of lesioning is mimicked by increasing the standard deviation of the noise distribution. Only moderate damage (standard deviation = 0.05) was applied for the eﬀects shown in this ﬁgure, which was Figure 9 in Harley and MacAndrew (1992, p. 382). The random lesioning into the weakening was such that the more severe the noise, the lower the probability of producing the target input (“cow” in these cases). Further, the more severe the noise, the higher the probability of producing other lexical items. This is the essence of the paradoxical phase suggested by Pavlov and Luria, although admittedly, the weaker element was “calf,” and not “dart.” The paradoxical nature of the phenomenon still holds. (Reproduced from Harley & MacAndrew, 1992, with permission to use the ﬁgure given by T. Harley, June 13, 2006).

oﬀ the map for all processing epochs. Note that /k/ has a much greater set of activation levels than /d/, for the obvious reason that both “cow” and “calf ” share that onset phoneme. The /d/ is actually more highly activated throughout the cyclings than is the word “dart.” This is most likely to be because a small number of occasionally activated unrelated words with /d/ onset were produced as well as “dart.”

Concluding remarks Here, we witness the ﬁnal link in the Pavlov to Luria to Harley/MacAndrew phenomenon of an inhibitory phase in pathology whereby normal laws of strength are reversed and strong and weak activation levels operate counterintuitively. The paradox has been shown to exist at distinct levels of “neural”

Uniﬁcation of explanatory paradigms in the neurosciences

39

description. Pavlov’s descriptions of the paradox were cast in the vocabulary of his physiological paradigm. This notion then was transferred to words and phonemes in the neuropsychological descriptive idiom of Alexander Luria, an idiom ﬁrmly implanted in the psychology of Hughlings-Jackson and Sigmund Freud (1891) and rather incongruous with the materialism of the Russian revolution and the Union of Soviet Socialist Republics (Homskaya, 2001). We now have witnessed how the phenomenon of the paradoxical state has unwittingly been simulated in a modern connectionist model, and therefore has been aligned with yet another level of neuroscientiﬁc description. Modern connectionism has provided the ﬁeld of neuropsychology with numerous computational simulations of both normal and abnormal human cognitive behavior. Before the advent of modern connectionism, Luria had borrowed much of the cortical neurodynamics of Pavlovian physiology. Luria, however, was incorporating the Pavlovian paradigm at a substantial remove from Pavlov, since Luria’s units were phonemes and words. Luria’s scientiﬁc descriptors drew heavily not only from Pavlov, but also from association psychology. By weakening connection strengths between the conceptual (semantic) level and the lexical level, and adding some random noise to the system, Harley and MacAndrew independently simulated a phase intriguingly similar to the paradoxical states of Pavlov and Luria. The independence of this simulation is all the more powerful, since at best they only tweaked the network so as to have it produce paraphasias. The paradox, as illustrated in their Figure 9, shows that the input target word “cow” strangely enough evoked “calf” and rarely if ever evoked “cow.” We note, however, that “dart” (totally unrelated) was almost never produced. But, there is nevertheless something puzzling about the surfeit of productions of “calf” for the target “cow.” One might suggest that “calf” was perseverated, in which case the argument for a paradoxical phase as it is described would be weakened. Harley and MacAndrew’s paradox-producing lesions did not involve slowing decay rates, or hampering with any cleanup units in the spirit of Plaut’s original suggestion for simulating perseveration (see Gotts & Plaut, 2004). In fact, the only alteration to decay rates they tested was speeding them up – not slowing them down. Harley and MacAndrew’s paradox lesions importantly involved weakening connections between the conceptual and the lexical levels plus the addition of random noise. More recent connectionist thinking has suggested that in fact decay rates need not be damaged to simulate perseverative production. Gotts and Plaut (2004) and Basso (2004) have suggested that weakened weight levels in one modality may indeed lead to perseveration, where the onus is on the weakened connectivity. Local weakened connections in a certain modality may be such that normal decay rates would in a sense not operate fast enough to avoid normal post-activation rebound, resulting in perseveration. Harley and MacAndrew did not have architectures such that they could set up simulations speciﬁcally for reading aloud, repeating, or naming, although these networks tend to extend more easily to the naming

40

Buckingham and Christman

situation, where the spreading activation begins at the semantic level. Many questions, however, remain in the interpretation of simulation correlations between normal and abnormal linguistic processing (e.g., Ruml, Caramazza, Capaso, & Miceli, 2005). Nevertheless, we have presented what we feel are some extremely interesting descriptions of inverted stimulus–response contingencies across three diﬀerent investigative paradigms in the neural sciences. Our view is again that we should resist any tendency to claim that the neuropsychological or the modern connectionistic theories should in any way reduce to Pavlov’s physiology. Rather we suggest that each explanatory account uniﬁes or comes more closely into alignment with the others in obvious ways, but each with its separate scientiﬁc methodologies and distinct vocabularies, cast as they are at diﬀerent levels of human cognition.

References Basso, A. (2004). Perseveration or the Tower of Babel. Seminars in Speech and Language, 25, 375–389. Buckingham, H. W. (forthcoming). Alexander Romanovich Luria: The man and his science. In N. Koertge (Ed.), New dictionary of scientiﬁc biography. Farmington Hills, MI: Charles Scribner’s Sons. Buckingham, H. W., & Christman, S. (2004a). Preface. Seminars in Speech and Language, 25, 291–293. Buckingham, H. W., & Christman, S. (2004b). Phonemic carryover perseveration: Word blends. Seminars in Speech and Language, 25, 363–373. Buckingham, H. W., & Finger, S. (1997). David Hartley’s psychobiological associationism and the legacy of Aristotle. Journal of the History of the Neurosciences, 6, 21–37. Buckingham, H. W., & Kertesz, A. (1976). Neologistic jargon aphasia. Amsterdam: Swets & Zeitlinger. Butterworth, B. (1979). Hesitation and the production of verbal paraphasias and neologisms in jargon aphasia. Brain and Language, 18, 133–161. Chomsky, A. N. (1994/2000). Language as a natural object. In A. N. Chomsky, New horizons in the study of language and mind (pp. 106–133). Cambridge, UK: Cambridge University Press. Chomsky, A. N. (2002). On nature and language. Cambridge, UK: Cambridge University Press. Code, C. (2000). Converging not fractionating. Brain and Language: Millennium Issue, 71, 44–45. Code, C., Lecours, A. R., Joanette, Y., & Wallesch, C.-W. (Eds.) (1996). Classical cases in neuropsychology (Vol. 1). Hove, UK: Psychology Press. Code, C., Rowley, D., & Kertesz, A. (1994). Predicting recovery from aphasia with connectionist networks: Preliminary comparisons with multiple regression. Cortex, 30, 527–532. Code, C., Wallesch, C.-W., Joanette, Y., & Lecours, A. R. (Eds.) (2003). Classical cases in neuropsychology (Vol. 2). Hove, UK: Psychology Press. Dell, G. S. (1986). A spreading-activation theory of retrieval in sentence production. Psychological Review, 93, 604–616.

Uniﬁcation of explanatory paradigms in the neurosciences

41

Dell, G. S., Schwartz, M. F., Martin, N., Saﬀran, E. M., & Gagnon, D. A. (1997). Lexical access in aphasic and non-aphasic speakers. Psychological Review, 104, 801–838. Freud, S. (1891/1953). On aphasia: A critical study (Trans. and introduction by E. Stengel). London: Image. Gotts, S. J., & Plaut, D. C. (2004). Connectionist approaches to understanding aphasic perseveration. Seminars in Speech and Language, 25, 323–334. Green, C. D. (2006). Classics in the history of psychology: “Conditioned reﬂexes: An investigation of the physiological activity of the cerebral cortex – Lecture XVI: Transition stages between the alert state and complete sleep: hypnotic stages.” Internet resource developed by Christopher D. Green, York University, Toronto, Ontario, Canada. Harley, T. A. (1993). Connectionist approaches to language disorders. Aphasiology, 7, 221–249. Harley, T. A., & MacAndrew, S. B. G. (1992). Modelling paraphasias in normal and aphasic speech. In Proceedings of the 14th Annual Conference of the Cognitive Science Society (pp. 378–383). Bloomington, Indiana. Hartley, D. (1746/1959). Various conjectures on the perception, motion, and generation of ideas (Trans. from the Latin by R. E. A. Palmer, and introduction with notes by M. Kallich). Los Angeles, CA: The Augustan Reprint Society, Publication No. 77–78. William A. Clark Memorial Library, University of California. Hartley, D. (1749). Observations on man, his frame, his duties and his expectations. London: S. Richardson. Hebb, D. O. (1949). The organization of behavior. New York: John Wiley. Homskaya, E. D. (2001). Alexander Romanovich Luria: A scientiﬁc biography (Trans. from the Russian by Daria Krotova. Ed., with a foreword, by D. E. Tupper). New York: Kluwer Academic/Plenum Publishers. James, W. (1890/1950). The principles of psychology. New York: Dover Publications. Kaczmarek, Bozydar L. J. (Ed.) (1995). Special Issue on Alexander R. Luria. Aphasiology, 9 (Mar–Apr). Lecours, A. R. (1982). On neologisms. In J. Mehler, E. Walker, & M. Garrett (Eds.), Perspectives on mental representations. Hillsdale, NJ: Lawrence Erlbaum Associates, Inc. Luria, A. R. (1962/1980). Higher cortical functions in man. New York: Basic Books. Luria, A. R. (1973). The working brain: An introduction to neuropsychology. New York: Basic Books. Miller, D., & Ellis, A. (1987). Speech and writing errors in “neologistic jargonaphasia”: A lexical activation hypothesis. In M. Coltheart, G. Sartori, & R. Job (Eds.), The cognitive neuropsychology of language. Hove, UK: Lawrence Erlbaum Associates Ltd. Pavlov, I. (1962). I. P. Pavlov: Psychopathology and psychiatry – Selected works (Trans. from the Russian by D. Myshne & S. Belsky. Compiled by Y. Popov & L. Rokhlin). Moscow: Foreign Languages Publishing House. Ruml, W., Caramazza, A., Capaso, R., & Miceli, G. (2005). Interactivity and continuity in normal and aphasic language production. Cognitive Neuropsychology, 22, 131–168.

4

The social and neuropsychological underpinnings of communication disorders after severe traumatic brain injury Skye McDonald

Preamble Chris Code has had a wide and varied research career. While well known for his research publications, Chis’s role as a mentor is possibly less acknowledged. With his innate curiosity, generosity and enthusiasm, Chris has a remarkable capacity to motivate his colleagues into the pursuit of collaborative projects. In my case these have led to signiﬁcant inroads into communication research, ongoing collaborations and enduring friendships. Furthermore, although Chris may be best known for his aphasia work, his interests have been more wide-ranging than this, delving into other kinds of communication disorders that are characterized less by problems of language, and more by problems of language use. When Chris Code ﬁrst arrived in Australia to take up the inaugural Chair of Communication Sciences and Disorders at the University of Sydney, he encouraged me to submit a review to Aphasiology, outlining the similarities and diﬀerences between communication disorders arising from damage to the frontal lobes of the brain as opposed to the right hemisphere (McDonald, 1993a). Not long after, he embarked on a collaboration with Leanne Togher examining communication patterns after traumatic brain injury, the result of which has been many innovative and inﬂuential published studies. In 1995 Chris initiated a meeting in which he proposed that the three of us join forces to produce an edited book entailing a comprehensive overview of the nature of communication disorders after traumatic brain injury from neuropsychological, linguistic, and social orientations. The book (McDonald, Togher, & Code, 1999) had contributions from many of the leading authorities of the time, all good friends of Chris’s. It is now a standard text in Psychology and Speech Pathology departments in over 20 universities across the USA, the UK and Australia. Research has moved on since that time and some fascinating new directions are emerging. It is timely, therefore, that in this tribute to Chris, the following chapter continues on from the themes of that text, to review some of the earlier work and to overview more recent innovations.

Underpinnings of communication disorders after TBI 43

Introduction The notion of communication disorders in people with severe traumatic brain injury (TBI) has developed signiﬁcantly over the past few decades and has been the impetus for a variety of innovative approaches to the way in which such disorders have been conceptualized and subsequently assessed. Such approaches were originally stimulated by important observational studies (Levin, Grossman, Rose, & Teasdale, 1979; Thomsen, 1975) that alerted the research community to the unique diﬃculties that people with TBI experienced when communicating. While aphasic disorders were found, these were clearly apparent in only the minority of cases (estimated between 2% and 30%; Heilman, Safran, & Geschwind, 1971; Sarno, 1980; Sarno & Levita, 1986). Far more prevalent were diﬃculties with communication, including problems of slowness, hesitancy, lack of initiative, reliance on set expressions, tangentiality, inappropriateness and over-talkativeness (Levin et al., 1979; Thomsen, 1975). These characteristics could not be clearly deﬁned as aphasia, although some were considered to represent a sub-clinical aphasic language disorder (e.g., Sarno, 1980; Sarno & Levita, 1986). In the ensuing decades, evidence has gradually accrued to suggest that such communication disturbances reﬂect underlying cognitive impairment rather than language per se. As such, they have represented an unparalleled opportunity to examine the intertwining of language and cognition that is inherent in any act of communication. More recently, the potential role of aﬀect in communication has begun to be addressed. Broadly speaking, problems in communication that emerge after traumatic brain injury have been conceptualized using three theoretical orientations: pragmatics and speciﬁcally speech act theory (Searle, 1975); discourse analyses, especially systemic functional linguistics (Halliday, 1985); and models of social skills (e.g., McFall, 1982). This chapter reviews advances in each of these and where possible, considers the neuropsychological underpinnings of communication diﬃculties as exposed by these approaches, as well as social and cultural implications.

Conceptualizing communicative ability using pragmatic theory Pragmatic theory addresses the role that contextual factors play in establishing the meanings associated with any given utterance. For example, it is argued that any utterance represents behaviour; that is, a speech act that is motivated by the desire to have some impact on the listener. Speech acts may be direct, in that the speaker states what is on his or her mind directly, as in “Please open the window”, or indirect although clearly transparent, as in “Can you please open the window”, whereby the speaker asks about the listener’s ability rather than making a direct request. The motivation to use indirect rather than direct speech acts is often the desire to be polite or to be otherwise thought well of by the listener (Brown & Levinson, 1978). Diﬀerent forms of

44

McDonald

politeness may be appropriate depending on the familiarity and status of the co-conversant as well as the import of the message. When high degrees of diplomacy are required, speech acts may be so indirect as to be opaque in their meaning (“It is hot in here!”). The idea that the speaker’s attitude towards the listener motivates their choice of utterance (e.g., the level of indirectness) suggests that, conversely, their attitude is revealed to the listener by that choice. Indeed, normal speakers have been shown to be sensitive to the relative politeness of various surface forms of the same underlying request (“Do you know where Jordan Hall is?” “Could you tell me where I might ﬁnd Jordon Hall?”, etc.) which varied systematically with the degree of indirectness and hesitancy they signalled (Clark & Schunk, 1980). Several issues arise from this conceptualization of speech acts. First, it suggests that, in order to be adept at understanding the social nuances of language, listeners must be able to comprehend and use politeness signals such as hesitancy. Second, it suggests that there must be some means by which opaque indirect speech acts (“It is hot in here!”) are decoded for the speaker’s intended meaning. Conversely, speakers must have the means to produce speech acts that convey their intended meanings via inference. There is clearly scope to examine pragmatic language competence in people with severe TBI, as they have often been described as both blunt and insensitive in their language use and concrete and literal in their general responses and understanding of information (Crosson, 1987; Milton & Wertz, 1986; Prigatano, 1986). Pragmatic understanding The comprehension of indirect language after TBI has been the focus of a number of studies in recent years, with a particular interest in sarcasm and irony. When being sarcastic, the speaker commonly says something that is literally the reverse, or at least diﬀerent from, what they mean, such as “What a great haircut” spoken to suggest the reverse. It is now well established that, in the absence of language deﬁcits, many adults and children with severe traumatic brain injury have great diﬃculty comprehending irony and sarcasm (Bara, Tirassa, & Zettin, 1997; Channon, Pellijeﬀ, & Rule, 2005; Channon & Watts, 2003; Dennis, Purvis, Barnes, Wilkinson, & Winner, 2001b; McDonald, 1992; McDonald & Flanagan, 2004; McDonald, Flanagan, Rollins, & Kinch, 2003; McDonald & Pearce, 1996; Turkstra, McDonald, & Kaufmann, 1996). This raises the question as to what deﬁcit is responsible for this diﬃculty. In 1975 Grice explained the conveyance of sarcasm within his broader conceptualization of the communication of conversational inference. According to Grice, conversational inferences are possible due to implicit agreements between speakers regarding the rules of conversation. It is assumed that, ﬁrst, speakers will cooperate with each other in the act of communication and, second, they will observe certain conventions (maxims) in speech by saying only as much as is required, saying this as clearly as possible, and saying only

Underpinnings of communication disorders after TBI 45 what is true and relevant to the context. These commonly shared assumptions can be exploited to vary the manner in which communication occurs. A blatant disregard of a conversational maxim will be noticed by the listener and will cause him or her to reconsider the utterance to make sense of why it was said in this manner. In doing so, he or she will inevitably take into account other contextual information, and the ﬁnal interpretation of the conversational meaning will be an inference drawn from both the utterance and the context in which it was said. By transgressing conversational maxims, speakers can thus communicate indirectly in the service of politeness or other social and cultural requirements (Brown & Levinson, 1978). Sarcastic statements transgress the maxim of quality (truthfulness). The listener, recognizing from the context that the literal truth of the remark contrasts with known facts, but assuming that the speaker said this for a reason (i.e., is attempting to communicate), reinterprets the statement to make it consistent with the context and thus derives the implied meaning, which is frequently opposite to that asserted. The process by which the listener comprehends the intended meaning was considered by Grice (1975, 1978) to be similar to that proposed for the interpretation of other indirect speech acts (Gordon & Lakoﬀ, 1975; Searle, 1975): (1) the literal meaning is comprehended; (2) some cue indicates this is not suﬃcient (e.g., the literal meaning is contradicted by the context); (3) inferential rules are implemented in order to derive the intended meaning from the literal meaning and from the context in which it occurred. Given that the majority of people with TBI do not suﬀer from basic language impairment, failure to understand sarcasm is unlikely to reﬂect an inability to comprehend the literal meaning, hence step 1 is unlikely to be problematic. Consequently deﬁcits must reside in other processes, either step 2 or step 3. In order to understand how these stages might be aﬀected it is necessary to consider the nature of neuropsychological disorders following traumatic brain injury. Neuropsychological underpinnings of pragmatic understanding 1. Common cognitive deﬁcits arising from traumatic brain injury While extremely variable, severe traumatic brain injuries typically produce lesions concentrated in the frontal and temporal lobes of the brain (Adams et al., 1985; Levin et al., 1987) with attendant diﬀuse axonal damage (Adams, Doyle, Ford, Gennarelli, Graham, & McLellan, 1989). Consistent with this, disorders of executive functioning (reﬂecting frontal system dysfunction), disorders of new learning (reﬂecting temporal and frontal dysfunction), and slowed information processing (reﬂecting diﬀuse axonal injury) are well documented sequelae of TBI (e.g., Tate, Fenelon, Manning, & Hunter, 1991). Executive functions are those that mediate and regulate other cognitive activities and behaviour in a purposeful and goal directed fashion, and are

46

McDonald

often conceptualized as representing either a loss of drive or a loss of control, although both may co-exist in the single individual with frontal system impairment (Tate et al., 1991). Disorders of drive will result in apathy and inertia, rigidity, inﬂexibility and perseveration. Disorders of control lead to impulsivity, disinhibition and distractiblity. In general, executive dysfunction signiﬁcantly impairs problem-solving capacity. Individuals may experience reduced attention and working memory capacity, fail to reason at an abstract level (draw inferences) and to develop eﬀective plans, and fail to monitor problem-solving behaviour eﬀectively or learn from mistakes (Darby & Walsh, 2005). Slowed information processing speed exacerbates these diﬃculties. Executive dysfunction is clearly implicated in the process of decoding indirect speech acts, as outlined by Gordon and Lakoﬀ and others. The integration of (verbal) information with the context (step 2) and the application of inferential rules (step 3) are processes that demand both working memory and abstract reasoning. INFERENTIAL REASONING

The extent to which individuals with TBI experience executive dysfunction varies enormously in both severity and kind. Nevertheless, there is a strong link between frontal injury after TBI and poor inferential reasoning (Dennis, Guger, Roncadin, Barnes, & Schachar, 2001a; Ferstl, Guthke, & von Cramon, 2002; MacDonald & Johnson, 2005) and also frontal injury and sarcasm comprehension (Shamay-Tsoory, Tomer, & Aharon-Peretz, 2005). It is possible, therefore, that pragmatic inferential reasoning represents a particular application of generic inferential reasoning skills. In support of this, measures of general inference making have been linked to poor pragmatic understanding in people with TBI (Martin & McDonald, 2005; McDonald, Bornhofen, Shum, Long, Saunders, & Neulinger, 2006). WORKING MEMORY

At a more reﬁned level, it is interesting to question what particular aspects of executive dysfunction contribute to poor inferential reasoning. Barnes and Dennis (2001) have argued that the problem with inferential reasoning may lie less in the computational aspects of inferencing (step 3 above) than in the working memory demands of integrating discourse meaning and world knowledge in real time (step 2). By a careful reduction of working memory demands, they demonstrated that deﬁcits in inferential reasoning could be correspondingly reduced in children with TBI. Independent studies have also reported correlations between poor working memory capacity and poor inferential reasoning (Dennis & Barnes, 1990) including the ability to understand sarcasm (Martin & McDonald, 2005; McDonald et al., 2006). Slowed information processing is linked to working memory deﬁcits and has, similarly, been associated with poor pragmatic understanding (McDonald et al., 2006).

Underpinnings of communication disorders after TBI 47 FLEXIBILITY

Inferential reasoning deﬁcits are not, however, likely to be completely explained by a disorder of working memory. Other executive deﬁcits may also play a role. For example, inﬂexible, perseverative thinking will impact on the ability to resolve pragmatic inference because rigid ﬁxation on the literal meaning will impede the capacity to understand the implied meaning, even if working memory demands are low. Empirical evidence for a link between pragmatic understanding and measures of ﬂexibility on standard neuropsychological measures is mixed. A relationship between the ability to understand sarcasm and performance on speciﬁc concept formation/shift tasks has been found in one study (McDonald & Pearce, 1996) but not in others (Martin & McDonald, 2005; McDonald et al., 2006; Turkstra et al., 1996). A speciﬁc measure of rigidity (i.e., perseverative errors) was found to be share a small amount of variance with scores on a sarcasm task (Martin & McDonald, 2005). IMPULSIVITY

Impulsivity (poor control) is also likely to impact on inferential reasoning because the participant reacts to initial meanings of conversational comments. There is even less research regarding this relationship, although a correlation between sarcasm and impulsivity has been found in the one study to examine this to date (Channon & Watts, 2003). NEW LEARNING

The capacity to learn is also likely to aﬀect pragmatic understanding as contextual information that is relevant to the conversational exchange may have occurred some time earlier. There is surprisingly little research that has been conducted into the eﬀects of poor new learning on pragmatic understanding following TBI (or indeed any clinical population). However, in one study it has been found that standard measures of new learning (taken from the Wechsler Memory Scale III) were correlated with poor understanding of sarcastic inference (McDonald et al., 2006). In sum, common cognitive sequelae of severe traumatic brain injury, including slowed information speed and working memory, rigidity and impulsivity, and poor new learning may each undermine the ability to understand pragmatic inferences. The impact of these executive abilities on inferential reasoning is consistent with the psycholinguistic account of how indirect speech acts are processed, suggesting that failure to recognize the conversational implicature occurs as a result of a failure to process and integrate language and the context in which it occurs in order to reject the literal meaning for another, inferred, meaning. Despite this, the three-stage model as advocated by Grice and others has

48

McDonald

been criticized as an inadequate explanation for how indirect speech acts are decoded. For example, some sarcastic comments can be both literally true and ironic. The mother who states “I love children who keep their rooms clean!” (Gibbs & O’Brien, 1991) may believe this to be true, but may also be speaking ironically (depending on the state of the bedroom). Sarcasm may also be manifested in the excessive politeness of the utterance “Oh I do beg your pardon most exalted one!” As a means to reconcile these issues it has been argued that sarcasm and irony may be better understood in terms of the (in)sincerity of the utterance rather than its truth value (Haverkate, 1990). This suggests that, in order to interpret such utterances, the hearer does not reject the literal meaning at all, but understands it in the context of the speaker’s attitude. Other kinds of pragmatic inference (e.g., hints) may also allude to issues that are on the speaker’s mind rather than in the patent context. These considerations suggest a diﬀerent kind of inference is required on the part of the listener; that is, an inference needs to be formed regarding the speaker’s intentions. 2. Theory of Mind The capacity to attribute mental states, such as thoughts, beliefs, desires and intentions, is considered pivotal to the ability to make sense of communication. This type of ability is known as having “Theory of Mind” (ToM) and has been thought to cause the communicative disorders seen in autism. Many individuals with high functioning autism or Asperger’s syndrome and normal IQ have ﬂuent and articulate speech but are, nonetheless, pedantic and overliteral (Happé & Frith, 1996), fail to interact normally in conversation, often talk at length on obscure or inappropriate topics (Ozonoﬀ & Miller, 1996), have inappropriate non-verbal communication and poor adherence to social rules (Bowler, 1992). They also fail to appreciate how utterances are used to convey information in a socially appropriate manner (Surian, BaronCohen, & Van der Lely, 1996) and misinterpret both metaphor and irony (Happé, 1993). Similar deﬁcits in social reasoning and social communication as seen in autism have also been reported in adults with TBI who have been reported as egocentric, self-focused, lacking interest in other people, displaying inappropriate humour, frequent interruptions, a blunt manner, overly familiar and disinhibited remarks or advances, and inappropriate levels of self-disclosure (Crosson, 1987; Flanagan et al., 1995; Levin et al., 1979; McDonald, Flanagan, Martin, & Saunders, 2004; McDonald & Pearce, 1998; McDonald & van Sommers, 1992). More particular reasoning deﬁcits that implicate ToM have also been found in people with TBI. For example, adults with TBI have diﬃculty ﬁlling in a questionnaire as though they were somebody else (Spiers, Pouk, & Santoro, 1994), ﬁnd it diﬃcult to identify the source of interpersonal conﬂict (Kendall, Shum, Halson, Bunning, & Teh, 1997) or otherwise interpret non-verbal interpersonal interactions (Bara, Cutica, &

Underpinnings of communication disorders after TBI 49 Tirassa, 2001; Cicerone & Tanenbaum, 1997). Deﬁcits on explicit ToM tasks have also been found in people with TBI, both adult and child (Bibby & McDonald, 2004; Dennis et al., 2001b; Milders, Fuchs, & Crawford, 2003; Santoro & Spiers, 1994; Stone, Baron-Cohen, & Knight, 1998). Furthermore, ToM performance has been linked to sarcasm comprehension. Speciﬁcally, those who experience diﬃculties understanding second order ToM inferences (i.e., what one person wants another person to believe) are also those most likely to experience problems understanding the meaning of sarcastic exchanges (Channon et al., 2005; McDonald & Flanagan, 2004). It is possible that problems with general inference-making secondary to executive deﬁcits in TBI aﬀect both non-social inferences and ToM. Studies that have examined this have reported a relationship between the two (Bibby & McDonald, 2004; Martin & McDonald, 2005). Working memory may also play a role. For example, a number of studies have shown that young children’s performances on false belief tasks are inﬂuenced by working memory capacity (Davis & Pratt, 1995; Gordon & Olson, 1998; Hughes, 1998; Keenan, 1998), although the evidence suggests that it is not the sole contributing factor (Tager-Flusberg, Sullivan, & Boshart, 1997). In acquired brain injury, working memory deﬁcits have been found to contribute to poor ToM performance (Bibby & McDonald, 2004; Stone et al., 1998) although it does not totally explain the diﬃculties seen (Bibby & McDonald, 2004). Performances on laboratory-based sarcasm tasks and conventional executive tests probably do have some underlying processes in common, but this does not exclude the possibility that inference-making such as ToM also calls on specialized systems for processing social information. Indeed, there is growing speculation (e.g., Adolphs, 2001, 2003; Bechara, 2002) that social problem solving may engage distinct neural systems. Social, interpersonal problems focus on quite diﬀerent information from the lists of words, numbers and simple ﬁgures that so often represent neuropsychological problemsolving tasks. For example, social information emphasizes individual rather than categorical diﬀerences and is dynamic, changing in response to the observer (Corrigan & Toomey, 1995). When relationships between executive measures and communication tasks requiring ToM are reported, these do not appear to represent exclusive relations. Correlations between pragmatic comprehension and indices of working memory, information processing speed, abstract reasoning and inhibition are modest at best (Channon & Watts, 2003; McDonald et al., 2006). Consequently, while there may be common processes required for social and non-social tasks, depending on the medium and response requirements (spoken, written, etc.), there may also be unique requirements called into play when solving social inferential tasks such as understanding sarcasm. Whether ToM represents a modular function that is diﬀerentially impaired in TBI, or a higher order ability reliant on generic executive skills, it is clearly related to impaired pragmatic understanding.

50

McDonald

3. Emotion A potential source of information when interpreting pragmatic inference is the emotional stance of the speaker. This is especially salient in the recognition of sarcasm, which is almost universally associated with a particular attitude of derision or scorn. Indeed a major criticism of the serial stage model of speech act comprehension as advocated by Grice is that such a model fails to account for the integral role that speaker attitude plays in the sarcastic retort. Nor does it specify how one inferential meaning is determined rather than another (Sperber & Wilson, 1986). As an alternative, Sperber and Wilson postulated a theory of irony within their larger thesis regarding the role of relevance in communication. They argued that every utterance has at most a single interpretation, which is a product of the listener’s search for the relevance the utterance has to the context, and therefore, unlike Grice’s proposition, Sperber and Wilson argued that there are no successive stages of interpretation. According to this position it is the recognition of the aﬀective stance of the speaker that alerts the listener to the sarcastic meaning of the comment. The potential role played by emotion recognition in pragmatic understanding in people with TBI needs to be considered. Over the past two decades there has been a surge of interest in emotion recognition. There is now a considerable body of evidence to suggest that emotion processing deﬁcits are prevelant in a substantial proportion of adults suﬀering from severe TBI. People with severe TBI have been found to have diﬃculties with emotion recognition across a range of media including photographs (Croker & McDonald, 2005; Green, Turner, & Thompson, 2004; Jackson & Moﬀat, 1987; Milders et al., 2003; Prigatano & Pribram, 1982; Spell & Frank, 2000), audiotaped remarks (Marquardt, Rios-Brown, Richburg, Seibert, & Cannito, 2001; McDonald & Pearce, 1996; Milders et al., 2003; Spell & Frank, 2000) and audiovisual displays (McDonald & Flanagan, 2004; McDonald et al., 2003). Interestingly, there appears to be relatively little association between the ability to recognize emotions and the ability to understand sarcasm (McDonald & Flanagan, 2004; McDonald & Pearce, 1996). Thus, despite the fact that sarcasm is usually associated with aﬀective states, the problems that people with TBI have in understanding sarcasm predominantly arise from their inability to make inferences, whether these are speciﬁcally about the non-literal meanings of the comment or the beliefs and attitudes of the speaker (McDonald & Flanagan, 2004). This is not to say that emotion deficits have no role in communication diﬃculties after TBI. Sarcasm, after all, is only one example of the rich repertoire of subtle meanings and innuendos available to speakers. Emotional cues may well play an important, possibly pivotal, role in many other communication contexts. But there is virtually no research in this area to date.

Underpinnings of communication disorders after TBI 51 Pragmatic language production: Politeness theory Disorders in the production of eﬀective communication have also been examined from a pragmatic theoretical perspective. First, the notion of politeness has proven useful to elucidate diﬃculties that arise following TBI in the use of diplomatic language to negotiate social situations. While adults with TBI appear to have an intact repertoire of strategies to moderate the politeness of their utterances (McDonald, 1993b) they are less ﬂexible than matched control speakers in their ability to use these across diﬀerent contexts (Togher & Hand, 1998). When faced with diplomatically challenging communication tasks such as hinting, or making requests to overcome a perceived reluctance on the part of the listener, adults with TBI have been found to have diﬃculty refraining from stating their desires directly (McDonald, 1993b) and making comments that were counter-productive to their desired outcome (McDonald & Pearce, 1998). These studies of politeness suggest that adults with TBI have diﬃculties producing language that utilizes pragmatic inference as a means of communication. A study of children with TBI suggests that younger speakers also have diﬃculties producing appropriate speech acts to meet contextual constraints (Dennis & Barnes, 2000). Neuropsychological underpinnings of politeness useage According to the pragmatic approaches outlined, certain predictions may be made concerning the contributions of co-existing cognitive impairments. Speciﬁcally, according to politeness theory, speakers need to appraise their conversational partners in order to determine their social and cultural standing (in relation to the speaker) as well as their particular attitude and sensitivities. Speakers need to have a repertoire of diﬀerent devices for moderating the politeness of their remarks, and they need to choose ﬂexibly between these in order to adapt to diﬀerent situational and inter-personal contexts. Finally, they need to be able to refrain from making their intentions explicit in the service of diplomacy and saving face. Deﬁcits in ﬂexibility, inhibition, theory of mind judgements and emotion perception are, therefore, likely to impact on the use of appropriately moderated, polite communication. Failure of restraint, or disinhibition, has already been discussed as a common sequel of frontal lobe injury secondary to TBI. Further, poor performance in the production of eﬀective requests has been found to be correlated with indices of disinhibition on formal neuropsychological tests (McDonald & Pearce, 1998) suggesting that more general disorders of control will impact on the ability to use language diplomatically. Although inﬂexibility with politeness has been documented (Togher & Hand, 1998) there has been no independent research linking politeness in discourse to other measures of rigidity in people with TBI. Similarly, there has been no research to date that links ToM and emotion recognition deﬁcits to failure to moderate politeness appropriately in either the TBI or other clinical populations. So, despite the potential

52

McDonald

contribution these deﬁcits make to the ability to use socially appropriate language, we await empirical conﬁrmation of this. Social knowledge An additional consideration is the role of social knowledge in communication. The notion that people with TBI have reduced access to social knowledge has been barely considered to date. Indeed, it is widely believed that people with circumscribed deﬁcits in either memory (learning) or executive function have relatively preserved access to knowledge and skills that were acquired premorbidly (Darby & Walsh, 2005). However, recent research challenges this belief in the area of social knowledge. Functional imaging of normal individuals suggests that ventromedial portions of the frontal lobes, in conjunction with the amygdalae, are involved in judgements concerning “trustworthiness” based on facial characteristics (Winston, Strange, O’Doherty, & Dolan, 2002). Patients with amygdala damage lose this ability (Adolphs, Tranel, & Damasio, 1998). Other social attributes also appear to be mediated by frontal–amygdala circuits. For example, personality judgements of extraversion, warmth, neuroticism, reliability and adventurousness that are based on the movements of light points on a walking ﬁgure are impaired in people with focal brain lesions (not TBI), with the relevant cortical region localized to the left frontal opercular cortices (Heberlein, Adolphs, Tranel, & Damasio, 2004). Similarly, adults with medial frontal damage appear to be less regulated by implicit gender stereotypes on a reaction time task than are people with dorsolateral frontal lesions and non-brain-injured controls (Milne & Grafman, 2001). Adults with focal ventromedial frontal lesions also appear to be less sensitive to dominance cues (based on gender, age, friendly facial expression and clothing) than adults with brain damage outside this region or without brain damage at all (Karaﬁn, Tranel, & Adolphs, 2004). Finally, preference judgements related to the visual attractiveness of faces activate the ventral striatum (Kampe, Frith, Dolan, & Frith, 2001) and the orbitofrontal cortex (O’Doherty, Winston, Critchley, Perrett, Burt, & Dolan, 2003), once again suggesting that the frontal, especially medial frontal, systems of the brain are involved in such social judgements. The orbitofrontal and medial temporal lobes are speciﬁcally vulnerable to the acceleration–deceleration forces of high impact TBI because of their proximity to the bony shelves of the anterior and middle fossa (Darby & Walsh, 2005). Consequently, disorders in social appraisal may accompany TBI. The relationship between such disorders and poor modulation of politeness is unknown. Pragmatic language production: Grice’s maxims As another means of utilizing pragmatic theory, the expressive communication of people with TBI has been characterized according to Grice’s maxims.

Underpinnings of communication disorders after TBI 53 Thus, in principle, language production should adhere to the maxims of quantity, quality, manner and relevance; that is, speakers should be precise, accurate, organized and relevant in their language production. Planned deviations from these maxims may be eﬀective in order to be diplomatic or dramatic in the right circumstances (as discussed with regard to politeness). Conversely, haphazard failures to adhere to these maxims will result in chaotic, socially unacceptable or ineﬀective language. Descriptions of discourse problems following TBI include lack of initiative, reliance on set expressions and general impoverishment in the amount and variety of language produced (Chapman et al., 1992; Erlich, 1988; Hartley & Jensen, 1991, 1992) or else over-talkativeness (Hagan, 1984; Milton, Prutting, & Binder, 1984), tangentiality and inappropriateness (e.g., Prigatano, Roueche, & Fordyce, 1986). These suggest that people with TBI do have problems adhering to implicit conversational maxims as outlined by Grice. A number of measures of communication have been developed using Grice’s maxims as a guide. In a study of two adults with TBI, “blind” raters evaluated how well two adults with severe TBI were able to explain how to play a game to a naive listener (i.e., a procedural narrative). Their productions were rated on scales that equated to the maxim of quantity (speciﬁcally “repetitiveness” and “amount of detail”) and manner (“clarity, “organization” and “eﬀectiveness”) and compared to those of demographically matched controls (McDonald, 1993b). The blind raters were able to clearly distinguish the productions of the participants with TBI from the control participants on these dimensions. A second study of a larger group of adults with TBI conﬁrmed problems with the demands of the procedural narrative. Typically, they failed to mention essential information, included irrelevant and therefore misleading information, repeated information and failed to sequence important steps in their correct chronological sequence (McDonald & Pearce, 1995). Similar problems with the orderly transfer of information have been reported when adults with TBI have been presented with diﬀerent procedural tasks (Galski, Tompkins, & Johnston, 1998; Prince, Haynes, & Haak, 2002; Snow, Douglas, & Ponsford, 1999). Other discourse genres have also been analyzed for characteristics that equate to the maxims of quantity and manner. Thus conversational topics have been reported as repetitive (Body & Parker, 2005), and as narratives insuﬃcient or inaccurate with respect to communicating essential content (Body & Perkins, 1998; Brookshire, Chapman, Song, & Levin, 2000; Snow et al., 1999). Grice’s maxims have also guided the development of checklists and questionnaires regarding communicative ability for people with TBI (Prutting & Kirchner, 1987). The Latrobe Communication Questionnaire (LCQ; Douglas, O’Flaherty, & Snow, 2000), for example, consists of 30 questions based on Grice’s maxims, as well as some additional questions tapping particular communication problems arising from cognitive deﬁcits (such as word retrieval, distractibility and impulsivity). The questionnaire has been found

54

McDonald

to be sensitive to discourse diﬃculties in people with TBI (Douglas, Bracy, & Snow, in press). Neuropsychological underpinnings of maxim violation Similar deﬁcits to those that are surmised to underpin pragmatic understanding may play a role in disrupting eﬀective expressive communication that meets Grice’s maxims. An individual with slow information processing, poor working memory, rigidity with associated loss of conceptual thought and/or disinhibition, as well as memory problems is likely to have diﬃculty planning an eﬀective communication strategy that enables information to be transferred in an orderly and eﬃcient manner. Interestingly, a factor analytic examination of the LCQ revealed that, while originally conceptualized along the lines of Grice’s maxims, the self-report questionaire appeared to cluster somewhat diﬀerently (Douglas et al., in press). Thus two factors seemed to represent “quantity”. On the one hand there appeared to be a constellation reﬂecting “too much”, suggesting the impact of disinhibition. On the other there was too little; that is, dysﬂuencies such as word-ﬁnding problems, hesitancies and failure to provide suﬃcient information, so suggesting a role for loss of drive and initiative. Another factor that emerged reﬂected attentional diﬃculties; that is, losing track when conversing and getting sidetracked. Yet another reﬂected the problem-solving, planning and monitoring aspect of executive function; that is, the ability to manage the task of communication, by selecting accurate information to meet the listener’s needs, keeping track of main details, putting ideas together logically, self-monitoring, adapting conversational style to different situations and knowing when to talk and when to listen. These results suggest that Grice’s maxims, while useful for highlighting the role of speaker expectations in communication, do not map directly onto psychological processes involved in eﬀective discourse. On the other hand, discourse diﬃculties do appear to correspond to common neuropsychological deﬁcits after TBI. Empirical evidence for a link between discourse errors and independent neuropsychological indices will be discussed in the following sections. Aspects of social cognition are also likely to have an impact on the ability to produce eﬀective communication that meets the listener’s needs. The ability to see the situation from the other’s perspective (ToM) is clearly important in order to formulate utterances that are meaningful for them. So, too, being able to read the emotional demeanour of others will be important in order to “pitch” one’s utterance at the right level. There has been no research, to date, examining these relationships.

Conceptualizing communication using discourse analysis Sophisticated linguistic frameworks have been applied in the ﬁeld of TBI to reveal discourse regularities by close examination of text (either written by

Underpinnings of communication disorders after TBI 55 the participant or transcribed from their speech) produced in response to speciﬁc communication tasks. A number of overviews of discourse analytic approaches in TBI have been written in recent years (e.g., Coelho, 1999; McDonald, 1998; Togher, Hand, & Code, 1999), which the interested reader should pursue. In general, discourse analyses are concerned with the discourse as a whole, its continuity, organization and the relation between structure and function. Thus discourse analytic methods provide the means to analyse meanings inherent in text across the conventional boundaries of sentences and clauses. Monologues such as telling a story or relating a procedure have been useful vehicles for analysing discourse. Two attributes of discourse that have been a major focus of investigation are eﬃciency and coherence. Eﬃciency Eﬃciency of discourse can be conceptualized as the rate of speech, or otherwise the amount of information imparted in the words produced. Early observational accounts of the communicative characteristics of people with TBI emphasized slow, hesitant, or conversely, over-talkative communication patterns. Analyses along the lines of Grice’s notion of “quantity” have similar revealed ineﬃcient information delivery. Analysis of the rate and nature of language produced has conﬁrmed these impressions. Adult and adolescent TBI patients have been found to speak more slowly (Hartley & Jensen, 1991; Stout, Yorkston, & Pimentel, 2000), produce fewer meaningful words (Brookshire et al., 2000; Chapman et al., 1992; Chapman, Levin, Matejka, Harward, & Kufera, 1995; Hartley & Jensen, 1991), more incomplete, ambiguous or uninterpretable utterances (Body & Perkins, 2004; Hartley & Jensen, 1991; Stout et al., 2000), as well as shorter information units (C-units) (Hartley & Jensen, 1991) and less information overall (Biddle, McCabe, & Bliss, 1996), per minute (Erlich, 1988; Stout et al., 2000) or, alternatively, per informational unit, expressed as either C-units (Wilson & Proctor, 2002) or T-units; that is, each independent clause plus associated subordinate clauses (Coelho, 2002; Coelho, Grela, Corso, Gamble, & Feinn, 2005) across both narrative and procedural discourse tasks. Coherence The coherence of discourse relies on the semantic continuity of the text (Patry & Nespoulous, 1990) and may reﬂect local or global coherence. At a “local” level there must be appropriate relations between adjacent propositions for coherence to occur. At a “global” or macrostructure level there is development and maintenance of an underlying discourse plan (Coelho, Liles, & Duﬀy, 1991b; Patry & Nespoulous, 1990). Both notions of coherence have been investigated in TBI subjects.

56

McDonald

1. Local coherence One measure of local coherence is provided by an estimate of textual cohesion created by the interdependence of linguistic items occurring in separate clauses in a text. A cohesive tie occurs wherever one linguistic item relies on another for its interpretation, via reiteration of semantically linked items “he brought the bag of apples in, placing the fruit in front of her”, or grammatical links such as that formed via pronominal reference “he had an apple but would not share it” (Halliday, 1985; Halliday & Hasan, 1985; Hasan, 1984, 1985). As noted in the earlier section, adults with TBI are frequently insuﬃciently informative, or else overtalkative, as well tangential and disorganized. The question arises, therefore, as to whether they have diﬃculties developing and maintaining textual cohesion. Despite the sophistication in (local) cohesion analyses that has developed in the past 10–15 years, results have produced a somewhat mixed picture. In general, adults with TBI remain sensitive to the demands of diﬀerent discourse requirements, such as procedural versus narrative discourse, varying the amount and type of lexicogrammatical cohesion accordingly (Coelho, 2002; Davis & Coelho, 2004; Hartley & Jensen, 1991; Liles, Coelho, Duﬀy, & Zalagens, 1989; Mentis & Prutting, 1987). However, whether the quality of cohesion is aﬀected is disputed. In some studies TBI speakers have been found to use less cohesive ties than non-brain-damaged control subjects (Davis & Coelho, 2004; Hartley & Jensen, 1991; Mentis & Prutting, 1987), but other studies have not found this (e.g., Coelho, 2002; Galski et al., 1998; Hough, 1990; Jordan, Murdoch, & Buttsworth, 1991; Leer & Turkstra, 1999; Wilson & Proctor, 2002). Similarly, there is disagreement as to whether or not TBI speakers produce more incomplete references where the source for interpretation of a given linguistic unit is missing or ambiguous (Hartley & Jensen, 1991; Hough & Barrow, 2003; Leer & Turkstra, 1999; Liles et al., 1989; McDonald, 1993b; Mentis & Prutting, 1987). This variability in study results may reﬂect the heterogeneity of the population under examination. After all, not all adults or children with TBI are expected to have deﬁcits in communication. There may also be diﬀerences in the way in which local coherence is calculated from one study to the next (see Davis & Coelho, 2004, for further discussion). An important additional issue is the need to carefully select the comparison group with respect to both socioeconomic status (see Snow & Douglas, 2000; Snow, Douglas, & Ponsford, 1997b, for discussion) and premorbid verbal abilities for any kind of discourse examination. Verbal ability and socioeconomic status have been clearly shown to inﬂuence the ability to produce coherent text (Brookshire et al., 2000; Coelho, 2002). But, in addition, it is not entirely clear that linguistic cohesion, thus measured, corresponds to subjective impressions concerning the coherence of the discourse (Glosser & Deser, 1991; McDonald, 1993b).

Underpinnings of communication disorders after TBI 57 2. Global coherence Global coherence has been gauged by identifying the nature and sequence of the propositional content, propositions being roughly equivalent to a predicate (i.e., verbs, modiﬁers and connectors) with one or more arguments (Kintsch & van Dijk, 1978; van Dijk & Kintsch, 1983). In story-telling tasks the propositional structure of TBI discourse has been characterized according to its organization into episodes deﬁned as sequences of events with speciﬁc beginnings, middles and ends (Brookshire et al., 2000; Chapman et al., 1992; Jordan et al., 1991; Liles et al., 1989; Mortensen, 2005). In procedural narratives, propositions are identiﬁed as to whether they represent essential, non-essential, ambiguous or irrelevant information, and whether they are positioned appropriately according to the sequence of the procedure (Galski et al., 1998; McDonald, 1993b; McDonald & Pearce, 1995; Snow, Douglas, & Ponsford, 1995, 1997b; Turkstra et al., 1996). Measures of global cohesion have also produced a rather mixed picture. Some studies suggest that, when relating a story, TBI speakers (child and adult) produce as many complete episodes and essential propositions as control speakers (Jordan et al., 1991; Liles et al., 1989; Snow et al., 1997b) while others suggest that they provide fewer episodes, less complex episodes and generally less essential information (Brookshire et al., 2000; Chapman et al., 1992; Coelho, 2002; Coelho, Liles, & Duﬀy, 1995; Liles et al., 1989). Arguably, propositional analyses of procedural narratives have been a bit more consistent. People with TBI, both adult and adolescent, have been reported to omit essential information, provide a disrupted sequence of explanation and include irrelevant and ambiguous material when explaining how to play a simple game (McDonald, 1993b; McDonald & Pearce, 1995; Turkstra et al., 1996) (although see Snow et al., 1997b). Raters’ impressions of procedural texts produced by TBI speakers support notions of disrupted global coherence by suggesting they are confused and disorganized (McDonald, 1993b). Neuropsychological contributions to failed eﬃciency and coherence after TBI Discourse analytic approaches arise from linguistic rather than psychological accounts of communication. As such, like Grice’s maxims, they would not necessarily directly address the role of cognitive or neuropsychological abilities in discourse production. Even so, the detailed characterization of language that such discourse analyses yield suggests a role for several important cognitive abilities, some of which have been examined empirically. Clearly word ﬁnding and word retrieval problems will impede the eﬃcient production of eﬀective discourse, and a link between the two has been reported within the child TBI literature (Brookshire et al., 2000). Second, coherent discourse

58

McDonald

requires continuous monitoring of verbal output in order to, for example, ensure that each pronominal reference used has an unambiguous source, and that ideas are inserted logically and eﬀectively into the language ﬂow. This is an on-line processing task that depends on good working memory capacity. Consistent with this there is empirical evidence for a relationship between impaired working memory and estimates of low eﬃciency and cohesion (Hartley & Jensen, 1991) and complexity of clauses within T-units (Youse & Coelho, 2005). The global coherence of text is likely to be aﬀected by executive disorders that impair the ability to plan and sequence behaviour to meet speciﬁed goals. In studies of adults and children with TBI (including mild and severe injuries) (Brookshire et al., 2000) the amount of essential information provided was associated with measures of conceptual thought, generativity and problem solving (Brookshire et al., 2000; McDonald & Pearce, 1995). Likewise, inability to transform the gist of written text was correlated with poor problem solving (Chapman et al., 2004). These results strongly suggest that deﬁcits in the ability to reason ﬂexibly and readily interfere with the orderly transmission of information. Furthermore, certain kinds of tasks may be more taxing of executive abilities than others. Story generation tasks, for example, wherein the speaker has no template for the structure and ﬂow of information, are likely to be more challenging for those with executive disorders than story recall based on prior exposure to an oral or pictorial story. In general, it appears that story generation tasks are more demanding for adult speakers, be they normal or suﬀering from TBI (Coelho, 2002). The ability to relate a narrative in a sensible sequence will also depend on the ability to recall the events to be narrated, as well as the events of the narration that have already unfolded. Thus, while story generation tasks may be more taxing of executive abilities, story recall tasks may rely more on intact memory capacity. Indeed, it appears that various indices of linguistic cohesion and coherence are more aﬀected by poor new learning capacity when the task requires someone retelling a previously heard story rather than generating one on the basis of a stimulus that remains in front of them (Brookshire et al., 2000; Youse & Coelho, 2005). Although it is less clear how social cognition (e.g., theory of mind and social knowledge) might be relevant to these particular dimensions of discourse production, emotion may represent a diﬀerent case. The ﬁnding of Leer and Turkstra (1999) that emotionally salient experiences are related by adolescents with and without TBI (and probably adults although this has not been examined) with better informational structure and coherence than less engaging tasks, raises the question as to whether emotional engagement facilitates coherent discourse and, if so, how. This is another fascinating avenue of exploration that awaits empirical research.

Underpinnings of communication disorders after TBI 59 Conversation The vast bulk of communication occurs as part of an interaction with one or more other speakers. Furthermore, it is in the social milieu that the problems experienced by speakers with TBI become most apparent. Consequently, methodologies are required that can characterize how verbal interaction between two or more participants is managed during spontaneous conversation. Broadly speaking, useful approaches for examining conversational skills following TBI have emerged from either linguistic (conversational) analyses (Patry & Nespoulous, 1990) or behavioural classiﬁcation based on models of social skills (McFall, 1982). 1. Linguistic approaches to analysing conversation Using a variety of linguistic approaches it has been found that TBI speakers elicit greater numbers of questions and prompts from their partners (Coelho, Liles, & Duﬀy, 1991a; Godfrey, Knight, Marsh, Monory, & Bishara, 1989). They have been rated as having poor topic maintenance (Drummond & Boss, 2004; Erlich, 1988; Milton et al., 1984), poor initiation (Drummond & Boss, 2004; Ehrlich & Barry, 1989) and providing information in an ineﬃcient and disorganized manner (Mentis & Prutting, 1987; Snow, Douglas, & Ponsford, 1997a, 1998). A particular theoretical approach that has been applied to interactive discourse in TBI has been Systemic Functional Linguistics (SFL). SFL is a theoretical approach developed by Halliday (1985) that addresses the relationship between the purpose and context of communication and its structure. According to this approach there are several levels of meanings within any discourse. Ideational meanings reﬂect the nature of the social interaction (shopping enquiry, social chit-chat, etc.) and are apparent in the vocabulary of the interaction. Interpersonal meanings reﬂect the nature of the social relationship between the speakers such as familiarity, power, and so on, and are realized in the choice of speech act. Thus speakers who have higher status may hold (and impart) more information, be in a position to make requests of their conversational partner and be able to be more direct in their communication (i.e., be less reliant on indirect politeness strategies). Finally, there are textual characteristics, that is, the connectedness of the discourse that reﬂects the mode of the language (e.g., spoken versus written). Cohesion analyses, for example, are based on Halliday and Hasan’s notion of textual coherence (Hasan, 1985). SFL, particularly as it pertains to interpersonal meanings, has been useful for examining conversation because it takes into account the discourse of the speaker with TBI in relation to their interlocutor as well as how that interlocutor behaves towards the speaker with TBI. Using this approach some similar patterns of discourse production to that already described have been revealed. For example, people with TBI tend to provide more information, including inappropriate information, to their

60

McDonald

conversational partner (Togher, Hand, & Code, 1997a, 1997b). But of potentially greater import, analyses have emphasized the role that conversational partners have in inﬂuencing the opportunities and choices that TBI speakers have when conversing. In general, it has been revealed that conversational partners often converse with speakers identiﬁed as having a TBI in a manner that has the eﬀect of disempowering them. Thus, compared to carefully matched control speakers, people with TBI were asked more questions for which the speaker already knew the answer, were subjected to repeated checking of the veracity of their responses, were given more information and were asked for less. (Togher et al., 1997a, 1997b). Togher and colleagues also demonstrated that, placed in an empowering situation, such as educating school children on the circumstances of their injury, speakers with TBI conversed in a manner that was indistinguishable from control speakers (with spinal injuries) (Togher, 2000; Togher & Hand, 1999). 2. Behavioural approaches to conversation Finally, communication disorders following TBI have been addressed from within the rubric of social skills (McFall, 1982). Notions of social skills have emerged primarily from a behavioural rather than a linguistic analysis. Checklists and rating scales based on this framework have ranged in focus from global measures of verbal and non-verbal behaviour such as “social performance” (Newton & Johnson, 1985; Spence, Godfrey, Knight, & Bishara, 1993) to intermediary measures such as “partner-directed behaviour” (Flanagan, McDonald, & Togher, 1995; McDonald et al., 2004) and “turntaking” (Drummond & Boss, 2004), to measures of speciﬁc and discrete attributes of communication such as “frequency of questions” (Godfrey et al., 1989). Using this behavioural approach, severe TBI speakers have been found to be generally less interesting, less rewarding and more eﬀortful to interact with than control speakers (Bond & Godfrey, 1997; Godfrey, Knight, & Bishara, 1991). They are reported to elicit higher rates of verbal facilitation from their conversational partner (Godfrey et al., 1989) and to be generally unskilled in their response to their partner’s questions (Spence et al., 1993). They have also been noted to be egocentric in their discussion and fail to actively involve their conversational partner, such as by asking questions or supporting them with the use of verbal reinforcers (Flanagan et al., 1995; Marsh & Knight, 1991; McDonald et al., 2004). Neuropsychological underpinnings of social skills Theoretical frameworks of social skills typically encompass three basic categories of social skills: (1) Encoding; that is, execution of behaviour including speech content, paralinguistic elements (e.g., voice volume), and non-verbal behaviour (e.g., facial expression), (2) decoding components such as attention, perception and interpretation of social cues, and “social intelligence”; that is,

Underpinnings of communication disorders after TBI 61 the identiﬁcation of problems and/or goals, and (3) decision making; that is, the generation of alternative plans of action and decisions concerning these (McFall, 1982). These relate very clearly to neuropsychological deﬁcits that have already been discussed in relation to communication disturbances after TBI as evaluated using other models. Thus executive dyscontrol and impulsivity will impact on the ability to formulate appropriate behavioural (including verbal) responses, and to monitor and regulate behavioural output. Attention to, processing and interpretation of social signals will be aﬀected by deﬁcits in emotion recognition, theory of mind, social knowledge and ability to think at a conceptual level and plan. Finally, executive dysfunction will also impede the ability to generate alternate plans and decisions. Once again, there has been little research to empirically test these hypothetical relationships.

Conclusions In conclusion, research into communication disorders after traumatic brain injury has advanced signiﬁcantly since the early observational studies of the 1970s. The use of linguistic theoretical approaches, such as pragmatics and systemic functional linguistics, as well as behavioural approaches emanating from a social skills perspective, has provided a sensitive means to elucidate disorders of communication. Although primary disorders of language are relatively infrequent after brain injury, it is apparent that for many people with severe TBI the task of communicating with others in a way that is clear and eﬀective, and sensitive to their conversational partner’s needs, is often compromised. The analytic approaches discussed in this chapter emphasize the social nature of communication. As such they represent an important advance over the “context-free” assessments of standard language batteries of the past. Social theories of communication expand notions of communicative competence to encompass the ability to use language in context and all that this entails. In doing so they have been shown to be sensitive to subtle but pervasive disorders of communication wherein basic language abilities remain intact but the ability to apply these sensitively and adaptively is impaired. Socially orientated theoretical approaches have also heightened awareness of cultural diﬀerences and reﬁned our notions of normality. For example, research by Togher, Snow, Body and colleagues (e.g., Body & Perkins, 1998; Snow et al., 1995; Snow & Douglas, 2000; Togher, 2000; Togher & Hand, 1999) highlights the importance of cohort eﬀects in what is considered normal and eﬀective conversational style. Studies such as these seriously challenge the assumption that professionally trained therapists can judge the competence of their clients’ communication skills by their own interactions (Ylvisaker, 2000). Socially oriented theories of language have provided the means to evaluate regularities in language use that may transcend conventional notions of “proper” talk and may vary from one context to the

62

McDonald

next, from one cohort to the next. They also reveal how important conversational partners are in terms of providing the speaker with TBI with adequate and/or normal opportunities to demonstrate communicative competence. Importantly, socially oriented theories of communication have also provided the means to consider how cognitive and emotional abilities interact with the language system to produce normal communicative ability. In the case of speech act theory (pragmatics), a psychologically based account of how indirect speech acts are understood emerged in the 1970s. This provided the impetus for a number of studies aimed at evaluating the model’s veracity in explaining disorders in the comprehension of irony relative to other competing notions (e.g., relevance theory, Sperber & Wilson, 1986). It has also pointed to a variety of potential mechanisms that align with our growing understanding of neuropsychological impairments commonly seen after traumatic brain injury. Other linguistic approaches have been less concerned with the psychological mechanisms underlying discourse ability but have, nonetheless, characterized communication disturbances in suﬃcient detail to enable clear speculation as to the underlying neuropsychological cause. As a result of these diﬀerent approaches it is possible to hypothesize about systematic relationships between a variety of neuropsychological impairments and communicative ability and to test these empirically. Thus deﬁcits in attention, working memory, information processing speed and learning have each been found to contribute to communication disorders as operationalized by these diﬀerent theoretical frameworks. So too, problems in conceptual reasoning and problem solving as well as the ability to monitor and regulate behavioural responses have been clearly implicated in both the ability to understand subtle communicative meanings and the ability to produce social skilled discourse. Despite this, not all studies have been able to demonstrate signiﬁcant associations between aspects of discourse and performance on standard neuropsychological tests, even when the constructs are clearly relevant (Brookshire et al., 2000; McDonald & Pearce, 1995; Turkstra et al., 1996). It is quite possible that discourse tasks represent ecologically valid tasks that are complex and unstructured relative to standard neuropsychological measures. The ecological validity of standard tests has often been criticized (Silver, 2000). It is also possible that discourse falls into the domain of social information processing and is therefore more relevantly compared to performance on other social problem-solving tasks. There are, however, few standard instruments in this domain – an issue that is increasingly recognized. But, in addition, recent advances in our understanding of social cognition identify entirely diﬀerent neuropsychological constructs that may be highly relevant to communication. The possibility that emotion recognition, theory of mind judgements and social attitudes are uniquely represented in the frontal systems of the brain and processed diﬀerently from non-social information opens a whole new avenue of research. The prevalence of psychosocial dysfunction following severe TBI is well known. It is becoming increasingly apparent that many

Underpinnings of communication disorders after TBI 63 people with TBI experience various deﬁcits in social information processing. New advances in our understanding of social cognition and how this becomes disordered following TBI, combined with sophisticated developments in characterizing discourse and communication as detailed in this chapter, thus provide us with exciting new directions for characterizing the neuropsychology of communication diﬃculties seen following brain injury.

References Adams, J. H., Doyle, D., Ford, I., Gennarelli, T. A., Graham, D. I., & McLellan, D. R. (1989). Diﬀuse axonal injury in head injury: Deﬁnition, diagnosis and grading. Histopathology, 15 (1), 49–59. Adams, J. H., Doyle, D., Graham, D. I., Lawrence, A. E., McLellan, D. R., Gennarelli, T., et al. (1985). The contusion index: A reappraisal in human and experimental non-missile head injury. Neuropathology and Applied Neurobiology, 11 (4), 299–308. Adolphs, R. (2001). The neurobiology of social cognition. Current Opinion in Neurobiology, 11, 231–239. Adolphs, R. (2003). Cognitive neuroscience of human social behaviour. Nature Reviews Neuroscience, 4 (3), 165–178. Adolphs, R., Tranel, D., & Damasio, A. R. (1998). The human amygdala in social judgement. Nature, 393, 470–474. Bara, B. G., Cutica, I., & Tirassa, M. (2001). Neuropragmatics: Extralinguistic communication after closed head injury. Brain and Language, 77 (1), 72–94. Bara, B. G., Tirassa, M., & Zettin, M. (1997). Neuropsychological constraints on formal theories of dialogue. Brain and Language, 59, 7–49. Barnes, M. A., & Dennis, M. (2001). Knowledge-based inferencing after childhood head injury. Brain and Language, 76 (3), 253–265. Bechara, A. (2002). The neurology of social cognition. Brain, 125 (8), 1673–1675. Bibby, H., & McDonald, S. (2004). Theory of Mind after traumatic brain injury. Neuropsychologia, 43, 99–104. Biddle, K. R., McCabe, A., & Bliss, L. S. (1996). Narrative skills following traumatic brain injury in children and adults. Journal of Communication Disorders, 29 (6), 446–469. Body, R., & Parker, M. (2005). Topic repetitiveness after traumatic brain injury: An emergent, jointly managed behaviour. Clinical Linguistics and Phonetics, 19 (5), 379–392. Body, R., & Perkins, M. R. (1998). Ecological validity in assessment of discourse in traumatic brain injury: Ratings by clinicians and non-clinicians. Brain Injury, 12 (11), 963–976. Body, R., & Perkins, M. R. (2004). Validation of linguistic analyses in narrative discourse after traumatic brain injury. Brain Injury, 18 (7), 707–724. Bond, F., & Godfrey, H. P. (1997). Conversation with traumatically brain-injured individuals: A controlled study of behavioural changes and their impact. Brain Injury, 11, 319–329. Bowler, D. M. (1992). “Theory of mind” in Asperger’s syndrome. Journal of Child Psychology and Psychiatry, 33, 877–893. Brookshire, B. L., Chapman, S. B., Song, J., & Levin, H. S. (2000). Cognitive and

64

McDonald

linguistic correlates of children’s discourse after closed head injury: A three-year follow-up. Journal of the International Neuropsychological Society, 6 (7), 741–751. Brown, P., & Levinson, S. (1978). Universals in language usage: Politeness phenomena. In E. N. Goody (Ed.), Questions and politeness: Strategies in social interaction. Melbourne: Cambridge University Press. Channon, S., Pellijeﬀ, A., & Rule, A. (2005). Social cognition after head injury: Sarcasm and theory of mind. Brain and Language, 93, 123–134. Channon, S., & Watts, M. (2003). Pragmatic language interpretation after closed head injury: Relationship to executive functioning. Cognitive Neuropsychiatry, 8 (4), 243–260. Chapman, S. B., Culhane, K. A., Levin, H. S., Harward, H., Mendelsohn, D., Ewing-Cobbs, L., et al. (1992). Narrative discourse after closed head injury in children and adolescents. Brain and Language, 43, 42–65. Chapman, S. B., Levin, H. S., Matejka, J., Harward, H., & Kufera, J. A. (1995). Discourse ability in children with brain injury: Correlations with psychosocial, linguistic and cognitive factors. Journal of Head Trauma Rehabilitation, 10 (5), 36–54. Chapman, S. B., Sparks, G., Levin, H. S., Dennis, M., Roncadin, C., Zhang, L., et al. (2004). Discourse macrolevel processing after severe pediatric traumatic brain injury. Developmental Neuropsychology, 25 (1–2), 37–60. Cicerone, K. D., & Tanenbaum, L. N. (1997). Disturbance of social cognition after traumatic orbitofrontal brain injury. Archives of Clinical Neuropsychology, 12, 173–188. Clark, H. H., & Schunk, D. H. (1980). Polite responses to polite requests. Cognition, 8 (2), 111–143. Coelho, C. A. (1999). Discourse analysis in traumatic brain injury. In S. McDonald, L. Togher, & C. Code (Eds.), Communication disorders after traumatic brain injury. Hove, UK: Psychology Press. Coelho, C. A. (2002). Story narratives of adults with closed head injury and non-brain-injured adults: Inﬂuence of socioeconomic status, elicitation task, and executive functioning. Journal of Speech, Language, and Hearing Research, 45 (6), 1232–1248. Coelho, C. A., Grela, B., Corso, M., Gamble, A., & Feinn, R. (2005). Microlinguistic deﬁcits in the narrative discourse of adults with traumatic brain injury. Brain Injury, 19 (13), 1139–1145. Coelho, C. A., Liles, B. Z., & Duﬀy, R. J. (1991a). Analysis of conversational discourse in head-injured adults. Journal of Head Trauma Rehabilitation, 6 (2), 92–98. Coelho, C. A., Liles, B. Z., & Duﬀy, R. J. (1991b). The use of discourse analysis for the evaluation of higher level traumatically brain injured adults. Brain Injury, 5, 381–392. Coelho, C. A., Liles, B. Z., & Duﬀy, R. J. (1995). Impairments of discourse abilities and executive functions in traumatically injured adults. Brain Injury, 9, 471–477. Corrigan, P. W., & Toomey, R. (1995). Interpersonal problem solving and information processing in schizophrenia. Schizophrenia Bulletin, 21 (3), 395–403. Croker, V., & McDonald, S. (2005). Recognition of emotion from facial expression following traumatic brain injury. Brain Injury, 19, 787–789. Crosson, B. (1987). Treatment of interpersonal deﬁcits for head-trauma patients in inpatient rehabilitation settings. The Clinical Neuropsychologist, 1 (4), 335–352, 366.

Underpinnings of communication disorders after TBI 65 Darby, D., & Walsh, K. W. (2005). Walsh’s neuropsychology: A clinical approach (5th ed.). Edinburgh, UK: Elsevier. Davis, G. A., & Coelho, C. A. (2004). Referential cohesion and logical coherence of narration after closed head injury. Brain and Language, 89 (3), 508–523. Davis, H. L., & Pratt, C. (1995). The development of children’s Theory of Mind: The working memory explanation. Australian Journal of Psychology, 47, 25–31. Dennis, M., & Barnes, M. A. (1990). Knowing the meaning, getting the point, bridging the gap, and carrying the message: Aspects of discourse following closed head injury in childhood and adolescence. Brain and Language, 39, 428–446. Dennis, M., & Barnes, M. A. (2000). Speech acts after mild or severe childhood head injury. Aphasiology, 14 (4), 391–405. Dennis, M., Guger, S., Roncadin, C., Barnes, M., & Schachar, R. (2001a). Attentionalinhibitory control and social-behavioral regulation after childhood closed head injury: Do biological, developmental, and recovery variables predict outcome? Journal of the International Neuropsychological Society, 7 (6), 683–692. Dennis, M., Purvis, K., Barnes, M. A., Wilkinson, M., & Winner, E. (2001b). Understanding of literal truth, ironic criticism, and deceptive praise following childhood head injury. Brain and Language, 78, 1–16. Douglas, J. M., Bracy, C. A., & Snow, P. C. (in press). Exploring the factor structure of the La Trobe communication questionnaire: Insights into the nature of communication deﬁcits following traumatic brain injury. Aphasiology. Douglas, J. M., O’Flaherty, C. A., & Snow, P. C. (2000). Measuring perception of communicative ability: The development and evaluation of the La Trobe communication questionnaire. Aphasiology, 14 (3), 251–268. Drummond, S. S., & Boss, M. R. (2004). Functional communication screening in individuals with traumatic brain injury. Brain Injury, 18 (1), 41–56. Ehrlich, J., & Barry, P. (1989). Rating communication behaviours in the head injured. Brain Injury, 3, 193–198. Erlich, J. S. (1988). Selective characteristics of narrative discourse in head-injured and normal adults. Journal of Communication Disorders, 21, 1–9. Ferstl, E. C., Guthke, T., & von Cramon, D. Y. (2002). Text comprehension after brain injury: Left prefrontal lesions aﬀect inference processes. Neuropsychology, 16 (3), 292–308. Flanagan, S., McDonald, S., & Togher, L. (1995). Evaluation of the BRISS as a measure of social skills in the traumatically brain injured. Brain Injury, 9, 321–338. Galski, T., Tompkins, C., & Johnston, M. V. (1998). Competence in discourse as a measure of social integration and quality of life in persons with traumatic brain injury. Brain Injury, 12 (9), 769–782. Gibbs, R. W., & O’Brien, J. (1991). Psychological aspects of irony understanding. Journal of Pragmatics, 16, 523–530. Glosser, G., & Deser, T. (1991). Patterns of discourse production among neurological patients with ﬂuent language disorders. Brain and Language, 40 (1), 67–88. Godfrey, H. D. P., Knight, R. G., Marsh, N. V., Monory, B., & Bishara, S. M. (1989). Social interaction and speed of information processing following severe head injury. Psychological Medicine, 19, 175–182. Godfrey, H. P., Knight, R. G., & Bishara, S. M. (1991). The relationship between social skill and family problem solving following very severe closed head injury. Brain Injury, 5, 207–211.

66

McDonald

Gordon, A. C. L., & Olson, D. R. (1998). The relation between theory of mind and capacity to hold in mind. Journal of Experimental Child Psychology, 68, 70–83. Gordon, D., & Lakoﬀ, G. (1975). Conversational postulates. In P. Cole & J. L. Morgan (Eds.), Syntax and semantics: Speech acts (Vol. 3). New York: Academic Press. Green, R. E. A., Turner, G. R., & Thompson, W. F. (2004). Deﬁcits in facial emotion perception in adults with recent traumatic brain injury. Neuropsychologia, 42, 133–141. Grice, H. P. (1975). Logic and conversation. In P. Cole & J. Morgan (Eds.), Syntax and semantics: Speech acts (Vol. 3). New York: Academic Press. Grice, H. P. (1978). Further notes on logic and conversation. In P. Cole (Ed.), Syntax and semantics: Pragmatics (Vol. 9). New York: Academic Press. Hagan, C. (1984). Language disorders in head trauma. In A. Holland (Ed.), Language disorders in adults. San Diego, CA: College Hill Press. Halliday, M. A. K. (1985). An introduction to functional grammar. Australia: Edward Arnold. Halliday, M. A. K., & Hasan, R. (1985). Language, context and text: Aspects of language in a social-semiotic perspective. Melbourne: Deakin University Press. Happé, F., & Frith, U. (1996). The neuropsychology of autism. Brain, 119 (4), 1377–1400. Happé, F. G. E. (1993). Communicative competence and theory of mind in autism: A test of relevance theory. Cognition, 48, 101–119. Hartley, L. L., & Jensen, P. J. (1991). Narrative and procedural discourse after closed head injury. Brain Injury, 5, 267–285. Hartley, L. L., & Jensen, P. J. (1992). Three discourse proﬁles of closed-head-injury speakers: Theoretical and clinical implications. Brain Injury, 6 (3), 271–281. Hasan, R. (1984). Coherence and cohesive harmony. In J. Flood (Ed.), Understanding reading comprehension. Newark, DE: International Reading Association. Hasan, R. (1985). The texture of a text. In M. A. K. Halliday & R. Hasan (Eds.), Language, context, and text: Aspects of language in a social-semiotic perspective. Victoria: Deakin University Press. Haverkate, H. (1990). A speech act analysis of irony Journal of Pragmatics, 14, 77–109. Heberlein, A. S., Adolphs, R., Tranel, D., & Damasio, H. (2004). Cortical regions for judgments of emotions and personality traits from point-light walkers. Journal of Cognitive Neuroscience, 16, 1143–1158. Heilman, K. M., Safran, A., & Geschwind, N. (1971). Closed head trauma and aphasia. Journal of Neurology, Neurosurgery and Psychiatry, 34, 265–269. Hough, M. S. (1990). Narrative comprehension in adults with right and left hemisphere brain damage: Theme organisation. Brain and Language, 38, 253–227. Hough, M. S., & Barrow, I. (2003). Descriptive discourse abilities of traumatic brain-injured adults. Aphasiology, 17 (2), 183–191. Hughes, C. (1998). Executive function in preschoolers: Links with theory of mind and verbal ability. British Journal of Developmental Psychology, 16, 233–253. Jackson, H. F., & Moﬀat, N. J. (1987). Impaired emotional recognition following severe head injury. Cortex, 23, 293–300. Jordan, F. M., Murdoch, B. E., & Buttsworth, D. L. (1991). Closed-head-injured children’s performance on narrative tasks. Journal of Speech and Hearing Research, 34 (3), 572–582.

Underpinnings of communication disorders after TBI 67 Kampe, K. K. W., Frith, C. D., Dolan, R. J., & Frith, U. (2001). Reward value of attractiveness and gaze. Nature, 413, 589. Karaﬁn, M. S., Tranel, D., & Adolphs, R. (2004). Dominance attributions following damage to the ventromedial prefrontal cortex. Journal of Cognitive Neuroscience, 16, 1796–1804. Keenan, T. (1998). Memory span as a predictor for false belief understanding. New Zealand Journal of Psychology, 27, 36–43. Kendall, E., Shum, D., Halson, D., Bunning, S., & Teh, M. (1997). The assessment of social problem solving ability following traumatic brain injury. Journal of Head Trauma Rehabilitation, 12, 68–78. Kintsch, W., & van Dijk, T. A. (1978). Toward a model of text comprehension and production. Psychological Review, 85, 363–394. Leer, E. V., & Turkstra, L. (1999). The eﬀect of elicitation task on discourse coherence and cohesion in adolescents with brain injury. Journal of Communication Disorders, 32 (5), 327–349. Levin, H. S., Amparo, E., Eisenberg, H. M., Williams, D. H., High, W. M. Jr., McArdle, C. B., et al. (1987). Magnetic resonance imaging and computerized tomography in relation to the neurobehavioral sequelae of mild and moderate head injuries. Journal of Neurosurgery, 66 (5), 706–713. Levin, H. S., Grossman, R. G., Rose, J. E., & Teasdale, G. (1979). Long term neuropsychological outcome of closed head injury. Journal of Neurosurgery, 50, 412–422. Liles, B. Z., Coelho, C. A., Duﬀy, R. J., & Zalagens, M. R. (1989). Eﬀects of elicitation procedures on the narratives of normal and closed head injured adults. Journal of Speech and Hearing Disorders, 54, 356–366. MacDonald, S., & Johnson, C. J. (2005). Assessment of subtle cognitivecommunication deﬁcits following acquired brain injury: A normative study of the functional assessment of verbal reasoning and executive strategies (FAVRES). Brain Injury, 19 (11), 895–902. Marquardt, T. P., Rios-Brown, M., Richburg, T., Seibert, L. K., & Cannito, M. P. (2001). Comprehension and expression of aﬀective sentences in traumatic brain injury. Aphasiology, 15 (10–11), 1091–1101. Marsh, N. V., & Knight, R. G. (1991). Behavioural assessment of social competence following severe head injury. Journal of Clinical and Experimental Neuropsychology, 13 (5), 729–740. Martin, I., & McDonald, S. (2005). Exploring the causes of pragmatic language deﬁcits following traumatic brain injury. Aphasiology, 19, 712–730. McDonald, S. (1992). Diﬀerential pragmatic language loss following closed head injury: Ability to comprehend conversational implicature. Applied Psycholinguistics, 13, 295–312. McDonald, S. (1993a). Major review. Viewing the brain sideways? Right hemisphere versus anterior models of non-aphasic language disorders. Aphasiology, 7, 535–549. McDonald, S. (1993b). Pragmatic language loss following closed head injury: Inability to meet the informational needs of the listener. Brain and Language, 44, 28–46. McDonald, S. (1998). Communication and language disturbances following traumatic brain injury. In B. Stemmer & H. A. Whitaker (Eds.), Handbook of neurolinguistics. (pp. 487–495). San Diego, CA: Academic Press. McDonald, S., Bornhofen, C., Shum, D., Long, E., Saunders, C., & Neulinger, K.

68

McDonald

(2006). Reliability and validity of “The Awareness of Social Inference Test” (TASIT): A clinical test of social perception. Disability and Rehabilitation, 28, 1529– 1542. McDonald, S., & Flanagan, S. (2004). Social perception deﬁcits after traumatic brain injury: The interaction between emotion recognition, mentalising ability and social communication. Neuropsychology, 18, 572–579. McDonald, S., Flanagan, S., Martin, I., & Saunders, C. (2004). The ecological validity of TASIT: A test of social perception. Neuropsychological Rehabilitation, 14, 285–302. McDonald, S., Flanagan, S., Rollins, J., & Kinch, J. (2003). TASIT: A new clinical tool for assessing social perception after traumatic brain injury. Journal of Head Trauma Rehabilitation, 18, 219–238. McDonald, S., & Pearce, S. (1995). The Dice game: A new test of organisational skills in language. Brain Injury, 9, 255–271. McDonald, S., & Pearce, S. (1996). Clinical insights into pragmatic language theory: The case of sarcasm. Brain and Language, 53, 81–104. McDonald, S., & Pearce, S. (1998). Requests that overcome listener reluctance: Impairment associated with executive dysfunction in brain injury. Brain and Language, 61, 88–104. McDonald, S., Togher, L. & Code, C. (Eds.) (1999). Communication disorders following traumatic brain injury. Hove, UK: Psychology Press. McDonald, S., & van Sommers, P. (1992). Diﬀerential pragmatic language loss following closed head injury: Ability to negotiate requests. Cognitive Neuropsychology, 10, 297–315. McFall, R. M. (1982). A review and formulation of the concept of social skills. Behaviour Assessment, 4, 1–33. Mentis, M., & Prutting, C. A. (1987). Cohesion in the discourse of normal and head-injured adults. Journal of Speech and Hearing Research, 30, 583–595. Milders, M., Fuchs, S., & Crawford, J. R. (2003). Neuropsychological impairments and changes in emotional and social behaviour following severe traumatic brain injury. Journal of Clinical & Experimental Neuropsychology, 25 (2), 157–172. Milne, E., & Grafman, J. (2001). Ventromedial prefrontal cortex lesions in humans eliminate implicit gender stereotyping. Journal of Neuroscience, 21 (12), 1–6. Milton, S. B., Prutting, C. A., & Binder, G. M. (1984). Appraisal of communication competence in head injured adults. In R. W. Brookshire (Ed.), Clinical aphasiology (Vol. 14, pp. 114–123). Minneapolis: BRK Publishers. Milton, S. B., & Wertz, R. T. (1986). Management of persisting communication deﬁcits in patients with traumatic brain injury. In B. P. Uzzell & Y. Gross (Eds.), Clinical neuropsychology of intervention. Boston, MA: Martinus Nijhoﬀ Publishing. Mortensen, L. (2005). Written discourse and acquired brain impairment: Evaluation of structural and semantic features of personal letters from a systemic functional linguistic perspective. Clinical Linguistics and Phonetics, 19 (3), 227–247. Newton, A., & Johnson, D. A. (1985). Social adjustment and interaction after severe head injury. British Journal of Clinical Psychology, 24, 225–234. O’Doherty, J., Winston, J., Critchley, H., Perrett, D., Burt, D. M., & Dolan, R. J. (2003). Beauty in a smile: The role of medial orbitofrontal cortex in facial attractiveness. Neuropsychologia, 41, 147–155. Ozonoﬀ, S., & Miller, G. A. (1996). An explanation of right hemisphere contributions to the pragmatic impairments of autism. Brain and Language, 52, 411–434.

Underpinnings of communication disorders after TBI 69 Patry, R., & Nespoulous, J.-L. (1990). Discourse analysis in linguistics: Historical and theoretical background. In Y. Joanette & H. H. Brownell (Eds.), Discourse ability and brain damage: Theoretical and empirical perspectives. New York: Springer-Verlag. Prigatano, G. P. (1986). Personality and psychosocial consequences of brain injury. In G. P. Prigatano, D. J. Fordyce, H. K. Zeiner, J. R. Roueche, M. Pepping, & B. Casewood (Eds.), Neuropsychological rehabilitation after brain injury. (pp. 29–50). Baltimore, MD: Johns Hopkins University Press. Prigatano, G. P., & Pribram, K. H. (1982). Perception and memory of facial aﬀect following brain injury. Perceptual and Motor Skills, 54, 859–869. Prigatano, G. P., Roueche, J. R., & Fordyce, D. J. (1986). Neuropsychological rehabilitation after brain injury. Baltimore, MD: Johns Hopkins University Press. Prince, S., Haynes, W. O., & Haak, N. J. (2002). Occurrence of contingent queries and discourse errors in referential communication and conversational tasks: A study of college students with closed head injury. Journal of Medical Speech Language Pathology, 10 (1), 19–39. Prutting, C. A., & Kirchner, D. M. (1987). A clinical appraisal of the pragmatic aspects of language. Journal of Speech and Hearing Disorders, 52, 105–119. Santoro, J., & Spiers, M. (1994). Social cognitive factors in brain injury associated with personality change. Brain Injury, 8 (3), 265–276. Sarno, M. T. (1980). The nature of verbal impairment after closed head injury. The Journal of Nervous and Mental Disease, 168, 685–692. Sarno, M. T., & Levita, E. (1986). Characteristics of verbal impairment in closed head injured patients. Archives of Physical Medicine Rehabilitation, 67, 400–405. Searle, J. R. (1975). Indirect speech acts. In P. Cole & J. L. Morgan (Eds.), Syntax and semantics: Speech acts. (Vol. 3). New York: Seminar Press. Shamay-Tsoory, S. G., Tomer, R., & Aharon-Peretz, J. (2005). The neuroanatomical basis of understanding sarcasm and its relationship to social cognition. Neuropsychology, 19, 288–300. Silver, C. H. (2000). Ecological validity of neuropsychological assessment in childhood traumatic brain injury. Journal of Head Trauma Rehabilitation, 15 (4), 973–988. Snow, P. C., Douglas, J., & Ponsford, J. (1995). Discourse assessment following traumatic brain injury: A pilot study examining some demographic and methodological issues. Aphasiology, 9 (4), 365–380. Snow, P. C., Douglas, J., & Ponsford, J. (1997a). Conversational assessment following traumatic brain injury: A comparison across two control groups. Brain Injury, 11 (6), 409–429. Snow, P. C., Douglas, J., & Ponsford, J. (1997b). Procedural discourse following traumatic brain injury. Aphasiology, 11 (10), 947–967. Snow, P. C., Douglas, J., & Ponsford, J. (1998). Conversational discourse abilities following severe traumatic brain injury: A follow-up study. Brain Injury, 12 (11), 911–935. Snow, P. C., & Douglas, J. M. (2000). Conceptual and methodological challenges in discourse assessment with TBI speakers: Towards an understanding. Brain Injury, 14 (5), 397–415. Snow, P. C., Douglas, J. M., & Ponsford, J. L. (1999). Narrative discourse following severe traumatic brain injury: A longitudinal follow-up. Aphasiology, 13 (7), 529–551.

70

McDonald

Spell, L. A., & Frank, E. (2000). Recognition of nonverbal communication of aﬀect following traumatic brain injury. Journal of Nonverbal Behavior, 24 (4), 285–300. Spence, S. E., Godfrey, H. P., Knight, R. T., & Bishara, S. (1993). First impressions count: A controlled investigation of social skill following closed head injury. British Journal of Clinical Psychology, 32, 309–318. Sperber, D., & Wilson, D. (1986). Relevance: Communication and cognition. Oxford, UK: Basil Blackwell. Spiers, M. V., Pouk, J. A., & Santoro, J. M. (1994). Examining perspective-taking in the severely head injured. Brain Injury, 8, 463–473. Stone, V. E., Baron-Cohen, S., & Knight, R. T. (1998). Frontal lobe contributions to theory of mind. Journal of Cognitive Neuroscience, 10 (5), 640–656. Stout, C. E., Yorkston, K. M., & Pimentel, J. I. (2000). Discourse production following mild, moderate, and severe traumatic brain injury: A comparison of two tasks. Journal of Medical Speech Language Pathology, 8 (1), 15–25. Surian, L., Baron-Cohen, S., & Van der Lely, H. (1996). Are children with autism deaf to Gricean maxims? Cognitive Neuropsychiatry, 1 (1), 55–71. Tager-Flusberg, H., Sullivan, K., & Boshart, J. (1997). Executive functions and performance on false belief tasks. Developmental Neuropsychology, 13, 487–493. Tate, R. L., Fenelon, B., Manning, M. L., & Hunter, M. (1991). Patterns of neuropsychological impairment after severe blunt head injury. Journal of Nervous and Mental Disease, 179, 117–126. Thomsen, I. V. (1975). Evaluation and outcome of aphasia in patients with severe closed head trauma. Journal of Neurology, Neurosurgery and Psychiatry, 38, 713–718. Togher, L. (2000). Giving information: The importance of context on communicative opportunity for people with traumatic brain injury. Aphasiology, 14 (4), 365–390. Togher, L., & Hand, L. (1998). Use of politeness markers with diﬀerent communication partners: An investigation of ﬁve subjects with traumatic brain injury. Aphasiology, 12 (7–8), 755–770. Togher, L., & Hand, L. (1999). The macrostructure of the interview: Are traumatic brain injury interactions structured diﬀerently to control interactions? Aphasiology, 13 (9–11), 709–723. Togher, L., Hand, L., & Code, C. (1997a). Analysing discourse in the traumatic brain injury population: Telephone interactions with diﬀerent communication partners. Brain Injury, 11 (3), 169–189. Togher, L., Hand, L., & Code, C. (1997b). Measuring service encounters with the traumatic brain injury population. Aphasiology, 11 (4–5), 491–504. Togher, L., Hand, L., & Code, C. (1999). Exchanges of information in the talk of people with traumatic brain injury. In S. McDonald, L. Togher, & C. Code (Eds.), Communication disorders after traumatic brain injury. Hove, UK: Psychology Press. Turkstra, L. S., McDonald, S., & Kaufmann, P. M. (1996). Assessment of pragmatic communication skills in adolescents after traumatic brain injury. Brain Injury, 10 (5), 329–345. van Dijk, T., & Kintsch, W. (1983). Strategies of discourse comprehension. New York: Academic Press. Wilson, B. M., & Proctor, A. (2002). Written discourse of adolescents with closed head injury. Brain Injury, 16 (11), 1011–1024. Winston, J. S., Strange, B. A., O’Doherty, J., & Dolan, R. J. (2002). Automatic and

Underpinnings of communication disorders after TBI 71 intentional brain responses during evaluation of trustworthiness of faces. Nature Neuroscience, 5 (3), 277–283. Ylvisaker, M. (2000). Reﬂections on dobermanns, poodles, and social rehabilitation for diﬃcult to serve individuals with traumatic brain injury. Aphasiology, 14 (4), 407–431. Youse, K. M., & Coelho, C. A. (2005). Working memory and discourse production abilities following closed-head injury. Brain Injury, 19 (12), 1001–1009.

5

Social validation of recovery in aphasia Leonard L. LaPointe and Kerry L. Lenius

Introduction Social validation of an outcome is achieved by assessing the social signiﬁcance of the goals, the social appropriateness of the procedures, and the social importance of the behavioral change (Kazdin, 1977; Wolf, 1978). This is essential if we are to generate meaningful conclusions regarding rehabilitation therapy. This chapter provides insights into the origins of social validation of change in the literature, and the application of this concept in aphasia therapy today. An excerpt from Talking about aphasia (Parr, Byng, Gilpin, & Ireland, 1997, p. 82) illustrates the frustration experienced by a person with aphasia while working on treatment goals. It aptly speaks to the need for social validation of therapeutic targets and strategies: Weekly group therapy involved quizzes and language games. At the time he [Vincent, the person with aphasia] was consumed with a desire to return to work and was extremely anxious about his ﬁnancial and home situation. While not being at all critical, Vincent points out that the weekly activities in speech and language therapy did not touch on these issues: “I personally had got a bit bored – I learned a lot of things that I didn’t know when I had the stroke, like the history of the Royals – The speech therapy didn’t give me information about help. The help they give me is to try and get better.” Vincent eventually left the group, but stays in touch with some of the people he met there. In this example, the consumer was less than satisﬁed with the services he received. If Vincent’s therapist had simply asked him, “What would you like to work toward in therapy? What is important to you?” Vincent’s statement might have gone something like this: Working in group therapy really helped me learn to socialize with others in a new way. I learned communication skills that I really needed to try to return to work. Despite the aphasia, I was able to use words, gestures, and drawings to make myself understood. This prepared me

Social validation of recovery in aphasia

73

for the communicative interactions I would be facing when I returned home. Social validation of the goals and outcomes of treatment can provide the framework for planning and implementing intervention that is salient and relevant to each of the individuals with whom we work.

Emergence of social validity in the literature As early as the 1950s social validation was present in a meager number of articles in medicine, psychotherapy, and business. It wasn’t until the 1970s that the term was more clearly deﬁned by behavioral therapists (Kazdin, 1977; Wolf, 1978). Wolf, the ﬁrst editor of the Journal of Applied Behavior Analysis (JABA), provided an entertaining description of the process and the perceived reluctance of the journal in coming to terms with the need to incorporate social importance with subjective assessments of social validity. He provided a delicate example of the need for this type of assessment by describing a manuscript submitted by Jones and Azrin (1969), who researched synchronized speech to reduce stuttering. Despite the reduction of the stuttering behavior, the speech sounded artiﬁcial. Jones and Azrin dealt with this problem by having judges rate the speech on the dimension of naturalness. Thus the researchers used social validation by having raters assess the social appropriateness of speech. If social validation was ignored and clients who stuttered were all instructed to use a regular beat pattern for speech, the stuttering might be extinguished; but the stigma of “abnormal” speech would remain. So what? This is the basis for testing social validity. If the changes we make in therapy are not impacting our clients at home and in the community, did we provide adequate service? If scores on standardized tests increase one standard deviation but consumers are unable to perceive a change, did we make a diﬀerence? When does a diﬀerence make a diﬀerence is an important question about any attempt to intervene and facilitate a change in behavior. Who cares? If we as professionals only use our own expertise and experience in setting up criteria for success, thereby neglecting the values and opinions of the other experts involved (the clients), we are implying that consumer opinions do not matter. This can be a serious ﬂaw in the successful realization of treatment goals. Wolf (1978, p. 210) states that “Behavioral treatment programs are designed to help someone with a problem. Whether or not the program is helpful can be evaluated only by the consumer.” This may be a little overstated, as the opinions of professionals and others in the community might indeed contribute to the determination of adequate outcomes, but certainly the opinion of the consumer should be paramount. Wolf also poses questions that might well be retained by every clinician during the phases and stages of treatment.

74

LaPointe and Lenius

1

Are the speciﬁc behavioral goals that have been generated really what society wants? Does the end justify the means? That is, do the participants, caregivers and other consumers consider the treatment procedure acceptable? Are the consumers satisﬁed with the results? This includes all results, even unpredicted ones.

2 3

Despite this growl by Wolf, trends in the use of social validity in behavioral modiﬁcation research remained ﬂat and low. Kennedy (1992) reviewed articles for inclusion of social validity in JABA from 1968 to 1990 and the journal Behavior Modiﬁcation from 1977 to 1990. His graphs show a sluggish trend toward increased use of social validity. Despite improvement, by 1990 social validation procedures were reported in only about 20 percent of the articles surveyed.

Implementing socially valid treatment Three main targets exist for the appropriate integration of social validation procedures in aphasia treatment. These are: • • •

developing socially valid goals using valid methods, and validating the outcomes.

Each of these areas needs to be addressed in order to achieve the result of providing treatment that is appropriate, meaningful, and eﬀective in enabling successful communication. Socially valid goals Traditionally a clinician may use a standardized test such as the Western Aphasia Battery (WAB) (Kertesz, 1982) to determine areas of impairment, select therapy goals, and possibly to document change. This focus on impairment is consistent with traditional approaches to disease characteristic of the medical model, but may not be the most eﬃcient way to determine socially relevant goals. The seemingly ever-changing terminology of the World Health Organization is being integrated into models of aphasia treatment (Rogers, Alarcon, & Olswang, 1999; Threats, 2002), but the concepts involved are important. Changes in social activities and participation are emerging as more relevant goals of treatment and are eroding the stone face of impairment-based approaches to intervention. The Life Participation Approach to Aphasia is having an impact on approaches to aphasia intervention and shaping the very core of the aphasia treatment model (LPAA Project Group, 2000). Most standardized tests of aphasia are predominantly impairment-based. Recently, some eﬀorts have been made to incorporate the

Social validation of recovery in aphasia

75

social model of aphasia into assessment procedures. The latest edition of Eisenson’s classic Examining for aphasia (LaPointe, 2006) incorporates principles of the social model of aphasia into the assessment in an eﬀort to guide clinicians in the quest to develop relevant participation-based treatment goals. This approach does not suggest that we discard the baby with the bathwater, as impairments and cognitive-linguistic processes also may need to be targeted for treatment; but for far too long it has been impairment or nothing, with little emphasis on reintegration of the person into an active, participating milieu. The traditional biographic standardized test interview needs to be supplemented or indeed replaced with speciﬁc information gathering as to the goals, values, hobbies, likes, dislikes, hopes, fears, anticipations, and motivations of each unique individual for whom we are planning treatment. This will assist the informed clinician with planning, delivering, and evaluating services (Pound, Parr, & Duchan, 2001). Lubinski (2001), Elman (2005), Simmons-Mackie (2001), Lyon and Shadden (2001), LaPointe (2002), and Worrall and her associates (Cruice, Worrall, Hickson, & Murison, 2005) all provide social model ﬂesh and humanity to the skeleton of treatment planning in aphasia. This entire movement, of course, harkens back to the birth and upbringing of language in context and person-centered concepts of aphasia intervention nurtured and inﬂuenced so thoroughly by Audrey Holland (Holland, 1982a, 1982b). Interview questions appropriate to determining and creating socially relevant and valid treatment goals can be gleaned, inferred, or directly created from all of the above sources and particularly from Lubinski (2001) and Simmons-Mackie (2001), and Elman (2005). The interview allows the client and any others present to express what life was like before the onset of aphasia, how life is impacted now, and what areas of communication breakdown generate the most stress on relationships. In an eﬀort to deﬁne socially valid aphasia therapy goals Ross and Wertz (2003) set out to determine the diﬀerence in quality of life as rated by people with and without aphasia. Two groups (people with aphasia for at least six months and non-brain-damaged individuals) completed quality of life measures. The greatest diﬀerence between the groups was evident in areas of activities of daily living, opportunities to acquire new information and skills, social support, mobility, and sexual activity. Of course it is imperative to customize treatment planning and weave speciﬁc treatment goals around the idiosyncracies of each person, but this study shows support for language therapy focusing on enhancing communication for speciﬁc functional situations and expanding participation in society. Sometimes we tend to err on the side of overzealous treatment planning and implementation. One of the authors of this chapter (LLL) remembers well an early treatment planning faux pas when a full court press of intervention (twice per day; intensive reading comprehension strategies integrated into the treatment schedule) was probably not in keeping with the personal goals of the person with

76

LaPointe and Lenius

aphasia. After two weeks of rather intensive treatment, I remember his words well: Doc, I thank you for all you’re trying to do here, but, you know, I never have completely read through a whole book. I don’t really care if I ever do. I just want to go up on the St. Johns River and live with my brother in the trailer there, and maybe sit out on the dock and ﬁsh a little. I know you’re trying real hard Doc, and I appreciate it, but I really don’t care if I can’t read very good. If the treatment goals of the person with aphasia are not built into the treatment plan, misguided expenditures of time, eﬀort, and money can be the result. This clinical lesson made it abundantly clear that precise activity and participation therapy must be harmonious with the expectations and needs of the person in therapy. Sometimes the people with whom we work are content to ﬁsh or plant cumquats. Socially valid methods In addition to determining goals that are vital to clients’ lives it is imperative to ensure the methods used to achieve the outcome are acceptable. Socially valid procedures can be facilitated by verifying that the materials being used are consistent with the patient’s expectations. An example of this is reported by Lustig and Tompkins (2002, p. 510), They state: “LG was presented with a list of possible conversation topics prior to the study and her preferences were taken into account when the ﬁnal stimulus sets were created.” By allowing the person with aphasia to aid in the selection of stimuli that are most relevant to him or her, we facilitate participation and ownership in the therapy. Validating the importance of the materials to each person can only help motivation and participation in rehabilitation. A ﬂy ﬁsherman probably would not respond as well to retelling the story of Cinderella as to creating instructions on how to match the insect hatch. A cake decorator may be more motivated to work on divorce cake designs than on conjugating the verb “to be.” Materials need to be not only age appropriate but person appropriate. Treatment procedures are another important consideration in generating socially valid intervention. Are the selected treatment procedures within the social or cultural norms or expectations of the person with aphasia? Working on paralinguistic nuances such as improving conversational eye contact may not be within the cultural norms of a young adult stroke victim who happens to be a Navajo American Indian. In the Navajo culture direct eye contact, particularly with an authority ﬁgure or older person, is considered bad manners. Naming the edible cuts of meat from a pig may not be a palatable activity for a Muslim or Orthodox Jew. Writing the stanzas of “What a friend we have in Jesus,” may be less appropriate for a Sri Lankan Buddhist than a

Social validation of recovery in aphasia 77 retired Baptist preacher from Dothan, Alabama. Reading statistics on comparative handgun violence in America and Australia may not sit well with a former oﬃcer of the National Riﬂe Association. Acceptable interventions that are socially appropriate also may take less time, are less unsettling, have fewer adverse or apathetic reactions, and are cost eﬃcient according to some research (Reimers, Wacker, Cooper, & DeRaad, 1992). Consumers of aphasia therapy have voiced dissatisfaction with treatment procedures that are not client centered or age appropriate. Clowns, balloons, circus animals, ﬂuﬀy puppies and kittens should be banished to the pediatric wards, unless of course one is working with a former clown or ﬂuﬀy puppy lover. We also need to explain why we are doing certain assessments or working on certain communication tasks. Explaining that we are evaluating coordination and control of the speech articulators (lips, front of the tongue, back of the tongue) fosters understanding; as opposed to the unexplained request to say “pa-ta-ka” over and over. Sometimes we assume too much and our clients wonder what we could possibly learn from the requests “smile; stick out your tongue; wiggle it from side to side; point to these pictures.” Possible client reactions are illustrated in the following observation: When asked about what speech and language therapy entails, people who have aphasia describe a number of diﬀerent activities . . . therapists seem to be poor at conveying information about what is being done in therapy, and why. As a result, to some aphasic people the rituals of therapy seem demeaning and made them feel stupid. Many people point out that therapy can feel like returning to the classroom. The association with school can sometimes be reinforced by the manner of the therapist. (Parr et al., 1997, p. 78) A prime example of the need to assure the selection and use of socially valid procedures is clearly demonstrated by consumers of augmentative alternative communication (AAC). Lasker and Beukelman (1999) measured peers’ perceptions of storytelling by an adult with aphasia to investigate if peers accepted an augmentative alternative communication device. In this study peers ranked the AAC digitized speech to be preferred over natural speech. However, this ﬁnding is not always the case. Shadden (2005) underscores this point when describing a stroke survivor with limited verbal output (only able to say “yes” and “no”) who was opposed to augmentative forms of communication. Through a support group he was encouraged to use a total communication approach (gestures, drawings, writing). Eventually he began using a DynaVox® and was successfully communicating with everyone except his wife. Despite the potential this man had for communicating with the device, no gains were made in communicating with his spouse. This highlights the importance of therapeutic relevance to all the principals in the

78

LaPointe and Lenius

constellation of treatment. If one of the principals is not buying into the procedures, the potential for improvement may be compromised.

Socially valid outcome measures When measuring treatment eﬀect, one of the pioneers of socially relevant intervention, Kazdin (1977), advocated two criteria by which to determine if treatment gains are socially valid: social comparison and consumer evaluation. Social comparison occurs when treatment is considered to be improved only when the target behavior is considered to be within “normal” functioning. This is considered one form of social validation since the rest of society performs in the same manner as the person with the now “normally” functioning behavior, therefore it is presumed that society would ﬁnd this behavior acceptable. The drawbacks to using social comparison as a criterion of social validity are fairly apparent. It is, expensive, time consuming, and intuitively ludicrous to be required to gather social norms for every speciﬁc treatment target. However, once norms have been established, clear criteria can be set without the obstacles posed by subjective measures. Goldstein (1990) makes a germane point by arguing that social comparison neglects to account for profound diﬀerences among clients prior to treatment, and that many clients and signiﬁcant others may be satisﬁed with smaller gains that still fall short of “normal.” Wells (1999, p. 912) asks, “What is the value of such an objective assessment when it is so unconﬁrmed by the perceptions of patients and carers?” Another problem is that social comparison only measures the change in level of impairment without considering changes in the ability to cope or compensate for problems. These issues may be why social comparison is not used as often as consumer evaluations. Kennedy (1992) reported that 91 percent of the JABA articles in 1983 that reported on social validity used subjective measures (i.e., consumer evaluation) and only 9 percent used normative comparison. Consumer evaluations These are the most common form of social validity used in determining treatment outcomes (Kennedy, 1992). Consumer evaluations typically take the form of rating scales of the person in treatment and/or caregiver. These may include quality of life (QOL) ratings, informal interviewing (which may include any of the principals involved), or speciﬁc judgments when comparing pre- to post-treatment abilities (i.e., comparing videotaped behaviors or writing samples). Sometimes, however, “anecdotal reports of client or family opinions are often not valued as ‘measures’ because they are considered subjective, unreliable, or unprofessional” (Simmons-Mackie & Damico, 2001, p. 22). In determining the social validation of treatment outcomes, many clinicians, however, value the opinions of the principals involved as much as

Social validation of recovery in aphasia

79

they value behavioral measures. Many researchers and clinicians use objective behavioral measures as primary dependent measures, and social validation as secondary measures of treatment outcomes (Schwartz & Baer, 1991). A clinical fact of life is that some signiﬁcant changes in behavioral measures may not signal a corresponding change as to the value of that change. When does a diﬀerence make a diﬀerence? That nagging outcome question needs to be addressed; and that is at the heart of social validation. Schlosser (1999) separates consumer reported outcomes into four groups: proximal, instrumental, intermediate, and distal. Proximal outcomes are directly related to the intervention, instrumental outcomes measure generalization, intermediate outcomes rate change in QOL, and distal outcomes rate changes on a larger level (i.e., national outcomes). Thus, when working on the ability to communicate information in conversation and measuring proximal outcomes, one could ask consumers, “How successful was Mr. R. at getting his message across?” If you choose to measure intermediate outcomes you could give a general QOL or well-being questionnaire to determine if the treatment improved psychosocial wellness. Outcomes also can be separated by activity limitation (previously referred to as disability in earlier WHO models) and participation restriction (previously termed handicap). For instance, if you plan to improve a person’s communicative interactions with a wide range of people, you would be attempting to reduce the participation restriction; and one option for a satisfaction measure would be to use the Communication Readiness and Use Index (CRUI) (Lyon et al., 1997) with any of the relevant principals involved. Multiple approaches may be used to measure consumer opinions. One option is forced choice (improved/not improved); another would be to provide a Likert scale (5 or 7 point), or use of a visual analogue scale (i.e., Communicative Eﬀectiveness Index, CETI) (Lomas, Pickard, Bester, Elbard, Finlayson, & Zoghaib, 1989). Additionally, consumer opinions could be measured by having raters view video clips of the targeted behavior before and after treatment, and rate the behavior that is more eﬀective. In humor, fruit-picking, and romance, timing is everything. Add successful therapy to the list. Perceptive clinicians begin with the end in mind. We need to plan ahead by determining the type of social validation measure that may be appropriate for the person enrolled in treatment. If a clinician plans to obtain ratings of pre/post ability one may want to videotape baseline ability before initiating treatment. Post-therapy ratings may be of limited value if pre-therapy behaviors are lost in the fog of history. Even if one does not intend to use video comparisons, it may be useful to have the person with aphasia and important others complete ratings of QOL or communication abilities (i.e., CETI) when treatment begins. Simmons-Mackie (2001) provides a comprehensive list of socially valid assessment tools to obtain stakeholder perspectives.

80

LaPointe and Lenius

The good, the bad, and the ugly Although consumer evaluations are extremely useful to gain insight into consumers’ perspectives, this is not a perfect science and not without its problems. Many of the subjective rating scales are inconsistent across studies. Validity and reliability of the scales are often unreported, and without the basics of adherence to psychometric principles, one runs the risk of producing measurements that have no real meaning. Schwartz and Baer (1991) provide advice on how to administer questionnaires to maximize validity and reliability. One common concern with subjective ratings is the risk of false positives. This occurs when people expect treatment to work, so they rate post measures more favorably. The placebo eﬀect can intrude when expectations of improvement are presumed. This may not always be a bad thing, but it makes it diﬃcult to attribute change to treatment procedures. One way to attempt to minimize this false positive bias is to counterbalance or “blind” the presentation of pre- and post-treatment samples when possible. Also, beware of potential social invalidity. Social invalidity occurs when consumers disapprove of some component of the program and are not direct or honest with their evaluations. Truthful opinions and responses that are unbiased by the desire to please or meet perceived expectations of an authority ﬁgure must be the goal as we gather data via our consumer opinion measures. We are not the ﬁrst to draw attention to these dilemmas; others have voiced similar apprehensions (Goldstein, 1990; Tompkins, 1994). Another issue that is speciﬁc to communication impairments in aphasia is the concern that persons with aphasia may experience diﬃculty comprehending questions or communicating their perceptions. It is acceptable, and even recommended, to provide any needed assistance to help people with aphasia complete perception ratings. This is a far superior tactic compared to pushing their opinions aside, and so overlooking the values of the person at the center of the illness. Worrall and Holland (2003) suggest several accommodations such as changing the format (interview instead of self-completed questionnaire); simplifying questions and responses (use simple language and allow the person with aphasia to answer in yes/no format); adding visual cues (pictographs); and prompting and personalizing questions. We can beneﬁt from the work of our colleagues in Canada, Australia, and the United Kingdom in generating and promoting “aphasia friendly” materials, and these can be used in harvesting valid opinions of treatment outcomes as well. An example of a pictorial QOL rating scale for people with aphasia is described by Engell, Hütter, Willmes, and Huber (2003). Maintenance of social validation Documenting maintenance has been an ongoing struggle in rehabilitation eﬀorts and it should not be overlooked in social validation measures. If consumers report treatment has improved aspects of QOL at termination of the

Social validation of recovery in aphasia

81

study, yet two months later QOL has trickled back to the original level, was treatment eﬀective? This is a concern voiced by Kennedy (2002) as he argues to incorporate maintenance as part of social validation before considering a treatment to be eﬀective.

Stakeholders Indeed, it appears that social validity may be measured only if direct consumers (persons receiving services), indirect consumers (such as the general public who may beneﬁt indirectly from the service), and service providers share in the evaluation of services. (Kozleski & Sands, 1992, p. 120) The stakeholders are the principals involved in aphasia treatment, and the principals can be deﬁned narrowly or as broadly as the community or society. These include the person with aphasia; spouses and caregivers; immediate and extended family members; acquaintances; friends and enemies; referring and co-working healthcare professionals; and third party payers. Maybe even pets. If a tail wags when a dog’s name is successfully emitted, that may be a form of cross-species social validation. Nearly everyone is aﬀected somehow, either directly or indirectly, by the services we provide. It is diﬃcult to determine the consequences of aphasia if we do not have a full appreciation of how the stakeholders perceive the consequences (Simmons-Mackie, 2001). Schwartz and Baer (1991) divide these consumers into four categories: direct, indirect, members of the immediate community, and members of the extended community. •

•

• •

Direct consumers are the primary stakeholders, the recipients of the intervention (i.e., the person with aphasia; or, when conducting caregiver training, the caregiver). This is a crucial target for social validity since understanding our clients’ perspectives of their own improvement on tasks or improved quality of life is crucial to determining the eﬀectiveness and eﬃcacy of our interventions. Direct consumers are the true focus of social validation of our services. They provide insight and direct information into their values; impressions of their well-being; and the impact of aphasia on their lives, expectations, hopes, and dreams (Worrall & Holland, 2003). Indirect consumers are strongly aﬀected by the intervention but are not the direct consumers. Indirect consumers include spouse or spouses (if polygamous), life partners, children, or close friends or relatives of the direct consumer. Members of the immediate community interact with the direct and indirect consumers on a regular basis (teacher, boss, co-worker, neighbor, grocery store clerk, massage therapist, bartender). Members of the extended community who do not interact with direct or

82

LaPointe and Lenius indirect consumers but may be aﬀected by the status of the direct consumer (other interventionists or professionals; third party payers; journal reviewers; taxpayers; newspaper writers; bass guitar players from Exeter; hillbillys; savants; the average man or woman on the street; and so on).

Diﬀerent consumers have diﬀerent viewpoints, expectations, and internal criteria for acceptability of outcomes. The measurement of quality of life is one area where this has been apparent. QOL is deﬁned by the World Health Organization (WHO) as “an individual’s perceptions of their position in life in the context of the culture and value systems in which they live and in relation to their goals, expectations, standards and concerns” (World Health Organization, 1996, p. 5). QOL is an elusive measure of life satisfaction, and it may not be totally accurate or valid for a healthcare professional (nurse, doctor, or clinician) to judge another person’s quality of life. To do so may be fraught with measurement pitfalls (LaPointe, 1999). This was reinforced in a recent study comparing quality of life ratings between self-ratings of people with aphasia and ratings from family members or healthcare providers who served as proxies for the people with aphasia (Cruice et al., 2005). These Antipodean researchers found that proxy respondents showed a signiﬁcant negative bias when rating QOL for the person with aphasia. According to these ﬁndings, we must be cautious in interpreting the evaluations of family members and healthcare providers’ ratings of treatment outcomes, especially when comparing these ratings with those of the direct consumer. Although QOL measures are best garnered directly from the patient, it is important to seek additional input from other stakeholders. Communication is not an isolated act except when sleep talking or mumbling in the bathroom. Procreation and communication are usually dependent on at least a social dyad. If we as clinicians ignore other consumers, the person with aphasia may experience continued isolation from the community and lose the chance for possible reintegration into the workforce.

Changing priorities in rehabilitation medicine While traditional health indicators are based on mortality (i.e. death) rates of populations, the ICF [International Classiﬁcation of Functioning, Disability, and Health] shifts focus to “life”, i.e., how people live with their health conditions and how these can be improved to achieve a productive, fulﬁlling life. (WHO press release, November, 2001) As is evident from earlier sections of this chapter, the traditional medical model of aphasia intervention and healthcare in general has been evolving toward a social model over the past few years. Traditional rehabilitation mainly focused on impairment measures (i.e., range of motion exercise, muscle strength, words per minute, etc.), with less consideration of the direct

Social validation of recovery in aphasia

83

consumer, family, and community perceptions. The neurolinguistic model of aphasia treatment included traditional stimulation and relearning techniques used in an attempt to improve language behaviors while perhaps recruiting or reorganizing new neuronal networks. More contemporary treatment principles attempt to generate increased attention on psychological and physical wellness (Lyon & Shadden, 2001). An example of this intervention emphasis is provided in the Life Participation Approach to Aphasia (LPAA; Chapey et al., 2001). In 2001 the WHO published the International Classiﬁcation of Functioning, Disability, and Health (ICF). This is a coding scheme model to identify interactions between health conditions, body functions and structures, activities and participation, environmental, and personal factors. The WHO instituted a shift from focusing on impairment to social perspectives and this was a natural opening for an increasing emphasis on social validation of treatment outcomes. The ICF has gained attention in our discipline because it connects communication and life skills. The American Speech-Language Hearing Association (ASHA) has incorporated the WHO model into its code of ethics (ASHA, 2001). Individual speech-language pathologists are also incorporating health classiﬁcation schemes (i.e., ICF) since they relate to the acquisition of funding, how we communicate to stakeholders, and how we converse within the profession (Threats & Worrall, 2004). The ICF framework is also appropriate to the application of clinical research, and can facilitate a bridge between clinical practice and current research (Threats, 2002). Patient-based measures in medicine With the tide of change in medicine and healthcare in general, and the evolution to patient-based outcomes, numerous health-related quality of life (HRQOL) rating scales are emerging. HRQOL measures typically include perceptions of social health, role functions, and general well-being. Interestingly, the new net of life features that are embraced by HRQOL measures may also incorporate spirituality, sexual function, life satisfaction, and aspects of the environment. These outcome measures may be generic for use across a broad range of medical conditions or speciﬁc to a select population. A few of the more common generic scales include the Sickness Impact Proﬁle, Quality of Well-Being scale, and the WHOQOL-100. Some examples of speciﬁc scales include the ALS (Amyoptrophic Lateral Sclerosis) Functional Rating Scale and the Parkinson’s Disease Questionnaire (Andresen & Meyers, 2000). Each type of scale (generic or speciﬁc) may have diﬀerent strengths and weaknesses (Guyatt, Feeny, & Patrick, 1993). Several of the popular scales used in the stroke population have been reviewed fairly extensively in the literature, with comparisons of the appropriateness, reliability, validity, responsiveness to change, and use in proxy assessments (Salter, Jutai, Teasell,

84

LaPointe and Lenius

Foley, Bitensky, & Bayley, 2005). However, there is no consensus on which scales are the gold standard for measuring societal perspectives of participation. Research and clinical validation of QOL scales continues at a feverish pace and no doubt the next ﬁve years will see some improvements and perhaps consensus on QOL scales that meet consumer, societal, and psychometric criteria.

Social validation in aphasia So far in this chapter we have reviewed the history, implementation, stakeholders, and health policy related to social validation. We now explore the underlying basis of social validation in aphasia therapy. If ever there was a middle earth in clinical aphasiology, this is it. Although some might conclude that the incorporation of social validation models to treatment outcomes in aphasia have been largely characterized by ignorance and apathy, over the past decade there have been stirrings that allow some optimism. The rising tide is apparently aﬀecting our small area of healthcare as well. Aphasiologists have introduced social validation measures in treatments for syntax, discourse, group therapy, caregiver training, and augmentative and alternative communication. In pioneering work, Doyle, Goldstein, and Bourgeois (1987) were among the ﬁrst to utilize social validation measures in aphasia. These investigators conducted a single subject design study to examine generalization and social validation of syntax training using the Helm Elicited Language Program for Syntax Stimulation (HELPSS). Five professional-level Veterans Administration employees who were naïve to the purposes of the study and the subjects served as judges. Pre- and post-treatment recordings were presented in a counterbalanced fashion, and raters judged if each response was adequate or inadequate. These rater judgments revealed that the syntax training improved trained grammatical constructs; however, there was no signiﬁcant generalization to new sentence structures. More recently, other studies also have utilized pre- and post-treatment comparisons with “naïve” raters to determine the social validity of a written communication strategy (Lustig & Tompkins, 2002), Linguistic Speciﬁc Treatment (LST) (Jacobs, 2001), conversational coaching (Hopper, Holland, & Rewega, 2002), volunteer training (Hickey, Bourgeois, & Olswang, 2004), and writing ability (LaPointe, Katz, & Braden, 1999). LaPointe et al. (1999) recruited a varied assembly of people from the community to rate perceived changes in writing. Unlike most other studies, these naïve raters were not restricted to healthcare workers or students but a diverse cross-section of community members in respect to occupation, age, and education. Among the large sample (n = 141) of raters were teachers, blue-collar workers, professionals, students, a preacher, IT experts, and a model. Raters were shown counterbalanced pairs of writing samples (one from baseline and one approximately six months later) and asked to judge

Social validation of recovery in aphasia

85

whether the ﬁrst item or the second item was “better,” or whether there was no diﬀerence between the two items. These judges were able to discern change in writing ability after six months that correlated with the improvement following therapy in multidimensional scoring of writing samples. A crosssection of people in the community from a sample that was diverse in education, occupation, age, and gender were able to discern and judge as “better” samples of writing taken from six months post-therapy. People could see a diﬀerence. Of course it remains for us to determine whether or not this perceived change makes a diﬀerence. And that is what the social validation process is all about. Who should be the direct or indirect consumers who validate treatment outcomes? Careful selection should be employed when determining which consumers to target. The work has only started. We need to know the opinions of physicians, nurses, rehabilitation specialists, insurance providers, as well as the direct and indirect segments of society. Hickey and Rondeau (2005) compared ratings from groups with diﬀerent knowledge of aphasia; one group was relatively unfamiliar with aphasia, and the other group consisted of second year speech-language pathology graduate students. Judges who were naïve to aphasia were more sensitive to change in pre- and posttreatment ratings, suggesting that members of the general public may provide more robust ratings. The most appropriate consumer groups to target should be carefully selected based on the treatment objectives. Raters who are naïve to the individual with aphasia cannot rate quality of life or broader change in daily communication abilities. Hinckley (2002) sought to describe the employment status and perceived life satisfaction of adults with chronic aphasia so she directly targeted persons with aphasia. In a unique alliance that included as a co-author the person with aphasia who was the focus of the study, Lasker, LaPointe, and Kodras (2005) described the progress of a professor with aphasia whose goal in therapy was to improve her teaching ability. She was an accomplished researcher and teacher in geography who specialized in geographic aspects of world hunger. Her over-riding objective was to return to the classroom to teach, and to continue her contributions to the university and her academic profession. The profundity of aphasia, particularly in verbal sentence formulation and production, in this professor was signiﬁcant. Treatment modalities and communication options included computer-based AAC to supplement her laborious attempts at verbal production. These strategies and other communication options that featured key word prompts were arrived at by consensus with powerful input from the person with aphasia. After some gratifying improvement and adaptation to using the AAC device to augment and supplement her lectures, we attempted some social validation of her communication changes. We selected a unique segment of indirect consumers by targeting this professor’s students as persons who would provide ratings of social validity. By selecting students who were expected to understand and learn from her lectures, we were able to target stakeholders who were

86

LaPointe and Lenius

signiﬁcantly impacted by the aphasia treatment outcome. The expectations of the students who needed to learn the class material would no doubt diﬀer from expectations of an outsider viewing brief video clips with no investment in the class. Changes in teaching and communication eﬀectiveness were reported by class members throughout the duration of a semester. This professor with aphasia continues to be reintegrated into the academic community and, despite persisting signiﬁcant verbal production diﬃculty, has been able to achieve her primary objective of returning to the classroom. We think she has improved, adapted, accommodated, and persisted in a way that is measurable and has clinical signiﬁcance to her and to us. A signiﬁcant segment of stakeholders, her students, agree. Researchers also have compared social validity ratings to changes on objective behavioral measures and standardized test scores. Doyle, Tsironas, Goda, and Kalinyak (1996) investigated the relationship between unfamiliar listeners’ judgments of connected discourse in people with aphasia and the correct information units (CIU) of the samples. In this study the two measures were strongly and positively correlated. Lyon and colleagues (1997) compared consumer ratings to standardized aphasia tests and found that, despite the lack of signiﬁcant improvement on the Boston Diagnostic Aphasia Examination (BDAE) and Communication Abilities in Daily Living (CADL) following communication training, caregivers and communication partners reported signiﬁcant gains in communication on the Communication Readiness and Use Index (CRUI) and Psychosocial Well-Being Index (PWI). Ross and Wertz (1999) studied the relationship between change in listener perceptions and standardized impairment and disability measures. They did not ﬁnd a signiﬁcant relationship when comparing scores on aphasia batteries and disability measures to listeners’ perceptions of change in overall communication ability. These ﬁndings reinforce the notion that both social validity measures and standardized test measures can be valuable indicators of clinical signiﬁcance and meaningful treatment outcomes. Psychosocial impact of aphasia: More than just language Aphasia does not aﬀect a person in isolation. This is a condition that aﬀects the entire constellation of those who orbit around the person with aphasia. With aphasia the aﬀected person and family members experience devastating and life-altering changes that alter their expectations and needs in therapy. Many of these changes have been described by those who have experienced the process ﬁrst hand (Hale, 2003; Montgomery-West, 1995). Concepts that are inherent in adapting to chronicity and the stages and phases of psychosocial eﬀects of the illness experience have been elucidated in some of the literature on aphasia. Adaptation, adjustment, accommodation, and the concept of Aristos (making the best of a given situation) are treated in depth in a recent book on aphasia (LaPointe, 2005). All these factors impact the person with aphasia and complicate the establishment and veriﬁcation of treatment

Social validation of recovery in aphasia

87

outcomes. Personal roles for an individual with aphasia may be drastically altered by the aphasia. The traditional breadwinner role may be transformed into a position of starkly increased dependence. Other long-held roles can be metamorphosed into those that are unfamiliar and frightening. Aphasia can shiver the soul. Speciﬁcally, it can dramatically alter the sense of self and torque identity. Shadden (2005) poignantly highlights some issues of re-establishing identity in aphasia. She writes from the expertise of both professional and caregiver, and provides insights that are illuminating to even the most experienced clinician. Lubinski (2001) provides a detailed inventory of potential eﬀects on the family, as well as family needs at diﬀerent patient stages (severe illness or crisis, recuperation, rehabilitation, post-rehabilitation, and institutionalization). Familiarity with this process is essential to a holistic appreciation of the psychosocial needs of the family with aphasia. Emotional and psychosocial changes can engulf aphasia recovery. No one has studied this and contributed more to it than Chris Code. His career is marked by signiﬁcant contributions to the science of aphasiology; and one of his most precious gifts may be that he has given us a richer understanding and appreciation of the psychosocial realm that accompanies the shock of aphasia. Code’s professional persona is a strange and wonderful amalgamation of Freud, Head, Schuell, Pogo, Ringo Starr, and Blind Lemon Jeﬀerson. His continuing contribution is evident in recent collaborations on the inﬂuence of psychosocial elements on aphasia recovery (Code & Herrmann, 2003). In addition to renegotiating identity roles, people with aphasia often are isolated from society. This leads to limited opportunities to participate in verbal communication. Socially valid treatment demands consideration of psychosocial elements. Unfortunately “emotional experience and personal perspectives, social roles and psychosocial perceptions are neither objective nor easy to measure and are not traditionally seen as well suited to experimental investigation. Consequently, issues of personal experience are often neglected in rehabilitation” (Code & Herrmann, 2003, p. 122). That should not deter us from studying this complex area of inter-related variables. We have a responsibility to all who have or will have aphasia to attempt to understand these inﬂuences and how they may aﬀect our interventions. Reimbursement This is a good time to reframe our thinking and restructure our treatments to create cost-eﬀective and beneﬁcial programs that are meaningful to patients, their families, and those paying the bills. (Carol M. Frattali, 1998, p. 242) Our late colleague and friend, Carol Frattali, captured our charge succinctly. Healthcare reimbursers have taken note of the need to provide therapy that inﬂuences life participation abilities. The new ICF health classiﬁcation scheme may be used to establish reimbursement decisions. Reporting progress

88

LaPointe and Lenius

using social validation outcomes demonstrates the utility of our service to third party payers (Threats & Worrall, 2004). In addition, direct consumers are becoming more involved in selecting healthcare plans and providers to seek an option that suits their needs (Frattali, 1998). Healthcare services for people with chronic conditions, especially in the United States, are still woefully inadequate. The reduction in services and reimbursement for rehabilitation that we have witnessed in the past two decades is shortsighted and some would say corrosive. Priorities seem to have elevated insurance, pharmaceutical, and other proﬁt-driven corporate interests above that of assuring a broad range of human services that are allowed and paid for as long as they are needed. We need social validation of rehabilitation eﬀorts for chronic conditions such as aphasia. We also need societal accountability that addresses the question of why these services are not readily available to those who need them. A civilized society may be judged by the way that it cares for its needy. When geopolitical agendas are ﬁnanced at the expense of human services in healthcare and education, the role of governments in serving public interests may indeed be questioned. History may not be kind. We can only hope that societal values become rebalanced, so that optimal regard can be paid to people in need of long-term healthcare; particularly those who struggle daily with the dreadfulness of aphasia.

Conclusion Social validation of treatment outcomes in aphasia has been relatively neglected, and we advocate that it should be an essential component of aphasia therapy. The principles of social validation can be incorporated during goal selection, establishment of priorities of treatment targets, selection of materials and procedures, determination of the context of treatment, and the measurement of socially relevant outcomes. Consumers represent a number of stakeholders, all of whom may hold diﬀerent perceptions of the success or failure of therapy. In this chapter we have advocated continued research and implementation of social validation strategies as a means for determining the clinical signiﬁcance of our services. Our ultimate objective is to enhance the quality of life and daily interactions of the people we serve. As has been noted before, this will advance the relevance of our interventions. Also it will facilitate socially relevant management by the clinicians who treat people with aphasia, as well as the future clinicians who are destined to treat us.

References Andresen, E. M., & Meyers, A. R. (2000). Health-related quality of life outcomes measurements. Archives of Physical Medicine and Rehabilitation, 81 (12, Suppl. 2), S30–S45. ASHA (2001). Scope of practice for speech-language pathology. Rockville, MD: ASHA.

Social validation of recovery in aphasia

89

Chapey, R., Duchan, J. F., Elman, R. J., Garcia, L. J., Kagan, A., Lyon, J. G., et al. (2001). Life participation approach to aphasia: A statement of values for the future. In R. Chapey (Ed.), Language intervention strategies in adult aphasia (4th ed., pp. 235–245). Baltimore, MD: Williams & Wilkins. Code, C., & Herrmann, M. (2003). The relevance of emotional and psychosocial factors in aphasia to rehabilitation. Neuropsychological Rehabilitation, 13, 109–132. Cruice, M., Worrall, L., Hickson, L., & Murison, R. (2005). Measuring quality of life: Comparing family members’ and friends’ ratings with those of their aphasic partners. Aphasiology, 19 (2), 111–129. Doyle, P., Goldstein, H., & Bourgeois, M. S. (1987). Experimental analysis of syntax training in Broca’s aphasia: A generalization and social validation study. Journal of Speech and Hearing Disorders, 52, 143–155. Doyle, P. J., Tsironas, D., Goda, A. J., & Kalinyak, M. (1996). The relationship between objective measures and listeners’ judgments of the communication informativeness of the connected discourse of adults with aphasia. American Journal of Speech-Language Pathology, 5 (3), 53–60. Engell, B., Hütter, B., Willmes, K., & Huber, W. (2003). Quality of life in aphasia: Validation of a pictorial self-rating procedure. Aphasiology, 17, 383–396. Elman, R. (2005). Social and life participation approaches to aphasia intervention. In L. L. LaPointe (Ed.), Aphasia and related neurogenic language disorders (3rd ed., pp. 39–50). New York: Thieme Medical Publishers. Frattali, C. (1998). Clinical care in a changing health system. In N. Helm-Estabrooks & A. Holland (Eds.), Approaches to the treatment of aphasia. San Diego, CA: Singular. Goldstein, H. (1990). Assessing clinical signiﬁcance. In L. B. Oswang, C. K. Thompson, S. F. Warren, & N. J. Minghetti (Eds.), Treatment eﬃcacy research in communication disorders (pp. 91–98). Rockville, MD: American Speech-Language Hearing Foundation. Guyatt, G. H., Feeny, D. H., & Patrick, D. L. (1993). Measuring health-related quality of life. Annals of Internal Medicine, 118 (8), 622–629. Hale, S. (2003). The man who lost his language. London: Penguin Books. Hickey, E. M., Bourgeois, M. S., & Olswang, L. B. (2004). Eﬀects of training volunteers to converse with nursing home residents with aphasia. Aphasiology, 18, 625–637. Hickey, E. M., & Rondeau, G. (2005). Social validation in aphasiology: Does judges’ knowledge of aphasia matter? Aphasiology, 19, 389–398. Hinckley, J. J. (2002). Vocational and social outcomes of adults with chronic aphasia. Journal of Communication Disorders, 35, 543–560. Holland, A. (1982a). Observing functional communication of aphasic adults. Journal of Speech and Hearing Disorders, 47, 50–56. Holland, A. (1982b). Remarks on observing aphasic people. In Clinical Aphasiology: Proceedings of the Conference 1982 (pp. 1–3). Minneapolis, MN: BRK Publishers. Also available online at http://aphasiology.pitt.edu/archive/00000749/ Hopper, T., Holland, A., & Rewega, M. (2002). Conversational coaching: Treatment outcomes and future directions. Aphasiology, 16, 745–761. Jacobs, B. J. (2001). Social validity of changes in informativeness and eﬃciency of aphasic discourse following linguistic speciﬁc treatment (LST). Brain and Language, 78, 115–127. Jones, R. J., & Azrin, N. A. (1969). Behavioral engineering: Stuttering as a function of stimulus duration during synchronization. Journal of Applied Behavior Analysis, 2, 223–230.

90

LaPointe and Lenius

Kazdin, A. E. (1977). Assessing the clinical or applied importance of behavior change through social validation. Behavior modiﬁcation, 1, 427–452. Kennedy, C. H. (1992). Trends in the measurement of social validity. The Behavior Analyst, 15, 147–156. Kennedy, C. H. (2002). The maintenance of behavior change as an indicator of social validity. Behavior Modiﬁcation, 26, 594–604. Kertesz, A. (1982). Western aphasia battery. New York: Grune & Stratton. Kozleski, E. B., & Sands, D. J. (1992). The yardstick of social validity: Evaluating quality of life as perceived by adults without disabilities. Education and Training in Mental Retardation, 27 (2), 119–131. LaPointe, L. (1999). Quality of life with aphasia. Seminars in Speech and Language, 20 (1), 5–17. LaPointe, L. L. (2002). The sociology of aphasia. Journal of Medical Speech-Language Pathology, 10 (1), vii–ix. LaPointe, L. L. (2005). Aphasia and related neurogenic language disorders. New York: Thieme Medical Publishers. LaPointe, L. L. (2006). Examining for aphasia-4. Austin, TX: Pro-ed. LaPointe, L. L., Katz, R. C., & Braden, C. L. (1999). Clinical signiﬁcance of change in language performance: Social validation of writing response improvement in aphasia. Aphasiology, 13, 787–792. Lasker, J., & Beukelman, D. R. (1999). Peers’ perceptions of storytelling by an adult with aphasia. Aphasiology, 13, 857–869. Lasker, J. P., LaPointe, L. L., & Kodras, J. E. (2005). Helping a professor with aphasia resume teaching through multimodal approaches. Aphasiology, 19, 399–410. Lomas, J., Pickard, L., Bester, S., Elbard, H., Finlayson, A., & Zoghaib, C. (1989). The communicative eﬀectiveness index: Development and psychometric evaluation of a functional communication measure for adult aphasia. Journal of Speech and Hearing Disorders, 54, 113–124. LPAA Project Group (2000). Life participation approach to aphasia: A statement of values for the future. The ASHA Leader, 5, 4–6. Lubinski, R. (2001). Environmental systems approach to adult aphasia. In R. Chapey (Ed.), Language intervention strategies in adult aphasia (4th ed., pp. 269–296). Baltimore, MD: Williams & Wilkins. Lustig, A. P., & Tompkins, C. A. (2002). A written communication strategy for a speaker with aphasia and apraxia of speech: Treatment outcomes and social validity. Aphasiology, 16, 507–521. Lyon, J. G., Cariski, D., Keisler, L., Rosenbek, J., Levine, R., Kumpula, J., et al. (1997). Communication partners: Enhancing participation in life and communication for adults in natural settings. Aphasiology, 11, 693–708. Lyon, J. G., & Shadden, B. B. (2001). Treating life consequences of aphasia’s chronicity. In R. Chapey (Ed.), Language intervention strategies in adult aphasia (4th ed., pp. 297–315). Baltimore, MD: Williams & Wilkins. Montgomery-West, P. (1995). A spouse’s perspective on life with aphasia. Topics in Stroke Rehabilitation, 2 (3), 1–4. Parr, S., Byng, S., Gilpin, S., & Ireland, C. (1997). Talking about aphasia: Living with loss of language after stroke. Buckingham, UK: Open University Press. Pound, C., Parr, S, & Duchan, J. (2001). Using partners’ autobiographical reports to develop, deliver, and evaluate services in aphasia. Aphasiology, 15, 477–493. Reimers, T. M., Wacker, D. P., Cooper, L. J., & DeRaad, A. O. (1992). Clinical

Social validation of recovery in aphasia

91

evaluation of the variables associated with treatment acceptability and their relation to compliance. Behavioral Disorders, 18 (1), 67–76. Rogers, M. A., Alarcon, N. B., & Olswang, L. B. (1999). Aphasia management considered in the context of the World Health Organization model of disablements. Physical Medicine and Rehabilitation Clinics of North America, 10 (4), 907–923. Ross, K. B., & Wertz, R. T. (1999). Comparison of impairment and disability measures for assessing severity of, and improvement in, aphasia. Aphasiology, 13, 113–124. Ross, K. B., & Wertz, R. T. (2003). Quality of life with and without aphasia. Aphasiology, 17, 355–364. Salter, K., Jutai, J. W., Teasell, R., Foley, N. C., Bitensky, J., & Bayley, M. (2005). Issues for selection of outcome measures in stroke rehabilitation: ICF participation. Disability and Rehabilitation, 27 (9), 507–528. Schlosser, R. W. (1999). Social validation of interventions in augmentative and alternative communication. AAC Augmentative and Alternative Communication, 15, 234–247. Schwartz, I. S., & Baer, D. M. (1991). Social validity assessments: Is current practice state of the art? Journal of Applied Behavior Analysis, 24, 189–204. Shadden, B. (2005). Aphasia as identity theft: Theory and practice. Aphasiology, 19, 211–223. Simmons-Mackie, N. (2001). Social approaches to aphasia intervention. In R. Chapey (Ed.), Language intervention strategies in adult aphasia (4th ed., pp. 246–268). Baltimore, MD: Williams & Wilkins. Simmons-Mackie, N., & Damico, J. S. (2001). Intervention outcomes: A clinical application of qualitative methods. Topics in Language Disorders, 21 (4), 21–36. Threats, T. T. (2002). Evidence-based practice research using a WHO framework. Journal of Medical Speech-Language Pathology, 10 (3), xvii–xxiv. Threats, T. T., & Worrall, L. (2004). Classifying communication disability using the ICF. Advances in Speech-Language Pathology, 6 (1), 53–62. Tompkins, C. A. (1994). Applying research principles to language intervention. In R. Chapey (Ed.), Language intervention strategies in adult aphasia (3rd ed., pp. 571–583). Baltimore, MD: Williams & Wilkins. Wells, A. (1999). Family support systems: Their role in aphasia. Aphasiology, 13, 911–914. Wolf, M. M. (1978). Social validity: The case for subjective measurement or how applied behavior analysis is ﬁnding its heart. Journal of Applied Behavior Analysis, 11, 203–214. World Health Organization (1996). WHOQOL-BREF introduction, administration, scoring, and generic version of the assessment. Geneva: Author. World Health Organization (2001). Press release, November. Retrieved February 2, 2006 from www.who.int/inf-pr-2001/en/pr2001–48.html Worrall, L. E., & Holland, A. L. (2003). Editorial: Quality of life in aphasia. Aphasiology, 17, 329–332.

6

Interactional aphasia Principles and practices oriented to social intervention Jack S. Damico, Martin J. Ball, Nina N. Simmons-Mackie and Nicole Müller

One of the real accomplishments during Chris Code’s tenure as Editor in Chief of Aphasiology: An International and Interdisciplinary Journal has been his consistent advocacy of psychosocial issues and social models of aphasia treatment. This chapter is intended to advance his eﬀorts and those of numerous other social scientists in clinical aphasiology by advocating a more direct focus on interactional aphasiology as a sub-discipline of clinical aphasiology. In the nineteenth century there was a ﬂourishing of research and clinical experience that gave way to the ﬁrst major focus on the human brain and its disabilities (Eling, 1994). Led by physicians and researchers who are now the recognized founders of medical and clinical aphasiology (e.g., Gall, Broca, Wernicke, Freud, Jackson), there occurred a great accumulation of knowledge regarding the brain and the consequences of brain damage. It took some time, however, before these data were placed within acceptable frameworks for various medical and clinical applications. John Hughlings Jackson, one of the founders of modern neurology, once discussed this problem of data overload. He suggested that although we have multitudes of facts, we require, as they accumulate, organizations of them into higher knowledge. He felt that we needed some better generalizations and working hypotheses (1882). Over the 125 years since this assertion, we can recognize both the problem that Jackson stated and several solutions that were eventually employed. With the formulation of neuropsychological approaches of brain functioning and damage pioneered by Lashley (1929) and Luria (1947), the focus on medical aphasiology led by Geschwind (1965), and the development of clinical aphasiology according to Schuell (1953), Darley (1975), and Porch (1967), the accumulated data over the last hundred years have been (somewhat) successfully applied to clinical populations. Despite these successes, however, there are problems with the ways in which the accumulating data are organized and employed within clinical populations. To an even greater extent than occurred in the nineteenth century, we are accumulating data and research ﬁndings that require additional generalizations and working hypotheses that are somewhat diﬀerent from those that have preceded us. As suggested by Jackson, we have to organize our data into

Interactional aphasia

93

higher levels of knowledge to create eﬀective working hypotheses of how these data ﬁt within the framework of individuals who are trying to negotiate the impact of aphasia. This chapter proposes one way to better organize some of the data that currently confront us, an orientation that will assist our understanding and focus on language, interaction, and aphasia. In this chapter, we propose that we move toward a more formal, explicit, and high proﬁle focus within our discipline of clinical aphasiology. A focus on authentic interactions in aphasia utilizing the research methodologies appropriate to these phenomena and the applications and practices drawn directly from theories and investigations directed to face-to-face interactions. We propose the creation of a sub-discipline of Interactional Aphasiology. Given the recent advances in clinical aphasiology toward a greater acceptance of qualitative research methods (e.g., Damico, Simmons-Mackie, Oelschlaeger, Elman, & Armstrong, 1999; Goodwin, 1995; Klippi, 1991; Wilkinson, 1999), and a growing focus on the functional and social considerations of aphasia (e.g., Ferguson, 1996; Holland, 1991; LeDorze & Brassard, 1995; Penn, 1987; Worrall, 1992), this proposal may not seem unusual or bold. Indeed, there have been a number of eﬀorts over the past few years toward a focus on aphasia as a clinical and practical impairment that results in extensive interactional consequences. Despite these recent advances within the history of aphasiology, attention to authentic interactional data and how they impact on social consequences has only minimally been advanced. It certainly has not been a major focus within the organized eﬀorts oriented toward clinical aphasiology. For example, in the loosely structured organization that holds the Clinical Aphasiology Conference every year, the vast majority of research papers presented have not focused on authentic interactional data or social consequences. Further, a reading of the current trends within the United States and within Europe shows they are far more oriented toward linguistic and processing approaches to intervention and to modular cognitive models, both to explain aphasia and to provide interventions. Those researchers who focus on authentic interaction in aphasia are certainly in the minority in the professions oriented to clinical aphasiology. This lack of orientation to interactional issues is surprising when the pervasiveness of the social and interactional consequences of aphasia is considered. One reason for this neglect appears to be that the issues of interaction in aphasia and of the social impact of aphasia are complex and involve numerous variables and considerations. When viewing this complexity, it is not surprising that the discipline of aphasiology with its medical and experimental orientations has not focused extensively on these issues. There are many areas of signiﬁcance still to be investigated within the realm of aphasia. Aphasia, however, is a large ﬁeld, capable of entertaining diverse orientations. The time is right for an explicit orientation embracing the complexity of authentic interaction and social action rather than ignoring it.

94

Damico et al.

To continue developing this line of research and its clinical implications, and more importantly, to get clinicians and researchers, professors and students to employ the work based on strong research and the principles and practices that result from this research, it is necessary to extend the awareness that the long-term consequences of aphasia are generally linked to the interactional realm. For, as Garﬁnkel (1967) and Goﬀman (1974) have stated, the genesis of society and social action is in the face-to-face interactions between individuals.

An operational framework To create the needed orientation, an operational framework is required. There are several reasons for such a framework. First, it will enable the development of an eﬀective set of principles or guidelines to direct future work and application within this proposed sub-discipline. To establish a disciplinary study, one must have a set of principles or constraints within which to operate. Second, once the framework is proposed and the principles developed, researchers oriented to this area can become more improvisational in their approaches to research and clinical application, and still be directed by the framework. This should enhance the creativity and originality of the research and clinical initiatives. Finally, an operational framework that represents an enhanced orientation will serve as an impetus to professionals interested in this area, so that they can adjust to the needs and opportunities of interactional aphasiology. Frankly, to incorporate people into a movement, you need a direction, people to advance and implement the movement, and, in eﬀect, a ﬂag or banner that others outside the vanguard will follow. The sub-disciplinary structure and its operational framework will supply such a “banner.” A sub-discipline of interactional aphasiology should consist of a set of principles and practices not just oriented to the social components or consequences of aphasia per se, but primarily to the interactional aspects that involve a focus on authentic face-to-face activities and the abilities and variables of interest within such authentic activities. The need to focus on face-to-face interaction can be accomplished in many ways; directly via methodologies like conversation analysis and other products of ethnomethodology, and indirectly as when we investigate the motivations, impact, and aﬀective issues involved with authentic interaction and when we set about creating applications generated by the data collected. Further, this framework – even as a working endeavor – should be advanced in ways that will enhance the objectives, data, implications, and applications of research regarding authentic interaction to other aphasiologists and to those interested in clinical aphasia. To formulate this framework, we can draw from a large knowledge base. Other realms of social science have targeted interaction as social action in all its authenticity and complexity, and have focused on how social action is eﬀectively established, negotiated, and

Interactional aphasia

95

sustained. Consequently, we can adopt some of this cross-disciplinary work into a study of social action that can enrich our appreciation of interaction in aphasia. This chapter discusses some of the social science research that may be outside the clinician’s typical experience, but is relevant to the establishment of interactional aphasiology. As a starting point, the following ten principles are suggested as the guiding values for the sub-discipline of interactional aphasiology.

Principles for interactional aphasiology Given the complexity of authentic interaction in all its various manifestations, it is important to have a set of principles available when engaging in data collection, analysis, and interpretation. These principles can guide how data are treated and what importance the data or patterns of data might hold. Further, a set of principles can inform the framework from which we operate to construct values, strategies, and techniques that can assist in increasing our knowledge and the applications of this knowledge in interactional aphasiology. Based on our research and a survey of the literature, there appear to be a number of interactional principles of social action that should be considered. Here is a list of those considered most important at present: Principle one: Authentic face-to-face interaction For the initial purposes of a framework in interactional aphasiology, there must be a clearly distinguished focus for our research and clinical endeavors. This focus should consist of a continual orientation of activity toward authentic face-to-face interaction in its various forms. That is, within this sub-discipline, the topic and context of interest should revolve around face-to-face interaction in terms of how it is systematically accomplished, what variables impact on face-to-face interaction, and the implications of neurological damage to this social dyad. In their classic sociology text, The Social Construction of Reality, Berger and Luckmann wrote, “The most important experience of others takes place in the face-to-face situation, which is the prototypical case of social interaction. All other cases are derivatives of it” (1967, p. 28). This principle suggests that people construct the meanings of objects and situations through their interactions with one another. That is, through their face-to-face interactions, individuals socially construct their behaviors, expectations, and beliefs (Gergen & Davis, 1985; Goﬀman, 1974; Rogers, 1980; Scheﬀ, 1990). This belief and its applications provide an eﬀective guide to determining what should be investigated, and what should become the object of descriptive assessment and compensatory intervention. The focus on face-to-face interaction is the basis for interactional sociology and it can serve us as a ﬁrst principle as well in interactional aphasiology.

96

Damico et al.

Principle two: The constructive nature of interaction Within the social sciences there is a pervasive idea that both orients our attention to the social world and, consequently, must serve as the actual rationale for our endeavors within the sub-discipline of interactional aphasiology. This is the principle of social constructivism. It suggests that the major work and accomplishment of face-to-face interaction is the construction of the meanings of objects and situations based on our interactions with one another. That is, through face-to-face interactions, individuals socially construct their behaviors, expectations, and beliefs. Based on this principle, many of the human behavioral traits and psychological processes like self-identity, competence, and the capacity and reactions to intimacy are viewed less as stable internal constructs and more as the products of external interactions with others (Berger & Luckmann, 1967; Kemper, 1991; Shotter, 1984). The signiﬁcance of this principle for interactional aphasiology lies in the fact that it provides one with a theoretical framework relating to the creation and preservation of both social and psychological behaviors. Rather than assuming that a particular trait or a speciﬁc behavior is due solely to a psychological construct or neurological module outside the social realm, this principle places the genesis of any trait, belief, or behavior squarely within the social sphere. Who we are and how we react is partially and importantly based on our previous and concurrent social interactions. In eﬀect, this principle provides us with the rationale for why we should study face-to-face interaction. There is a social component to all human behaviors and traits, and to understand this phenomenon in aphasic patients, to understand how this phenomenon is modiﬁed and re-constructed, we must study where the social construction occurs – within face-to-face interaction.

Principle three: Local negotiation of social action Consistent with the ﬁrst two principles, a third interactional principle also places the emphasis on the actual activities that occur during face-to-face interaction. This principle is based on the widely documented ﬁnding within ethnomethodology that successful social action is accomplished at the local level (Duranti & Goodwin, 1992; Garﬁnkel, 1967; Heritage, 1984). This means that any social phenomenon as it unfolds is locally and immediately constituted through the observable activities of the participants. This principle is consistent with the expectation that an individual’s “common-sense” knowledge during interaction is employed on an instance-by-instance basis to construct social action. In this sense, what participants in a social interaction will do in their next interactive turn is related to what their partners have done in the immediate prior turn. This reliance on the immediate and local actions and context such that one action helps determine the next creates a conditional relevance, so that a ﬁrst action helps determine what may occur as a second action, and the second

Interactional aphasia

97

actually depends on what occurred as the ﬁrst action (Goodwin & Heritage, 1990; Wilkinson, 1999). In any social action the importance of this local negotiation can be generally stated as a condition where actions project next actions. Said another way, the presence and impact of participants in an interaction impinge on each other as the face-to-face situation continues. In eﬀect, authentic interaction is constructed through a continuous reciprocity of expressive acts. Consequently, when researchers and clinicians orient to face-to-face interaction, they can focus on the actual behaviors and possible interpretations as revealed in the actual data before them. This provides a mechanism for understanding social action without having to delve too far outside the actual interactional dyad. For our part in interactional aphasiology, we should orient the aspects of the local management of interaction to discover how and when this occurs. Principle four: The complexity of face-to-face interaction The fourth guiding principle provides us with a realistic set of assumptions regarding our task of trying to study, account for, and understand the impact of aphasia on face-to-face interaction. We should expect, recognize, and embrace the complexity of the authentic interaction as a human phenomenon. In authentic contexts, the reactions and interactions, the personalities and beliefs, the objective behaviors and subjective interpretations are emphatically close and local. During face-to-face activities, the skills, traits, and behaviors of each participant are continually interacting, and we must attempt to describe and account for them as best we can. Indeed, that is the objective of a research agenda focusing on interaction in aphasia. Without attention to the complexity, our eﬀorts, our implications and our applications will fall short of the needs of our patients and clients. Damico et al. (1999) have discussed this issue, and the fact that one of the problems with much of the current experimental research in clinical aphasiology is that it doesn’t account for the complexity of the neurological and social phenomenon known as aphasia. The experimental research in the ﬁeld is eﬀective – as far as it goes – but it is simply not suﬃcient to account for authentic social interaction. In the sub-discipline of clinical aphasiology, the complexity must be recognized and various ways to account for the impact of aphasia in all its complexity must be a priority when designing and carrying out any research agenda. Principle ﬁve: The multiplicity of manifestations Keeping with the complexity theme, the ﬁfth principle strives to emphasize and then guide the investigation of all the potential manifestations of semiotic, cognitive, social, and psychological activity that make up the tapestry of face-to-face communication. Within authentic interaction, we should expect that there are a number of potential manifestations needed to create the

98

Damico et al.

social action. That is, there might be linguistic resources, various types of cognitive skills and traits, social strategies and knowledge resources, verbal and non-verbal behaviors, neurological traits, and other potential semiotic systems that might be employed to create the emergent phenomena that we know as social action within face-to-face interaction. As an individual attempts to negotiate within face-to-face interaction, he or she employs a number of these manifestations to accomplish the desired objectives and the resultant interactional behavior – one that creates comprehensibility, predictability, and successful expectations – is most likely to be the emergent property of interactions between some of this multiplicity of manifestations (Perkins, 1998, 2001, 2002). To use a metaphor employed by Janet Emig (1983), the individual uses these manifestations to “weave a web of meaning.” For our purposes, then, we must be prepared to engage in an objective and detailed analysis of our data to determine what variables or manifestations produce the observed social actions (e.g., Simmons-Mackie & Damico, 1997). Principle six: Orient to the functional goal In order to best address the complexity and to keep a handle on the plentitude of symptoms and manifestations in face-to-face interaction, it is best to maintain that the catalyst for interaction is to accomplish social action. We should orient our ﬁrst question to “how was an interaction (or an aspect of it) accomplished?” If we adopt this functional and strategic approach, then we can better handle the complexity of the phenomenon and its potential emergence via the resources available to the interactants in the dyad or social group. This focus on the functional aspects of face-to-face interaction is consistent with a emerging emphasis in clinical aphasiology over the past 15 years. Work by clinical researchers like Holland (1991, 1998; Holland & Thompson, 1998), Lyon (1996) and Elman (Elman & Bernstein-Ellis, 1995) have advocated a more functional approach to the description, assessment, and intervention in aphasia and these initiatives have greatly inﬂuenced the ﬁeld. Within the sub-discipline of interactional aphasiology, a practical and functional orientation to face-to-face interaction and how it impacts on eﬀectiveness should serve as the medium within which the data are interpreted. Principle seven: Social action as collaborative Another interactional principle necessary in interactional aphasiology is a reasonable consequence of most of the principles discussed thus far – social action is always a collaborative enterprise. In eﬀect, face-to-face social action is always collaborative and so we should always remember to incorporate this characteristic. Indeed, it should be our watchword. If social construction is accomplished at the local level, then all social actions are active and dynamic

Interactional aphasia

99

enterprises wherein (at least) two participants are involved in a process of coconstruction. Social actions of all sorts (e.g., conversation, arguments, ﬁghts, nonverbal posturing) are not a series of discrete behaviors or messages that pass from an active individual to a passive one. Rather, all face-to-face interaction is a process of participants actively constructing and negotiating meaning in a coordinated and joint manner as the social action proceeds. In practice, we can focus on the aphasic or the non-aphasic interactant, the dyad or the group, but eventually any analysis or its interpretation should orient to the collaborative impact needed to construct an interaction (Goodwin & Heritage, 1990; Oelschlaeger & Damico, 1998; Perkins, 1995). Principle eight: The dynamic character of interaction Building on the previous point, the construction of our relations with others – especially due to the local management of the interaction – is highly ﬂexible. Whatever patterns and strategies are introduced during an interaction, they will always be dependent on the interactions and reactions of the other participant. Consequently, the behaviors and goals, interactions and reactions will be continually modiﬁed through the exceedingly variegated and subtle interchange that goes on when accomplishing social action. We must always be aware of this fact. It is possible that this characteristic will eventually limit the wholesale applications of some of our research. But it is equally possible that we may ﬁnd that, although individual manifestations change across contexts, individuals, and over time, general and underlying principles will be discerned. For the moment, however, the dynamic character of face-to-face interaction should serve as the caveat of the sub-discipline. Principle nine: Contextual impact Although some social researchers have tried to focus exclusively on conversation as the prime face-to-face interaction, there are other equally valid and authentic social dyads and groupings that may also require investigation depending on various contextual issues. Harvey Sacks (1992) and others (e.g., Goodwin & Heritage, 1990; Scheﬀ, 1990; Schegloﬀ, 1968), focusing on conversation, acknowledged this in their writings and their research foci. To determine which social dyads should be the focus of attention, one must recognize the contextual relevance of social action. Not only do the various manifestations of social action change depending on the local context, but, as with all aspects of human semiotic systems, context determines the prime social dyads and groups from one interactional opportunity to another. Therefore, we should employ an awareness of contextual relevance when determining what kind of face-to-face interaction should be the focus of our attention in various settings.

100

Damico et al.

Principle ten: Adopting methods suitable to the phenomena we study The last principle I want to discuss as necessary for the sub-discipline of interactional aphasiology involves the tools and methods that we should use to investigate authentic face-to-face interaction. That is, what kinds of research methodologies are adequate for conducting research on complex and authentic social action like this? For a host of reasons, the answer is that we should adopt qualitative research methodologies. Over the last few decades, there has been a trend in the philosophy of science to recognize that research and systematic investigation becomes scientiﬁc by adopting the methods of study appropriate to its subject matter. This stance is called “scientiﬁc realism” and is currently a dominant philosophical position rather than the formerly dominant neo-positivistic approach (Okasha, 2002; Papineau, 1996). Among other things, scientiﬁc realism suggests that science is deﬁned by the results and ﬁndings not the methodology. Within this focus, qualitative research – by deﬁnition – appears to be the most appropriate research paradigm for interactional aphasiology. Basically, qualitative research refers to a variety of analytic procedures designed to systematically collect and describe authentic, contextualized social phenomena with the goal of interpretive adequacy (Damico et al., 1999). The idea of interpretive adequacy – what Graham Button has described as explication of social action – should be the goal of interactional aphasia, and so qualitative research methodologies are best employed within this subdiscipline. Of course, this qualitative research paradigm involves a number of traditions of inquiry. While we may be most familiar and even prefer – within this context – to employ the most analytic of the qualitative methodologies – conversation analysis, it is not the only tradition of inquiry we should employ. In fact, to completely investigate and understand authentic interactional data, its variables, complexity, and implications, conversation analysis is not suﬃcient by itself. Other qualitative traditions of inquiry are more appropriate in some instances. Other traditions of inquiry include biographical study, case study research, ethnography and ethnographic methodologies, grounded theory, historical methodology, and other types of naturalistic data collection strategies like participant observation, ethnographic interviewing, discourse analysis, artifactual analysis, focus groups, and lamination research and phenomenology (Damico & Simmons-Mackie, 2003; Damico el al., 1999). Within a sub-discipline of interactional aphasiology, this paradigm and these traditions of inquiry and the various naturalistic data collection strategies can assist us in achieving the other nine principles within the previously described operational framework.

Conclusion These ten principles should help orient us to an understanding of how social action is achieved in face-to-face interaction, and how it impacts on the social

Interactional aphasia

101

accomplishments and consequences of individuals with aphasia. Of course, we still have to develop the implications and applications that might arise from the sub-discipline of interactional aphasiology. For example, we must ask: “How do we get others to understand and focus on the interactional complexity of face-to-face interaction?” and “How can the practices resulting from this research be applied in clinical settings?” It is certainly possible that the principles proposed in this chapter are preliminary and naïve. In the ﬁnal analysis, however, whether we adopt an approach consisting of these or other principles, whether we strive to create a sub-discipline or not, there is a need to embrace the complexity of aphasia and its implications within a social action framework. For, when addressing the issues and concepts in clinical aphasia, regardless of what we theorize and discuss about language and processing, grammar and modular cognitive systems, the real signiﬁcance of all of these areas means nothing unless we see these abstract conceptions played out in the arena of authentic face-to-face interaction. After all, that is where the human creature exists.

References Berger, P. L., & Luckmann, T. (1967). The social construction of reality. A treatise in the sociology of knowledge. New York: Anchor Books. Damico, J. S., & Simmons-Mackie, N. N. (2003). Qualitative research and speechlanguage pathology: Impact and promise in the clinical realm. American Journal of Speech Language Pathology, 12, 131–143. Damico, J. S., Simmons-Mackie, N., Oelschlaeger, M., Elman, R., & Armstrong, E. (1999). Qualitative methods in aphasia research Aphasiology, 13, 651–665. Darley, F. L. (1975). Aphasia. Philadelphia: Saunders. Duranti, A., & Goodwin C. (1992). Rethinking context: Language as an interactive phenomenon. Cambridge, UK: Cambridge University Press. Eling, P. (Ed.) (1994). Reader in the history of aphasia. From Franz Gall to Norman Geschwind. Amsterdam: John Benjamins. Elman, R., & Bernstein-Ellis, E. (1995). What is functional? American Journal of Speech-Language Pathology, 4, 115–117. Emig, J. (1983). The web of meaning: Essays on writing, teaching, learning, and thinking. Portsmouth, NH: Heinemann. Ferguson, A. (1996). Describing competence in aphasic/normal conversation. Clinical Linguistics and Phonetics, 10, 55–63. Garﬁnkel, H. (1967). Studies in ethnomethodology. Englewood Cliﬀs, NJ: Prentice Hall. Gergen, K. J., & Davis, K. E. (Eds.) (1985). The social construction of the person. New York: Springer Geschwind, N. (1965). Disconnection syndromes in animals and man. Brain, 88, 585–644. Goﬀman, E. (1974). Interaction ritual: Essays in face to face behavior. Garden City, NY: Doubleday. Goodwin, C. (1995). Co-constructing meaning in conversations with an aphasic man.

102

Damico et al.

In S. Jacoby & E. Ochs (Eds.), Research in language and social interaction (Special issue of Construction), 28, 233–260. Goodwin, C., & Heritage, J. (1990). Conversational analysis. Annual Review of Anthropology, 19, 283–307. Heritage, J. (1984). Garﬁnkel and ethnomethodology. Cambridge, UK: Polity Press. Holland, A. L. (1991). Pragmatic aspects of intervention in aphasia. Journal of Neurolinguistics, 6, 197–211. Holland, A. L. (1998). Why can’t clinicians talk to aphasic adults? Comments on supported conversation for adults with aphasia: Methods and resources for training partners. Aphasiology, 12, 844–847. Holland, A., & Thompson, C. (1998). Outcomes measurement in aphasia. In C. Frattali (Ed.), Measuring outcomes in speech-language pathology (pp. 245–266). New York: Thieme. Jackson, J. H. (1882). On some implications of dissolution of the nervous system. In Selected Writings (Vol. 2, pp. 29–44). New York: Basic Books (reprinted 1958). Kemper, T. D. (Ed.) (1991). Research agendas in the sociology of emotions. New York: State of New York University Press. Klippi, A. (1991). Conversational dynamics between aphasics. Aphasiology, 5, 373–378. Lashley, K. S. (1929). Brain mechanisms and intelligence. Chicago: University of Chicago Press. LeDorze, G., & Brassard, C. (1995). A description of the consequences of aphasia on aphasic persons and their relatives and friends, based on the WHO model of chronic diseases. Aphasiology, 9, 239–255. Luria, A. R. (1947). Traumatic aphasia. The Hague: Mouton. Lyon, J. G. (1996). Optimizing communication and participation in life for aphasic adults and their prime caregivers in natural settings: A use model for treatment. In G. Wallace (Ed.), Adult aphasia rehabilitation (pp. 137–160). Boston, MA: Butterworth-Heinemann. Oelschlaeger, M. L., & Damico, J. S. (1998). Joint productions as a conversational strategy in aphasia. Clinical Linguistics and Phonetics, 12, 460–480. Okasha, S. (2002). Philosophy of science. A very short introduction. Oxford, UK: Oxford University Press. Papineau, D. (Ed.) (1996). The philosophy of science. Oxford, UK: Oxford University Press. Penn, C. (1987). Compensation and language recovery in the chronic aphasic patient. Aphasiology, 1, 235–245. Perkins, L. (1995). Applying conversational analysis to aphasia: Clinical implications and analytic issues. European Journal of Disorders of Communication, 30, 372–383. Perkins, M. R. (1998). Is pragmatics epiphenomenal? Evidence from communication disorders. Journal of Pragmatics, 29, 291–311. Perkins, M. R. (2001). Compensatory strategies in SLI. Clinical Linguistics and Phonetics, 15, 67–71. Perkins, M. R. (2002). An emergentist approach to pragmatic impairment. In F. Windsor, M. L. Kelly, & N. Hewlett (Eds.), Investigations in clinical linguistics and phonetics (pp. 1–14). Mahwah, NJ: Lawrence Erlbaum Associates, Inc. Porch, B. E. (1967). The Porch index of communicative ability. Palo Alto, CA: Consulting Psychologists Press. Rogers, M. F. (1980). Goﬀman on power, hierarchy and status. In J. Ditton (Ed.), The view from Goﬀman (pp. 100–133). New York: St. Martin’s Press.

Interactional aphasia

103

Sacks, H. (1992). Lectures on conversation. Volume I. Oxford, UK: Blackwell. Scheﬀ, T. J. (1990). Microsociology: Discourse, emotion and social structure. Chicago: University of Chicago Press. Schegloﬀ, E. (1968). Sequencings in conversational openings. American Anthropologist, 70, 1075–1095. Schuell, H. M. (1953). Aphasic diﬃculties understanding spoken language. Neurology, 3, 176–184. Shotter, J. (1984). Conversational realities: Constructing life through language. Newbury Park, CA: Sage. Simmons-Mackie, N. N., & Damico, J. S. (1997). Reformulating the deﬁnition of compensatory strategies in aphasia. Aphasiology, 11, 761–781. Wilkinson, R. (1999). Introduction. Aphasiology, 4–5, 251–258. Worrall, L. (1992). Functional communication assessment: An Australian perspective. Aphasiology, 6, 105–111.

Part II

Research considerations

7

From the study of language dysfunction and handicap to a better understanding of linguistic processing in normality Jean-Luc Nespoulous and Jacques Virbel

Introduction There are certainly several ways of paying tribute to a scholar and a friend such as Chris Code. Rather than referring explicitly to speciﬁc contributions he has made to aphasiology, we have chosen to oﬀer him a chapter dealing with a somewhat new deﬁnition of the notion of “handicap” which, we thought, he might like, knowing how attached he has been throughout his career to a clinical approach such as the one we adopt here. Doing so, we hope Chris will react to our proposals, thus pursuing an interaction which began during a sabbatical year he partly spent in our laboratory, in Toulouse, a decade ago.

Deﬁcits, normality, cognitive ﬂexibility and adaptive and/or palliative strategies Probably for etymological reasons, the ﬁrst deﬁnition given by dictionaries of the word handicap is related to horse-races and the equalization of the chances of success between riders by the imposition on the best horses of heavier weights to carry or of longer distances to run. According to this earliest deﬁnition, the word handicap has a proper “positive” sense since it refers to a horse, and more generally, to a sportsman or a player whose superiority is recognized and whose advantage is being attenuated in order to produce a more equitable competition with those less powerful than him. According to these same dictionaries, it is only in second place that, in a ﬁgurative sense, the word handicap has come to indicate all “deﬁciency, physical or mental”, likely to aﬀect somebody in any activity whatsoever. With regard to the word handicapped – adjective, past participle, turned substantive – these same dictionaries frequently reverse the order of the meanings, so giving priority to the latter, with its “negative” semantic attributes. In the ﬁeld of language, as in a good many other ﬁelds which will not be the subject of this article, the handicap – in the last acceptation of the

108

Nespoulous and Virbel

term – usually evokes a certain type of deﬁcit or dysfunction, lasting or momentary, compared to a state known as stable, or “normal”. The origin of such a dysfunction, as indicated above, is classically regarded as resulting from intrinsic physical and/or mental deﬁciencies (see above) but no one has yet extended the scope to the social sphere, thus agreeing to take into account various extrinsic or environmental parameters in the characterization of the handicap and those who suﬀer from it (Bernstein, 1975; Besse, de Gaulmyn, Ginet, & Lahire, 1992; Nespoulous, 1978). It is within this latter framework, non-restrictive and open, that we shall be positioning this article, convinced that at one time or another, to a greater or lesser extent, temporarily or permanently, all human beings – speaker and/or interlocutor – might ﬁnd themselves in a situation of linguistic (or other) handicap. In this context, the observation and the ﬁne characterization of such a dysfunction is not only able to provide invaluable information about the nature of the disturbances highlighted, but also to make it possible to better apprehend, through after-eﬀect, (a) the full details of the functioning of language in a subject considered “normal” as well as (b) the strategies – “spontaneous” or induced, “natural” or technologically relayed – brought about to (try to) “adapt” to the dysfunction and to compensate as well as possible for the deﬁciencies aﬀecting a speaking subject (Nespoulous, 1996). Our argumentation will be based primarily on data obtained from aphasic patients with whom one of us has been working for about 30 years, but we will frequently widen the range of our remarks to other populations (of handicapped persons) and to other (“handicapping”) situations so as to characterize the handicap in as general and as large a way as possible and to extract a maximum of information, particularly as regards cognitive ﬂexibility, of the observation of degradations of communication, whatever the origins might be: pathological or not, occasional or durable, and so on. Some “central” dysfunctions of language in aphasia and their palliative strategies The cerebral lesion that causes aphasia creates at the same time a deﬁcit and a communication handicap, making any verbal interaction diﬃcult. Generally, the components of the language as a whole are not aﬀected by the lesion and there are even cases where only one component proves to be dysfunctional. Comparisons of diﬀerent patients presenting diﬀerent selective deﬁcits and showing evidence of “double dissociations” allow for the identiﬁcation of various speciﬁc, and relatively autonomous, functional components, in the functional architecture of language in the human brain-mind, even with so-called “normal” subjects. It is on such bases, particularly over the past 40 years, that the traditional neuropsychological approach to language, also called cognitive neuropsycholinguistics, has developed (Nespoulous, 2004). Parallel to the generation of a deﬁcit and a communication handicap,

From language dysfunction and handicap to normal linguistic processing

109

the cerebral lesion in handicapped subjects develops, often unconsciously, various palliative strategies that, in the best cases, allow subjects to circumvent the deﬁcit and to overcome their handicap, at least partially. It is this tendency that makes Audrey Holland (1977, p. 173) state: “aphasics communicate better than they speak”. However, from the start, aphasiology has been much more concerned with the characterization of the underlying deﬁcit (see above) than with the strategic and adaptive potential of the patient confronted with this deﬁcit. It is certainly not a question of radically opposing the two approaches, insofar as they seem to be complementary: the ﬁrst makes it possible to identify (a) the direct “negative” manifestations of the deﬁcit (“linguistic symptoms”), as well as (b) the “positive” manifestations relating to the aspects of the linguistic function that have remained intact; and the second makes it possible to apprehend (c) the palliative strategies built up by the patient in spite of this deﬁcit and thus his or her cognitive ﬂexibility in the processing of linguistic information (Nespoulous, 1994). If one agrees to adopt such a double, or even triple, approach, with regard to aphasiology, one is ineluctably led to reject all characterization of verbal behaviour in (binary) terms of respect or violation by an individual of the canonical properties of his or her language, in favour of an adaptive vision of this behaviour. Speaking and understanding – just like acting and perceiving – become adapting to (or attempting to adapt to) the constraints of the situation in which one ﬁnds oneself, albeit more or less successfully, depending on whether one is aphasic or a so-called normal speaker (see the diagram below).

We will now give some examples to help illustrate our argument. Temporal adverbs to the rescue of deﬁcient verbal inﬂections There are certain people with aphasia – called agrammatic – who are characterized by major diﬃculties in the management of grammatical morphemes

110

Nespoulous and Virbel

and/or syntactic structuring of verbal messages. Among other symptoms, these patients present a reduction of inﬂexional morphology that leads them, in languages like French or English, to produce inﬁnitives, in the ﬁrst case, and gerunds (sleeping, walking . . .) in the second, instead of conjugated forms of the verbs. Such a reduction, likely to particularly disturb the temporal marking of utterances is, however, frequently compensated for by resorting to adverbs of time (yesterday, tomorrow . . .) or by employing phrases carrying temporal information (next week, last summer . . .). This type of strategy makes it possible for the patient to circumvent the deﬁcit mentioned above and the communication can then continue eﬀectively, at least on this point, all the more since there is more semantic precision in these lexical markers of time than in temporal inﬂections of the present, past or future (Nespoulous, 1973). Circumlocutions and gestures to the rescue of the missing word Inability to recall a word, or problems of access to the mental lexicon (or anomia) is a particularly frequent symptom of aphasia, whatever the clinical category may be. Although it is possible to observe a patient absolutely unable to ﬁnd and/or to produce an adequate word – in a naming task (from pictures) or in spontaneous language – it is extremely rare that this lexical deﬁciency results in total mutism and an absolute absence of speech production. Usually, indeed, the patient will resort – just like a normal subject who has a transitory lexical diﬃculty – either to periphrastic strategies (i.e., he or she tries to formulate a deﬁnition of the word he or she is not able to recall), or to mimo-gestural strategies (i.e., the patient tries to mime the use of the object referred to by the word he or she is not able to ﬁnd in his or her mental lexicon: Nespoulous, 1979). In so doing, these patients provide, moreover, the proof of the integrity of underlying semantic representations: they know what they want to say but cannot say it (see below). Phonemic paraphasias and “repair strategies” In nearly all the work relating to phonetic and/or phonemic disturbances in aphasia, as in preceding domains, clinicians and researchers have generally characterized the patients’ deﬁciencies negatively in terms of “performance errors”. More recently, however, and on the basis of new theoretical frameworks in phonology, the approach to such pathological phenomena has been greatly renewed (Béland, 1985; Moreau, 1993; Nespoulous, 1998; Nespoulous & Moreau, 1997; Paradis, 1988). Therefore, instead of resorting to a strictly descriptive taxonomy of the phonetic and/or phonemic “errors” (i.e., in terms of omissions, additions, substitutions and displacements of segments), it became possible (a) to predict the nature of the disturbances according to the canonical structure of the words the patient had to produce in a particular

From language dysfunction and handicap to normal linguistic processing

111

task, and (b) to apprehend them as the consequence of the use of “repair strategies” applied to a word of which the phonological structure was inaccessible to the patient, certainly because it was too complex. Thus, in the presence of a word like “brouette” (/bwεt/, which is “wheelbarrow”, in English), – certainly diﬃcult to produce for an aphasic person just as for a child in the learning period because of the presence of the consonantal cluster /b/ – clinicians and researchers often simply spoke about (a) errors of omission, when the subject said /bwεt/, or (b) errors of addition, when he said /bewεt/. Considering such phenomena, the “theory of constraints and repair strategies” (Paradis, 1988) aims at considering that, faced with a consonant cluster like /b/, the patient who has diﬃculty in producing such a group makes use of at least two universal strategies of “repair”, which he can apply to simplify the syllabic structure of a word like “brouette”: the syncope, which leads the patient to delete the liquid consonant //, and the epenthesis, which leads him to insert a vowel between the two consonants. Certain patients thus showed that they resorted preferentially to one or the other of these two strategies, while others sometimes used one and sometimes the other of these two strategies, even on the same words (Nespoulous, 1998). Towards a new distribution of roles in dialogue . . . Since Bally (1942), it has been agreed to regard any speech act as the combination of “referential” elements (Bally’s dictum) and of “modalizing” elements (the same linguist’s modus). Thanks to the former, speakers set up the elements of the information they wish to communicate; they encode a “proposition”, according to the logicians’ deﬁnition of this term (i.e., the explicit relation of a predicate and its arguments); and they refer to people, objects, ideas, and so on that are part of the socio-cultural context of the community to which they belong. Thanks to the latter, the same speakers this time formulate the position they wish to adopt in relation to the above referential content; giving their speech their own particular “signature”. They thus express a doubt or a certainty; make comments; accept or refuse the propositional content that they themselves have set up or that has been set up by their interlocutors. However, several studies in aphasiology have clearly shown that cerebral lesions aﬀect these two types of elements in unequal ways (Nespoulous, 1980, 1981; Nespoulous, Code, Virbel, & Lecours, 1998). So, while the wording of the referential elements of speech poses a major problem to aphasic patients, the great majority of them remain able to manage the modalizing elements. Thus an aphasic patient can say: “I cannot say it” (see above), but at the same time cannot say: “she cannot sing it”, to take two sentences that have, apart from anything else, the same lexical and syntactic characteristics (Nespoulous & Lecours, 1989). In “strategic” terms, it appears possible to exploit this kind of dissociation in order to consider recourse to a particular type of verbal interaction likely

112

Nespoulous and Virbel

to improve the transmission of information between the patient and those close to him or her, in particular in a dialogue situation. Thus if the therapist or a member of the patient’s family addresses – in the context of a question requesting an opinion – the essential part, or even the totality, of the necessary referential elements, the patient should, in most cases, be able to produce the adequate modalizing elements in his or her answer, thus guaranteeing the success of the verbal exchange. This procedure is certainly not ideal. It has its limitations; but it must allow, at least initially, the freeing up of many communication situations that would be doomed to failure without the use of such strategies. Adapting like this to the constraints of the situation – here pathological – is by no means original: what do we do when we address somebody who does not have a good understanding of our language? What do we do when we speak to a child who is not yet proﬁcient in the use of his or her mother tongue? What do we do if not to give a maximum of informative elements in our question so that our “non-expert” interlocutor can answer us, parsimoniously, but no less eﬀectively? In the four illustrations above, the range of the concept of strategy diﬀers, certainly. Thus, for example, the ﬁrst three types appear to emerge spontaneously from the patient, because they would seem to be part of the general semiotic potential anchored (without their knowledge) in any human being; the fourth requires, at least partially, an inter-individual adjustment, which certainly will not escape the protagonist’s awareness. In all these cases, however, the verbal behaviour does not appear (or no longer appears) as a stereotyped human response but rather as a highly adaptive and ﬂexible cognitive activity. We shall return to this later. Some “peripheral” dysfunctions of language and their palliative strategies In what precedes, we endeavoured to illustrate our introductory remarks by drawing our examples from a “central” pathology such as aphasia; a pathology that aﬀects some of the components at the heart of human linguistic activity (phonological, lexical, morpho-syntactic processing, and so on). There are, however, other linguistic dysfunctions that, although only aﬀecting the more “peripheral” components of the functional architecture of language, are still of interest for our purposes. These dysfunctions, sensory and/or motor, can be highlighted in certain aphasic patients, diﬀerent from those considered up to now, as a result of cerebral lesions, which, too, are diﬀerent. They can however also be observed among patients whose central nervous system is intact but who suﬀer from certain attacks that block the functioning of aﬀerent (e.g., vision, hearing) or eﬀerent (phonation, manual dexterity) systems. Contrary to the palliative strategies previously evoked in the context of “central” pathologies – strategies whose range, although real, remains limited

From language dysfunction and handicap to normal linguistic processing

113

– the “peripheral” dysfunctions sometimes lead the patients to develop whole systems of substitution: for example, the replacement of the audio-phonatory loop by a visuo-gestural system, sign language for the profoundly deaf; the replacement of visual information intake by tactile means, via Braille, for the blind (e.g., O’Regan & Noe, 2001). In such a context, resorting to external palliatives, produced by recent technological advances, proves to be crucial and not only because such palliatives are likely to facilitate the adaptation of certain patients to their deﬁcit but because they raise, in return, important questions (a) as to the “deterministic” hardwiring of the human nervous system, and/or (b) as to its adaptive ﬂexibility (Lenay & Pfaender, 2004).

Technological palliatives Data processing and linguistic handicaps The relationship between data processing and linguistic handicaps is circumscribed by that which relates, on the one hand, to the treatment of statements (in “natural” language), and on the other hand, by the consideration of users of computerized devices. To simplify, it is possible to determine two situations, or classes of cases, that in fact are very closely related, are even interlinked, in reality. The ﬁrst situation is that of the design and development of speciﬁc devices providing computerized assistance. The principle mainly at work here is that, as previously indicated, of semiological substitution: substitution of the modality of existence of information simultaneous with the sensory substitution of access to this new form of information. Thus text to speech synthesis systems and computerized Braille come to the assistance of the partially sighted or blind; conversely, vocal dictation that transforms (oral) speech into text compensates for the handicap of the hard of hearing or deaf; vocal commands or special keyboards compensate for diﬃculty in or impossibility of writing or typing resulting from certain motor handicaps of the upper limbs. The principal problems encountered in this class of application are partly ‘classic’, related to language: the objective of automation imposes a level of extent and detail of the linguistic data and of formalization of the models often over and above what the descriptions and the linguistic or psycholinguistics models propose, at all levels of language. For example (Maurel, Lemarié, Vigouroux, Virbel, Mojahid, & Nespoulous, 2004) on the one hand, the apparently very modest question of oral interpretation (or “translation”) of certain visual structures of the texts is much more complex than one might think (especially if one views writing as a non-pertinent “code” from a signiﬁcant point of view), and, on the other hand, not many data have been gathered yet on this phenomenon (Virbel, 1989). But in addition, such data, as extended as necessary, must also be pertinent on the cognitive level. The procedure then aims at developing interdisciplinary

114

Nespoulous and Virbel

research where the researchers of the disciplines concerned inter-react, and among them, as a recent new element, are researchers who are themselves handicapped. But it is the very notion of substitution that covers the greatest complexity, because in the end, it mobilizes that of identity or equivalence of contents. It can be noted that intra-modal substitution is already attested on diﬀerent levels in the case of translations, summaries, transliterations and lists of contents. In addition, objects like logigrammes, used for example in the ﬁeld of technical instructions, combine discursive and ﬁgurative aspects (in particular diagrammatic), and thus undoubtedly generate representations of diﬀerent natures: propositional and analogical. Thus the question of knowing whether two messages of identical or diﬀerent modality really are equivalent (questions which are the basis of the transpositions evoked here) constitutes a formidable problem of nature, both logical and cognitive, if one aims at least at introducing a form of guarantee of this equivalence reminiscent of a theorematic demonstration. This type of question is central in semantics, logic and philosophy of language, where major theoretical divergence exists, bringing into play the very design of language and of its relationships with the world and the mind. This is a crucial but rather speculative question, but which here leads to experimental possibilities relating to multimodal communication, not much studied until recently, but central in the context of the communication of handicapped people. “Information for all” and handicaps Another situation is that where, like anyone else, handicapped people need access to, and use of computerized devices: word processing, the Internet, databases, on-line services, computerized physical environments (domestic apparatus, cars, houses, etc.), be it for professional or private reasons (training, purchases, amusement, administrative procedures, reservations, etc.). Research in this area encounters questions of appreciably the same order, with an emphasis on the fundamental problem posed here, that of accessibility to information and to physical objects related to various cognitive or physiological deﬁcits. Some of the problems experienced by handicapped people in the access to these devices are caused by the modes of interface used (screens, keyboards, the mouse) and of interactivity (for example: doubleclick on highlighted zones), which are not convenient, or even simply not practicable for the blind or partially sighted, or for those who have insuﬃcient mobility in their hands. And, for example, on the ﬁrst point, many new techniques are being developed as access interfaces (special keyboards, scanning, voice recognition, piloting by ocular movements, monitoring of facial expressions, interpretation of biological electric signals, laser stimulation of the retina, voice synthesis, multidimensional sound, tactile stimulation, return of eﬀort, etc.). It may seem at ﬁrst that this is a speciﬁc case of what has already been

From language dysfunction and handicap to normal linguistic processing

115

discussed, in the following sense: data processing, contributing to aid the exercise of the faculty of variously handicapped language, also does so when this faculty is exercised in relation to and through computerized devices. But in fact it goes far beyond a simple speciﬁc case. Indeed, what deeply characterizes the situation evoked is that it aims at constituting a particular case called “information for all”, by which is meant all users, all uses and all types of information. This point is very important because it appears as of now that it is the source of deep conceptual and methodological reformulations. For computing, this is indeed a challenge without precedent, which is at the origin of the recent foundation of the (in French) STIC: Sciences et Technologies de l’Information et de la Communication (Science and Technology of Information and Communication) for the structuring of research. In this movement, the consideration of the characteristics of users no longer comes at the end, but at the beginning and is situated at the centre of the design of cooperative, interactive systems, provided with certain dialogical aptitudes. Concepts such as those just mentioned, and others like utilizability, accessibility, adaptivity and adaptability are given new simultaneously operational definitions, for the conceptions of applications, and based on knowledge formed with the disciplines of human and social sciences or of the life concerned (and concernable). The work of J. Carrol (Carrol, 2002) is very representative of such developing knowledge in connection with “utilizability”. Another example is the case of the notion of assistance, which is not unrelated to our subject. The conceptual, logical and philosophical growth of knowledge brought to the concept of handicap, by J. Perry (and colleagues), one of the founders of the “semantic of situations” can also be appreciated (Perry, Macken, & Israel, 2004). According to him, handicap should not be considered in a static way, solely in opposition to performances considered normal, but in relation to a complex function of capacities and aptitudes, targeted tasks, and circumstances, by which is meant environment (infrastructural, artefactual): disability, inability and handicap thus receive relative deﬁnitions that bring into play a “circumstantial” conception, making it possible to conceptualize the background of the normal–pathological opposition, and to relativize this kind of opposition. With regard to linguistic handicaps in particular, a very great number of situations necessitate the reconsideration of the notions of deﬁcit or variation compared to a supposed “normality” or an equally problematic “average”: the diminutions of performances due to ageing, fatigability, cognitive overload, professional crisis situations, incidents or accidents, ineptitudes relating to the learning capacities of the users, cannot merely be viewed as simple limits or suspensions of the success of conduct and performance, but must be studied in the light of more subtle theories of error and failure. Models of direct or mediated inter-human communication, like models of action and decision, must incorporate this kind of design of potential failure or error; all the more since, as we have already seen, the users in situations of

116

Nespoulous and Virbel

failure develop palliative activities that may succeed only partially, or even not at all, but that must in no way be confused with other forms of failure. Here the central factor, in a normal, pathological or handicapped situation, is adaptation (of which learning is a part).

Communication, information and handicap Faced with this new situation, the STIC has resorted to two types of procedure, which are ideally inter-articulated, the limits of one calling on the other. One, which could also be called, as it is in psychology, “domain speciﬁc”, generalizes the classic conception of user “proﬁles”, and includes both the domains in the strict sense, as well as the processes concerned and the mechanisms of adaptation (of the users and the systems). The other, and this is what we shall concentrate on, aims to exploit and/or develop cognitive theories of information and communication, making it possible to highlight all the necessary conceptualizations in all cases. These theories, we emphasize, do not pretend to oﬀer ready-made solutions to the problems that concern us here, but they can make it possible to situate the handicapped use of data processing and/or communication, both in an enlightening manner on the theoretical level and in an exploitable way on a more practical level. One of these, the speech acts theory (SAT), in addition to this ﬁrst prerequisite, satisﬁes two others that are very important. For one thing, the SAT can stand up to formalization eﬀorts of a logical nature essential to any automated treatment (Grice: Logic and Conversation, 1975 in Grice, 1989; Searle & Vanderveken, 1985). This remark leads us to the second prerequisite: research relating to SAT is being developed in an extremely wide interdisciplinary context (Champagne, Herzig, Longin, Nespoulous, & Virbel, 2002; Tsohatzidis, 1994; Vanderveken & Kubo, 2002): not only logic, as indicated (of mental states and action), but also linguistics, psycholinguistics and neurosciences of language, the philosophy of the mind and language, and several sub-specialities of computer science (design of cooperative systems, interactive systems, etc.), a set of domains tending to constitute contemporary pragmatism. The handicap “situated” in speech acts theory We had concluded (see above) with the need for an adaptive (in particular with reference to the constraints of the situation and the nature of the linguistic tasks) and non-stereotyped vision of communication, with the relativity of success and failure and with the existence of palliative activities in the handicapped subject. We would like to show how the reference to SAT can inform the preceding analyses of linguistic handicaps. First of all the SAT, as its name indicates, considers communication as an activity. This apparent truism in fact covers deep elements of renewal of the communication approach. In this:

From language dysfunction and handicap to normal linguistic processing •

•

•

117

Like any action, communication does not abide by the true/false opposition, as propositions do, but that of success and failure. And as for most other types of action, this realm is not governed by an all-or-nothing principle (discrete), but on the contrary by gradualism, and it is also multi-source. The conditions for success and failure of speech acts are naturally particular in comparison to physical actions, for example (see below), nevertheless it may be noted that a general theory of error like that of J. Reason (Reason, 1993) proposes concepts that are relevant here: the concept of latent error (introduced surreptitiously right from conception and not dependent on the quality of subjects’ performances) and that of error caused by an attempt to recover an earlier error. Contrary to an “algorithmic” (and angelic) vision of action, we thus notice that communication is inherently and not anecdotally subject to risks, and risks it is only partially possible to anticipate. Like many other acts, communication is also an intentional activity (Cohen, Morgan, & Pollock, 1990) and the intentionality is, in this case, reﬂexive. Since the founding article of P. Grice (Meaning, 1956 in Grice, 1989), which associated the problem of intentionality with that of signiﬁcance, and the later work of Strawson (Strawson, 1964) and Searle (Searle, 1969; 1981) on this question, it is considered that by an utterance u, a speaker does not simply aim to have his interlocutor recognize his intention to communicate the contents of u to her, but he also intends, through the use of adequate linguistic resources, to have her recognize this intention. It is by this feature of the demonstration of intentionality (which can also be expressed as intention to draw attention to such an intention) that communication marks its particular form of cooperation. Finally, like a number of intentional actions, the communicational action depends on necessary (but not suﬃcient) preconditions; and it is decomposable into sub-actions whose sequence comes back to the action concerned. In the technical sense, it is therefore liable to planning, and one can, for example, represent this planning both in terms of a “cognitive task analysis” (Salembier & Pavard, 2004) and in terms of a computer planning system (Pollock, 1990).

We thus note that the few aspects evoked – intention to attract attention, request for cooperation, satisfaction of preconditions, planning of the action – to characterize in-depth communicational activity can be also the cause of the characterization of multiple possibilities of failures of relative importance. Moreover, SAT can be considered a pioneer in this ﬁeld: the initial work of J. Austin (Austin, 1962) was founded (inter alia) on a typology of the various ways of not succeeding in a speech act, and Searle’s later developments led him to develop the concept of conditions of success of speech acts, as distinct from that of conditions of satisfaction of their propositional content. There, too, proof was found that there are only a limited number of ways of not succeeding in a speech act and in a characteristic manner

118

Nespoulous and Virbel

(because a speech act constitutes a structure). This was not without consequence for the conceptions of adaptation in communication situations, or, moreover, for the conceptions of language acquisition. Communication is thus successful only in so far as it avoids risks of failure that it is at least partly possible to anticipate, and one can seek to deﬁne an overall illocutionary structure on the classes of performance of speech acts (direct, indirect and implicit), linked to a structure of the classes of risks of failure of the same acts. One of the possibilities of communication failure lies in the plurality of linguistic resources for the same communicational goal. This phenomenon is well known for lexemes (synonymy) or more extended expressions (periphrases, deﬁnitions), or between certain syntactical structures (active vs. passive, full verb vs. verb support + nominalization, for example). SAT shines an interesting light on this question for our purposes, showing that this source of potential failure is also what gives language its ﬂexibility. One can take the example of the reference (but the demonstration can extend to predicative and illocutory acts). As Frege established, the possibility of referring to an entity by several diﬀerent expressions is not a deﬁciency of the language, but on the contrary a necessary property (Frege, 1952): one cannot not refer to this entity according to a particular experience we have had. But all the same, the classes of linguistic expressions of these (classes of) possible experiences are not unlimited, but in fact quite restricted: there are generally less than a dozen types, going from proper name to pronoun, with various kinds of determination in between (Charolles, 2002). Lastly, the cooperative nature of the reference (see Clark & Wilkes-Gibbs, 1990) forces us to take into account what we may know of our interlocutor’s experience of the whole. This aspect is fundamental, and, it would seem, the source of the most serious errors of appreciation; but in addition, it has been shown that if the manifestation of the intention to refer to a certain entity were suﬃciently successful, it could overcome possible determinative referential improprieties: “the young woman at the end of the room who is holding a glass of Martini in her hand is the mayor’s daughter” can carry out a successful act of reference even if she is holding a glass of Coke. The theory of speech acts provides all the knowledge required, but in fact only within the framework of the untroubled use of language. It thus predicts the existence of several forms of relationship between the meaning of an utterance and the meaning aimed at by the speaker of this statement (in addition to the ordinary case where both coincide) such as irony, metaphor, implicature (a particular form of inference), indirect speech acts, and so on. (It acts as a prediction in that the theory provides an organized and exhaustive enumeration of all the possible cases with regard to a model.) However, research pertaining to the comprehension of this type of speech act in subjects aﬀected with lesions of the right hemisphere showed that these distinctions are less clear-cut than envisaged and do not observe as clearly as was thought the hierarchy of complexity supposed between these types of speech

From language dysfunction and handicap to normal linguistic processing

119

act (Champagne et al., 2002; Champagne, Virbel, Nespoulous, & Joanette, 2003). Moreover, the situation is appreciably the same in normal subjects. One is then led to reconsider the right versus left hemisphere opposition in the treatment of language by the mind-brain; and at same time, these data suggest reasons for the choice of a formal model of representation among other logically equivalent models. Linguistic information The exact nature of linguistic information is without doubt important. It is easy to perceive that such information is structured in a complex fashion, and one might hope to ﬁnd that linguistic theories oﬀer profound and enlightening insights permitting the enrichment of reﬂection about hypotheses on the treatment of information by the mind-brain. One such theory was formulated by Z. Harris, whose most recent work, entitled A theory of language and information, speaks for itself (Harris, 1991). Harris, among many other contributions, deﬁnes four types of syntactic constraint that contribute to giving its “sentencehood” to a sequence of words, over which 11 types of informational constraint operate, which indicate “how sentences carry information”. These two classes of constraints are interdependent, the strongest among them being the relative order of introduction (what dependence operates on the products of the eﬀect of which other?). Two points seem pertinent here: •

•

each application of a constraint contributes simultaneously to the structure of the sequence, and to a type of information carried by the sentence. Through its structured character, the notion of information deﬁned within this framework is very distant from that deﬁned in 1949 by C. Shannon and W. Weaver in The mathematical theory of communication (1949); the intermediate outputs of the diﬀerent levels of application of the constraints are not dissimilar, at ﬁrst sight, from childish or pidgin statements. So the constraint referred to as dependence on dependencies comprises only the predicative structure of a sentence. The constraint of linearization ﬁxes the mutual order of the words according to their (types of) dependencies. Finally “actualizers” (noun determinants, person/tense of the verb, etc.) apply to this resulting structure, as products of the constraint of form reductions. Harris regarded these actualizers as traces of the reduction of metaphrases; that is, of sentences having elements of the basic sentence as arguments. Thus an intermediate state of a sentence (i.e., a sentence in a state where all the constraints have not yet been applied) such as “Max met Lea” would be, for example: “Max meet Lea before me say Max meet Lea”, which can be represented as: before(meet(Max, Lea), say(me, meet(Max, Lea))).

120

Nespoulous and Virbel

We see that verbal morphology is not the only way of conveying information relating to time (see above). Another attraction of Z. Harris’ informational theory of language is that it provides a concept of the basic sentence (founded on the dependence on dependencies introduced above) operational in various contexts. The following summary of an experiment serves as illustration. The evaluation of performances of comprehension/memorization of texts of the narrative type relies on tests known as “cued recall”, where the subjects are invited to answer questions relative to a text read or heard beforehand. With the aim of formalizing this test (which questions to ask subjects, how, which responses to expect, which of those obtained are signiﬁcant) a new semantic concept has been introduced, that of the question/answer (Q/A) structure associated with a text, a structure suggested by, but independent of, its exploitation in this test (Virbel, 1997). Such a concept is in fact already the product of two independent approaches (which have been shown to be compatible with other pre-existing semantic models, like the Rhetorical Structure Theory; RST; Mann & Thompson, 1988): Z. Harris’ linguistic theory, and more precisely its concept of basic sentences entering into the composition of textual sentences; and the logical theory known as “set of answers”, where the meaning of a clause is represented by the set of the clauses making up the responses to a question supported by the clause considered. Moreover, and perhaps especially, one can predict certain semantic properties of a text according to formal properties of the Q/A graph (e.g., the aspects of coherence), and it seems that far from being an experimental artefact, this Q/A structure possesses cognitive reality: textual units more densely attached to others by virtue of this Q/A relation would be more easily memorized. Thanks to a recent collaboration with researchers of the Institute of Psychology of the University of Rio Grande do Sol (De Mattos Pimenta Parente, Holderbaum, Virbel, & Nespoulous, 2003), the questionability of narratives; that is, the fact that the question–answer relationship between sentences is a good predictor of the memorization of an account, has been highlighted: the contents of the sentences most densely connected to the Q/A graph tend to be retained best. This result can be exploited not only in the development of experimental protocols, but also in that of various types of documents where the communicational eﬃciency is of prime importance (instructions in the event of incidents or accidents, for example). This research appears to be a good illustration of the mutual contributions of work done in “normal” and handicapped situations, and of the various subjects concerned.

Conclusion: Flexibility and adaptability of human verbal behaviour We have already emphasized the non-stereotypical nature of human verbal behaviour. Speaking and understanding, in this context, clearly require the best possible use of one’s semiotic potential to communicate with others,

From language dysfunction and handicap to normal linguistic processing

121

often in new situations. So communication constitutes a real challenge in that success is never guaranteed. The extent of the challenge varies in direct proportion to the “novelty”, and thus to the inherent diﬃculty of the new situation with which the protagonists are confronted. It also varies according to the momentary or durable nature of the situation. Thus, a pathological subject, aﬀected with an often durable deﬁcit, must face this challenge permanently, and with varying degrees of success according to whether the deﬁcit is central or peripheral (see above). In the case of so-called ‘normal’ subjects, they will be confronted with many communicational challenges, more so if their pragmatic interactions are multiple and varied. They can also have diﬃculty with “degraded” situations, for example, an impoverishment of perceived signals or ignorance of modern technological media: knowing how to read is not a suﬃcient condition for being able to consult Web pages or surf the Internet; and knowing how to write is not the only skill needed to handle a word processor eﬀectively! Even subjects said to be experts in certain complex linguistic tasks, like simultaneous interpretation, are nevertheless constrained – within the framework of their profession – to deploy various strategies of adaptation to deal with the cognitive diﬃculty relating to the task they have to achieve; and being bilingual is not the sole requirement for a good interpreter. We see from the above that the novelty and/or the diﬃculty of a situation of the types we have enumerated make the use of adaptive or palliative strategies essential in the pathological subjects who have served as initial illustrations, as well as in anyone engaged in unusual or complex situations. Consequently, the linguistic competence of a speaker/listener – pathological as well as normal – can no longer merely be reduced to the control of a certain number of rules – as has long been advocated by many linguistic models; it must integrate a certain number of pragmatic parameters relating to the contexts of use with linguistic tasks, all within the framework of what some call “situated cognition”. As a result, the diagram presented at the beginning of the chapter can be reformulated, in more general and inclusive terms, in the following way:

Therefore, the linguistic handicap, whatever its origin, has a somewhat amended status compared to the one it usually has in contemporary society.

122

Nespoulous and Virbel

Instead of the variation from an increasingly illusive, not to say illusory, norm, it becomes at once (a) the situation experienced, to diﬀering degrees certainly, by someone in certain circumstances, and (b) a crucial element in the characterization of the outcome of verbal behaviour as well as the functional architecture of language in human beings. In other words, it teaches us much more about the functional dynamics of this linguistic capacity that is said to be “Man’s domain” than the too mechanical computational metaphor prevalent at the time of the creation of cognitive science. Echoing the preceding diagram, the following could illustrate the road travelled:

References Austin, J. (1962). How to do things with words. Oxford, UK: Oxford University Press. Bally, Ch. (1942). Syntaxe de la modalité explicite. Cahiers Ferdinand de Saussure, 2, 3–13. Genève: Droz. Béland, R. (1985). Contraintes syllabiques sur les erreurs phonémiques dans l’aphasie. Thèse de Doctorat, Université de Montréal. Bernstein, B. (1975). Langage et classes sociales: Codes socio-linguistiques et contrôle social. Paris: Les Editions de Minuit. Besse, J.-M., de Gaulmyn, M.-M., Ginet, D., & Lahire, B. (1992). L’illétrisme en questions. Lyon: Presses de l’Université de Lyon. Carrol, J. M. (2002). Making use is more than a matter of task analysis. Interacting with Computers, 14, 619–627. Champagne, M., Herzig, A., Longin, D., Nespoulous, J.-L., & Virbel, J. 2002). Formalisation pluridisciplinaire de l’inférence de certains types d’actes de langage non littéraux. In Information – Interaction – Intelligence (pp. 197–225). Toulouse: Cépaduès-Editions. Champagne, M., Virbel, J., Nespoulous, J.-L., & Joanette, Y. (2003). Impact of right hemispheric damage on a hierarchy of complexity evidenced in young normal subjects. Brain and Cognition, 53, 152–157. Charolles, M. (2002). La référence et les expressions référentielles en français. Paris: Ophrys. Clark, H. H., & Wilkes-Gibbs, D. (1990). Refering as a collaborative process. In

From language dysfunction and handicap to normal linguistic processing

123

P. Cohen, J. Morgan, & M. Pollock (Eds.), Intentions in communication (pp. 463–493), Cambridge, MA: MIT Press. Cohen, P. H., Morgan, J., & Pollock, M. (1990). Intentions in communication. Cambridge, MA: MIT Press. De Mattos Pimenta Parente, M. A., Holderbaum, C. S., Virbel, J., & Nespoulous, J.-L. (2003). Text questionability as a predictor of story recall. Thirteenth Annual Meeting of the Society for Text Understanding. Madrid, June 26–28. Frege, G. (1952). On sense and reference. In P. Geach & M. Black (Eds.), Writings of Gottlob Frege (pp. 56–78). Oxford, UK: Blackwell. Grice, P. (1989). Studies in the way of words. Cambridge, MA: Harvard University Press. Harris, Z. (1991). A theory of language and information. A mathematical approach. Oxford, UK: Clarendon Press. Holland, A. (1977). Some practical considerations in aphasia rehabilitation. In M. Sullivan & M. S. Kommers (Eds.), Rationale for adult aphasia therapy (pp. 167–180). Lincoln, NE: University of Nebraska Medical Center Print Shop. Lenay, Ch., & Pfaender, F. (2004). Sens de la spatialisation de l’information et prothèses perceptives. Revue Parole, 29–30, 63–88. Mann, W., & Thompson, S. (1988). Rhetorical structure theory: Towards a functional theory of text organization. Text, 8 (3), 243–281. Maurel, F., Lemarié, J., Vigouroux, N., Virbel, J., Mojahid, M., & Nespoulous, J.-L. (2004). De l’adaptation de la présentation oralisée des textes aux diﬃcultés perceptives et mnésiques du langage. Revue Parole, 29–30, 153–188. Moreau, N. (1993). Apport de la théorie des contraintes et des stratégies de réparation à l’étude des paraphasies phonémiques dans l’aphasie. Thèse pour le Doctorat en Sciences du Langage, Université de Toulouse-Le Mirail. Nespoulous, J.-L. (1973). Etude linguistique de divers phénomènes d’agrammatisme. Thèse de Doctorat, Université de Toulouse-Le Mirail. Nespoulous, J.-L. (1978). Du “handicap linguistique” au “retard de langage”: Réﬂexions sur les imperfections survenues au cours du développement du langage chez l’enfant. Rééducation Orthophonique, 101, 209–232. Nespoulous, J.-L. (1979). Geste et discours: Étude du comportement gestuel spontané d’un aphasique en situation de dialogue. Etudes de Linguistique Appliquée, 36, 100–121. Nespoulous, J.-L. (1980). De deux comportements verbaux de base: Référentiel et modalisateur. De leur dissociation dans le discours aphasique. Cahiers de Psychologie, 23, 195–210. Nespoulous, J.-L. (1981). Two basic types of semiotic behavior: Their dissociation in aphasia. Publication Series of the Toronto Semiotic Circle, II et III, 173–213. Nespoulous, J.-L. (1994). Le langage: Introduction. Linguistique, Neurolinguistique et Neuropsycholinguistique. Un parcours en quatre étapes. In M. Jeannerod & X. Seron (Eds.), Neuropsychologie humaine (pp. 317–319). Bruxelles: Mardaga. Nespoulous, J.-L. (1996). Les stratégies palliatives dans l’aphasie. Rééducation Orthophonique, 34, (188), 423–433. Nespoulous, J.-L. (1998). Segmental errors as (psycho)linguistic evidence of the nature of phonological representations. In W. Ziegler & K. Deger (Eds.), Clinical phonetics and linguistics (pp. 323–335). London: Whurr Publishers. Nespoulous, J.-L. (2004). Linguistique, pathologie du langage et cognition: Des dysfonctionnements langagiers à la caractérisation de l’architecture fonctionnelle du

124

Nespoulous and Virbel

langage. In C. Fuchs (Ed.), La linguistique cognitive (pp. 171–194). Paris: Ophrys & Editions de la MSH. Nespoulous, J.-L., & Lecours, A. R. (1989). Pourquoi l’aphasique peut-il dire: “Je ne peux pas le dire” et pas “Elle ne peut pas la chanter”? (De l’intérêt des dissociations verbales dans l’étude du comportement verbal des aphasiques). Cahiers du Centre Interdisciplinaire des Sciences du Langage (pp. 135–182). Mélanges oﬀerts à J. Verguin. Toulouse: Université de Toulouse-Le Mirail. Nespoulous, J.-L., & Moreau, N. (1997). Repair strategies and consonantal cluster production in Broca’s production. In Y. Lebrun (Ed.), From the brain to the mouth: Acquired dysarthria and dysﬂuency in Adults (pp. 71–80). Dordrecht: Kluwer Academic Publishers. Nespoulous, J.-L., Code, Ch., Virbel, J., & Lecours, A. R. (1998). Hypotheses on the dissociation between “referential” and “modalizing” verbal behaviour in aphasia. Applied Psycholinguistics, 19, 311–331. O’Regan, J. K., & Noe, A. (2001). A sensorimotor account of vision and visual consciousness, Behavioral and Brain Sciences, 24, 5. Paradis, C. 1988). On constraints and repair strategies. The Linguistic Review, 6, 71–97. Perry, J., Macken, E., & Israel, D. (2004). Prolegomena to a theory of disability, inability and handicap. Revue Parole, 29/30, 43–62. Pollock, M. (1990). Plans as complex mental attitudes. In P. Cohen, J. Morgan, & M. Pollock, Intentions in communication (pp. 77–104). Cambridge, MA: MIT Press. Reason, J. (1993). Human error. Cambridge, UK: Cambridge University Press. Salembier, P., & Pavard, B. (2004). Analyse et modélisation des activités coopératives situées. Activités, 1 (1), 87–99 (Revue électronique: http://www.activites.org/) Searle, J. (1969). Speech acts. Cambridge, UK: Cambridge University Press. Searle, J. (1981). Expression and meaning: Studies in the theory of speech acts. Cambridge, UK: Cambridge University Press. Searle, J., & Vanderveken, D. (1985). Foundations of illocutary logic. Cambridge, UK: Cambridge University Press. Shannon, C. E., & Weaver, W. (1949). The mathematical theory of communication, Urabana, IL: The University of Illinois Press (reprinted 1964). Strawson, P. (1964). Intention and convention in speech acts. Philosophical Review, 73, 439–460. Tsohatzidis, S. L. (1994). Foundations of speech act theory: Philosophical and linguisitc perspectives. London & New York: Routledge. Vanderveken, D., & Kubo, S. (2002). Essays in speech acts theory. Amsterdam: John Benjamins. Virbel, J. (1989). The contribution of linguistic knowledge to the interpretation of text. In J. Andre, V. Quint, & R. Furuta (Eds.), Structured documents (pp. 181–190). Cambridge, UK: Cambridge University Press. Virbel, J. (1997). Aspects du contrôle des structures textuelles. In J. Lambert & J.-L. Nespoulous (Eds.), Perception auditive et compréhension du langage (pp. 251–272), Marseille: Solal.

8

Production and perception of word tones in patients with brain damage Inger Moen

Chris Code, in his introduction to Classic cases in neuropsychology emphasizes the importance of the single case study: “Developments in neuropsychology owe much to the discovery and careful examination of sometimes rare and remarkable individuals” (Code, Wallesch, Joanette, & Lecours, 1996, p. 1). One of the many contributions of Chris Code to the development of neuropsychology, aphasiology and clinical linguistics is his remarkable ability to bring to light, and as editor of books and journals make available to the research community, single case studies that have provided new insight into the relationship between language, mind and brain (e.g., Code 1991; Code et al., 1996; Code, Wallesch, Joanette, & Lecours, 2002). The interest of clinical linguists in the prosodic features of speech goes back to a case study by Monrad-Krohn (1947) of a patient whose “melody of language”, rhythm and pitch variation, was disturbed as a result of left hemisphere damage, while her ability to sing was not aﬀected. “The variations of pitch had by no means disappeared. On the contrary they were rather greater than usual in Norwegian, but they were neither adequate nor quite constant in their inadequacy” (Monrad-Krohn, 1947, p. 411). Monrad-Krohn’s patient had suﬀered left hemisphere damage, but the clinical-perceptual impression is that damage to either hemisphere may lead to deviations of sentence prosody. Acoustic investigations have revealed both normal and abnormal characteristics in the intonation of patients with Broca’s and Wernicke’s aphasia and right-hemisphere-damaged patients (Cooper & Klouda, 1987; Cooper, Soares, Nicol, Michelow, & Goloskie, 1984; Danly & Shapiro, 1982; Ryalls, 1982; Shapiro & Danly, 1985). It is, however, unclear to what extent these abnormalities are linguistic in nature and to what extent they are caused by poor control of the physiological mechanisms associated with phonation and fundamental frequency variation, or whether they are the result of a deﬁciency in the long-range planning of linguistic units (for a review and discussion, see Ryalls & Behrens, 1988). Speech prosody includes the linguistic categories of stress, rhythm, tone, duration, and intonation. In addition to having strictly linguistic functions, prosody can also be used to signal the speaker’s attitudes and emotions. The auditory correlates of prosody are variations in pitch, loudness, tempo,

126

Moen

and rhythm. These features have a primary relationship with the physical dimensions of fundamental frequency, intensity, and time. A key issue in the investigation of prosody in the brain-damaged population is the search for the neuroanatomical underpinnings of the various prosodic functions. If the physical correlates of prosody – fundamental frequency, intensity, and time – are of primary importance when it comes to determining hemispheric specialization, we would expect unilateral brain lesions to result in the same type of behaviour, regardless of the linguistic functions of the disturbed physical features. We would, for instance, expect disturbed ability to modulate fundamental frequency to be evident as deviant pitch throughout a patient’s speech, regardless of the linguistic functions of fundamental frequency in the particular language. If, on the other hand, the linguistic functions are crucial when determining hemispheric specialization, we would expect the behavioural eﬀect of unilateral lesions to vary depending on the linguistic functions of the physical correlates in the patient’s language. We might expect, for instance, that it would be possible for a patient with unilateral lesions to produce diﬀerences in pitch to signal intonational variation, but not to signal variation in lexical tone. A third possibility would be that both hemispheres are engaged in the processing of prosody, but that they process diﬀerent acoustic features, for instance that one hemisphere processes fundamental frequency and the other hemisphere processes time (Gandour, 1998). During the last decades data have accumulated on prosodic disorders as a result of brain damage, data that have produced several major hypotheses concerning the neuroanatomical regions active in prosodic processing (for a review, see Baum & Pell, 1999). The most straightforward of these hypotheses assumes that all aspects of prosody are processed in the right hemisphere and integrated with linguistic information from the left hemisphere via the corpus callosum (Klouda, Robin, Graﬀ-Radford, & Cooper, 1988). Van Lancker (1980) proposes a hypothesis which posits that aﬀective or emotional prosody is controlled by the right hemisphere, whereas the left hemisphere is specialized for linguistic prosody. This is referred to as the functional lateralization hypothesis. This hypothesis assumes that there is a scale of prosodic features from the most linguistically structured (e.g., Chinese and Norwegian tones) associated with left-hemisphere specialization to the least linguistically structured (e.g., emotional tone, voice quality) associated with right-hemisphere specialization. A third major hypothesis assumes that the perception and production of prosody are mainly subserved by subcortical regions and are not lateralized to either of the hemispheres (e.g., Cancelliere & Kertesz, 1990). Several recent studies have supported the hypothesis that individual acoustic cues to prosody may be independently lateralized (e.g., Van Lancker & Sidtis, 1992).

Production and perception of word tones after brain damage

127

Tone languages Pitch variation is a property of all natural languages. No language is spoken on a monotone. But pitch diﬀerences function diﬀerently in diﬀerent languages. In tone languages diﬀerences in pitch at syllable or word level are used to distinguish the lexical meaning of words. In these languages pitch variations are contrastive in the lexicon. In nontone languages pitch may be used to signal intonation at the level of the phrase and the sentence. Tone languages also exhibit sentence intonation, but generally with fewer possibilities of variation than nontone languages because of the use of pitch at the syllable and word level. There is general agreement that the primary acoustic correlates of tone are states and movements of the fundamental frequency of the voice (F0), although there may be concomitant changes in time, intensity and phonation. Tone languages are quite numerous. According to Fromkin and Rodman (1993) there are more than 1000 tone languages in Africa alone. However, when it comes to the investigation of language as a result of brain damage, the data from tone languages come from only a limited number of languages, to be presise, from diﬀerent dialects of Chinese, from Thai and from Norwegian (for a review see Gandour, 1998). Tone languages diﬀer with regard to number and shape of lexical tones. Mandarin Chinese, for instance, has four lexical tones: high level, rising, low level, and falling (Liang & van Heuven, 2004). Cantonese has six tones: high level, high rising, high-mid level, low level, low rising, low-mid level. In many tone languages there are sets of words that diﬀer only in tone. In Thai, for instance, a language with ﬁve tones: mid, low, falling, high, and rising, a set of ﬁve words can be distinguished by variation in tone only: /khaa/, to be stuck; /khàa/, a kind of spice; /khâa/, to kill; /kháa/, to engage in trade; /khàá/, leg (Gandour, 1998). In Norwegian, a so-called pitch accent language, where the tonal contrast is restricted to one syllable in a word, pitch and stress are closely linked. The accented syllable is also stressed. The accented syllable carries one of two phonemically contrastive tones, referred to as Accent1 and Accent2. There are a number of minimal pairs diﬀering only in tone: for example, vannet /1vane/ (the water); vanne /2vane/ (to water); skuﬀen /1skufen/ (the drawer); skuﬀen /2skufen/ (the showel) (Moen & Sundet, 1996).

The perception of tone after unilateral brain damage Studies of the perception of tonal contrasts in brain-damaged speakers of tone languages point to a left-hemisphere dominance in tonal perception. Hughes, Chan and Su (1983) in a study of 12 Mandarin Chinese patients with right-hemisphere lesions found that only ﬁve of the patients showed a mild defect in a tonal identiﬁcation task. The majority of the patients achieved a perfect score.

128

Moen

In another study of Mandarin Chinese Naeser and Chan (1980) found that the perception of Mandarin Chinese tones was impaired for their nonﬂuent mixed aphasic patient, a bilingual speaker of Mandarin Chinese and Cantonese. She scored only 55% correct on a listening identiﬁcation test of the four Mandarin Chinese tones, whereas a normal control scored 100%. Her performance was poor across all four tones. A CT scan showed extensive cortical and subcortical damage to the left hemisphere. The right hemisphere was not aﬀected. Yiu and Fok (1995) reported on the results of a tonal perception test in 21 right-handed Cantonese aphasic speakers: 11 anomic, 2 conduction and 2 Wernicke’s, 2 Broca’s and 4 transcortical motor aphasic patients. There were two control groups, a normal group of eight persons and a non-cortical brain-damaged non-aphasic group consisting of three dysarthric patients. Except for four of the anomic patients, where no CT scan was available, the other aphasic patients had left-hemisphere damage demonstrated on CT scans. The aphasic group performed signiﬁcantly worse than the normal control group and the dysarthric patients. The performance of the normal controls and the dysarthric group was very similar. The aphasic subjects demonstrated errors with all tones, but they had more diﬃculty with the level than with the falling tones. The scores were not signiﬁcantly diﬀerent among the aphasic groups, and the scores did not correlate signiﬁcantly with severity of aphasia or post-onset time. The normal performance of the dysarthric subjects suggests that the aphasic group’s perception problem can be attributed to left-hemisphere lesions and not to a general brain-damage eﬀect. Gandour and Dardarananda (1983) studied the perception of tonal contrasts in a group of four Thai aphasic speakers, two Broca aphasic patients, one transcortical motor aphasic patient, and one conduction aphasic patient. In addition there were two controls, one right-brain-damaged nonaphasic patient and a normal speaker. The results of the perception test indicated that all four aphasic patients performed signiﬁcantly worse than either of the controls. The right-hemisphere-damaged control achieved near perfect scores. This result is further support for the assumption that the tonal perception deﬁcit in aphasic speakers of tone languages is not due to a general brain-damage eﬀect. No diﬀerence in performance among the aphasic patients could be attributed to a speciﬁc aphasia syndrome. The aphasic patients’ tonal confusions were similar to those of normals, and their perception errors indicated that the perception deﬁcit was general to all ﬁve tones rather than selective to individual tones. Moen and Sundet (1996) investigated the perception of the two tonal contrasts in East Norwegian in eight brain-damaged speakers, four lefthemisphere-damaged aphasic speakers and four right-hemisphere-damaged nonaphasic speakers. The aphasic speakers included two Broca’s and two anomic aphasic patients. There was a control group of ten normal speakers. The control group identiﬁed all the words correctly. The right-hemispheredamaged group’s performance was comparable to that of the normal controls:

Production and perception of word tones after brain damage

129

only one incorrect identiﬁcation. In the left-hemisphere-damaged group, on the other hand, only one of the four patients identiﬁed all the target words correctly. The other three patients identiﬁed from 50% to 92% of the words correctly. The confusion between the two accents was bidirectional: 17% of Accent1 stimuli and 20% of Accent2 stimuli were reported as the other accent. The general unimpaired performance of right-hemisphere-damaged patients is not unexpected in view of the fact that dichotic listening experiments have demonstrated a right ear superiority in the perception of tonal contrasts (Moen, 1993; Van Lancker & Fromkin, 1973, 1978). Whether the reduced, but not completely disrupted, performance of the left-hemispheredamaged patients is due to residual mechanisms still operating within the damaged left hemisphere, to mechanisms in the right hemisphere, or to subcortical mechanisms is a moot point. There is little evidence in the studies reported here for a selective deﬁcit in the perception of particular lexical tones. All tones seem to be equally diﬃcult. The exception is Yiu and Fok’s study (1995). They found that falling tones were easier to identify than level ones. Gandour (1998) points out that the tones that seem to be most susceptible to confusion, for aphasic patients as well as for normal subjects, are those that are phonetically similar in height and shape to other tones in the same tonal system. The current evidence indicates that, on the whole, the aphasic patients make more of the same kinds of perceptual errors that the normal subjects make. There is a quantitative rather than a qualitative diﬀerence between the errors made by the two groups.

The perception of tone after general brain damage Moen, Simonsen, Oksengaard and Engedal (2004) investigated the ability of ten elderly patients with dementia of the Alzheimer’s type (AD) and ten age-matched normal control subjects to distinguish perceptually between the two Norwegian word tones. AD patients suﬀer from a progressive neurodegenerative disorder aﬀecting both cerebral hemispheres. It is therefore possible that their perception of tonal distinctions might diﬀer from that of patients with unilateral cerebral damage and from normal controls. The test stimuli were a set of drawings illustrating minimal pairs of words diﬀering only in word tones. The test words were read by the examiner, and the subjects were asked to point to the pictures corresponding to the stimulus word. The test scores of half the AD patients matched those of the normal controls. The other ﬁve patients’ performance was impaired. The AD patients had all been tested with the Mini Mental State Examination, a test of cognitive ability. Low cognitive test scores corresponded on the whole to impaired performance on the word tone test, with one notable exception. The patient with the highest cognitive test scores made most mistakes on the word tone test. A possible contributing factor to his impaired performance might be

130

Moen

linked to the distribution of his cerebral lesions. It is possible that the damage included areas implicated in semantic processing. He may have had problems distinguishing the meanings of the word pairs presented to him, in addition to a possible accent discrimination problem. In order to understand a spoken word, the listener has to convert acoustic input into meaning. This involves at least two distinct processes: phonetic and phonemic decoding, and lexical activation. If the ability to distinguish between two diﬀerent phonological strings is impaired, this may lead to the activation of a wrong word in the mental lexicon. This is presumably the reason why some patients with aphasia fail to distinguish between minimal pairs of words diﬀering only in word tones. If the distinction between diﬀerent lexical items is reduced due to a breakdown in semantic memory, the ability to diﬀerentiate between pairs of words will also be reduced, and a wrong lexical item may be activated. Lexical semantic impairment is a well-documented characteristic of many AD patients (Bayles & Kaszniak, 1987), and the behaviour of the AD patients during the word tone test also indicated a semantic problem. Whereas patients with aphasia, who had been tested with the same test previously, pointed relatively unhesitatingly to one of the two pictures when the stimulus word had been presented, the AD patients talked about the pictures, and commented on similarities and diﬀerences in the drawings before they made their choice. In some cases they repeated the stimulus word, looked at the pictures and said, “There is no diﬀerence.” It is, however, not possible on the basis of this test alone to decide whether the AD patients’ problem was purely semantic or a combination of blurred semantic distinctions and reduced phonological perception.

The production of tone after unilateral brain damage Studies of tone production in the speech of aphasic speakers of Mandarin, Cantonese, Thai, and Norwegian indicate that left-hemisphere damage may lead to deviant tone production, whereas the tone production of righthemisphere-damaged patients is relatively spared. Deﬁcient tone production also seems to depend on type and severity of aphasia and time since onset of brain damage. A production deﬁcit is most evident in the severly aphasic patients and more evident shortly after onset of brain damage than later. Non-ﬂuent Broca’s aphasic patients have more problems producing correct tonal contrasts than ﬂuent Wernicke’s or conduction aphasic patients (Gandour, 1987; Gandour, Petty, & Dardarananda, 1988; Gandour et al., 1992; Moen & Sundet, 1996; Naeser & Chan, 1980; Packard, 1986; Ryalls & Reinvang, 1986). There is, however, no indication of a particular pattern of tonal disruption in any speciﬁc type of aphasia. The evidence for a selective deﬁcit in the production of particular tones is inconclusive at present. Investigations of Cantonese and Mandarin seem to indicate that static (level) tones may be more resistant to disruption than dynamic (contour) tones. Yiu and Fok (1995) found that their aphasic

Production and perception of word tones after brain damage

131

subjects made mistakes in the production of all six Cantonese tones, though Tone 6 (low level) was the easiest to produce. Liang and van Heuven (2004) studied a Mandarin aphasic subject. In their study, out of the four lexical tones, the least compromised tone was Tone 1 (high level, 88% correct). The second best production was Tone 3 (low dipping, 20% correct). According to Liang and van Heuven, Tone 1 and Tone 3 can both be analysed as static tones: the high level tone and the low level tone, respectively. The dynamic tones, Tone 4 (the falling tone, 16% correct) and Tone 2 (the rising tone, 9% correct) were the most diﬃcult to produce. On the other hand, evidence from Thai seems to indicate that falling tones are easier to produce than level tones. Gandour et al. (1988, 1992), in a series of acoustic phonetic studies on tonal disruption in brain-damaged subjects in Thai, found that almost all tonal substitutions resulted in mid, low, or falling tones. The mid, low, and falling tones are all characterized by a falling fundamental frequency contour throughout their duration, whereas the high and rising tones are not (Gandour, 1998). As a result of the reduction of transglottal air pressure, the pitch has a tendency to drop over the course of an utterance. It may be the same mechanism that makes a rising pitch contour more diﬃcult to produce than a falling one. This mechanism cannot, however, account for the superior production of the level tones in the Chinese aphasic speakers. East Norwegian diﬀers from the Asian tone languages under review in having only two tones, Accent1 and Accent2. Both accents are associated with a low pitch level. The diﬀerence between them is located in the beginning of the syllable, before the pitch reaches its lowest level. Accent2 has an extensive fall in pitch from the beginning of the syllable to its lowest pitch level. Accent1 may either have an initial narrow fall or a constant low level. The pitch pattern may be described as high-low in Accent2 syllables and as low in Accent1 syllables. Accent1 is the unmarked accent, the pitch pattern used when the opposition between the two accents is neutralized, and it is the accent given to new loanwords. An investigation of tonal production in East Norwegian aphasic patients (one Broca and two anomic) tested the ability to diﬀerentiate between minimal pairs of words diﬀering only in tone. The test material was a set of drawings illustrating minimal pairs of this type. The target words were written below each drawing. The three aphasic patients all failed to produce correct distinctions between the two accents in some of the minimal pairs (Moen & Sundet, 1996). It is noteworthy that most of the mistakes involved the substitution of Accent1 for Accent2. There may be two possible explanations for these unidirectional mistakes, an articulatory explanation and a phonological one. From an articulatory point of view, Accent2, with a high fall, may be more diﬃcult to produce than Accent1, with a limited fall or a low level. From a phonological point of view most of the accent mistakes involve the replacement of a marked feature by an unmarked one. According to the theory of phonological underspeciﬁcation (e.g., Kenstowicz, 1994) only the marked accent will be speciﬁed in the lexical phonological representation. The patients’ accent substitutions could then be

132

Moen

accounted for by assuming that Accent2 words occasionally are retrieved from the mental lexicon without accent speciﬁcation. These words will then, by default, be assigned Accent1. If the substitution of Accent1 for Accent2 reﬂects an articulatory problem and not a phonological one, it would be expected that Accent1 would not only replace Accent2 in words that are members of minimal pairs. One of the patients from the study, the Broca aphasic person, was also tested in a reading test that did not consist of minimal pairs. In this test he produced a clear distinction between the two accents. It is therefore unlikely, in the case of this patient, that the problem was an articulatory one (Moen & Sundet, 1999). The theory of underspeciﬁcation cannot alone account for this patient’s accent production. If phonological underspeciﬁcation was the only mechanism at work, one would expect some Accent1 contours on Accent2 words regardless of whether they were members of minimal pairs or not. In addition to a theory of phonological underspeciﬁcation, a connectionist model of lexical access might account for the patient’s tonal productions. This type of model assumes that when a target word is accessed, the target word together with phonologically similar words will be activated (e.g., Dell, 1988). If the target word is the member of a minimal accent pair, two identical segmental phonological structures with diﬀerent prosodic patterns will be activated. The patient then has to choose between these two. When the target word is not a member of a minimal pair, the patient does not have to make a choice between two identical segmental structures with diﬀerent pitch patterns. As a result, the correct accent is also produced on Accent2 words. Studies of intonation in nontone languages have shown a narrowing of the fundamental frequency range in the speech of aphasic patients (Cooper et al., 1984; Ryalls, 1982). Gandour et al. (1992), however, in their investigation of tonal production in brain-damaged Thai speakers, found that the patients’ deviant tone production could not be attributed to a compressed tone space. Not only was there no compression of the fundamental frequency range, but the patients’ tone space was actually wider than the normal range. Liang and van Heuven (2004), on the other hand, in their study of a Mandarin speaker, found the patient’s F0 range to be less than half that of a normal control. And Moen (2004), in a study of three Norwegian patients with Broca’s aphasia, arrived at a similar result. There was a phonological distinction between the two word tones in the speech of all the patients, but phonetically the F0 variation in the aphasic patients covered a narrower frequency span than in the speech of the normal controls. Why these studies have arrived at such diﬀerent results is unclear.

Conclusions Investigations of the tonal perception and production in brain-damaged speakers of tone languages have demonstrated reduced ability in both tasks in left-hemisphere-damaged patients, whereas tonal production and

Production and perception of word tones after brain damage

133

perception is spared in right-hemisphere-damaged nonaphasic patients, indicating that the processing of lexical tones is the property of the left hemisphere. Whether the reduced, but not disrupted, performance of the left-hemisphere-damaged patients is due to residual mechanisms in the left hemisphere, to mechanisms in the right hemisphere, or to subcortical mechanisms, is unclear. There is little evidence of a selective deﬁcit, a rank order of diﬃculty, in the perception of particular types of tones. The exception is Yiu and Fok’s study of Cantonese tones, which found that falling tones were easier to identify than level ones. There is no indication of diﬀerent perceptual deviations depending on type and severity of aphasia. In general, aphasic patients make the same kind of perceptual errors as normal subjects do, but they make more errors. When it comes to the tonal production of brain-damaged patients, the results of the investigations are in some respects less clear. The ability to produce, like the ability to perceive, tonal contrasts is normal in the righthemisphere-damaged subjects and reduced in the aphasic left-hemispheredamaged subjects. The severity of the tonal production disability seems to depend on type of aphasia and on time post-onset of brain damage. Anterior Broca’s aphasic patients have more problems than posterior ﬂuent aphasic patients. And the problems are most severe in the period shortly after brain damage. There is no indication of a particular type of tonal disruption associated with a speciﬁc type of aphasia. There is no clear evidence of selective production deﬁcits of particular tones. But there are indications that a falling tone may be easier to produce than a rising or level tone, possibly due to the general tendency to reduce the transglottal air pressure during an utterance.

Directions for future research Although the nature of the mechanisms underlying reduced tonal perception and production are at present unclear, the current evidence indicates that tonal processing is impaired following left hemisphere damage in tone languages. There are, however, few investigations of tonal processing in patients with subcortical damage, such as patients with Parkinson’s disease. Further investigations of this patient group might expand our knowledge of the neuroanatomical bases for the processing of tonal contrasts. Most studies of tones in the brain-damaged population have focused on single words or short utterances in relatively few languages. Future research will, it is hoped, include longer stretches of speech and data from a wider range of the numerous tone languages of the world.

134

Moen

References Baum, S. R., & Pell, M. D. (1999). The neural bases of prosody: Insights from lesion studies and neuroimaging, Aphasiology, 13 (8), 581–608. Bayles, K. A., & Kaszniak, A. W. (1987). Communication and cognition in normal aging and dementia. London: Taylor & Francis. Cancelliere, A., & Kertesz, A. (1990). Lesion localisation in acquired deﬁcits of emotional expression and comprehension, Brain and Cognition, 13, 133–147. Code, C. (1991). The characteristics of aphasia. Hove, UK: Lawrence Erlbaum Associates Ltd. Code, C., Wallesch, C.-W., Joanette, Y., & Lecours, A. R. (1996). Classic cases in neuropsychology. Hove, UK: Psychology Press. Code, C., Wallesch, C.-W., Joanette, Y., & Lecours, A. R. (2002). Classic cases in neuropsychology: Vol 2. Hove, UK: Psychology Press. Cooper, W. E., & Klouda, G. V. (1987). Intonation in aphasic and right-hemispheredamaged patients. In J. H. Ryalls (Ed.), Phonetic approaches to speech production in aphasia and related disorders (pp. 59–77). Boston/Toronto/San Diego: Little, Brown & Co. Cooper, W. E., Soares, C., Nicol, J., Michelow, D., & Goloskie, S. (1984). Clausal intonation after unilateral brain damage, Language and Speech, 27, 17–24. Danly, M., & Shapiro, B. E. (1982). Speech prosody in Broca’s aphasia. Brain and Language, 16, 171–190. Dell, G. S. (1988). The retrieval of phonological forms in production: Tests of predictions from a connectionist model. Journal of Memory and Language, 27, 124–142. Fromkin, V., & Rodman, R. (1993). An introduction to language (5th ed.). New York: Harcourt Brace Jovanovich. Gandour, J. (1987). Tone production in aphasia. In J. H. Ryalls (Ed.), Phonetic approaches to speech production in aphasia and related disorders (pp. 45–57). Boston/Toronto/San Diego: Little, Brown & Co. Gandour, J. (1998). Aphasia in tone languages. In P. Coppens, Y. Lebrun, & A. Basso (Eds.), Aphasia in atypical populations (pp. 117–142). Hove, UK: Lawrence Erlbaum Associates Ltd. Gandour, J., & Dardarananda, R. (1983). Identiﬁcation of tonal contrasts in Thai aphasic patients. Brain and Language, 18 (1), 98–114. Gandour, J., Petty, S. H., & Dardarananda, R. (1988). Perception and production of tone in aphasia. Brain and Language, 35, 201–240. Gandour, J., Ponglorpisit, S., Khunadorn, F., Dechongkit, S., Boongird, P., Boonklam, R., et al. (1992). Lexical tones in Thai after unilateral brain damage. Brain and Language, 43, 275–307. Hughes, C. P., Chan, J. L., & Su, M. S. (1983). Aprosodia in Chinese patients with right cerebral hemisphere lesions. Archives of Neurology, 40, 732–736. Kenstowicz, M. (1994). Phonology in generative grammar. Oxford, UK: Blackwell Publishers. Klouda, G. V., Robin, D. A., Graﬀ-Radford, N. R., & Cooper, W. E. (1988). The role of callosal connections in speech prosody. Brain and Language, 35, 154–171. Liang, J., & van Heuven, V. J. (2004). Evidence for separate tonal and segmental tiers in the lexical speciﬁcation of words: A case study of a brain-damaged Chinese speaker. Brain and Language, 91, 282–293.

Production and perception of word tones after brain damage

135

Moen, I. (1993). Functional lateralization of the perception of Norwegian word tones – Evidence from a dichotic listening experiment. Brain and Language, 44, 400–413. Moen, I. (2004). Dysprosody in Broca’s aphasia: A study of Norwegian brain damaged patients. In L. Verbitskaya & T. Chernigovskaya (Eds.), Teoreticheskije problemy jazykoznanija. Sbornik statej k 140-letiju kafedry obshchego jazykoznanija ﬁlologicheskogo fakul’teta Sankt-Peterburgskogo gosudarstvennogo universiteta (pp. 341–356) [Theoretical problems of linguistics. Papers dedicated to 140 years of the Department of General Linguistics of St Petersburg State University]. St Petersburg: Philological Faculty of St Petersburg State University Publishing House. Moen, I., Simonsen, H. G., Oksengaard, A. R., & Engedal, K. (2004). Perception of the Norwegian word tones in patients with Alzheimer’s disease (AD). In B. Murdoch, J. Goozee, B.-M. Whelan, & K. Docking (Eds.), Proceedings of the 26th International Association of Logopaedics and Phoniatrics (IALP) 2004 Congress. Brisbane: IALP. Moen, I., & Sundet, K. (1996). Production and perception of word tones (pitch accents) in patients with left and right hemisphere damage. Brain and Language, 53, 267–281. Moen, I, & Sundet, K. (1999). An acoustic investigation of pitch accent contrasts in the speech of a Norwegian patient with a left-hemisphere lesion (Broca’s aphasia). In B. Maassen & P. Groenen (Eds.), Pathologies of speech and language: Advances in clinical phonetics and linguistics (pp. 221–228). London: Whurr Publishers. Monrad-Krohn, G. H. (1947). Dysprosody or altered melody of language, Brain, 70, 405–423. Naeser, M. A., & Chan, S. W.-C. (1980). Case study of a Chinese aphasic with the Boston Diagnostic Aphasia Exam. Neuropsychologia, 18, 389–410. Packard, J. L. (1986). Tone production deﬁcits in nonﬂuent aphasic Chinese speech. Brain and Language, 29, 212–223. Ryalls, J. H. (1982). Intonation in Broca’s aphasia. Neuropsychologia, 20, 355–360. Ryalls, J. H., & Behrens, S. J. (1988). An overview of changes in fundamental frequency associated with cortical insult, Aphasiology, 2, 107–115. Ryalls, J., & Reinvang, I. (1986). Functional lateralisation of linguistic tones: Acoustic evidence from Norwegian. Language and Speech, 29, 389–398. Shapiro, B. E., & Danly, M. (1985). The role of the right hemisphere in the control of speech prosody in propositional and aﬀective contexts, Brain and Language, 25, 19–36. Van Lancker, D. (1980). Cerebral lateralization of pitch cues in the linguistic signal. International Journal of Human Communication, 13, 227–277. Van Lancker, D., & Fromkin, V. (1973). Hemispheric specialization for pitch and “tone”: Evidence from Thai. Journal of Phonetics, 1, 101–109. Van Lancker, D., & Fromkin, V. (1978). Cerebral dominance for pitch contrasts in tone language speakers and in musically untrained and trained English speakers. Journal of Phonetics, 6, 19–23. Van Lancker, D., & Sidtis, J. J. (1992). The identiﬁcation of aﬀfective-prosodic stimuli by left- and right-hemisphere-damaged subjects: All errors are not created equal. Journal of Speech and Hearing Research, 35, 963–970. Yiu, E. M.-L., & Fok, A. Y.-Y. (1995). Lexical tone disruption in Cantonese aphasic speakers. Clinical Linguistics and Phonetics, 9 (1), 79–92.

9

Subcortical aphasia Historical perspective and contemporary thinking Bruce E. Murdoch

Introduction The concept that structures lying below the level of the cerebral cortex in the subcortical regions of the brain may be involved in language processing has been the subject of controversy for more than a century. In recent years evidence provided primarily through cliniconeuroradiological investigations has greatly increased awareness and acceptance that subcortical structures such as the basal ganglia and thalamus have a role to play in language. This evidence to a large extent has come from a relatively small group of researchers who have provided theories and mechanisms by which subcortical structures may inﬂuence language processing, backed up by empirical evidence. The work of these researchers would not have come into the public domain without the support of journal editors with suﬃciently open minds to accept and publish work that ran counter to contemporary thinking. One such journal editor has been Chris Code. Chris has always kept an open mind on all aspects of brain function relating to the occurrence of aphasic disorders and through his editorship of the journal Aphasiology has always provided a forum where new theories relating to language processes and language disorders can be espoused and debated. Without Chris Code and his willingness to support and publish work relating to new aspects of brainrelated function, much of the progress towards furthering our understanding of subcortical language mechanisms would have been greatly retarded. The present chapter discusses subcortical language mechanisms and subcortical aphasia from a historical perspective, and presents the latest thinking in relation to how subcortical structures may inﬂuence language and language disorders. The progress made towards greater enlightenment of subcortical language processes can in many ways be linked to encouragement provided by Chris Code and other editors of journals prepared to extend the boundaries of contemporary theory and practice.

Subcortical aphasia

137

Historical perspective Ever since the era of “phrenological science” the cerebral cortex has been considered the neural substrate of higher psychological function, including language. In keeping with this view, the standard “associationist” anatomofunctional model of language organization was deeply rooted in cortical areas and their ﬁbre connections (Lichtheim, 1885; Wernicke, 1874). According to this still inﬂuential model, linguistic representations are stored in discrete cortical areas, and consequently subcortical brain lesions were thought to only produce language deﬁcits if they disrupted the white matter ﬁbres that connect the various cortical language centres (e.g., disruption of the arcuate fasciculus in instances of conduction aphasia). Despite the emphasis on the cerebral cortex, evidence to suggest the occurrence of aphasia associated with subcortical brain lesions has been available since the late nineteenth century. More than a century ago Broadbent (1872) proposed that words were “generated” as motor acts in the basal ganglia. Marie (1906) challenged the traditional view of aphasia and described a clinical syndrome that he called “anartria,” secondary to dysfunction of a speciﬁc subcortical region involving the caudate nucleus, putamen, internal capsule and thalamus (Marie’s quadrilateral space). Monakow (1914) also championed the participation of the lentiform nucleus in the pathogenesis of aphasia. Perusal of the monumental anatomoclinical summaries published in the early twentieth century, such as those by Moutier (1908), Henschen (1922) and Nielsen (1946) also reveals a number of cases of language disturbances associated with lesions apparently limited to subcortical structures. Unfortunately, these empirical data were subjected to radically diﬀerent interpretations by the various authors. Moutier supported the “quadrilatèrè” proposed by his teacher Pierre Marie. In contrast Nielsen explicitly denied any role of subcortical structures in mental activities, interpreting his observations in strict adherence to the traditional Wernicke–Lichtheim model. Later, Fisher (1959) described aphasia as a clinical feature in a patient with left thalamic haemorrhage. Penﬁeld and Roberts (1959) suggested that the thalamus had an integrative function in language processing. Since the late 1970s, the traditional view of language processing in the brain has been challenged by the ﬁndings of an increasing number of cliniconeuroradiological correlation studies that have documented the occurrence of adult language disorders in association with apparently subcortical vascular lesions. The introduction in recent decades of new neuroradiological methods for lesion localisation in vivo, including computed tomography in the 1970s and more recently magnetic resonance imaging, has led to an increasing number of reports in the literature of aphasia following subcortical lesions (for reviews of in vivo correlation studies see Alexander, 1989; Cappa & Vallar, 1992; Murdoch, 1996). In particular, these new neuroimaging techniques have allowed more precise identiﬁcation and localization of subcortical lesion parameters (Alexander, Naesar, & Palumbo, 1987; Cappa & Wallesch, 1994),

138

Murdoch

and hence the ability to evaluate the inﬂuence of speciﬁc lesions in producing motor and cognitive anomalies. Therefore, although the concept of subcortical aphasia remains controversial, recent years have seen a growing acceptance of a role for subcortical structures in language and the development of a range of models that attempt to explain the nature of that role. Prior to discussing models of subcortical participation in language, however, it is necessary to ﬁrst review the relevant subcortical neuroanatomy and the reported clinical features of subcortical aphasia.

Neuroanatomy of the subcortical region The basal ganglia, thalamus and subcortical white matter pathways represent the subcortical structures that have been aﬀorded the most consideration within contemporary models of subcortical participation in language. More recently, studies based on deep brain stimulation have also suggested a possible role for the subthalamic nucleus in language processes (Whelan, Murdoch, Theodoros, 2003; Whelan, Murdoch, Theodoros, Silburn, & Hall, 2004a). Further, a role for the cerebellum in language has also been suggested (Docking, Murdoch, & Ward, 2003; Leiner, Leiner, & Dow, 1993). Clinically, the basal ganglia represent a functional system of interconnected components that typically include the corpus striatum (i.e., caudate nucleus, putamen and internal [GPi] and external [GPe] segments of the globus pallidus), subthalamic nucleus and substantia nigra (pars compacta [SNPC] and pars reticulata [SNPR]). Anatomically, this system is largely positioned at the cortico-subcortical boundary, and functionally has been hypothesized to be composed of a number of neural circuits subserving motor, cognitive and limbic functions (Alexander & Crutcher, 1990; Alexander, Crutcher, & De Long, 1990). In general, the basal ganglia can be considered to comprise a group of “input structures” (the caudate nucleus, putamen and ventral striatum) that receive direct input essentially from all areas of the cerebral cortex and “output” structures (the GPi, the SNPR and the ventral pallidum) that project back to the cerebral cortex via the thalamus. Contemporary thinking is that the striatum acts as a “multi-laned” throughway that forms part of a series of multi-segmented circuits connecting the cerebral cortex, basal ganglia and thalamus (Alexander, De Long, & Strick, 1986; Graybiel & Kimura, 1995; Middleton & Strick, 2000). Thus basal ganglia anatomy is characterized by their participation in multiple “loops” with the cerebral cortex, each of which follows the basic route of: cortex → striatum → globus pallidus/substantia nigra → thalamus → cortex in a unidirectional fashion. Within contemporary theories of subcortical participation in language, it has been suggested that the basal ganglia mediate linguistic processes by way of these cortico-striato-pallido-thalamo-cortical pathways (Crosson, 1985; Wallesch & Papagno, 1988). Consequently, these loops constitute the neuroanatomical basis of subcortical participation in language.

Subcortical aphasia

139

Syndromes of subcortical aphasia The majority of studies that have attempted to explore the notion of subcortical participation in language have investigated the impact of vascular thalamic and striatocapsular lesions on linguistic abilities (Murdoch, 1990), giving rise to syndromes of thalamic and striatocapsular aphasia. Despite the fact that the aphasic symptom complex associated with thalamic lesions appears to approximate a more uniform syndrome than its striatocapsular counterpart, heterogeneity within each aphasic category has been documented with respect to language proﬁles and recovery rates (Murdoch, 1996). This inconsistency has been partly attributed to methodological limitations including the wide-ranging scope of assessments utilized and experimental designs employed. Kennedy and Murdoch (1990) emphasized that general measures of language function typically utilized in the assessment of subcortical aphasia, may have lacked the requisite sensitivity to detect more subtle, high-level linguistic deﬁcits within this population. Furthermore, it has been suggested that the complexity of circulatory dynamics and the protean nature of spontaneous vascular lesions may have also contributed to the inherent variability of symptoms observed (Graﬀ-Radford, Eslinger, Damasio, & Yamada, 1984). Thalamic aphasia Numerous studies have documented aphasia after dominant thalamic lesions, the function of the thalamus in language being described in terms of an integrative role (Penﬁeld & Roberts, 1959; Schuell, Jenkins, & Jiménez-Pabón, 1965), arousal mechanisms (Luria, 1977; McFarling, Rothi, & Heilman, 1982; Riklan & Cooper, 1975), modulation and integration of cortical areas to permit language processing (Ojemann, 1983), semantic veriﬁcation of formulated cortical language segments in verbal production (Cappa & Vignolo, 1979; Wallesch & Papagno, 1988), managing of verbal memory (Reynolds, Turner, Harris, Ojemann, & Davis, 1979) or a selective engagement of cortical mechanisms leading to an impairment in the semantic–lexical interface (Nadeau & Crosson, 1997a, 1997b). Commonly, language disturbances resulting from lesions of the thalamus are of a mixed transcortical sensory aphasia (Crosson, 1992; Murdoch, 1996) and characterized by word ﬁnding diﬃculties, paraphasias, neologistic output, perseveration and reduced spontaneous speech output in the presence of relatively preserved repetition and variable, but often good, auditory comprehension abilities (Crosson, 1984; Jonas, 1982). This proﬁle, however, has been documented to vary (Cappa & Vignolo, 1979; Crosson, 1984), including reports of normal language abilities in individuals following thalamic haemorrhage (Cappa, Papagno, Vallar, & Vignolo, 1986). Despite this variability, language disturbances following thalamic lesions do present a more uniform clinical picture than those associated with striatocapsular lesions, and it is

140

Murdoch

generally accepted that a typical thalamic aphasia can be characterized by the clinical presentation. Striatocapsular aphasia Although in vivo correlation studies have documented beyond reasonable doubt that language impairments may occur in association with lesions conﬁned to the striatocapsular region of the dominant hemisphere, manifestations of language pathology subsequent to lesions of the basal ganglia and internal capsule have failed to establish a homogeneous symptom complex with no unitary striatocapsular aphasia being identiﬁed (Crosson, 1985; Kennedy & Murdoch, 1993; Nadeau & Crosson, 1997a, 1997b). Furthermore, the eﬀects of striatocapsular lesions on language abilities appear, in general, to be more enduring than the impact associated with thalamic lesions (Wallesch, Kornhuber, Brunner, Kunz, Hollerbach, & Suger, 1983). Indeed, reported language proﬁles extend from normal to severe impairments on the parameters of auditory and reading comprehension, spontaneous speech, repetition, naming and writing (Alexander & LoVerme, 1980; Damasio, Damasio, Rizzo, Varney, & Gersh, 1982; Vallar, Papagno, & Cappa, 1988). Although language disorders are common subsequent to dominant hemisphere striatocapsular lesions, it has been suggested that the more overt language symptoms in such cases may be related to concomitant cortical dysfunction (Nadeau & Crosson, 1997a). Mega and Alexander (1994) showed that the basal ganglia play a more subtle role in the generation of words. More recent evidence indicates that the basal ganglia have a broader role in complex aspects of language, that is, executive language functions (Copland, Chenery, & Murdoch, 2000b). Despite the documented variability of language disturbances associated with striatocapsular aphasia, some researchers have identiﬁed a distinct pattern of impairment that conforms to the anterior-nonﬂuent/posterior-ﬂuent cortical dichotomy (Cappa, Cavallotti, Guidotti, Papagno, & Vignolo, 1983). Other authors have also identiﬁed three patterns of language disturbance associated with putaminal and internal capsule lesions, including: (1) Broca’s type or transcortical motor aphasia with dysarthria, following lesions of the striatocapsular region with anterior extension; (2) Wernicke’s type aphasia subsequent to striatocapsular lesion with posterior extension; and (3) global aphasia following combined anterior and posterior lesions of the basal ganglia and/or internal capsule, plus extension (Murdoch, Thompson, Fraser, & Harrison, 1986; Naeser, Alexander, Helm-Estabrooks, Levine, Laughlin, & Geschwind, 1982). Despite this apparent consensus, several other studies have questioned the accuracy and utility of the anterior–posterior dichotomy by describing a number of cases in which the patterns of language impairment could not be accounted for in terms of this anatomical distinction (Kennedy & Murdoch, 1993; Wallesch, 1985).

Subcortical aphasia

141

Theoretical models of subcortical participation in language The possible existence of subcortical aphasia as a clinical entity has catalyzed the development of contemporary language theories that proﬀer functional roles for subcortical nuclei, including the striatum, globus pallidus and thalamus. These theoretical constructs speciﬁcally promote a network model of language organization (Cappa & Vallar, 1992), whereby cortico–subcortical– cortical pathways represent the neural basis of linguistic processing, in preference to exclusive cortical–cortical connections. The work of Alexander and colleagues (1986, 1990) provides the basis for our understanding of the anatomical and functional organization of cortico–subcortical–cortical circuits. Seminal schemas proposed parallel yet functionally segregated basal ganglia–thalamocortical pathways to underlie skeletomotor, occulomotor, cognitive and limbic functions. To date, the skeletomotor circuit has proﬀered the greatest contribution to the conceptualization of basal ganglia–thalamocortical organizational substrates. As such, contemporary models of subcortical participation in language have largely evolved from theories of motor control, the foundations of which were established within studies of basal ganglia dysfunction in primates with experimentally induced 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) toxicity (Starr, Vitek, & Bakay, 1998). Based on clinicoanatomical evidence thus far, three major basal ganglia– thalamocortical circuits have been speculated to participate in the mediation of linguistic processes (Cappa & Vallar, 1992): (1) the anterior “complex” loop (i.e., dorsolateral prefrontal and lateral orbitofrontal circuits (Alexander et al., 1986): frontal association cortex–caudate nucleus–globus pallidus– ventral anterior thalamus–frontal association cortex; (2) the anterior “motor” loop (i.e., skeletomotor circuit; Alexander et al., 1986): sensory motor cortex– putamen–globus pallidus–ventral lateral thalamus–sensory motor cortex; and (3) the posterior loop (Van Buren & Borke, 1969): temporoparietal cortex–pulvinar–temporoparietal cortex. The anterior “complex” and “motor” pathways were hypothesized to mediate lexical–semantic expression and articulation respectively, and the posterior loop to facilitate auditory comprehension (Cappa & Vallar, 1992). Additional subcortical–cortical pathways have also been postulated to participate in the regulation of language (Cappa & Vallar, 1992), including: temporal auditory cortex–caudate nucleus pathway facilitating auditory comprehension (Damasio et al., 1982; Van Hoesen, Yeterian, & Lavizzo-Mourey, 1981); amygdala–temporal neocortex–dorsomedial thalamus (Cappa & Sterzi, 1990) and caudate nucleus– supplementary motor area–anterior (Naeser, Palumbo, Helm-Estabrooks, Stiassny-Eder, & Albert, 1989) regulating speech production. The functional speciﬁcity of language-dedicated subcortical circuits to date has been largely restricted to the elementary linguistic faculties of auditory comprehension and verbal expression (Alexander et al., 1986). It is anticipated, however, that contemporary research may serve to expose functional subdivisions within

142

Murdoch

nonmotor basal ganglia–thalamocortical circuits, which reﬂect a similar level of organizational complexity to that of the somatotopic channels identiﬁed within subcortical motor circuitry (Alexander et al., 1986). Indeed, this disclosure may potentially involve the elucidation of the neural substrates underpinning language at both single word and sentential levels of processing. Several theories have attempted to explicate the subcortical neural mechanisms underlying receptive and expressive linguistic abilities. These include: the subcortical white matter pathways (Alexander, Naeser, & Palumbo, 1987), response–release semantic feedback (Crosson, 1985), lexical decision making (Wallesch & Papagno, 1988), and selective engagement (Nadeau & Crosson, 1997a) models. Subcortical white matter pathways model The subcortical white matter pathways model (Alexander et al., 1987) dismisses a role for the subcortical nuclei in language and advocates cortico– cortico, corticostriatal, thalamocortical and corticobulbar white matter pathways as critical to the facilitation of auditory comprehension and verbal expression. The fulcrum of this theoretical schema developed from a series of robust clinical-neuroradiological studies that highlighted an array of receptive and expressive language deﬁcits in individuals with large striatal lesions, extending into the surrounding white matter pathways (Alexander et al., 1987). This proﬁle was in stark contrast to that observed in patients with relatively circumscribed lesions of the putamen and caudate nucleus, which resulted in covert or nominal disturbances to language such as mild word ﬁnding diﬃculties and hesitant verbal output. This ﬁnding consequently supported a minimal function hypothesis for basal ganglia participation in language and directed discussion towards the white matter pathways linking cortical–cortical and subcortical–cortical regions. Vascular lesions of the striatum that extended beyond the lateral boundary of the anterior limb of the internal capsule, incorporating the anterior, extra anterior, anterior superior, superior or posterior periventricular white matter (PVWM), temporal isthmus, insular cortex and/or external capsule, were documented to produce a range of expressive and receptive language deﬁcits (Alexander et al., 1987). More speciﬁcally, nonthalamic lesions with extensions into the anterior superior PVWM were reported to result in transcortical motor aphasia, largely evidenced as sparse verbal output and diﬃculty initiating speech. This symptom complex was hypothesized to result from damage to the ﬁbre pathways connecting the supplementary motor area and Broca’s area. Anterior superior PVWM pathway disconnection was postulated to restrict limbic inputs to cortical language centres, resulting in reduced speech drive. Repetition deﬁcits were reported to arise from lateral and/or superior lesion extensions relative to the putamen, which implicate the external and extreme capsules and, potentially, the arcuate fasciculus. In relation to

Subcortical aphasia

143

speech motor control, corticobulbar ﬁbres within the superior PVWM and genu of the internal capsule, in addition to corticocerebellar and thalamocortical ﬁbres within the anterior portion of the superior PVWM and anterior limb of the internal capsule, were inculpated. The temporal isthmus, linking the medial geniculate nucleus of the thalamus to the primary auditory association cortex, and the auditory association callosal pathway connecting Wernicke’s area and the right temporal association cortex were identiﬁed as the subcortical white matter pathways integral to auditory comprehension. Posterior striatal lesion extension incorporating these structures typically resulted in comprehension deﬁcits and neologistic output. Furthermore, wide-ranging lesion extension relative to the putamen, including the anterior limb of the internal capsule, extra anterior PVWM, anterior PVWM, anterior superior PVWM and temporal isthmus was reported to result in global language impairment. Alexander et al. (1987) avoided attributing a role in language functioning to the thalamus on the basis that language deﬁcits resulting from thalamic and putaminal lesions are subserved by disparate pathophysiological mechanisms. Given that white matter pathways provide the means by which components of the language system communicate with each other, the importance given to these pathways in the model proposed by Alexander et al. (1987) would, on the surface, appear reasonable. However, the ﬁndings of more recent studies refute the notion that white matter pathway disconnection provides a valid datum for clinical manifestation of subcortical damage (Cappa & Vallar, 1992). Response-release semantic feedback model A postulated thalamo-cortical alerting system (Ojemann, 1976) represents the plinth of the response-release semantic feedback (RRSF) (Crosson, 1985) model. The model proposes a role for subcortical structures in regulating the release of preformulated language segments from the cerebral cortex. According to this model, the conceptual, word-ﬁnding and syntactic processes that fall under the rubric of language formulation occur in the anterior cerebral cortex. The monitoring of anteriorly formulated language segments, as well as the semantic and phonological decoding of incoming language, occurs in the posterior temporoparietal cortex. Language segments are conveyed from the anterior language formulation centre to the posterior language centre via the thalamus prior to release for motor programming. This operation allows the posterior semantic decoding centres to monitor the language segment for semantic accuracy. If an inaccuracy is detected, then the information required for correction is conveyed via the thalamus back to the anterior cortex. If the language segment is found to be accurate during monitoring, then it is released from a buﬀer in the anterior cortex for subsequent motor programming. In addition to subcortical structures participating in the preverbal semantic monitoring process, the model also speciﬁes that the

144

Murdoch

striatocapsular structures are involved in the release of the formulated language segment for motor programming. Speciﬁcally, it is suggested that this release occurs through the cortico-striato-pallido-thalamo-cortical loop in the following way. Once the language segments have been veriﬁed for semantic accuracy, the temporoparietal cortex releases the caudate nucleus from inhibition. The caudate nucleus then serves to weaken inhibitory pallidal regulation of thalamic excitatory outputs in the anterior language centre, which in turn arouses the cortex to enable generation of the motor programmes for semantically veriﬁed language segments. According to this model, Crosson (1985) hypothesized that subcortical lesions within the cortico-striato-pallido-thalamo-cortical loop would produce language deﬁcits conﬁned to the lexical–semantic level. The original conception of the response-release mechanism in Crosson’s (1985) model has since been revised and elaborated in terms of the neural substrates involved (Crosson, 1992). Although the actual response-release mechanism in the modiﬁed version resembles that in the original conception, the route for this release is altered. The formulation of a language segment causes frontal excitation of the caudate, which increases inhibition of speciﬁc ﬁelds within the globus pallidus. However, this level of inhibition alone is not suﬃcient to alter pallidal output to the thalamus. An increase in posterior language-cortex excitation to the caudate, which occurs once a language segment has been semantically veriﬁed posteriorly, provides a boost to the inhibition of the pallidum. The pallidal summation of this anterior and posterior inhibitory input allows the release of the ventral anterior thalamus from inhibition by the globus pallidus, causing the thalamic excitation of the frontal language cortex required to trigger the release of the language segment for motor programming. Overall, the revised model provides an integrated account of how subcortical structures might inﬂuence language output through a neuroregulatory mechanism that is consistent with knowledge of cortical–subcortical neurotransmitter systems and structural features. Lexical decision making model In line with the RRSF model, the lexical decision making (LDM) model (Wallesch & Papagno, 1988) also proposes a cortico-striato-pallido-thalamocortical loop as the neural platform for linguistic operations, including a speciﬁc thalamocortical arousal mechanism, consistent with Ojemann’s (1976) theorem. Despite evident parallels, however, distinct incongruities prevail between these theoretical constructs with respect to functional cortical organization viewpoints, and the nature of proposed subcortical mechanisms. Wallesch and Papagno (1988) postulated that the subcortical components of the loop constitute a “frontal lobe system” comprising parallel modules with integrative and decision-making capabilities rather than the simple neuroregulatory function proposed in Crosson’s (1985) model. Speciﬁcally,

Subcortical aphasia

145

the basal ganglia system and thalamus were hypothesized to process situational as well as goal-directed constraints and lexical information from the frontal cortex and posterior language area, and subsequently to participate in the process of determining the appropriate lexical item, from a range of cortically generated lexical alternatives, for verbal production. The most appropriate lexical alternative is then released by the thalamus for processing by the frontal cortex and programming for speech. Cortical processing of selected lexical alternatives is made possible by inhibitory inﬂuences of the globus pallidus on a thalamic gating mechanism. This most appropriate lexical alternative has an inhibitory eﬀect on the thalamus, promoting closure of the thalamic gate, resulting in activation of the cerebral cortex and production of the desired response. Cortical processing of subordinate alternatives is suppressed as a consequence of pallidal disinhibition of the thalamus, and the inhibition of cortical activity. Selective engagement model Selective engagement (SE) theory represents the most contemporary schema of subcortical participation in language and principally proposes a frontal– inferior thalamic peduncle (ITP)–nucleus reticularis (NR)–centrum medianum (CM) system to subserve the “engagement” of cortical components that mediate attentional and behavioural processes, including language (Nadeau & Crosson, 1997a). This proposed linguistic frontal lobe system complied with the tenets of the LDM model, with the exception of two distinct anomalies. In particular, selective engagement theory disputes a role for the basal ganglia in language and redeﬁnes nonspeciﬁc thalamic nuclei (i.e., NR, CM and parafascicular nucleus) as critical to the mediation of linguistic processes. Nadeau and Crosson (1997b) considered ventral anterior (VA) and ventral lateral (VL) thalamic participation in language an insolvent hypothesis. This postulate was largely fuelled by two lines of evidence, including: (1) an observed decline in the incidence of aphasia following surgically induced lesions of the VA and VL thalamus, concomitant with enhanced stereotactic technique accuracy (Fox, Ahlskog, & Kelly, 1991), and (2) the fact that aphasia resulting from tuberothalamic territory infarcts involving the VA nucleus typically resembles that following paramedian territory lesions, which spare the VA thalamus. Postulated thalamic engagement of the cortex, however, was in line with Ojemann’s (1976) proposed ventral thalamic focal altering mechanism in addition to Crosson’s (1985) VA responserelease system, relative to the galvanization of verbal output channels. The expansion of these postulates to consider the activation of more extensive language-dedicated cortical mosaics (Ojemann, 1983), largely under NR control (Nadeau & Crosson, 1997a), accommodated manifestations of receptive as well as expressive language deﬁcits observed subsequent to lesions of the thalamus. The RRSF and LDM models previously discussed focused primarily on output versus input mechanisms, providing no discernible explanation

146

Murdoch

for comprehension deﬁcits. In contrast, the structural complexity of the neural system subserving SE mechanisms accommodates the spectrum of aphasic characteristics observed following lesions of the dominant thalamus (Nadeau & Crosson, 1997b), perhaps approximating a more cogent axiom of subcortical participation in language than its antecedents. An important feature of the selective engagement theory is that it discounts a role for the basal ganglia in language. A variable symptom complex with respect to observed manifestations of language pathology in the presence of classically deﬁned striatocapsular lesions formed the basis of this postulate. In more detail, Nadeau and Crosson (1997a) analysed the linguistic proﬁles of 50 cases subsequent to relatively uniform striatocapsular infarctions, including the caudate head, putamen, anterior limb of the internal capsule and portions of the globus pallidus. Vast heterogeneity relative to the severity and incidence of language deﬁcits including ﬂuency, articulation, comprehension, repetition and naming was reported. Nadeau and Crosson (1997a) hypothesized that an integral role for the basal ganglia in language would be fortiﬁed by a coherent aphasic syndrome, in the event of uniform damage. Based on the above evidence, therefore, a minimal function hypothesis with respect to the contribution of the basal ganglia to language functions was promoted. Nadeau and Crosson (1997a) largely attributed language disturbances subsequent to lesions of the basal ganglia to cortical hypoperfusion. Thrombotic or embolic occlusions primarily of the middle cerebral artery (MCA), or less commonly the internal carotid artery, were identiﬁed as precursors to striatocapsular infarction (Weiller, Ringelstein, Reiche, Thron, & Buell, 1990). More importantly, circulatory dynamics pertaining to the rate of arterial recanalization and the eﬃciency of anastomotic circulation following basal ganglia infarction, were considered integral factors in determining the presence or absence of aphasia. Perisylvian cortex ischaemia by way of MCA occlusioninduced cystic infarction, neuronal drop out or generalized tissue dysfunction (Nadeau & Crosson, 1997a), provided a tenable explanation for the variable array of expressive and receptive language deﬁcits associated with striatocapsular infarcts. Furthermore, haemorrhagic basal ganglia lesions were also postulated to disturb cortical circulatory dynamics relevant to language functions. Pressure eﬀects inducing cortical ischaemia were held responsible for consequent manifestations of aphasia. Evidence is available that disputes Nadeau and Crosson’s (1997a) claim that lesions of the striatocapsular region fail to establish a homogeneous aphasic syndrome. A coherent aphasic syndrome relative to generative aspects of language, including verbal ﬂuency, sentence generation and extended discourse, has been reported (Mega & Alexander, 1994). This ﬁnding suggests a need to revisit the notion of basal ganglia aphasia, paying particular attention to the scope and sensitivity of linguistic assessments utilized in addition to circulatory dynamics (Crosson, Zawacki, Brinson, Lu, & Sadek, 1997). Indeed, this evidence supports a potential role for the basal

Subcortical aphasia

147

ganglia in mediating linguistic processes. In all probability, this role may entail the regulation of thalamocortical engagement. Proposed mechanisms include the switching of engagement between neural nets (Malapani, Pillon, Dubois, & Agid, 1994). Limitations of theoretical models of subcortical participation in language Each of the models outlined above has a number of limitations and consequently no one model has achieved uniform acceptance. A major limitation of these models is that they fail to fully explain the considerable variability in clinical presentation of subcortical aphasia. According to Cappa (1997), a further problem is that the models suggest such extensive and widely distributed systems subserving lexical processing that speciﬁc predictions appear to be diﬃcult to disprove on the basis of pathological evidence. In other words, these models do not lend themselves readily to empirical testing. Yet another limitation arises from the nature of the research on which these models are based. The available models of subcortical participation in language are largely based on the observation that certain contrasting deﬁcits of language production arise in subjects with particular subcortical vascular lesions when tested on traditional tests of language function. These language measures were typically designed for taxonomic purposes regarding traditional cortical-based aphasia syndromes and may be inadequate for developing models of brain functioning. It has also been argued that language deﬁcits associated with subcortical vascular lesions may actually be related to concomitant cortical dysfunction via various pathophysiological mechanisms. For instance, due to limitations inherent to currently available neuroimaging techniques, cortical infarction may not have been detected by neuroimaging. Consequently, inaccurate lesion parameters may have served to contaminate our conceptualization of subcortical aphasia thus far. In addition to the recognized shortcomings of current neuroimaging techniques, a number of physiological mechanisms have also been proposed that potentially attribute manifestations of subcortical aphasia to cortical dysfunction. Subcortical lesions have been reported to exert distance eﬀects on the cerebral cortex, including cortical hypoperfusion and hypometabolism (Perani, Valler, Cappa, Messa, & Fazio, 1987). Reduced cerebral blood ﬂow results in ischaemia-induced neuronal loss (Lassen, Olsen, Hojgaard, & Skriver, 1983) and ischaemic penumbra (i.e., maintenance of tissue viability in the presence of neuronal dysfunction), both mechanisms having the potential to disable cortical activity. Also, subcortical lesions may result in diaschisis or the functional deactivation of distance-related cortical structures (Metter et al., 1983). As yet, however, the relationship between the structural site and aetiology of subcortical lesions, the extent of diaschisis, cortical hypometabolism and hypoperfusion, and associated language function remains to be fully elucidated.

148

Murdoch

Overall, the validity of the aforementioned operative models of subcortical participation in language remains largely unattested due primarily to a previous incapacity to strictly deﬁne the extent of vascular neuropathology. A further encumbrance to empirical ratiﬁcation rests with the inadequacy of animal models in providing an appropriate linguistic platform for investigation (Crosson, 1992). The value of model-driven and theoretically founded studies of cognition cannot be overestimated in quests to extricate the subcortical–cortical mechanisms underpinning language (Cappa & Sterzi, 1990). The utilization of existing frameworks, however, in the context of advancing scientiﬁc techniques is considered critical to their ultimate interpretation. In line with this proposal, a recent resurgence in functional neurosurgery to treat the motor symptoms of Parkinson’s disease, involving the generation of discrete surgically induced lesions of the subcortical nuclei, would appear to provide an unprecedented opportunity to empirically test contemporary theories of subcortical participation in language.

Pallidotomy, thalamotomy and deep brain stimulation Over the course of the past decade or so, primate research has served to catalyse the development of a sound theoretical framework that has enhanced our understanding of the pathophysiology underlying movement disorders, such as those seen in Parkinson’s disease. This, combined with advances in neuroimaging and neurosurgical techniques and a degree of disillusionment with drug treatments for movement disorders, has led to a revival of stereotactic neurosurgical procedures such as pallidotomy (involving lesioning of speciﬁc components of the globus pallidus) and thalamotomy (involving lesioning of speciﬁc nuclei in the thalamus) in the treatment of Parkinson’s disease. In addition to their patent therapeutic value, the discrete circumscribed lesion sites provided by these procedures aﬀord an unprecedented opportunity to empirically test contemporary subcortical language theories. More recent, as an alternative to ablative procedures such as pallidotomy and thalamotomy that overtly destroy neural tissue, deep brain stimulation (DBS) involving implantation of electrodes within a range of subcortical targets such as the subthalamic nucleus (STN), has gained increasing support as the preferred method of treatment for Parkinson’s disease. In that DBS has been documented to simulate the eﬀects of ablative lesions (i.e., block neuronal activity at the target site), this technique also provides an opportunity to test models that implicate structures such as the STN and thalamus in language. The majority of studies reported to date pertaining to the impact of pallidotomy (Lombardi, Gross, Trepanier, Lang, Lozano, & Saint-Cyr, 2000; Scott et al., 2002; Trepanier, Saint-Cyr, Lozano, & Lang, 1998), and thalamotomy (Fukuda, Kameyama, Yoshino, Tanaka, & Narabayashi, 2000) on cognitive function have been largely neuropsychologically based. Assessment batteries have typically included measures of attention, memory,

Subcortical aphasia

149

concentration, visuospatial abilities and executive functioning. In regard to language, the domains of confrontation naming, verbal learning, semantic and phonemic ﬂuency have been aﬀorded considerable scrutiny, however, indepth linguistic analyses were not included. Recently, a series of studies by Whelan, Murdoch and colleagues have addressed this problem by utilizing a battery of high-level language tests to examine the eﬀects of pallidotomy (Murdoch, Whelan, & Theodoros, 2003; Whelan, Murdoch, Theodoros, Silburn, & Hall, 2004b; Whelan, Murdoch, Theodoros, Silburn, & HardingClark, 2000), thalamotomy (Whelan, Murdoch, Theodoros, Silburn, & Hall, 2002) and DBS of the STN (Whelan et al., 2003, 2004a) on linguistic function. Overall these studies provided evidence to suggest that the concatenation of subcortical nuclei comprising basal ganglia–thalamocortical circuits plays a fundamental role in high-level linguistic processes potentially underpinning the recruitment and directed interplay of frontal and temporoparietal cortical regions. With regard to the STN, the ﬁndings of Whelan et al. (2003, 2004a) highlighted the need to modify contemporary theories of subcortical participation in language to incorporate the STN. More speciﬁcally, the outcomes of their research challenged unilateral models of functional basal ganglia organization with the proposal of a potential interhemispheric regulatory function for the STN in the mediation of high-level linguistic processes. Indeed, the STN may contribute to the mediation of linguistic processes by indirectly regulating thalamocortical outputs within the cortico–subcortical–cortical language circuits.

Functional neuroimaging Further clariﬁcation of the role of subcortical structures in language is likely to come through the use of functional neuroimaging techniques and neurophysiological methods such as electrical and magnetic evoked responses. Functional neuroimaging techniques such as functional magnetic resonance (fMRI) and positron emission tomography (PET) enable brain images to be collected while the subject is performing various language production tasks (e.g., picture naming, generating nouns) or during language comprehension (e.g., listening to stories). These techniques therefore enable visualization of the brain regions involved in a language task, with a spatial resolution as low as a few millimetres. Although functional neuroimaging does therefore oﬀer a tool to unravel the role of subcortical structures in language, results from functional neuroimaging studies to date have proven less than deﬁnitive (Cabeza & Nyberg, 2000). These studies have, however, revealed a number of cortical and subcortical structures beyond the perisylvian cortex to be active during linguistic processing (Crosson et al., 1999; Peterson, Fox, Posner, Mintum, & Raichle, 1989; Warburton et al., 1996), providing support for a distributed network model of language organization (Mesulam, 2000). In particular, word generation studies have shown consistent activation of medial frontal cortex, usually near the boundary of pre-supplementary motor

150

Murdoch

area (SMA) and the rostral cingulated zone. Although the pre-SMA is known to have extensive subcortical connections, including projections to the striatal grey matter spanning the internal capsule and to the caudate nucleus and putamen, as well as receiving connections from ventral anterior and dorsal medial thalamus in the majority of functional neuroimaging studies, these subcortical components have not shown consistent activity in functional neuroimaging studies of word generation. This reported inconsistency in activation of the basal ganglia and thalamus may be the product of limitations in numbers of subjects studied, number of trials during functional neuroimaging and experimental design. Recently Crosson et al. (2003), using fMRI, observed signiﬁcant activity in the subcortical structures during lexical generation tasks but not during nonsense syllable generation. They inferred the existence of a left pre-SMA–dorsal caudate–ventral anterior thalamic loop involved in lexical retrieval. Further, Crosson et al. (2003) hypothesized “that activity in this loop was related to maintaining a bias toward the retrieval of one lexical item versus competing alternatives for each response during word generation blocks” (p. 1075). Several PET studies have also demonstrated activation of the thalamus and basal ganglia during completion of language tasks such as picture naming (Price, Moore, Humphreys, Frackowiak, & Friston, 1996a) and word repetition (Price et al., 1996b).

Conclusion Speculation has existed since the end of the nineteenth century that subcortical brain structures have a role in language. Although it is generally accepted that the thalamus has a role in language, little consensus has been reached regarding the involvement, not to mention the role, of the basal ganglia in language. In particular controversy still exists as to whether the structures of the striatocapsular region participate directly in language processing or play a role as supporting structures for language. Consequently, the important question that remains to be answered is: Do the subcortical structures have an inherent language function that contributes a speciﬁc cognitive function beyond that of the cortex, or do they simply participate in regulating and enhancing functioning of the cortical language centres? Contemporary theories suggest that the role of subcortical structures in language is essentially neuroregulatory, relying on quantitative neuronal activity. Recently reported ﬁndings suggest that subcortical structures may be involved in maintaining response biases across time that are set by the cortical components of cortical–subcortical–cortical loops (Copland, Chenery, & Murdoch, 2000a). Hypotheses generated by these theories of subcortical participation in language require testing in order to advance our understanding of the importance of subcortical brain mechanisms to language function.

Subcortical aphasia

151

References Alexander, G. E., & Crutcher, M. D. (1990). Functional architecture of basal ganglia circuits: Neural substrates of parallel processing. Trends in Neuroscience, 13, 266–271. Alexander, G. E., Crutcher, M. D., & De Long, M. R. (1990). Basal gangliathalamocortical circuits: Parallel substrates of motor, oculomotor, prefrontal and limbic functions. Progress in Brain Research, 85, 119–146. Alexander, G. E., De Long, M. R., & Strick, P. L. (1986). Parallel organization of functionally segregated circuits linking basal ganglia and cortex. Annual Review of Neuroscience, 9, 357–381. Alexander, G. E., & LoVerme, S. R. (1980). Aphasia after left hemisphere induced haemorrhage. Neurology, 30, 1193–1202. Alexander, G. E., Naeser, M. A., & Palumbo, C. L. (1987). Correlations of subcortical CT lesion sites and aphasia proﬁles. Brain, 110, 961–991. Alexander, M. P. (1989). Clinico-anatomical correlations of aphasia following predominantly subcortical lesions. In F. Boller & J. Grafman (Eds.), Handbook of neuropsychology (pp. 47–66). Amsterdam: Elsevier. Broadbent, G. (1872). On the cerebral mechanism of speech and thought. London: Longmans. Cabeza, R., & Nyberg, L. (2000). Imaging cognition II: An empirical review of 275 PET and fMRI studies. Journal of Cognitive Neuroscience, 12, 1–47. Cappa, S. F. (1997). Subcortical aphasia: Still a useful concept? Brain and Language, 58, 424–426. Cappa, S. F., Cavallotti, G., Guidotti, M., Papagno, C., & Vignolo, L. A. (1983). Subcortical aphasia: Two clinical-CT scan correlation studies. Cortex, 19, 227–241. Cappa, S. F., Papagno, C., Vallar, G., & Vignolo, L. A. (1986). Aphasia does not always 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. Cappa, S. F., & Vallar, G. (1992). Neuropsychological disorders after subcortical lesions: Implications for neural models of language and spatial attention. In G. Vallar, S. F. Cappa, & C.-W. Wallesch (Eds.), Neuropsychological disorders associated with subcortical lesions (pp. 7–41). Oxford, UK: Oxford University Press. Cappa, S. F., & Vignolo, L. A. (1979). Transcortical features of aphasia following left thalamic haemorrhage. Cortex, 15, 121–130. Cappa, S. F., & Wallesch, C.-W. (1994). Subcortical lesions and cognitive deﬁcits. In A. Kertesz (Ed.), Localisation and neuroimaging in neuropsychology (pp. 545–566). San Diego, CA: Academic Press. Copland, D. A., Chenery, H. J., & Murdoch, B. E. (2000a). Processing lexical ambiguities in word triplets. Evidence of lexical–semantic deﬁcits following dominant nonthalamic subcortical lesions. Neuropsychology, 14, 379–390. Copland, D. A., Chenery, H. J., & Murdoch, B. E. (2000b). Persistent deﬁcits in complex language function following dominant nonthalamic subcortical lesions. Journal of Medical Speech-Language Pathology, 8, 1–15. Crosson, B. (1984). Role of the dominant thalamus in language: A review. Psychological Bulletin, 96, 491–517. Crosson, B. (1985). Subcortical function in language: A working model. Brain and Language, 25, 257–292.

152

Murdoch

Crosson, B. (1992). Subcortical functions in language and memory. New York: Guilford Press. Crosson, B., Beneﬁeld, H., Cato, M. A., Sadek, J. R., Moore, A. B., Wierenga, C. E., et al. (2003). Left and right basal ganglia and frontal activity during language generation: Contributions to lexical, semantic and phonological processes. Journal of the International Neuropsychological Society, 9, 1061–1077. Crosson, B., Sadek, J. R., Bobholz, J. A., Gokay, D., Mohr, C. M., Leonard, C. M., et al. (1999). Activity in the paracingulate and cingulate sulci during word generation: An fMRI study of functional anatomy. Cerebral Cortex, 9, 307–316. Crosson, B., Zawacki, T., Brinson, G., Lu, L., & Sadek, J. R. (1997). Models of subcortical functions in language: Current status. Journal of Neurolinguistics, 10, 277–300. Damasio, A. R., Damasio, H., Rizzo, M., Varney, N., & Gersh, F. (1982). Aphasia with non-hemorrhagic lesions in the basal ganglia and internal capsule. Archives of Neurology, 29, 15–20. Docking, K., Murdoch, B. E., & Ward, E. C. (2003). Cerebellar language and cognitive functions in childhood: A comparative review of the clinical research. Aphasiology, 17, 1153–1161. Fisher, C. M. (1959). The pathologic and clinical aspects of thalamic hemorrhage. Transections of the American Neurological Association, 84, 56–59. Fox, M. W., Ahlskog, J. E., & Kelly, P. J. (1991). Stereotaxic ventrolateralis thalamotomy for medically refractory tremor in post-Levodopa era Parkinson’s disease patients. Journal of Neurosurgery, 75, 723–730. Fukuda, M., Kameyama, S., Yoshino, M., Tanaka, R., & Narabayashi, H. (2000). Neuropsychological outcome following pallidotomy and thalamotomy for Parkinson’s disease. Stereotactic and Functional Neurosurgery, 74, 11–20. Graﬀ-Radford, N. R., Eslinger, P. J., Damasio, A. R., & Yamada, T. (1984). Nonhaemorrhagic infarction of the thalamus: Behaviour, anatomic and physiological correlates. Neurology, 34, 14–23. Graybiel, A. M., & Kimura, M. (1995). Adaptive neural networks in the basal ganglia. In J. C. Houk, J. L. Davis, & D. G. Beiser (Eds.), Models of information processing in the basal ganglia (pp. 103–116). Cambridge, MA: MIT Press. Henschen, S. E. (1922). Klinische und anatomishe beitrage zur pathologic des gehirns. Stockholm: Almquist and Wiksell. Jonas, S. (1982). The thalamus and aphasia, including transcortical aphasia: A review. Journal of Communication Disorders, 15, 31–41. Kennedy, M., & Murdoch, B. E. (1990). Cortical dysfunction subsequent to subcortical vascular lesions: An explanation for subcortical aphasia? Journal of Neurolinguistics, 5, 31–54. Kennedy, M., & Murdoch, B. E. (1993). Chronic aphasia subsequent to striatocapsular and thalamic lesions in the left hemisphere. Brain and Language, 44, 284–295. Lassen, N. A., Olsen, T., Hojgaard, K., & Skriver, E. (1983). Incomplete infarction: A CT negative irreversible ischaemic brain lesion. Journal of Cerebral Blood Flow and Metabolism, 3 (Suppl. 1), 602–603. Leiner, H. C., Leiner, A. L., & Dow, R. S. (1993). Cognitive language functions of the human cerebellum. Trends in Neuroscience, 16, 444–447. Lichtheim, L. (1885). On aphasia. Brain, 7, 433–484. Lombardi, W. J., Gross, R. E., Trepanier, L. L., Lang, A. E., Lozano, A. M., &

Subcortical aphasia

153

Saint-Cyr, J. A. (2000). Relationship of lesion location to cognitive outcome following microelectrode-guided pallidotomy for Parkinson’s disease: Support for the existence of cognitive circuits in the human pallidum. Brain, 123, 746–758. Luria, A. R. (1977). On quasi-aphasic speech disturbances in lesions of the deep structures of the brain. Brain and Language, 4, 432–459. Marie, P. (1906). The third left frontal convolution plays no special role in the function of language. In M. F. Cole & M. Cole (Eds.), Pierre Marie’s papers on speech disorders. New York: Hafner (reprinted 1971). Malapani, C., Pillon, B., Dubois, B., & Agid, Y. (1994). Impaired simultaneous cognitive task performance in Parkinson’s disease: A dopamine-related dysfunction. Neurology, 44, 319–326. McFarling, D., Rothi, L. J., & Heilman, K. M. (1982). Transcortical aphasia from ischaemic infarcts of the thalamus: A report of two cases. Journal of Neurology, Neurosurgery and Psychiatry, 45, 107–112. Mega, M. S., & Alexander, M. P. (1994). Subcortical aphasia: The core proﬁle of capsulostriatal infarction. Neurology, 44, 1824–1829. Mesulam, M. M. (2000). Behavioural neuroanatomy: Large scale networks, association cortex, frontal syndromes, the limbic system, and hemispheric specialisations. In M. Mesulam (Ed.), Principles of behavioural and cognitive neurology (pp. 1–120). Oxford, UK: Oxford University Press. Metter, E. J., Riege, W. H., Hanson, W. R., Kuhl, D. E., Phelps, M. E., Squire, L. R., et al. (1983). Comparison of metabolic rates, language and memory in subcortical aphasias. Brain and Language, 19, 33–47. Middleton, F. A., & Strick, P. L. (2000). Basal ganglia output and cognition. Evidence from anatomical, behavioural and clinical studies. Brain and Cognition, 42, 183–200. Monakow, C. von (1914). Die Lokalisation im Grosshirn und der Obbau der Funktion durch Kortikale Herde. Wiesbaden: Bergmann. Moutier, F. (1908). L’Aphasie de Broca. Doctoral dissertation, Paris. Murdoch, B. E. (1990). Acquired speech and language disorders: A neuroanatomical and functional neurological approach. London: Chapman & Hall. Murdoch, B. E. (1996). The role of subcortical structures in language: Cliniconeuroradiological studies of brain damaged subjects. In B. Dodd, R. Campbell, & L. Worrall (Eds.), Evaluating theories of language: Evidence from disordered communication (pp. 137–160). London: Whurr Publishers. Murdoch, B. E., Thompson, D., Fraser, W., & Harrision, L. (1986). Aphasia following non-haemorrhagic lesions in the left striato-capsular region. Australian Journal of Human Communication Disorders, 14, 5–21. Murdoch, B. E., Whelan, B.-M., & Theodoros, D. G. (2003). Subcortical aphasia: Evidence from stereotactic surgical lesions. In I. Papathanasiou & R. De Bleser (Eds.), The sciences of aphasia: From theory to therapy (pp. 65–92). Oxford, UK: Pergamon. Nadeau, S. E., & Crosson, B. (1997a). Subcortical aphasia. Brain and Language, 58, 355–402. Nadeau, S. E., & Crosson, B. (1997b). Subcortical aphasia: Response to reviews. Brain and Language, 58, 436–458. Naeser, M. A., Alexander, G. E., Helm-Estabrooks, N., Levine, H. L., Laughlin, S. A., & Geschwind, N. (1982). Aphasia with predominantly subcortical lesion sites: Description of three capsular/putaminal aphasia syndromes. Archives of Neurology, 39, 2–14.

154

Murdoch

Naeser, M. A., Palumbo, C. L., Helm-Estabrooks, N., Stiassny-Eder, D., & Albert, M. (1989). Severe non-ﬂuency in aphasia: Role of the medial subcallosal fasciculus and other white matter pathways in the recovery of spontaneous speech. Brain, 112, 1–38. Nielsen, J. M. (1946). Agnosia, apraxia, aphasia. New York: Hoeber. Ojemann, G. (1976). Subcortical language mechanisms. In H. A. Whitaker & H. Whitaker (Eds.), Studies in neurolinguistics (pp. 103–138). New York: Academic Press. Ojemann, G. (1983). Brain organization for language from the perspective of electrical stimulation mapping. Behavioural and Brain Sciences, 2, 189–230. Penﬁeld, W., & Roberts, L. (1959). Speech and brain mechanisms. Princeton, NJ: Princeton University Press. Perani, D., Vallar, G., Cappa, S. F., Messa, C., & Fazio, F. (1987). Aphasia and neglect after subcortical stroke: A clinical/cerebral perfusion correlation study. Brain, 110, 1211–1229. Peterson, P. M., Fox, P. T., Posner, M. I., Mintum, M., & Raichle, M. E. (1989). Positron emission tomographic studies of the processing of single words. Journal of Cognitive Neuroscience, 1, 153–170. Price, C. J., Moore, C., Humphreys, G. W., Frackowiak, R. S., & Friston, K. J. (1996a). The neural signs sustaining object recognition and naming. Proceedings of the Royal Society of London, B, 263, 1501–1507. Price, C. J., Wise, R. J., Warburton, E. A., Moore, C. J., Howard, D., Patterson, K., et al. (1996b). Hearing and saying: The functional neuroanatomy of auditory word processing. Brain, 119, 919–931. Reynolds, A. F., Turner, P. T., Harris, A. B., Ojemann, G. A., & Davis, L. E. (1979). Left thalamic hemorrhage with dysphasia: A report of ﬁve cases. Brain and Language, 7, 62–73. Riklan, M., & Cooper, I. S. (1975). Psychometric studies of verbal functions following thalamic lesions in humans. Brain and Language, 2, 45–64. Schuell, H., Jenkins, J. J., & Jiménez-Pabón, E. (1965). Aphasia in adults. New York: Harper Row. Scott, R. B., Harrison, J., Boulton, C., Wilson, J., Gregory, R., Parkin, S., et al. (2002). Global attentional-executive sequelae following surgical lesions to globus pallidus interna. Brain, 125, 565–574. Starr, P. A., Vitek, J. L., & Bakay, R. A. E. (1998). Ablative surgery and deep brain stimulation for Parkinson’s disease. Neurosurgery, 43, 989–1105. Trepanier, L. L., Saint-Cyr, J. A., Lozano, A. M., & Lang, A. E. (1998). Neuropsychological consequences of posteroventral pallidotomy for the treatment of Parkinson’s disease. Neurology, 51, 207–215. Vallar, G., Papagno, C., & Cappa, S. F. (1988). Latent dysphasia after left hemisphere lesions: A lexical-semantic and verbal memory deﬁcit. Aphasiology, 2, 463–478. Van Buren, J. M., & Borke, R. C. (1969). Alterations in speech and the pulvinar: A serial section study of cerebrothalamic relationships in cases of acquired speech disorders. Brain, 92, 255–284. Van Hoesen, G. W., Yeterian, E. H., & Lavizzo-Mourey, R. (1981). Widespread cortico-striate projections from temporal cortex of the Rhesus monkey. Journal of Comparative Neurology, 199, 205–219. Wallesch, C.-W. (1985). Two syndromes of aphasia occurring within ischaemic lesions involving the left basal ganglia. Brain and Language, 25, 357–361.

Subcortical aphasia

155

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 function. Brain and Language, 20, 286–304. Wallesch, C.-W., & Papagno, C. (1988). Subcortical aphasia. In F. C. Rose, R. Whurr, & M.A. Wyke (Eds.), Aphasia (pp. 256–287). London: Whurr Publishers. Warburton, E., Wise, R. J. S., Price, C. J., Weiller, C., Hadar, U., Ramsey, S., et al. (1996). Noun and verb retrieval by normal subjects: Studies with PET. Brain, 119, 159–179. Weiller, C., Ringelstein, E. B., Reiche, W., Thron, A., & Buell, U. (1990). The large striatocapsular infarct: A clinical and pathological entity. Archives of Neurology, 47, 1085–1091. Whelan, B.-M., Murdoch, B. E., & Theodoros, D. G. (2003). Deﬁning a role for the subthalamic nucleus with operative theoretical models of subcortical participation in language. Journal of Neurology, Neurosurgery and Psychiatry, 74, 1543–1550. Whelan, B.-M., Murdoch, B. E., Theodoros, D. G., Silburn, P. A., & Hall, B. (2002). Role for the thalamus in language? A linguistic comparison of 2 cases subsequent to unilateral thalamotomy procedures in the dominant and non-dominant hemispheres. Aphasiology, 16, 1213–1226. Whelan, B.-M., Murdoch, B. E., Theodoros, D. G., Silburn, P. A., & Hall, B. (2004a). Re-appraising contemporary theories of subcortical participation in language: Proposing an interhemispheric regulatory function for the subthalamic nucleus in the mediation of high level linguistic processing. Neurocase, 10, 345–352. Whelan, B.-M., Murdoch, B. E., Theodoros, D. G., Silburn, P. A., & Hall, B. (2004b). Redeﬁning functional models of basal ganglia organization: A role for the posteroventral pallidum in linguistic processing. Movement Disorders, 19, 1267–1278. Whelan, B.-M., Murdoch, B. E., Theodoros, D. G., Silburn, P. A., & Harding-Clark, J. (2000). Towards a better understanding of the role of subcortical nuclei participation in language. The study of a case following bilateral pallidotomy. Asia Paciﬁc Journal of Speech, Language and Hearing, 5, 93–112. Wernicke, C. (1874). De aphasische Symtomencomplex. Breslau: Cohn & Weigert.

10 Mechanisms of lexical selection and the anomias Tobias Bormann, Gerhard Blanken and Claus-W. Wallesch

Introduction “Aphasia can be approached from several directions, reﬂecting the range of interdisciplinary interest, and each approach has its own story to tell” (Code, 1989, p. ix). Chris Code, to whom this chapter is dedicated, has used a variety of approaches to aphasia and the aphasic person, including the neurolinguistic, psychosocial, brain science, historical and therapeutic perspective. Chris’s personality and scope of interest are a major reason for the success of Aphasiology – the journal he edits. GB and CWW came into contact with Chris Code through our common interest in recurring utterances (Blanken, de Langen, Dittmann, & Wallesch, 1989; Blanken, Dittmann, Haas, & Wallesch, 1988; Blanken, Wallesch, & Papagno, 1990; Code, 1982a, 1982b). As we also did related research on the psychosocial impact of aphasia on the person and his or her family, Chris spent some (at least for us) scientiﬁcally fruitful and socially rewarding months with us in Freiburg in the early 1990s. With regard to recurring utterances, we took diﬀerent perspectives: Whereas Chris was mainly interested in their pathophysiological basis, we focused on their meaning for neurolinguistic models of word production. Using the “classic approach” of model-based cognitive neurolinguistics, the group of GB, ﬁrst in Freiburg, then in Magdeburg, and now in Erfurt, have broadened their scope to include other phenomena of deﬁcient word production into their research and modelling. This chapter reﬂects their present state of insight. Chris Code summarized the strengths and weaknesses of the cognitive approach: Occasionally people ﬁnd themselves at a loss with cognitive theories, especially when more than one theory or model can be applied to a single symptom complex (e.g., paraphasia, dyslexia) in a given patient, producing diﬀerent interpretations and predictions. [. . .] Single case investigations were championed in early cognitive neuropsychology, but they have fallen out of favour with some in recent years, although theory development is constrained by data from single cases and their theory-driven investigation. (Code & Wallesch, 2006, p. 821)

Mechanisms of lexical selection and the anomias

157

We would like to encourage further model-driven research into the phenomenology of aphasia, and present this chapter as an example of the use of the cognitive approach. For virtually every aphasic patient, speech production is a diﬃcult task. Deﬁcits of single word production aﬀect, to varying degrees, patients with all aphasic syndromes, and have been studied extensively. Frequently, patients show phonological errors by substituting, adding, deleting or exchanging target sounds. It is assumed that, in these cases, the patient has usually been successful in accessing the intended word form, but is, however, unable to appropriately prepare this abstract phonological form for output (e.g., Butterworth, 1992). Other patients already have diﬃculties retrieving the correct phonological word form from the mental lexicon. The mental lexicon is a long-term store containing entries of a speaker’s words. For written language, an independent orthographic lexicon is assumed, which may be accessed independently of phonological lexical access (e.g., Rapp, Benzing, & Caramazza, 1997). In some models, the word’s syntactic features (so-called lemma information, e.g., syntactic category or gender) are part of the speaker’s lexical knowledge as well (see Levelt, Roelofs, & Meyer, 1999). It is widely agreed that lexical access in speech production is controlled by semantics, a memory system, which has either been fractionated into verbal and other modality-speciﬁc parts (e.g., Shallice, 1988) or which may be a single modality-neutral unitary system (e.g., Hillis, Rapp, Romani, & Caramazza, 1990). Evidence for the independent access to semantic and phonological information can be observed in aphasic patients. Often, they indicate that they know an object and can give details on how and in which contexts it is encountered. This suggests that the patient has successfully processed, for example, the picture and that the semantic system is working adequately to allow access to semantic knowledge about the object. Often, these patients can be cued to correctly name the object by giving them the word’s ﬁrst phoneme or onset (e.g., “ti” for “tiger”). Patients with diﬃculties accessing the correct word form in their mental lexicon are usually called “anomic” (Goodglass & Baker, 1976). The respective anomia has also been termed “phonological anomia”, or “classical anomia” (Geschwind, 1967). In contrast, diﬃculties at the semantic level give rise to a condition termed “semantic anomia” (Howard & Orchard-Lisle, 1984; see Nickels, 1997, for a review). The underlying diﬃculty is assumed to aﬀect the semantic system, either as a consequence of progressive degeneration of brain structures thought to support semantic memory, or as the consequence of a stroke (Hillis et al., 1990). These two conditions may be identiﬁed by confronting the patient with other tasks that are supposed to involve the semantic system (e.g., word–picture matching). This “cognitive” approach in neurolinguistics is guided by a set of assumptions, namely that a brain lesion can selectively aﬀect some processing components of the cognitive apparatus while sparing others, and that a

158

Bormann et al.

patient’s performance is based on the formerly intact and now (often selectively) lesioned cognitive structure (e.g., Caramazza, 1984, 1986). The “cognitive” approach has proven most fruitful in revealing the cognitive architecture of language processing. In a careful analysis, a patient’s performance is related to a model of normal word processing, and the functional lesion within this model is inferred from performance in diﬀerent tasks as well as from variables aﬀecting this performance (e.g., Rapp, 2001; Shallice, 1988). In addition, patients may display dissociations among tasks that are not observed in normal subjects. If such performance cannot be reconciled with existing models of word processing, these models need revision. A patient’s performance may thus, for example, contribute to models of lexical processing (Caramazza, 1997; Dell, Schwartz, Martin, Saﬀran, & Gagnon, 1997).

Models of word production Most psycholinguistic models of word production have been based on normal individuals’ slips of the tongue (Dell, 1986; Fromkin, 1971; Garrett, 1975) and on reaction time studies with healthy subjects (Levelt et al., 1999). All models distinguish between semantic, syntactic, and phonological information, and most authors conceive of the lexicon as some sort of network. Lexical entries are thought to be nodes in the network that receive activation from other nodes, usually those representing semantic information. In most models, selection occurs when a lexical node receives activation above a certain threshold. However, models diﬀer considerably with regard to the way the respective information is represented and how information at the diﬀerent levels may interact. Modular models assume discrete, non-overlapping processing and very limited interaction. A successful model of this type has been advocated by Levelt and co-workers (Levelt, 1989; Levelt et al., 1999; Roelofs, 1992, 1997). It conceives of lexical access as a two-stage process. In the ﬁrst step, a cohort of meaning-related lemmas is activated based on the available semantic information. Lemmas are assumed to be modality-independent representations of a word’s syntactic features. They receive activation from their respective lexical concepts at the semantic level. The lemma that receives most activation is selected from this cohort, and activation spreads down to the next level, the level of word form. Usually, only one lemma is being selected and subsequently activates its corresponding word form. Thus, while lemmas may be activated in parallel, word forms are not. Only in the (rare) cases of near-synonyms, which are very similar in meaning (sofa, couch), does the model allow for parallel activation of more than one word form (Jescheniak & Schriefers, 1998; Levelt et al., 1999). Within this two-stage model, semantic errors are attributed to mis-selection at the lemma level or substitutions at the level of lexical concepts (Levelt et al., 1999). On the other hand, errors of omission are supposed to result

Mechanisms of lexical selection and the anomias

159

from a block at the level of word form. As there is no feedback between the word form level and the lemma level, the phonological word form level is not assumed to inﬂuence lexical selection, and the two error types, semantic errors and errors of omission, are considered independent events. In contrast with this discrete serial model of lexical access, other models allow for parallel activation of word forms and for an inﬂuence of phonological information on lexical selection. Cascading models have rejected the idea of discrete serial processing and allow for parallel processing at diﬀerent levels of the system, including the word form level (Caramazza, 1997; Humphreys, Riddoch, & Quinlan, 1988). Processing at a later stage may operate despite incomplete information from earlier levels and does not have to wait until processing at these earlier levels is completed. In the model of Caramazza and co-workers (Caramazza, 1997; Caramazza & Miozzo, 1997) the idea of a lemma level is explicitly rejected. Semantic information activates a cohort of meaning-related word forms. Syntactic information is assumed to be represented in an independent network. Another type of model is the interactive model of Dell and colleagues, which assumes a semantic feature level, a lemma level and a phoneme level (Dell, 1986; Dell et al., 1997). It diﬀers from the previous models in that it assumes feedback connections between adjacent levels of representation. Selection occurs at the lemma level after activation has spread between the levels for some time, thus allowing both semantic and phonological information to inﬂuence lexical selection. Figure 10.1 provides a sketch of (a) the discrete serial model (of Levelt and co-workers), (b) the cascading model (of Caramazza and co-workers), and (c) the interactive model (of Dell and co-workers). The “nodes” at the semantic level represent holistic lexical concepts in the discrete serial model and semantic features in the cascading and interactive models.

Figure 10.1 Sketch of three diﬀerent models of word production (see text).

160

Bormann et al.

Variables inﬂuencing lexical access In accordance with the postulated levels of processing, a number of variables have been identiﬁed that inﬂuence processing at the diﬀerent levels within the system. These variables are important in inferring the functional lesion of an individual. For example, Butterworth (1992) suggested that a frequency eﬀect points to a lexical deﬁcit, while an inﬂuence of word length on phonological paraphasias suggests a post-lexical origin. This has been termed the “critical variable approach” (Shallice, 1988, p. 72). It may, however, be of interest not only to investigate the inﬂuence of diﬀerent variables on correct responses but also to investigate the inﬂuences of the diﬀerent variables on the respective errors. In most patients, at least those with phonological anomia, lexical entries are not consistently unavailable. First, providing a cue often helps patients to overcome temporary diﬃculties. Second, when item-consistency across several administrations of a naming test is assessed, there is usually great variability. Thus anomia seems to aﬀect access to a lexical entry, but not to indicate permanent loss of lexical entries (however, see the case of Howard, 1995). Naming performance has been shown to be aﬀected by a target’s concreteness as well as its familiarity. These variables are thought to aﬀect semantic processing. Concrete targets are supposed to have richer and more robust semantic representations than abstract ones (e.g., “honour”, “faith”). Consequently, patients with semantic impairments are often found to be sensitive to abstractness and familiarity. Furthermore, a word’s syntactic category may determine ease of lexical access. It has often been reported that patients have more diﬃculties producing verbs compared to nouns (e.g., Miceli, Silveri, Villa, & Caramazza, 1984). On the other hand, patients have been reported who demonstrate selective sparing of verbs or nouns, even in only one modality. For example, Caramazza and Hillis (1991) presented two aphasic patients who seemed to have selective diﬃculties producing verbs only in the oral or written modality, respectively. Most impressively, these patients also exhibited diﬃculties producing a homophone when it referred to actions (“to watch”), but not when it referred to an object (“the watch”). Other patients revealed intact access to function words but impaired access to content words in speaking, and the reverse dissociation in writing (Rapp & Caramazza, 1997). One of the most important factors inﬂuencing processing at the lexical level is word frequency. It has been reported to aﬀect access to a word’s phonological form. Healthy subjects are faster at producing words of higher frequency (Jescheniak & Levelt, 1994), and aphasic patients are better at naming words of higher frequency than words of lower frequency. This “frequency eﬀect” in aphasia has been taken as a strong clue to a lexical deﬁcit (e.g., Butterworth, 1992). In cognitive models, the advantage for frequent words may be simulated by a lower threshold, which means, the more

Mechanisms of lexical selection and the anomias

161

often a word is encountered during everyday life, the lower its threshold and the easier its selection. Some authors have suggested that age of acquisition (i.e., the age at which a word was ﬁrst learned) is a stronger predictor of ease of lexical access. Age of acquisition is highly correlated with word frequency, but studies carefully controlling for this correlation reported an independent inﬂuence of age of acquisition for healthy subjects (e.g., Barry, Hirsh, Johnston, & Williams, 2001) as well as for aphasic speakers (Hirsh & Ellis, 1994). Aphasia may result in temporarily or permanently raised thresholds of the lexical entries. In many cases, then, no entry may receive activation above the threshold level and thus no entry will be selected. In this case, the patient would give no response (see Dell, Lawler, Harris, & Gordon, 2004). It has indeed been demonstrated that patients produce more errors of omission in response to pictures of low frequency words (Kremin et al., 2003). In contrast, semantic errors have been shown to be relatively independent of word frequency. For example, Nickels and Howard (1994) did not ﬁnd an inﬂuence of frequency on semantic errors. They did, however, report an eﬀect of imageability on naming for some of their patients. On the other hand, Caramazza and Hillis (1990) observed that in one patient, RGB, semantic errors were more numerous for low frequency target words.

Semantic neighbourhood Recently, Blanken, Dittmann, and Wallesch (2002) have identiﬁed another, relatively neglected, variable that inﬂuences lexical access. Semantic concepts diﬀer with respect to the size of the semantic category they belong to. For example, a lemon is part of the relatively large semantic category of “fruits”. In contrast, other items may come from a small or no speciﬁc semantic category, such as “cage” or “anchor”. The size of the semantic neighbourhood should inﬂuence the chance of semantic errors as, for items from large semantic categories, semantic competition is higher and mis-selections are more likely. Blanken et al. (2002) presented the case of MW, a German globally aphasic subject with relatively preserved oral naming skills. MW’s responses revealed a clear dependency on semantic neighbourhood: With items from large semantic categories, he produced many semantic errors and fewer omissions. In contrast, when a target word was a “low competition” item, the patient showed few semantic errors and more omissions. Under both conditions, the sum of both error types was comparable, indicating that the items did not diﬀer in their overall diﬃculty. The results were proposed to be incompatible with Levelt’s discrete two-stage model of lexicalization. In this model, both error types are assumed to be independent of each other. Particularly, the number of omissions should not be related to the previous occurrence of a semantic error.

162

Bormann et al.

We tested six further patients with aphasia following a stroke to replicate MW’s pattern of performance. These six patients were part of a larger group (Bormann, Kulke, Wallesch, & Blanken, 2006). Three patients were diagnosed as suﬀering from Wernicke’s aphasia and three were diagnosed with amnesic aphasia, according to the Aachen Aphasia Test (AAT; Huber, Poeck, Weniger, & Willmes, 1983). They were shown 33 pictures of objects with many and clear semantic competitors and 33 object pictures having few or weak semantic rivals. Both target groups were matched for frequency, age of acquisition, length and normed picture name agreement. The 66 pictures were presented in a pseudorandomized order. Their ﬁrst response within 5 seconds was scored as correct, omission, semantic error, or other. The average frequencies of semantic errors and errors of omission for both types of items were submitted to an analysis of variance with repeated measures. For the analysis by subjects, error type and item type were within-subject variables. For the analysis by items, item type was a between-item factor, while error type was a within-item factor. Both analyses resulted in a signiﬁcant main eﬀect for error type, with omissions being more frequent than semantic errors, F1(1, 5) = 10.74, p < .05; F2(1, 64) = 20.76, p < .01. The other main eﬀect, item type, did not reach signiﬁcance (both F < 0). The interaction of both variables was signiﬁcant, F1(1, 5) = 9.68, p <.05; F2(1, 64) = 11.55, p < .01. Planned comparisons revealed that semantic errors were more frequent for target words with many competitors, while omissions dropped in frequency for low competitive target words. For every patient, the sums of both error types under both conditions did not diﬀer signiﬁcantly as assessed by chi square tests. We discuss the implications below.

Semantic dementia: Progressive semantic impairment Another population that encounters frequent diﬃculties in naming single objects is patients with a progressive loss of semantic knowledge. A progressive loss of conceptual knowledge has been reported for a large number of patients suﬀering from probable Alzheimer’s disease (e.g., Hodges & Patterson, 1995). Diﬃculties in naming everyday objects are among the ﬁrst symptoms, and Hodges, Salmon, and Butters (1991) demonstrated that most naming errors in patients with Alzheimer’s disease are semantic in nature. In most cases of probable Alzheimer’s disease, other cognitive functions are aﬀected as well. In contrast, there now exist a considerable number of case reports of patients showing a rather selective decline in conceptual knowledge with few accompanying cognitive deﬁcits. Progressive ﬂuent aphasia, or semantic dementia (SD), is a variant of the fronto-temporal lobar atrophies (Salmon & Hodges, 2001; Snowden, Goulding, & Neary, 1989). The cognitive diﬃculties are associated with atrophy of the temporal lobes, most often the temporal poles and the inferior-lateral temporal areas. In semantic dementia, atrophy usually aﬀects the left temporal lobe or the temporal lobes of both hemispheres. Clinically, patients exhibit poor single word

Mechanisms of lexical selection and the anomias

163

comprehension and poor naming, while other components of language, such as syntax and phonology, are well preserved. Naming errors of patients with semantic dementia have been reported to be semantic or errors of omission (Hodges, Patterson, Oxbury, & Funnell, 1992) with some patients showing a tendency towards more general semantic responses during the course of the illness (Hodges, Graham, & Patterson, 1995). Hirsh and Funnell (1995) reported naming performance in a patient with SD to be aﬀected by concept familiarity. On the other hand, for a patient with probable Alzheimer’s disease, only age of acquisition was a signiﬁcant predictor of naming success. Hirsh and Funnell took this as evidence for a modular architecture of semantic processing and lexical access. While semantic dementia was assumed to aﬀect semantic processing, the patient with Alzheimer’s disease was supposed to have impaired access to the lexicon. Lambon Ralph, Graham, Ellis, and Hodges (1998), in contrast, reported the naming ability of nine patients with semantic dementia to be inﬂuenced by familiarity, word frequency and age of acquisition. Within an interactive model, they claimed, semantic and lexical variables all inﬂuence lexical access: Familiarity may reﬂect a concept’s robustness to impairment, while frequency and age of acquisition correlated with ease of access to a lexical entry. More robust concepts should be better able to activate their respective lexical entries. More easily accessible entries, on the other hand, may require less input from the semantic system to reach their selection threshold. We tested a patient, ZC, with progressive word ﬁnding diﬃculties in the face of relatively spared general cognitive functioning. ZC complained about word ﬁnding diﬃculties lasting for more than 2 years. In line with this, CT scans showed atrophy of left frontal and left temporal areas. ZC was fully orientated for time and space and could give an adequate account of her recent past. Her forward and backward digit spans were normal or even above average. ZC was confronted with the same 66 pictures as the aphasic group and was asked to name the respective object using a single word. Responses were rated as correct, semantic errors, errors of omissions, and circumlocutions. In a regression analysis, we found rated familiarity and age of acquisition to be signiﬁcant predictors of her naming success. These results replicate the observations of Lambon Ralph et al. (1998). The patient’s diﬃculties were not restricted to the semantic system and, instead, seemed to aﬀect semantic processing and access to the lexicon. Lambon Ralph et al. had taken their results as evidence for an interactive type of architecture. The results from the high–low competition naming test point in the same direction: For low competitive items, ZC showed one semantic error and 14 errors of omission. In contrast, for targets with many lexical competitors, we observed 12 semantic errors and 6 omissions. For semantic errors, the diﬀerence between high and low competitive items was signiﬁcant (p < .01) while the diﬀerence between these item categories for omissions was in the right direction and approached signiﬁcance (p < .12). In contrast, there was

164

Bormann et al.

no diﬀerence in the overall number of correct responses for the two groups of items.

Discussion The results of the two studies replicate Blanken et al.’s (2002) ﬁndings with a globally aphasic patient, MW. When items have many semantic competitors, more semantic errors occur, while for target items with few competitors, more errors of omission are being observed. As the items from both conditions were comparable in their overall diﬃculty, a common source of both error types is suggested. The results speak against the proposal of Levelt and co-workers that lexical selection is carried out at the lemma level and independently of the word form level. Thus, semantic errors and errors of omission are not independent events. Instead, the comparable amounts of overall errors implicate a functional locus that is relevant for both types of errors to occur. The data are thus easier to reconcile with cascading or interactive models of lexical access. Within a cascading type of model, the results may be explained by assuming that in aphasia and progressive semantic disorders a larger set of lexical candidates is activated. Activation then cascades from the semantic level through the lemma level down to the word form level. It is here that the errors, semantic or omission, arise. However, meaning-related errors are preceded by broad semantic activation and thus may be the result of an inability to restrict the number of candidates. A similar account has been proposed by Nickels and Howard (1994) and Gerhand and Barry (2000). Further evidence for an involvement of modality-speciﬁc representations in lexical selection comes from a number of single-case studies comparing oral and written naming. One of the most suggestive observations was the case PW of Rapp et al. (1997). PW was asked to react to pictures by saying, then writing, then again saying their name (called the “triple naming task”). He gave diﬀerent responses in his oral and written response but, within a modality, his responses were the same. If lexical selection had been carried out at the modality-independent lemma level, he should have given the same response across diﬀerent modalities. If, on the other hand, he had started the whole selection process anew, he should have exhibited a tendency to produce yet another response in the third naming trial, again in the oral modality. Thus his consistent responses within one modality speak against this alternative explanation. Together with other reports of patients showing semantic errors in only one modality (Caramazza & Hillis, 1990, 1991), this suggests that the idea of lexical selection as occuring exclusively at the lemma level is too narrow. In contrast, modality-speciﬁc word forms seem to be involved in lexical selection. On the other hand, this does not necessarily imply that this is always the case. Our argument applies to aphasic speakers, and it is not clear whether it holds for lexical access of non-aphasic speakers. For these,

Mechanisms of lexical selection and the anomias

165

activation of more than one phonological form has been demonstrated for near-synonyms; that is, words with extreme semantic similarity. These have also been shown to be involved in a speciﬁc type of speech error, blends (e.g., Garrett, 1993). Thus Levelt’s model allows for parallel activation of phonological forms in some narrowly circumscribed situations of lexical processing. In general, the distribution of the patterns of semantic substitutions and omissions within aphasic naming errors can fairly be predicted by properties of the semantic environment of a given target. Our results therefore point to the necessity to control test items for the potential impact of a further variable aﬀecting aphasic naming performance: the targets’ semantic neighbourhood.

References Barry, C., Hirsh, K. W., Johnston, R. A., & Williams, C. L. (2001). Age of acquisition, word frequency, and the locus of repetition priming of picture naming. Journal of Memory and Language, 44, 350–375. Blanken, G., de Langen, E. G., Dittmann, J., & Wallesch, C. W. (1989). Implications of preserved written language for the functional basis of speech automatisms (recurring utterances): A single case study. Cognitive Neuropsychology, 6, 211–249. Blanken, G., Dittmann, J., Haas, J. C., & Wallesch, C. W. (1988). Producing speech automatisms (recurring utterances): Looking for what is left. Aphasiology, 2, 545–556. Blanken, G., Dittmann, J., & Wallesch, C.-W. (2002). Parallel or serial activation of word forms in speech production? Neurolinguistic evidence from an aphasic patient. Neuroscience Letters, 325, 72–74. Blanken, G., Wallesch, C.-W., & Papagno, C. (1990). Dissociations of language functions in aphasic patients with speech automatisms (recurring utterances). Cortex, 26, 41–63. Bormann, T., Kulke, F., Wallesch, C.-W. & Blanken, G. (2006). Omissions and semantic errors in aphasic naming: Is there a link? Manuscript submitted for publication. Butterworth, B. (1992). Disorders of phonological encoding. Cognition, 42, 261–286. Caramazza, A. (1984). The logic of neuropsychological research and the problem of patient classiﬁcation in aphasia. Brain and Language, 21, 9–20. Caramazza, A. (1986). On drawing inferences about the structure of normal cognitive systems from the analysis of patterns of impaired performance: The case for single-patient studies. Brain and Cognition, 3, 41–66. Caramazza, A. (1997). How many levels of processing are there in lexical access? Cognitive Neuropsychology, 14, 177–208. Caramazza, A., & Hillis, A. E. (1990). Where do semantic errors come from? Cortex, 26, 95–122. Caramazza, A., & Hillis, A. E. (1991). The organization of nouns and verbs in the brain. Nature, 349, 788–790. Caramazza, A., & Miozzo, M. (1997). The relation between syntactic and phonological knowledge in lexical access: Evidence from the “tip-of-the-tongue” phenomenon. Cognition, 64, 309–343.

166

Bormann et al.

Code, C. (1982a). Neurolinguistic analysis of recurrent utterances in aphasia. Cortex, 18, 141–152. Code, C. (1982b). On the origins of recurrent utterances in aphasia. Cortex, 18, 161–164. Code, C. (1989). Preface. In C. Code (Ed.), The characteristics of aphasia (pp. ix–x). London: Taylor & Francis. Code, C., & Wallesch, C.-W. (2006). The form of representation of language in the brain and the inﬂuence of John C. Marshall. Aphasiology, 20, 819–822. Dell, G. (1986). A spreading activation theory of retrieval in sentence production. Psychological Review, 93, 283–321. Dell, G. S., Lawler, E. N., Harris, H. D., & Gordon, J. K. (2004). Models of errors of omission in aphasic naming. Cognitive Neuropsychology, 21 (2/3/4), 125–145. Dell, G. S., Schwartz, M. F., Martin, N., Saﬀran, E. M., & Gagnon, D. A. (1997). Lexical access in aphasic and nonaphasic speakers. Psychological Review, 104 (4), 801–838. Fromkin, V. (1971). The non-anomalous nature of anomalous utterances. Language, 47, 27–52. Garrett, M. F. (1975). The analysis of sentence production. In G. Bowers (Ed.), The psychology of learning and motivation (pp. 133–177). New York: Academic Press. Garrett, M. F. (1993). Errors and their relevance for models of language production. In G. Blanken, J. Dittmann, H. Grimm, J. C. Marshall, & C.-W. Wallesch (Eds.), Linguistic disorders and pathology (pp. 72–92). Berlin: De Gruyter. Gerhand, S., & Barry, C. (2000). When does a deep dyslexic make a semantic error? The roles of age-of-acquisition, concreteness, and frequency. Brain and Language, 74, 26–47. Geschwind, N. (1967). The varieties of naming errors. Cortex, 3, 96–112. Goodglass, H., & Baker, E. (1976). Semantic ﬁeld, naming and auditory comprehension in aphasia. Brain and Language, 3, 359–374. Hillis, A. E., Rapp, B., Romani, C., & Caramazza, A. (1990). Selective impairment of semantics in lexical processing. Cognitive Neuropsychology, 7 (3), 191–243. Hirsh, K. W., & Ellis, A. W. (1994). Age of acquisition and lexical processing in aphasia: A case study. Cognitive Neuropsychology, 11 (4), 435–458. Hirsh, K., & Funnell, E. (1995). Those old, familiar things: Age of acquisition, familiarity and lexical access in progressive aphasia. Journal of Neurolinguistics, 9, 23–32. Hodges, J. R., Graham, N., & Patterson, K. (1995). Charting the progression of semantic dementia: Implications for the organization of semantic memory. Memory, 3, 463–495. Hodges, J. R., & Patterson, K. (1995). Is semantic memory consistently impaired early in the course of Alzheimer’s disease? Neuroanatomical and diagnostic implications. Neuropsychologia, 33 (4), 441–459. Hodges, J. R., Patterson, K., Oxbury, S., & Funnell, E. (1992). Semantic dementia. Progressive ﬂuent aphasia with temporal lobe atrophy. Brain, 115, 1783–1806. Hodges, J. R., Salmon, D. P., & Butters, N. (1991). The nature of the naming deﬁcit in Alzheimer’s and Huntington’s disease. Brain, 114, 1547–1558. Howard, D. (1995). Lexical anomia: Or the case of the missing lexical entries. Quarterly Journal of Experimental Psychology, 48A (4), 999–1023. Howard, D., & Orchard-Lisle, V. (1984). On the origin of semantic errors in naming:

Mechanisms of lexical selection and the anomias

167

Evidence from the case of a global aphasic. Cognitive Neuropsychology, 1 (2), 163–190. Huber, W., Poeck, K., Weniger, D., & Willmes, K. (1983). Aachener Aphasietest (AAT). Göttingen: Hogrefe. Humphreys, G. W., Riddoch, M. J., & Quinlan, P. T. (1988). Cascade processes in picture identiﬁcation. Cognitive Neuropsychology, 5 (1), 67–103. Jescheniak, J., & Levelt, W. (1994). Word frequency eﬀects in speech-production: Retrieval of syntactic information and of phonological form. Journal of Experimental Psychology: Learning, Memory, and Cognition, 20, 824–843. Jescheniak, J. D., & Schriefers, H. (1998). Discrete serial versus cascaded processing in lexical access in speech production: Further evidence from the co-activation of near-synonyms. Journal of Experimental Psychology: Learning, Memory, and Cognition, 24, 1256–1274. Kremin, H., Lorenz, A., de Wilde, M., Perrier, D., Arabia, C., Labonde, E., et al. (2003). The relative eﬀects of imageability and age-of-acquisition on aphasic misnaming. Brain and Language, 87, 33–34. Lambon Ralph, M. A., Graham, K. S., Ellis, A. W., & Hodges, J. R. (1998). Naming in semantic dementia – what matters? Neuropsychologia, 36 (8), 775–784. Levelt, W. J. M. (1989). Speaking. From intention to articulation. Cambridge, MA: MIT Press. Levelt, W. J. M., Roelofs, A., & Meyer, A. S. (1999). A theory of lexical access in speech production. Behavioral and Brain Sciences, 22, 1–75. Miceli, G., Silveri, M. C., Villa, G., & Caramazza, C. (1984). On the basis for agrammatics’ diﬃculty in producing main verbs. Cortex, 20, 207–220. Nickels, L. (1997). Spoken word production and its breakdown in aphasia. Hove, UK: Psychology Press. Nickels, L., & Howard, D. (1994). A frequent occurrence? Factors aﬀecting the production of semantic errors in aphasic naming. Cognitive Neuropsychology, 11 (3), 289–320. Rapp, B. (Ed.) (2001). Handbook of cognitive neuropsychology: What deﬁcits reveal about the human mind. Philadelphia, PA: Psychology Press. Rapp, B., Benzing, L., & Caramazza, A. (1997). The autonomy of lexical orthography. Cognitive Neuropsychology, 14 (1), 71–104. Rapp, B., & Caramazza, A. (1997). The modality-speciﬁc organization of grammatical categories: Evidence from impaired spoken and written sentence production. Brain and Language, 56, 248–286. Roelofs, A. (1992). A spreading-activation theory of lemma retrieval in speaking. Cognition, 42, 107–142. Roelofs, A. (1997). The WEAVER model of word-form encoding in speech production. Cognition, 64, 249–286. Salmon, D. P., & Hodges, J. R. (2001). Frontotemporal dementia (Pick’s disease). In J. R. Hodges (Ed.), Early onset dementia: A multidisciplinary approach (pp. 47–73). Oxford, UK: Oxford University Press. Shallice, T. (1988). From neuropsychology to mental structure. Cambridge, UK: Cambridge University Press. Snowden, J. S., Goulding, P. J. & Neary, D. (1989). Semantic dementia: A form of circumscribed cerebral atrophy. Behavioral Neurology, 2, 167–182.

11 Repetitive verbal behaviours in PML An exploratory study of conversation Nicole Müller, Alana Kozlowski and Pattie Doody Introduction The science of repetitive verbal behaviours is only one of numerous areas to which Chris Code has made contributions that are impossible to ignore (see e.g., Code, 1982a, 1982b, 1989; Code & Ball, 1994). Repetitive verbal behaviours (RVBs) occur in the presence of a variety of neurological dysfunctions. There is, moreover, a multitude of taxonomies and characterizations that incorporate various parameters of description. Table 11.1 (adapted from Wallesch, 1990, p. 134; see also Guendouzi & Müller, 2006, pp. 169–170) gives an indication of the variety of terminologies and deﬁnitions encountered in the available literature. Literature on RVBs in progressive neurological conditions, including various types of dementia, shows that RVBs such as echolalia and perseverations tend to be more common in the more advanced stages of the disease in question (e.g., dementia of the Alzheimer’s type), and relatively uncommon in earlier stages (see e.g., Cummings, Benson, Hill, & Read, 1985; Shindler, Caplan, & Hier, 1984; Sjogren, Sjogren, & Lindgren, 1952; Wallesch, 1990, pp. 143, 149). Whereas the studies cited so far classify RVBs mainly on the basis of form and structure, there is also a body of literature that focuses more on the repetition and redundancy of ideas, information and topics (see e.g., the studies described in Ulatowska & Chapman, 1995). The dominant perspective on RVBs in the available literature can be described as taxonomic and symptomatic. In other words, the impetus for research is the search for motor and neurological correlates of diﬀerent types of RVBs, and the research paradigms are, of necessity, experimental and quantitative, leading to a distillation of generalizable characteristics and classiﬁcations of RVBs across distinguishable neurological impairments. To date, there is less work that investigates the communicative context of RVBs, their contributions (detrimental or facilitating) to how conversations are maintained and managed, and their emergence as conversations unfold (see e.g., Body & Parker, 2005; Guendouzi & Müller, 2006; Müller & Guendouzi, 2005; Perkins, Body, & Parker, 1995; Perkins, Whitworth, & Lesser, 1998). Continuing eﬀorts in this

Repetitive verbal behaviours in PML 169 Table 11.1 Types and deﬁnitions of RVBs, with sources Type and deﬁnition Echolalia “the automatic and compulsive repetition of words by the patient in the absence of the understanding of their meaning” “a reﬂex automatism of verbal response, providing an empty, stereotyped quality to speech”

Sources

“repetition of the investigator’s utterances with or without mild changes in position and choice of words”

Brain (1965, p. 105) Hecaen and Albert (1978, pp. 74–75) Huber et al. (1982, p. 80)

Iteration repetition of parts of words (sounds or syllables), included in Ludlow et al.’s deﬁnition of palilalia

Machetanz et al. (1988)

Palilalia “the involuntary repetition two or more times of a terminal word, phrase or sentence” “a disorder of speech characterized by compulsive repetition of a phrase or word that the patient reiterates with increasing rapidity and with a decrescendo of voice volume” “the reiteration of single or partial syllables or combinations of syllables many times with increasing rate” Perseveration “the recurrence, out of context and in the absence of the original stimulus, of some behavioral act” Recurring/recurrent utterances “a subgroup of speech automatisms which consist exclusively of syllables or sequence of syllables which are linked up in their production” “an utterance made up of either real words or a non-meaningful string of speech sounds which some aphasic patients produce either every time they produce speech or just sometimes” “The term recurrent utterance is most usually reserved to describe repeated and unchanging utterances made up of recognizable words which some aphasic individuals produce either every time they attempt speech, or almost every time they attempt speech” Stereotypy “a permanent stereotyped verbal expression with or without linguistic meaning unconsciously and involuntarily uttered” “set phrases that are used recurrently but usually communicatively adequate” Speech automatism “a constantly recurring utterance which is formally rigid, consists of neologistic sequences of syllables, interchangeable words or phrases, does not ﬁt into the linguistic context either lexically or syntactically, and which the patient produces in contrast to the intention expected by his interlocutors” Speech tics: (a) coprolalia: “all unprovoked swearing using single words or phrases” (b) word tics: “any meaningful word interjected into speech and not part of communicative speech or hesitation phenomena”

Critchley (1970, p. 201) Boller et al. (1973, p. 1117) Ludlow et al. (1982, p. 353) Buckingham et al. (1979, p. 329) Huber et al. (1982, p. 81) Code (1982a, p. 141) Code (1989)

Alajouanine (1956, p. 6) Huber et al. (1982, p. 82) Huber et al. (1982, p. 81)

Ludlow et al. (1982, p. 353) Ludlow et al. (1982, p. 353)

170

Müller et al.

direction are necessary, since any impairment of communicative functioning has an immediate impact on quality of life. This chapter investigates the occurrence of RVBs in the spoken language of a person with progressive multifocal leukoencephalopathy (PML) in the context of AIDS (see below for more detail). According to McCabe, Sheard and Code (2002), there are numerous studies that cite impaired communication skills in the context of HIV/AIDS. However, few studies have investigated language or speech impairment in a comprehensive, contextually embedded and function-oriented manner. McCabe et al.’s study demonstrates that a wide-ranging array of acquired communicative diﬃculties arise out of HIV/ AIDS, and calls for “[f]urther investigation to explore the functional use of language by people with HIV and their pragmatic skills”. This chapter is intended as a small contribution to this area of inquiry.

RVBs in PML: A case study Method Participants This study involves the analysis of conversational behaviours between two participants (see below for details concerning data collection and analysis), A and D. A is the second author of this chapter, a speech-language pathologist and clinical instructor, and currently a doctoral student. D is a male aged 38 years, diagnosed with progressive multifocal leukoencephalopathy consequent to Acquired Immune Deﬁciency Syndrome (AIDS). PML is a demyelinating disease of the central nervous system, caused by the JC virus (named after the initials of the person in whom it was found) (Wyen, Lehmann, Fatkenheuer, & Hoﬀmann, 2005). It is estimated that in excess of 70% of adults harbour the virus; however it remains harmless in persons with healthy immune systems, but in persons with immune systems compromised by the Human Immunodeﬁciency Virus (HIV) or AIDS, the JC virus causes PML. The lesions associated with PML typically occur in the hemispheric white matter, but have also been documented in the basal ganglia, the brain stem, the cerebellum (Berger, 2004) and, exceptionally, in the spinal cord (Wyen et al., 2005). The multiple, somewhat unpredictable lesion sites cause a wide variety of cognitive and behavioural symptoms, many of which impact communication. D’s speech communication is severely impaired, owing to hypokinetic dysarthria and frequent RVBs. His speech is characterized by decreased vocal intensity, harsh and breathy voice quality, reduced prosodic contours (both in amplitude and variety), and short, rapid rushes of speech with imprecise articulation. Conversational speech ranges from a whisper, to a quiet strained voice with obvious pitch breaks, to falsetto productions. Reduced intensity is a primary contributor to communication breakdown. Overall, there is lack of

Repetitive verbal behaviours in PML 171 control over pitch contours, and little variability. D does not repair a communication breakdown by adjusting stress on a misunderstood phrase or word. RVBs include the repetition of the pitch contour, as well as the linguistic content. Overall, speech is perceptually fast, with some parts of utterances (including RVBs, but not restricted to them) having an accelerated rate of production. These “rushes” are accompanied by decreased articulatory precision. The range of movement of visible articulators is reduced during speaking tasks (compared to non-speech tasks). No adjustment of speaking rate or articulatory amplitude or precision is noted when D is aware of communication breakdown. Micrographia aﬀects D’s writing to the extent that he is no longer willing to use writing as a communicative tool. He rarely produces gestures to aid communication, and those that occur only infrequently aid in clarifying the intended message. Facial aﬀect varies, is ﬂat at times, but at other times unremarkable. D has been participating, inconsistently, in speech therapy for approximately 18 months. The intelligibility of his speech has progressively worsened to the point that he was found 0% unintelligible on the single word portion of the Assessment of Intelligibility of Dysarthric Speech (Yorkston & Beukelman, 1981). It was noted during therapy that D could produce loud vocalizations, and often intelligible speech when the task was non-communicative (such as producing a long [] vowel, which he can sustain for 4.5 s, at 80 dB) and/or involves rote (such as counting, or producing other over-learned phrases). Data The conversation between A and D that forms the basis of analysis for this chapter took place in the speech and hearing clinic D has been attending. It was recorded approximately 2 years after D’s diagnosis with PML. A and D have known each other for approximately 18 months, during which time A has been D’s speech therapist. While there are some elements of “therapy” in the conversation (such as A prompting D to monitor and attempt to raise his vocal intensity, or scaﬀolding D’s turn by prompting him to produce “big key words”), there is no focused therapy activity, much less any therapeutic “drill”. In all, approximately 27 minutes of conversation were recorded and transcribed orthographically. This conversation was closely analysed, and the patterns arising from this micro-analysis were compared with two other recorded conversations between the same interlocutors, and were found to be conﬁrmed. The focus of analysis is the linguistic interactional aspects of the conversation, rather than the quality of the speech signal, the prosodic or gestural characteristics. While it is of course understood that those characteristics are integral parts of conversational interaction, limitations of space prohibit a detailed holistic analysis of all component systems of the conversation and their interaction.

172

Müller et al.

Descriptive and analytic framework The descriptive framework for the linguistic and interactional characteristics of D’s RVBs is provided by systemic functional linguistics (SFL). In recent years, SFL has become an increasingly popular tool with which to approach disordered speech and language in a variety of social contexts. Among the characteristics that make SFL relevant to clinical contexts, Halliday (2005, p. 134) suggests that: [it] presents language as a semogenic (meaning-making) resource, one governed by tendencies not rules, and whose categories (as is typical of semiotic systems) are “fuzzy” rather than determinate. It is formulated in terms of strengths, rather than of deﬁcits or constraints: what the speaker can do (and what the language “can do”). Thus SFL has a social, context-embedded orientation, its focus is the linguistic choices an individual makes to construct meaning in social interactions (Halliday & Matthiessen, 2004; Martin, Matthiessen, & Painter, 1997). This social-functional orientation is particularly relevant if one wishes to do justice to persons whose oral or written language is impaired, and who, consequently, suﬀer signiﬁcant disempowerment in cultures that highly value these skills (Armstrong, 2005). In the course of this chapter, we present a structural characterization of D’s RVBs, and analyse how they function in conversation. To this end, we use the categories of Theme/Rheme, and Given/ New information. Patterns Structural characteristics of D’s RVBs D produces 69 verbal utterances that are at least partially intelligible and thus lend themselves to analysis. In these utterances, 99 RVBs of various types occur (mean: 1.43 per utterance). Table 11.2 lists the types of RVBs encountered in this sample. Single word repetitions clearly dominate, and also have the highest range of repetition (with a maximum of ﬁve, encountered once; the highest proportion being a single repetition of a single word, encountered 28 times). Table 11.2 Types of RVBs, and range of repetitions Type Single word N 55 % 55.5 Range 1–5

Elliptical Expanclause sion

Part Noun False Clause Prepositional word group start phrase

Synonym

14 14.14 1–3

6 6.06 1–4

1 1.01 1

12 12.12 1

4 4.04 1–2

4 4.04 1

2 2.02 1

1 1.01 1

Repetitive verbal behaviours in PML 173 The most common single word repetitions are “yes” and “no” (22 times altogether), followed by nouns (N = 16) and adjectives (N = 12). Verbs are far less frequent (N = 4), and there is a single instance of “where”. Thus single word RVBs in D’s speech are content words, rather than reiterations of function words.1 Diﬀerent types of RVBs often occur in the same utterance, as illustrated in the examples described later. As discussed in detail by Wallesch (1990), classifying RVBs is not altogether straightforward. The closest category of those quoted in Table 11.1 is that of palilalia (or iteration, included under palilalia, see above). However, many of D’s RVBs are not terminal, or utterance-ﬁnal (as speciﬁed in Critchley, 1970). The deﬁnitions of palilalia make no reference to the contextual embedding, or linguistic contribution, of RVBs. To this end, an examination of RVBs in their linguistic context is necessary, which is undertaken in the following sections. Theme and Rheme, and Given versus New information Theme and Rheme are categories in the analysis of a clause as message. According to Halliday and Matthiessen (2004, p. 58), a “clause has meaning as a message; the Theme is the point of departure for the message. It is the element that the speaker selects for ‘grounding’ what he is going to say.” In English, as in many other languages, Theme and Rheme are signalled by position: the Theme occupies the initial position in the clause; the Rheme consists of the rest of the clause (see Halliday & Matthiessen, 2004, p. 64; Martin et al., 1997, pp. 23–24). The boundary between Theme and Rheme is drawn such that the Theme of a clause “ends with the ﬁrst constituent [of a clause] that is either participant, circumstance, or process” (Halliday & Matthiessen, 2004, p. 79).2 This participant, circumstance, or process in thematic position is referred to as the topical Theme, and this is what our analysis focuses on. SFL treats information structure as a system that is separate from thematic structure; however, in terms of language use, the two systems are closely linked. Whereas Theme and Rheme are constituents of the clause, Given and New information are constituents of what in SFL is referred to as the information unit, which may be coextensive with a clause, but may also extend beyond a single clause. The typical, unmarked state of aﬀairs is in fact that the information unit maps onto a single clause, and that Given information corresponds to the topical Theme, and New information to the Rheme. Thus the unmarked sequence of information is Given before New (Halliday & Matthiessen, 2004, pp. 87–89). While acknowledging that Theme/Rheme and Given/New information are two separate systems and conceptually diﬀerent categories, we present their analyses together, since the patterns in our data support this step. Having said that information structure and thematic structure map closely onto each other, we also have to keep in mind that it is characteristic of conversational

174

Müller et al.

language that many utterances do not consist of complete clauses. The productions in our data are no exception to this tendency. Of D’s 69 at least partially intelligible utterances, 21 consist of minor clauses (“yes”, “no”, or “right”, typically repeated at least once). From the rest of his utterances, some interesting patterns emerge. Many of D’s utterances consist of clause fragments that lack a Theme, and consist of New information only. The ellipsed, “understood” Theme is typically represented by the Rheme of a clause in A’s preceding utterance, or by information that is easily recoverable in the context of the conversation (such as a reference to either D himself, or to another person known to both interlocutors). Example 1 illustrates this pattern: Example 1 1 A: how was your weekend? 2 D: boring steroid shot got a steroid shot steroi- steroid shot st- steroid shot 3 A: I think you just told me it was boring and you got a steroid shot 4 D: yes yes The Rheme of A’s initial clause represents new information; the “weekend” has not been mentioned previously. This becomes the “understood”, ellipsed Theme, now Given information, of D’s ﬁrst clause fragment, with a quasiRheme representing New information: “boring”. The repetitive sequence that begins with “steroid shot” contains a clause fragment consisting of Process + Goal (“got a steroid shot”), with the Actor ellipsed (“I”). The ellipsed element, structurally the Actor-subject of the clause fragment, is easily recoverable from the situational context, hence can be treated as Given information, and can therefore justiﬁably be ellipsed. D’s repetition only encompasses the focus of New information, the most salient part of the quasi-Rheme of his clause fragment (“got” as a Process is semantically “light” in the sense that it does not contribute information that cannot be treated as recoverable from the Goal; the default relationship between ellipsed subject and Goal-complement is one of “getting”, or “receiving”). In turn 3, A expands on D’s utterance, and by means of projection (“I think you just told me”) recasts the information received from D into two clauses with complete Theme–Rheme structures, which are conﬁrmed as an accurate representation of a state of aﬀairs by D in turn 4. Thus the two interlocutors collaborate at arriving at the default, unmarked Theme–Rheme, Given–New sequence. D’s utterance in Example 2 shows the same pattern of Theme-less clause fragments, and expansion of clause fragments:3 Example 2 7 A: what does what do the steroid shots do? 8 D: P pump me up p^ p^ p^ pump (unintelligible) me strong strong dick hard dick hard make your dick hard dick hard make your dick hard

Repetitive verbal behaviours in PML 175 D’s utterance begins with what we have classiﬁed as a false start, which turns into a clause fragment representing a New Rheme to an ellipsed Given Theme (“steroid shots”, or “they”). The second clause fragment (“me strong strong”) contains neither Actor-Subject nor Process-Verb group. Again, the Actor is easily recoverable as Given information (“they” / “steroid shots”). Both the process and the participant roles of “me” and “strong” are inferable, because of the default semantic relationship between “steroid shots”, “me” and “strong”, which is one of causing (“make” or the like) an eﬀect of being “strong” (hence the participant role of Attribute) on a person, “me” (hence the participant role of Goal). What is reiterated in this clause fragment is again the focus of New information; “me” is Given. The repetitive sequence that starts with “dick hard” shows a similar internal structure. The participant roles are the same as with “me” and “strong”; that is, Goal and Attribute, and both represent the focus of New information in an incomplete Rheme to an ellipsed, Given Theme. The Rheme is completed by the addition of the Process (“make”), and the sequence of partial and completed Rheme is repeated. Example 3 represents a similar pattern of expansion and RVBs in relation to thematic and information structure: Example 3 142 A: you’re telling me the kids down the street pushed you and you ended up with this bruise on your knee 143 D: yes yes bad bruise purple purple 144 A: yeah it’s awful 145 D: purple purple it’s pur pur purple 146 A: give me a nice= ((low pitch, moderately loud)) 147 A: =pur pur pur purple it’s purple and green green In turn 143, D conﬁrms A’s summary of previous turns by reiterating part of the shared information, “bad bruise”, and then proceeds to expand with a repeated New element of information, which again can be construed as the New Rheme to a Given Theme (“it”, or “the bruise”). D appears to treat A’s turn 144 as an indication that she has not understood him (and correctly so). This is probably due to A’s prevailing strategy of providing expanded, completed clause structures based on D’s utterances, for D to conﬁrm (illustrated in Examples 2 and 3). Therefore, while “purple” in turn 145 is strictly speaking not New information as regards the text as a whole (in hindsight, as it were), it can be treated thus for the purposes of reconstructing the unfolding text, the achievement of meaning creation between the interactants. Thus D treats “purple” as New, and completes the Given Theme + New Rheme structure after a repetition of the themeless Rheme. In fact, as indicated by A’s therapy cue in turn 146, there is still no mutual understanding, and D produces another turn with the by now familiar sequence of repetition and expansion: This time, part-word repetitions of “purple” are followed by a

176

Müller et al.

completed and, here, expanded Given Theme + New Rheme sequence, where “purple” is expanded on by the addition of a further adjective, which is in turn repeated. In most of his turns, D only attempts to introduce one or two New elements of information. Example 4 shows a diﬀerent structure: All the information is new, and is not “latched onto” contextually inferable or Given information: Example 4 44 D: (unintelligible) sex sex sex T T T-cells ((holding up 3, then 4 ﬁngers)) three eleven Cooper Cooper Cooper tol my mom Cooper Cooper Cooper Dr Cooper tol my mom (unintelligible) ((shakes 4 ﬁngers)) Cooper Cooper Cooper 45 A: I know who we are talking about, Dr Cooper 46 D: Cooper ((very high pitched voice; close to crying?)) you’re doing great D is unable to integrate the ﬁrst four New items into any kind of meaning sequence, and changes tack, beginning again with “Cooper”, which he is able after two reiterations to expand into a Theme + Rheme sequence (containing New information only). However, this is still not successful, since the information necessary to complete the verbal Process “told” (in SFL terms, the “verbiage”) is not forthcoming. After another attempt, starting again with three productions of “Cooper”, D gives up and A takes over, conﬁrming understanding of “Dr Cooper”, which in turn is re-conﬁrmed by D in turn 46 by a single production of “Cooper”. Of the 99 RVBs in this conversation, only 9 contain Given information as regards the text (in other words, information that has been previously introduced). However, of these, three contain information that cannot be treated as Given, or shared for the purposes of the exchange, since in each case, A’s preceding utterance signals that she still requires conﬁrmation, as in Example 5. Further, three examples represent a rephrasing of a Theme–Rheme sequence oﬀered by A (using pronouns and ellipsis of the Predicator); these serve as ﬁnal conﬁrmation of shared information; see Example 6: Example 5 104 A: are we talking about Fran or your dad? 105 D: Fran Fran Fran Fran Example 6 128 A: kids pushed you. I just heard you D 129 D: you did you did ((smiles)) The tendency for RVBs to associate with New information is also conﬁrmed by the fact that there are only ﬁve instances in the text where D introducing

Repetitive verbal behaviours in PML 177 New information does not co-occur with either an identiﬁable RVB, or the deterioration of his speech to such an extent that it becomes unintelligible (and may therefore have contained RVBs; there are two such instances). One instance of non-repeated New information is represented by “you’re doing great” in Example 4 above, and we may speculate whether it is signiﬁcant that this example represents a direct quotation from another speaker, and that the clause “you’re doing great” is highly formulaic; both factors may assist in its ﬂuent production. However, these questions await further investigation.

Discussion The severe dysarthria, as well as the high proportion of RVBs in D’s speech pose a considerable challenge to communicative success. In order to understand how these challenges are met and dealt with, it makes sense to analyse these speech patterns in the context of a real communicative event. The detailed analysis of a conversation between D and A has shown a pattern of D consistently violating the unmarked Given Theme + New Rheme structure that is the default for English clause structure. The ellipsis of Given Themes is not an uncommon feature of English conversational speech. In fact, the consistent reiteration of Given Themes where they are clearly and unambiguously recoverable would make for very strange conversations indeed. However, D’s utterances show a pattern where a single New item is introduced, and then expanded into a “virtual” complete Rheme to an ellipsed topical Theme. Further, we found that RVBs pattern with New information. In addition, we noted a strategy on the part of A to expand and integrate the New information provided by D into unmarked Given Theme + New Rheme sequences for D to conﬁrm. Examples 3 and 5 above illustrate that D actively uses this collaborative pattern to advance the conversation. It therefore appears that D’s presentation of New information utterances initially is a strategy that emerged out of his severe communication impairment. D’s ability to sustain phonation and maintain articulatory precision is limited, as is his ability to vary pitch. The association of RVBs with New information introduces a further complication, because RVBs take up some of the available phonation resources in an utterance, thus further limiting D’s meaning output. In this light, starting utterances with the most salient item, the focus of New information, and relying on an interlocutor to “ﬁll in the gaps” either mentally or out loud, makes a lot of sense. The dialogue can be advanced collaboratively, while D avoids expending voice on information that is already Given, or inferable from the situational context. In this context, the positional constraints for palilalia described in some sources are interesting. Critchley (1970) and Singh and Kent (2000) state in their deﬁnitions that the reiterations of words and phrases typically occur towards the middle and end of utterances. A re-examination of the data that gave rise to these deﬁnitions might well conﬁrm the pattern we found with D, namely that there is a strong association with New information and repetitiveness, if the

178

Müller et al.

speakers’ productions largely followed the unmarked Given Theme + New Rheme sequence of English clauses. D’s RVBs are not restricted to utterance internal or utterance ﬁnal position, but as we have seen, they do not follow “canonical” clause structure. Garratt, Bryan, and Maxim (1999) noted that palilalia in their participants was more evident in utterances with increased propositional load. In other words, more “meaningful” speech contained more instances of palilalia, while automatic speech tasks had none, which led the authors to conclude that processing demands relate to the emergence of palilalia, and to hypothesize that additional processing demands “stress” the damaged motor speech system. In contrast, Boller et al. (1973) characterized palilalia as a disturbance of speech, rather than language, with no defect in the abilty to handle the linguistic and symbolic aspects of communication. D’s RVBs, which appear to structurally fall under the category of palilalia as deﬁned above (Table 11.1), make us inclined to prefer Garratt et al.’s view over Boller et al.’s. Whether utterance patterns in a person with compromised speech ability are the result of deliberate choices to structure his or her output to maximum eﬀect, or whether they are an emergent product of multiple interacting factors, an awareness of the patterns (and how they may further or hinder communication) on the part of interlocutors is crucial in order to maximize communicative success, and the ability of the individual with impaired speech to participate in society. Eggins (1994) points out that it is through sustained dialogue that individuals are able to establish and maintain social roles and identities. It is particularly important to give individuals with progressively worsening conditions, such as D, the wherewithal to maintain the ability to “speak for themselves”, and as themselves (if with the help of others) for as long as possible. The linguistic behaviours documented here on the basis of a single conversation were conﬁrmed in other interactions. It became clear that D constructed the client–clinician relationship as essentially one of equal power and control, and in fact he is able to “turn the tables” on the clinician and teases her for her lack of understanding, in eﬀect reconstructing and repositioning the communicative impairment from a problem of production to one of reception.

Notes 1 We include “yes”, “no” and “where” in the category of content words (although they also clearly have grammatical functions), on the grounds that they can stand alone in conversational speech, and thus carry the content of a message, unlike function words (such as determiners). 2 A full discussion of diﬀerent types of themes (topical, interpersonal, and metafunctional) is beyond the scope of this chapter. For further detail, see Halliday and Matthiessen (2004, chapter 3). 3 We in no way intend to shock any of our readers by the choice of examples. The data are what the data are. Those accustomed to working with neurologically impaired populations frequently encounter language that may be considered

Repetitive verbal behaviours in PML 179 oﬀensive by some, or not suitable for persons below a certain age. In fact, D takes great delight in A’s misunderstanding of the potentially oﬀensive item (A interprets it as “dig”; “I was picturing gardening”, turn 42) and having to rely on D’s mother to clarify. Thus D is not only able but willing to use the breakdown of communication to humorous eﬀect.

References Alajouanine, T. (1956). Verbal realization in aphasia. Brain, 79, 1–28. Armstrong, E. (2005). Language disorder: A functional linguistic perspective. Clinical Linguistics and Phonetics, 19, 137–153. Berger, J. (2004). Progressive multifocal leukoencephalopathy in the AIDS era. Journal of Neurovirology, 10, 37. Body, R., & Parker, M. (2005). Topic repetitiveness after traumatic brain injury: An emergent, jointly managed behaviour. Clinical Linguistics and Phonetics, 19, 379–392. Boller, F., Boller, M., Denes, G., Timberlake W. H., Zieper, I., & Albert, M. (1973). Familial palilalia. Neurology, 23, 1117–1125. Brain, R. (1965). Speech disorders. London: Butterworth. Buckingham, H. W., Whitaker, H., & Whitaker, H. A. (1979). On linguistic perseveration. In H. Whitaker & H. A. Whitaker (Eds.), Studies in neurolinguistics (Vol. 4, pp. 328–352). New York: Academic Press. Code, C. F. S. (1982a). Neurolinguistic analysis of recurrent utterance in aphasia. Cortex, 18, 141–152. Code, C. F. S. (1982b). On the origins of recurrent utterances in aphasia. Cortex, 18, 161–164. Code, C. F. S. (1989). Speech automatisms and recurring utterances. In C. F. S. Code (Ed.), The characteristics of aphasia (pp. 155–177). London: Taylor & Francis. Code, C. F. S., & Ball, M. J. (1994). Syllabiﬁcation in aphasic recurring utterances: Contributions of sonority theory. Journal of Neurolinguistics, 8, 257–265. Critchley, M. (1970). Aphasiology and other aspects of language. London: Arnold. Cummings, J. L., Benson, D. F., Hill, M. A., & Read, S. (1985). Aphasia in dementia of the Alzheimer’s type. Neurology, 35, 394–397. Eggins, S. (1994). An introduction to systemic functional linguistics. London: Pinter. Garratt, H., Bryan, K, & Maxim, J. (1999). Palilalia in progressive supranuclear palsy: Failure of the articulatory buﬀer and subcortical inhibitory systems. In B. Maassen & P. Groenen (Eds.), Pathologies of speech and language: Advances in clinical phonetics and linguistics (pp. 245–252). London: Whurr. Guendouzi, J. A., & Müller, N. (2006). Approaches to discourse in dementia. Mahwah, NJ: Lawrence Erlbaum Associates, Inc. Halliday, M. A. K. (2005). Guest contribution. A note on systemic functional linguistics and the study of language disorders. Clinical Linguistics and Phonetics, 19, 133–135. Halliday, M. A. K., & Matthiessen, C. M. I. M. (2004). An introduction to functional grammar (3rd ed.). London: Arnold. Hecaen, H., & Albert, M. L. (1978). Human neuropsychology. New York: Wiley. Huber, W., Poeck, K., & Weniger, D. (1982). Aphasie. In K. Poeck (Ed.), Klinische neuropsychologie. Stuttgart: Thieme. Ludlow, C. L., Polinsky, R. J., Caine, E. D., Bassich, C. J., & Ebert, M. H. (1982).

180

Müller et al.

Language and speech abnormalities in Tourette syndrome. Advances in Neurology, 35, 351–361. McCabe, P., Sheard, C., & Code, C. (2002). Acquired communication impairment in people with HIV. Journal of Medical Speech-Language Pathology, 10, 183–199. Machetanz, J., Schönle, P. W., & Benecke, R. (1988). Iterative Dysarthrie beim M. Parkinson. Nervenarzt, 59, 559–661. Martin, J. R., Matthiessen, C. M. I. M., & Painter, C. (1997). Working with functional grammar. London: Arnold. Müller, N., & Guendouzi, J. A. (2005). Order and disorder in conversation: Encounters with dementia of the Alzheimer’s type. Clinical Linguistics and Phonetics, 19, 393–404. Perkins, L., Whitworth, A., & Lesser, R. (1998). Conversing in dementia: A conversation analytical approach. Journal of Neurolinguistics, 11, 33–53. Perkins, M., Body, R., & Parker, M. (1995). Closed head injury: Assessment and remediation of topic bias and repetitiveness. In M. Perkins & S. Howard (Eds.), Case studies in clinical linguistics (pp. 293–320). London: Whurr. Shindler, A. G., Caplan, L. R., & Hier, D. B. (1984). Intrusions and perseverations. Brain and Language, 23, 148–158. Singh, S., & Kent, R. D. (2000). Singular’s illustrated dictionary of speech-language pathology. San Diego, CA: Singular. Sjogren, T., Sjogren, H., & Lindgren, A. G. H. (1952). Morbus Alzheimer and morbus Pick. A genetic, clinical and pathoanatomical study. Acta Psychiatrica Neurologica Scandinavica, (Suppl.), 82, 1–152. Ulatowska, H. K., & Chapman, S. B. (1995). Discourse studies. In R. Lubinski (Ed.), Dementia and communication (pp. 115–130). San Diego, CA: Singular. Wallesch, C.-W. (1990). Repetitive verbal behaviour: Functional and neurological considerations. Aphasiology, 4, 133–154. Wyen, C., Lehmann, C., Fatkenheuer, G., & Hoﬀmann, C. (2005). AIDS-related progressive multifocal leukoencephalopathy in the era of HAART: Report of two cases and review of the literature. AIDS Patient Care and STDs, 19, 486–494. Yorkston, K. M., & Beukelman, D. R. (1981). Assessment of intelligibility of dysarthric speech. Tigard, OR: CC Publications.

12 Multiparty interactions in aphasia Alison Ferguson

This chapter describes a line of future enquiry in relation to understanding how people with aphasia communicate in groups, and is inspired by two of the major foci of Chris Code’s work in aphasiology, namely his long-standing concern that services provided for people with aphasia be directed to the individual needs of the person (Code & Müller, 1995, pp.1–2), and that emotional response and support is integral to recovery in aphasia (Code, Hemsley, & Herrmann, 1999). Code has played an important role in drawing together the diverse range of approaches to the assessment and treatment of aphasia, which have included group therapy, both in his edited books (Code & Müller, 1995) and through his role as journal editor for Aphasiology, and more recently for the International Journal of Language and Communication Disorders. He has been a strong advocate for the need for an eclectic approach to aphasia therapy, for example, he states, “The major ability of the therapist involved in the treatment of aphasia is to be able to carefully select the most appropriate approach to help support those individuals with aphasia in achieving their goals.” (Code & Müller, 1995, p. 46). In his own research he continues to underscore the surprisingly low proportion of services that provide this eﬃcacious and eﬃcient method of service delivery (Katz et al., 2000). Group processes work to re-establish the sense of identity and selfesteem of participants, and Chris has always had considerable commitment to the role of self-help groups in this regard both at a personal level,1 and professionally (Code, Eales, Pearl, Conan, Cowin, & Hickin, 2001), with the development of a simple tool through which counseling support could be oﬀered (Code & Müller, 1992; Code, Müller, Hogan, & Herrmann, 1999). This chapter takes these two notions (that group therapy is an important way to provide services and that group interactions provide emotional support for recovery) as foundational “givens,” and seeks to push our understanding one step further through attempting to identify those key elements within the myriad of interactional processes that make groups work. Understanding these processes allows us to develop our skills in running groups, to educate others to run groups, and to facilitate the interactions of others who may be involved in group interactions with people with aphasia.

182

Ferguson

Sampling interaction through monologue? Previous research on interaction involving people with aphasia has focused on one-to-one interactions, and these interactions have often been more monologic than dialogic, involving, for example, clinicians facilitating storytelling by the person with aphasia. However, there are questions regarding the representativeness of monologue. In a study that involved a monologic story-telling task (about a frightening experience), Ulatowska and colleagues (2001) looked at a range of discourse measures, quantitatively looking at the number of propositions, and qualitatively rating global structure, temporal sequence, reference, suspense, coherence, and clarity on a set of rating scales. They found no signiﬁcant relationship between discourse performance on these measures and measures of impairment (Western Aphasia Battery Aphasia Quotient and Cortical Quotient, and Token Test) or on functional measures (ASHA Functional Assessment of Communication Skills for Adults) (Ulatowska et al., 2001). This ﬁnding raises a number of questions. If we relate these ﬁndings to the World Health Organisation (WHO) ICF model of impairment, limitations on communication activity, and restrictions on social participation (WHO, 2001), then it would appear that monologic discourse performance is not related to impairment level measures or functional participation level measures. It might be argued that monologic performance describes communication at the level of activity solely, but ﬁndings such as these suggest that for the study of aphasia in the future, it is important that we move beyond monologic discourse sampling and consider more valid discourse tasks (Armstrong, 2000).

From monologue to dialogue Research on conversation has investigated more interactive exchanges, and with more usual communication partners, such as spouses, or volunteers. This type of research into interaction allows us to look at what might be regarded as the outstanding feature of conversations involving people with aphasia, which is trouble due to word-ﬁnding diﬃculty, and the repair work that is undertaken by the interactants to deal with the trouble and keep the conversation going (Booth & Perkins, 1999; Ferguson, 1994, 1998; Hengst, 2003; Lindsay & Wilkinson, 1999; Perkins, Crisp, & Walshaw, 1999). The adjustment that occurs between speakers in dyadic communication challenges our notions as to what constitutes the nature of aphasic impairment (Heeschen & Schegloﬀ, 1999; Helasvuo, Klippi, & Laakso, 2001). Beeke, Wilkinson, and Maxim (2001) present a brief description of two excerpts from interactions between moderate-severely aphasic speakers (one with a therapist, the other with a partner). Their analysis illustrates how the speakers combine co-occurring gesture with talk built on the previous utterances in order to convey meaning, despite substantial language impairment, and they suggest that the observed language performance demonstrates

Multiparty interactions in aphasia

183

adaptation rather than the impairment of aphasia itself (Beeke et al., 2001). Similar adaptation is discussed by Oelschlaeger and Damico (2003), who present a detailed conversation analysis of a series of eight conversations recorded at home between a man with aphasia and his wife over a 2-month period, illustrating the systematic use of conversational resources for collaboration. Their ﬁndings highlight adaptation by both partners in the exchange. The partner is shown to adapt her responses and repair work to the nature of the diﬃculties the person with aphasia is experiencing, and the person with aphasia is also suggested to be using repetition of his wife’s guesses of the word he is searching for as both an interactive strategy (e.g., as conﬁrmation, or disconﬁrmation, or as turn place-holder in the absence of being able to make an alternative contribution), as well as possibly a reauditorization strategy to assist his language processing (Oelschlaeger & Damico, 2003). As soon as we start to look at dyadic communication we begin to recognize the importance of the other partner and their way of communicating as a factor aﬀecting the aphasic language use. While this presents problems with control for reliability purposes, it reﬂects the fundamental nature of conversational exchange, and so presents a challenge that needs to be explored rather than minimized (such as occurs through elicitation strategies that minimize the partner’s contribution, such as monologic discourse elicitation). What we want to know is which partner communicative behaviors are more or less helpful, and to investigate this we need to try to observe and systematically describe these communicative behaviors rather than eliminate them from assessment.

Group interactions involving aphasic speakers Social participation typically involves conversational exchanges among groups of speakers rather than one-to-one dyadic talk. There is relatively little previous research that has looked closely at the communication of aphasic speakers and others within group settings. Early work by Wilcox and Davis (1977) compared the use of speech acts by people with aphasia in individual and group therapy, and found that aphasic speakers used more questions in the group situation than in individual sessions. They suggested that group therapy is more facilitative of the use of a greater variety of pragmatic behaviors (Wilcox & Davis, 1977). Klippi’s work in the area presents the most detailed account currently available of naturally occurring interactions in groups involving aphasic speakers, using conversation analysis methodology, identifying the multi-modal resources used by people with aphasia in group interactions, and their systematic use of the turn-taking and repair resources available (Klippi, 1996, 2003; Laakso & Klippi, 1999). Just as dialogue shows us a diﬀerent set of communicative behaviors from those we can observe in monologic discourse, group interaction will similarly provide an opportunity to observe how the person with aphasia manages

184

Ferguson

a distinctly diﬀerent set of communication challenges. However, an issue that arises in looking at the previous research on aphasia group interactions is how diﬀerent the group situations are – some involve chat, some involve more structured activities, and so on (Aten, Caligiuri, & Holland, 1982; Avent, 1997; Bollinger, Musson, & Holland, 1993; S. Brumﬁtt, 1995; S. M. Brumﬁtt & Sheeran, 1997; Drummond & Simmons, 1995; Glindemann & Springer, 1995; McCarney & Johnson, 2001; Wilcox & Davis, 1977; Worrall, 1995). What we have to recognize is that “group therapy” is likely to be diverse, both externally, in the sense that diﬀerent groups will be set up for diﬀerent purposes and diﬀerent mixes of participants, and also internally, in the sense that because there are multiple participants there will always be multiple agendas during the period in which groups of people meet. It can be useful to think of group therapy as an “activity type” in the sense that Levinson describes as: “any culturally recognized activity . . . a fuzzy category whose focal members are goal-deﬁned, socially constituted, bounded, events with constraints on participants, setting, and so on, but above all on the kinds of allowable contributions” (Levinson, 1992, p. 69). From this perspective, we can start looking at relevant aspects of setting, participants, goals, speech acts/sequences, how language is used (what is “allowable”), and the genres that occur within this activity.

Multiparty interaction The term “multiparty” interaction is being used increasingly to describe interactions involving multiple participants. The term is neutral as to whether the participants are in fact a “group”, for example a conversation among people waiting for a bus is a multiparty interaction, but not necessarily a group interaction in the sense that the people are not aﬃliated in any way. Nor does the interaction necessarily have a shared focus, for example students conversing among themselves in a classroom before a lecture starts may all be talking at once, but in many diﬀerent combinations and sub-groupings. The advantage of making the multiparty nature of the interaction the starting point is that it allows the analysis to explore potential issues such as the extent of group membership and shared focus, for example. On the other hand, if only two people within a larger group are talking, is this “multiparty,” or is it essentially no diﬀerent from a dialogue, and hence is there no need to invoke other analytic frameworks? One answer is that a multiparty interaction is occurring when there is at least one other listener to an exchange between at least two participants at any moment; that is, an actively engaged third-party is required to consider an interaction as “multiparty.” An example comes from Osvaldsson (2004) who analyzed laughter in two conferences involving clients, family, and staﬀ from youth detention homes. Osvaldsson noted that while in a two-party exchange laughter ﬁts into the turn-taking structure (Sacks, Schegloﬀ, & Jeﬀerson, 1974) in the sense that one party initiates and the other follows, in the multiparty interaction the

Multiparty interactions in aphasia

185

non-speaking participants use laughter as their contribution – they can use laughter to initiate, to join in unison, or to indicate disagreement by withholding laughter, that is, “The initiation of laughter by the other participants provides for the multiparty aspects of these exchanges” (Osvaldsson, 2004, p. 542, italics as per original). Multi-modal resources such as eye-gaze, facial and other movement, and other vocal behaviors that regulate turn-taking and provide information about emotional/attitudinal states, including laughter, provide an important resource for people with aphasia participating in groups (Klippi, 2003). Just as interactants can use these non-verbal resources adaptively, so too can they make verbal adaptations in multiparty interactions (as previously discussed with regard to dialogue). Goodwin, for example, discusses the analysis of how a speaker adjusts one sentence in an unfolding turn as he shifts his attention to each of three hearers successively (Goodwin, 1981). When we recognize group therapy interactions as a particular activity type within a wider frame of multiparty interactions, then we can see that within any group interaction there is going to be monologue, dialogue, and what Eggins and Slade describe as “multilogue” (Eggins & Slade, 2004/1997, p. 20). In analyzing the multiparty interactions that occur in aphasia group therapy we can focus our attention on each particular type of interaction. For example, while some group activities use rotating turns for monologue elicitation, others can be structured for dialogic exchange, and other group activities allow for the multilogue facilitators that are neatly summed up in Elman’s description of this type of interaction as “jazz music” (i.e., dynamic, improvised; Elman, 2004). The many diﬀerent types of discourse may occur not just over the period of the group session but also over the “life” of the group. While attention to the diﬀerent types of interaction is useful, it is important not to compartmentalize the diﬀerent interactions. As an example, caution needs to be taken when abstracting, for instance, a short monologue from within a group interaction. Wilkinson talks about how we often remove such previously occurring co-text from our analysis of what is going on, and miss how both the speaker and the hearer are using what has gone before to provide important context for what they are meaning/interpreting (Wilkinson, 1999).

Mediation in multiparty interaction People with aphasia by the very nature of their communication disability ﬁnd that often they are accompanied by another person (e.g., carer, family member) into social situations that may involve a group of people. Previous research in aphasia has focused on the types of strategies and training needed to support the communication of volunteers and carers when talking directly with people with aphasia, for example “supported communication” (Kagan, 1998, 1999; Kagan, Black, Duchan, Simmons-Mackie, & Square, 2001), but the role that such communication partners take in “mediating” interaction

186

Ferguson

between the person with aphasia and third parties has received little attention. The term “mediating” is used here in the sense of acting as a “medium” for the communication, and a focus on multiparty interactions highlights the importance of this role in this particular type of “multilogue.” Also, as the access to both social and therapy groups for people with aphasia increases, people with aphasia are increasingly in situations where they themselves mediate the interactions between other group participants. This mediation role is familiar to us all; for example when you take someone with you into an interaction (particularly one who knows you better than do the people in the group), then that person may end up at times “mediating” the interaction, such as by explaining what you meant, or taking over the telling of a oftentold story. “Mediation” is distinctively associated with multiparty interaction – in the sense that it requires a third party, and so cannot be observed in monologue or dialogue – and its facilitative power makes it of key interest to speech-language pathologists. The notion of mediation provides an alternative way to view the role of the clinician in facilitating group therapy interactions, and I explore this further in the following section. So, what communication resources might someone in a mediator role use? Candlin and Maley (1994) talk about the discoursal strategies used in mediating legal disputes. These strategies involve the more “textual” aspects of providing the “gist” of what has just been said, or providing the “upshot” (Heritage & Watson, 1979), but they suggest that what is achieved beyond this is a cognitive reframing (Goﬀman, 1974). The “frame” essentially aligns or reinforces the current thinking, while “reframing” involves widening or narrowing, or changing, the current thinking – that is, reframing is trying to change people’s view of the situation. They note the similarities of this mediation process with the therapy process, and note how mediation draws on therapy practices, but they also note the diﬀerences in which therapy aims to explore the personal aspects, whereas mediation of conﬂict aims to depersonalize, to objectify the situation for the participants. What is relevant for the purposes of this chapter is the intermediary’s discoursal role and strategies, in the sense that the role of group leader, for example, or the role of carer in group interactions with people who have aphasia, involves this cognitive process of working out what the person with aphasia is meaning, then working out what others might have understood or misunderstood (i.e., the frame), and judging when to add any additional provision of gists or upshots (i.e., reframing) through textual processes. For the speech-language pathologist working as a group leader there is also the therapeutic counseling role in the reframing process to serve the psychosocial or interpersonal goals of the group. For the carer in a social interaction this aspect also exists, as there is a goal for interpersonal harmony, for communication to be successful, to facilitate the person with aphasia’s sense of contribution/being valued in the interaction. Ideally, the person in this mediation role manages to assist when necessary, and to draw back when the person with aphasia is able to communicate independently. However, this can be a ﬁne line to judge, and the

Multiparty interactions in aphasia

187

intermediary runs the risk of potentially disempowering the person with aphasia in the interaction. The example that follows is drawn from an aphasia group therapy session, in which A5 (a 59-year-old man with moderate ﬂuent aphasia) is taking on the “mediation” role, through the telling of another group member’s story (A4), who had fallen while she and A5 were on a train trip. As well as A5’s mediation role, we can also see three points where the speech-language pathologist (SP1) mediates the story for the other group members through providing the gist of the story (asterisked). Note that at these points A5 himself is not seeking assistance, but rather the speech-language pathologist appears to have judged that other members of the group may not have the same shared knowledge regarding the extent of the trip (“coming back from Melbourne”), and may have needed a précis or gist of A5’s fairly lengthy circumlocution about the numbers of onlookers (“everyone suddenly came”), and might not have caught A5’s implicit meaning in his description of the railway oﬃcials being “scared” (“worried about getting sued”).

Example: The story of A4’s fall (3.5 minute excerpt, from aphasia group therapy session) The interaction involves 12 people seated around a large rectangular table, with two video cameras recording from each end of the room. There are eight people with aphasia (from left cerebrovascular accidents), two female speech-language pathologists aged between 40 and 50 years, and two speech pathology students (one male ST1, and one female ST2) aged between 20 and 25 years. The details of the participants with aphasia are provided in Appendix 12.1 A5 *SP1 A5 A4 SP1 A5 A4 A5

*SP1 A5 SP1 A5 A4 A5 A7

We w w when we went to aphasia, when we went to come back here, we got to Central When you were coming back from Melbourne Yeah, we got oﬀ at Central, so I got the bags, and A4 wanted to go to the toilet Yes, I know, embarrass {GENERAL LAUGHTER} No secrets! What happened there was one part to the street, when she touched, er the leg er twisted, she went down. There was people everywhere, weren’t there! Security guards! {SIMULTANEOUS} Oh yes And then there was about six, and they come around and say how are you. And they try to say how are you, can’t hear you. And A4 couldn’t talk properly. And there I am, you know when I start to talk, I can’t talk sometimes, and I said hang on, we both had stroke, we don’t quite understand, slow down, and get away, give us a bit of room, and we understand. Oh gee we got a lot of work! {GENERAL LAUGHTER} Everyone suddenly came. And all we wanted to do You didn’t have to make them cups of tea? {JOKING} They wanted to send us oﬀ in an ambulance, to hospital. Embarrassed, embarrass, embarrass. All we wanted to do was get on the Newcastle train. I suppose, but it’s nice when people are kind, it was really kindness.

188 A5

A7 A5

A4 A5 *SP1 A5 A7 A3 A5 A7 A5 SP1

Ferguson They were scared, because they had to, they put us on to the train, make sure we were safe. When the train stopped at Wyong, we had to go on a bus from there to Cardiﬀ, so the railway bloke come, how are you, all right? Took us out, carry our bags. {GENERAL LAUGHTER} I don’t think they were scared, I think they were kind. No, have a listen, the whole story was, we got to Cardiﬀ, they sent out the driver looked out and checked us, the railway bloke ended up there too. (turns to A4) They were ready to meet your son. And then she ended up getting a letter, didn’t you, from the railway. Oh yes Saying, they said, how are you, you all right, did you need anything. Do you think they were worried about getting sued? Yes. I don’t mind, but other people were (to A3) Ah the cynicism! True But some people would No, you’re probably right It was good that it was helped. It was probably a combination.

Such mediation will be very familiar to speech-language pathologists, and I suggest that we can usefully describe this interactive work on a continuum, from interpreting (e.g., other language interpreting, or within same language “interpreting”) through collaborative production (e.g., saying the word for someone), to facilitation (e.g., cues, prompts). The notion of “interpreting” for someone with aphasia is problematic in that it raises important ethical questions regarding gray areas of advocacy and the extent to which supporting communication ﬁts within our scope of practice (Ferguson, Worrall, McPhee, Buskell, Armstrong, & Togher, 2004). These ethical issues are well known to interpreters of other languages, when cultural “interpretation” is also required. Friedland and Penn’s research provides a number of insights into the issues that arise when interpreting is less about linguistic translation and more about mediation (Friedland & Penn, 2003). They used conversation analysis to analyze in detail a 45-minute interview with Zulu-speaking parents of an 8-year-old child who had been injured in a motor vehicle accident. Their identiﬁcation of facilitators and inhibitors in this setting would apply to other “mediated” interactions, and these chieﬂy revolved around role issues. Facilitators were observed to include that the mediator was an active participant (initiates, questions) and ﬂexibly switched between interpreting and information gathering, and that there was shared knowledge between the mediator and the other participants. Inhibitors were observed to include diﬀerent agendas held by participants, interruptions, complicated repair trajectories, and misinterpretation. Speaking for another person, supplying words for them, and ﬁnishing their sentences are all everyday occurrences, and are used frequently when interacting with people with aphasia in two-way interactions as well as multiparty interactions (Ferguson, 1993; Oelschlaeger & Damico, 2003). The shared knowledge of familiar communication partners plays an important role in

Multiparty interactions in aphasia

189

successful collaborative production, and is probably essential for those taking on the role of mediating communication between a person with aphasia and a third party to be able to assist with word searches. However, such shared knowledge need not be built on personal familiarity, as shared world knowledge can be created by speech-language pathologists building up a group activity based on particular topics, for example. In real-world situations, the particular knowledge of the context for communication will provide communication partners with a constrained and hence predictable set of resources that will assist the necessary guesswork, for example for a solicitor taking instructions for a will (Ferguson, Worrall, McPhee, Buskell, Armstrong, & Togher, 2003). Klippi provides a good example of collaborative team work between two people with aphasia in a group interaction, where the speaker cannot ﬁnd the word and writes it down (Klippi, 2003). The speaker cannot read, and so is unsure as to whether what he has written is the word he is looking for, but one of the other members of the group with aphasia can read, and she reads the word aloud for him, which allows him to conﬁrm the word (p. 125). Most of the available literature that addresses facilitation in group interactions focuses on the speech-language pathologist’s role. Bernstein-Ellis and Elman present a clear summary of ways a clinician can increase conversational initiation (e.g., through directing questions to particular group members, explicitly seeking participation or the help of other members to assist participation), and ways a clinician can increase exchange of information (e.g., through supported conversation methods, including pictures, gestures) (Bernstein-Ellis & Elman, 1999, pp. 52–53). Garrett’s approach to group therapy provides for extensive use of facilitation, through a topic/ activity-centered role-play of interactions, in which the clinician provides scaﬀolding and “language mediation” to assist in the rehearsal stages (Garrett & Ellis, 1999). However, the work by people with aphasia in facilitating group interaction has also been recognized. McCarney and Johnson (2001) include the description of facilitative contributions in their rating system. Their description of a rating of 0, 1, or 2 mentions that the contributions were not facilitating (of discussion); but for a rating of 3 the “content of utterance(s) likely facilitates discussion” (p. 1028), a rating of 4 is described as “facilitating,” and a rating of 5 “shows some creative ability to further expand the conversation” (p. 1028). However, they discuss that identifying this aspect of facilitation appeared to cause problems for raters, and aﬀected reliability (which however they report to be satisfactory). Describing the work of mediation is an analytic challenge, as much of what is going on is conducted covertly by participants, and to a large extent unconsciously. Mediation makes use of the resources typically used for dealing with communication breakdown retrospectively (e.g., repair), in order to act prospectively and preventively to avoid trouble in communication. The research on repair in aphasic interactions suggests that clinicians may

190

Ferguson

conduct overt repair less frequently than spouses (Lubinski, Duchan, & Weitzner-Lin, 1980), and spouses may conduct overt repair less frequently than less familiar communication partners (Ferguson, 1994). Possibly, spouses are prepared to risk endangering the onward ﬂow of conversation more than less familiar partners, preferring to get the message straight even though the conversation may be halted. Less familiar partners, through provision of overt correction (including collaborative production), provide quick repair work that poses less threat to the onward ﬂow of conversation. Clinicians in conversation with people with aphasia appear to be very focused on maintaining the ﬂow of conversation, and it is this forward-looking work that appears to be at the heart of mediation in multiparty interactions.

Conclusion The challenge for the future is in the frameworks and methods of analysis to capture the complex and dynamic nature of multiparty interactions involving people with aphasia, and there are a number of well-developed sociolinguistic methodologies that will assist in this (Gumperz, 1999; Halliday & Matthiessen, 2004; Norris & Jones, 2005; Prevignano & Thibault, 2003). In this chapter I have suggested that multiparty interactions warrant our attention as part of increasing the validity of assessment, and have drawn attention to the mediation of communication as a particular feature of multiparty interaction. Further research into the nature and factors inﬂuencing the success of mediation will contribute to the future development of assessments that capture the impact of aphasia on people’s lives, and the future development of therapy that aims to facilitate their social interaction.

Acknowledgements The contributions of Megan Alston, Sue Sherratt, Judy Vajak, and Julie Hengst to the thoughts that have been developed in this chapter are gratefully acknowledged. Many thanks are also owed to the members of the Aphasia Group Therapy program for sharing their experiences.

Note 1 A favorite personal reminiscence of mine is seeing Chris carefully balancing the cheese platter he had prepared for his local aphasia group among the pile of research papers on the back seat of his car – a rather precarious positioning given the narrow winding roads of the English countryside!

References Armstrong, E. (2000). Aphasic discourse analysis: The story so far. Aphasiology, 14 (9), 875–892.

Multiparty interactions in aphasia

191

Aten, J. L., Caligiuri, M. P., & Holland, A. L. (1982). The eﬃcacy of functional communication therapy for chronic aphasic patients. Journal of Speech and Hearing Disorders, 47, 93–96. Avent, J. R. (1997). Group treatment in aphasia using cooperative learning methods. Journal of Medical Speech-Language Pathology, 5 (1), 9–26. Beeke, S., Wilkinson, R., & Maxim, J. (2001). Context as a resource for the construction of turns at talk in aphasia. Clinical Linguistics and Phonetics, 15 (1&2), 79–83. Bernstein-Ellis, E., & Elman, R. J. (1999). Aphasia group communication treatment: The Aphasia Center of California approach. In R. J. Elman (Ed.), Group treatment of neurogenic communication disorders: The expert clinician’s approach (pp. 47–56). Woburn, MA: Butterworth-Heinemann. Bollinger, R. L., Musson, N. D., & Holland, A. L. (1993). A study of group communication intervention with chronically aphasic persons. Aphasiology, 7 (3), 301–313. Booth, S., & Perkins, L. (1999). The use of conversation analysis to guide individualized advice to carers and evaluate change in aphasia: A case study. Aphasiology, 13 (4/5), 283–303. Brumﬁtt, S. (1995). Psychotherapy in aphasia. In C. Code & D. Müller (Eds.), The treatment of aphasia: From theory to practice (pp. 18–28). London: Whurr. Brumﬁtt, S. M., & Sheeran, P. (1997). An evaluation of short-term group therapy for people with aphasia. Disability and Rehabilitation, 19 (6), 221–230. Candlin, C. N., & Maley, Y. (1994). Framing the dispute. International Journal for the Semiotics of Law, 7 (19), 75–98. Code, C., Eales, C., Pearl, G., Conan, M., Cowin, K., & Hickin, J. (2001). Proﬁling the membership of self-help groups for aphasic people. International Journal of Language & Communication Disorders, 36 (41–45). Code, C., Hemsley, G., & Herrmann, M. (1999). The emotional impact of aphasia. Seminars in Speech & Language, 20 (1), 19–31. Code, C., & Müller, D. (Eds.) (1995). Treatment of aphasia: From theory to practice. London: Whurr. Code, C., & Müller, D. J. (1992). The Code-Müller Protocols: Assessing perceptions of psychosocial adjustment to aphasia and related disorders. Kibworth: Far Communications. Code, C., Müller, D. J., Hogan, A., & Herrmann, M. (1999). Perceptions of psychosocial adjustment to acquired communication disorders: Applications of the Code-Müller protocols. International Journal of Language & Communication Disorders, 34 (2), 193–207. Drummond, S. S., & Simmons, T. P. (1995). Linguistic performance of female aphasic adults during group interaction. Journal of Neurolinguistics, 9 (1), 47–54. Eggins, S., & Slade, D. (2004/1997). Analysing casual conversation. London/New York: Equinox/Cassell. Elman, R. J. (2004). Group treatment and jazz: Some lessons learned. In J. Duchan & S. Byng (Eds.), Challenging aphasia therapies: Broadening the discourse and extending the boundaries (pp. 130–133). Hove, UK: Psychology Press. Ferguson, A. (1993). Conversational repair of word-ﬁnding diﬃculty. In M. L. Lemme (Ed.), Clinical aphasiology (Vol. 21, pp. 299–310). Austin, TX: Pro-Ed. Ferguson, A. (1994). The inﬂuence of aphasia, familiarity and activity on conversational repair. Aphasiology, 8 (2), 143–157.

192

Ferguson

Ferguson, A. (1998). Conversational turn-taking and repair in ﬂuent aphasia. Aphasiology, 12 (1), 1007–1031. Ferguson, A., Worrall, L., McPhee, J., Buskell, R., Armstrong, E., & Togher, L. (2003). Testamentary capacity and aphasia: A descriptive case report with implications for clinical practice. Aphasiology, 17 (10), 965–980. Ferguson, A., Worrall, L., McPhee, J., Buskell, R., Armstrong, E., & Togher, L. (2004). Autonomy in life decisions for people with aphasia: Issues for speech pathologists. Paper presented at the 26th World Congress of the International Association of Logopedics & Phoniatrics, Brisbane, 29 August–2 September. Friedland, D., & Penn, C. (2003). Conversation analysis as a technique for exploring the dynamics of a mediated interview. International Journal of Language and Communication Disorders, 38 (1), 95–111. Garrett, K. L., & Ellis, G. J. (1999). Group communication therapy for people with long-term aphasia: Scaﬀolded thematic discourse activities. In R. J. Elman (Ed.), Group treatment of neurogenic communication disorders: An expert clinician’s approach (pp. 85–96). Boston, MA: Butterworth-Heinemann. Glindemann, R., & Springer, L. (1995). The assessment of PACE therapy. In C. Code & D. Müller (Eds.), The treatment of aphasia: From theory to practice (pp. 90–107). London: Whurr. Goﬀman, E. (1974). Frame analysis: An essay on the organization of experience. New York: Harper & Row. Goodwin, C. (1981). Conversational organization: Interaction between speakers and hearers. New York: Academic Press. Gumperz, J. J. (1999). On interactional sociolinguistic method. In S. Sarangi & C. Roberts (Eds.), Talk, work and institutional order: Discourse in medical, mediation and management settings (pp. 453–471). Berlin: Mouton de Gruyter. Halliday, M. A. K., & Matthiessen, C. M. I. M. (2004). An introduction to functional grammar (3rd ed.). London: Arnold. Heeschen, C., & Schegloﬀ, E. A. (1999). Agrammatism, adaptation theory, conversation analysis: On the role of so-called telegraphic style in talk-in-interaction. Aphasiology, 13 (4–5), 365–405. Helasvuo, M., Klippi, A., & Laakso, M. (2001). Grammatical structuring in Broca’s and Wernicke’s aphasia in Finnish. Journal of Neurolinguistics, 14, 231–254. Hengst, J. (2003). Collaborative referencing between individuals with aphasia and routine communication partners. Journal of Speech, Language, and Hearing Research, 46 (4), 831–848. Heritage, J. C., & Watson, D. R. (1979). Formulations as conversational objects. In G. Psathas (Ed.), Everyday language (pp. 123–162). New York: Wiley. Kagan, A. (1998). Supported conversation for adults with aphasia: Methods and resources for training conversation partners. With introduction by R. C. Marshall, commentary by S. Byng, A. Holland, S. Parr, C. Penn, and N. Simmons-Mackie. Aphasiology, 12, 811–864. Kagan, A. (1999). Communication strategies used by “good” versus “poor” speaking partners of individuals with aphasia. Aphasiology, 13, 807–820. Kagan, A., Black, S. E., Duchan, J. F., Simmons-Mackie, N., & Square, P. (2001). Training volunteers as conversation partners using “Supported Conversation for Adults with Aphasia” (SCA): A controlled trial. Journal of Speech, Language, and Hearing Research, 44, 624–638. Katz, R. C., Hallowell, B., Code, C., Armstrong, E., Roberts, P. M., Pound, C., et al.

Multiparty interactions in aphasia

193

(2000). A multinational comparison of aphasia management practices. International Journal of Language and Communication Disorders, 35 (2), 303–314. Klippi, A. (1996). Conversation as an achievement in aphasics (Studia Fennica, 6). Helsinki: Suomalaisen Kirjallisuuden Seura. Klippi, A. (2003). Collaborating in aphasic group conversation: Striving for mutual understanding. In C. Goodwin (Ed.), Conversation and brain damage (pp. 117–143). Oxford, UK: Oxford University Press. Laakso, M., & Klippi, A. (1999). A closer look at the “hint and guess” sequences in aphasic conversation. Aphasiology, 13, 345–363. Levinson, S. C. (1992). Activity types and language. In P. Drew & J. Heritage (Eds.), Talk at work: Interaction in institutional settings (pp. 66–100). Cambridge, UK: Cambridge University Press. Lindsay, J., & Wilkinson, R. (1999). Repair sequences in aphasic talk: A comparison of aphasic–speech and language therapist and aphasic–spouse conversations. Aphasiology, 13, 305–325. Lubinski, R., Duchan, J., & Weitzner-Lin, B. (1980). Analysis of breakdowns and repairs in aphasic adult communication. In R. H. Brookshire (Ed.), Clinical Aphasiology Conference Proceedings (pp. 111–116). Minneapolis, MN: BRK. McCarney, C. T., & Johnson, A. F. (2001). Examining conversational characteristics of persons with chronic aphasia during three group conversations. Aphasiology, 15 (10/11), 1017–1028. Norris, S., & Jones, R. H. (Eds.) (2005). Discourse in action: Introducing mediated discourse analysis. London: Routledge. Oelschlaeger, M., & Damico, J. S. (2003). Word searches in aphasia: A study of the collaborative responses of communicative partners. In C. Goodwin (Ed.), Conversation and brain damage (pp. 211–227). Oxford, UK: Oxford University Press. Osvaldsson, K. (2004). On laughter and disagreement in multiparty assessment talk. Text, 24 (4), 517–545. Perkins, L., Crisp, J., & Walshaw, D. (1999). Exploring conversation analysis as an assessment tool for aphasia: The issue of reliability. Aphasiology, 13 (4–5), 259–282. Prevignano, C. L., & Thibault, P. J. (Eds.). (2003). Discussing conversation analysis. Amsterdam: John Benjamins. Sacks, H., Schegloﬀ, E. A., & Jeﬀerson, G. (1974). A simplist systematics for the organization of turn taking for conversation. Language, 50, 696–735. Ulatowska, H. K., Olness, G. S., Wertz, R. T., Thompson, J. L., Keebler, M. W., Hill, C. L., et al. (2001). Comparison of language impairment, functional communication, and discourse measures in African-American aphasic and normal adults. Aphasiology, 15 (10/11), 1007–1016. WHO (2001). ICF: International classiﬁcation of functioning, disability and health. Geneva: World Health Organisation. Wilcox, J., & Davis, G. A. (1977). Speech act analysis of aphasic communication in individual and group settings. In R. H. Brookshire (Ed.), Clinical Aphasiology Conference Proceedings (pp. 166–174). Minneapolis, MN: BRK. Wilkinson, R. (1999). Sequentiality as a problem and resource for intersubjectivity in aphasic conversation: Analysis and implications for therapy. Aphasiology, 13, 327–343. Worrall, L. (1995). The functional communication perspective. In C. Code & D. Muller (Eds.), The treatment of aphasia: From theory to practice (pp. 47–69). London: Whurr.

194

Ferguson

Appendix 12.1: Description of group participants with aphasia Client

Gender

Age

A1 A2 A3 A4 A5 A6 A7 A8

F M M F M F F F

93 78 57 58 59 53 60 73

TPO (mths) 10 46 26 38 >72 >72 13 12

Nature of aphasia Non-ﬂuent Non-ﬂuent Non-ﬂuent Non-ﬂuent Fluent Non-ﬂuent Fluent Fluent

BDAE 1 severity 1 2 2 3 3 3 5 5

CETI 2

VASES 3

12.90 23.59 63.25 61.18 73.0 59.50 85.68 94.87

33 22 22 31 37 30 36 40

1 Goodglass, H., & Kaplan, E. (1983). Assessment of aphasia and related disorders (Boston Diagnostic Examination for Aphasia). Philadelphia: Lea & Febiger. 2 Lomas, J., Pickard, L., Bester, S., Elbard, H., Finlayson, A., & Zoghaib, C. (1989). The Communicative Eﬀectiveness Index: Development and psychometric evaluation of a functional communication measure for adult aphasia. Journal of Speech & Hearing Disorders, 54, 113–124. 3 Brumﬁtt, S., & Sheeran, P. (1999). VASES: Visual Analogue Self-Esteem Scale. Bicester, UK: Winslow.

13 Stroke stories Conveying emotive experiences in aphasia Elizabeth Armstrong and Hanna K. Ulatowska When patients suﬀer a loss of language, must they also lose their sense of self ? (Oliver Sacks, 2005)

Introduction For many years, Professor Chris Code has worked in both clinical and academic capacities highlighting the impact of aphasia on the individuals involved and their family/carers, and has investigated reactions and “adjustment” to aphasia. He has also mentored many research students and academics, and facilitated the description of aphasia from numerous angles, including linguistic approaches. The current chapter encapsulates both of these areas that he has inﬂuenced signiﬁcantly, addressing the ways in which people with aphasia describe emotional experiences, using a variety of linguistic tools to achieve expression of attitudes, opinions, and feelings. Language as a system of meaning serves many functions, including the conveying of information and the obtaining of goods and services, as well as social bonding and the construction and expression of identity. As one of our most powerful social tools, language enables us to engage other people in our lives and to participate in theirs. In order to do this, we employ a variety of linguistic resources that not only relate our experiences in a factual manner, but also convey our particular stance on those experiences, so that our opinions, feelings, judgements and values are apparent and ultimately negotiable, that is, can lead to dialogue in which these aspects are discussed. We also aim to make our conversation interesting to others, but perhaps most importantly, we also use our language to organize and make sense of our reality (Hydén, 1997). Individuals with aphasia are potentially disadvantaged in all of these endeavours because of their language impairment. To date, studies of aphasic language have predominantly focused on the information-giving function of language, that is, the imparting of relatively concrete information in terms of naming objects or descriptions of pictures. It is the purpose of this chapter to raise issues related to evaluative language and associated linguistic resources,

196

Armstrong and Ulatowska

and to discuss ways in which they are relatively impaired or preserved in aphasia. We present discourse samples of aphasic speakers analysed from the perspectives of both the nature of evaluative language in aphasia, and its vital role in the expression and construction of identity. We also discuss implications of such discourse analysis that would include taking clinicians and their aphasic clients beyond the realm of factual language in the therapy situation.

Evaluative language The role of evaluative language in social interaction has been of interest to linguists concerned with the role of language in social life for a number of years. In a summary of this work, Hunston and Thompson (2003) suggest three functions of evaluative language: 1 2 3

to express the speaker’s or writer’s opinion, and in doing so to reﬂect the value system of that person and their community; to construct and maintain relations between the speaker or writer and hearer or reader; to organize the discourse.

In order to achieve these functions, a variety of linguistic and nonlinguistic devices are employed that enable individuals to express their attitudes, feelings and judgements. Labov (1972) cites various methods of evaluation used to “signal salience” of information that is separate from the speciﬁc ongoing action involved in the recount. Such information could involve the speaker’s reﬂection on the action in question, providing direct speech for illustrative purposes, or use of forceful language such as heavily emotive words, intensiﬁers, superlatives, and comparatives. Prosodic patterns related to evaluative language, including marked changes in volume, speech rate and pitch have also been investigated (Peterson & McCabe, 1983). The importance of evaluative language has been acknowledged in many applied linguistic ﬁelds already, including media studies, education, second language learning, and sociolinguistic studies of culturally diverse groups (Biber & Finegan, 1989; Carter & Nash, 1990; Labov, 1972; Martin, 1995; Stubbs, 1986). Its centrality to meaning is highlighted by Cortazzi and Jin (2003), who discuss its role in narratives, noting that “Evaluation is held to be the key to narrative: through evaluation, speakers show how they intend the narrative to be understood and what the point is” (p. 103) and that “the evaluation makes the narrated events reportable, repeatable, and relevant” (p. 105). Labov and Waletsky (1967) similarly point out that it is the evaluative function of a narrative that communicates the meaning of the narrative by establishing some point of personal involvement. Throughout many diﬀerent genres, speakers articulate who they are through the use of evaluative language. In eﬀect, they are expressing their identity

Stroke stories 197 through providing the listener with an insight into how they view their world.

The role of evaluation in narrative and identity One of the main contexts in which evaluative language has been explored is the narrative. For several years now, there has been signiﬁcant interest in the ﬁeld of social science in the function of narratives. This has occurred in relation to the individual’s construction of his or her reality and identity, as shared with others in life stories, as that individual attempts to reﬂect and “makes sense” of his or her life experiences. Hydén (1997, p. 49) writes: The narrative’s importance lies in its being one of the main forms through which we perceive, experience, and judge our actions and the course and value of our lives. Ochberg (1988, p. 174) also suggests that the stories can actively impact on individuals’ futures: They shape how we conduct our lives, how we come to terms with pain, what we are able to appropriate of our own experience, and what we disown – at the familiar price of neurosis. The role of narratives as a coping mechanism has also been acknowledged through the way we put our emotions into words (Smyth & Pennebaker, 1999). In recent years, medical sociologists and anthropologists have focused on illness narratives in the exploration of how individuals experience and “deal with” disruptive life changes as the result of a variety of chronic illnesses (e.g., Becker & Kaufman, 1995; Faircloth, Boylstein, Rittman, Young, & Gubrium, 2005; Jordens, Little, Paul, & Sayers, 2001; McKevitt, 2000). Re-construction of identity following the onset of chronic illness and in the ensuing years has been of particular interest, and is said to be revealed, among other ways, through the organization of, and the language used in illness narratives (Bury, 1982; Hydén, 1997). Much of the literature on illness narratives to date, however, has focused on illnesses where the person involved has resultant physical changes/impairments/disabilities. Because of the very nature of their impairment (i.e., impaired communication), the stories of people with aphasia or other cognitive impairments have rarely been explored.

Evaluative language and aphasia To date, as noted above, studies of language use in aphasic speakers have largely concerned themselves with factual language. Such language has involved the speaker naming concrete objects and actions, or producing

198

Armstrong and Ulatowska

discourse dealing with descriptions of pictures, retelling stories or speciﬁc practical activities, such as catching a bus, or paying bills. And yet, as mentioned, individuals with aphasia are especially vulnerable to issues of identity change and related psychosocial issues (Code, Hemsley, & Herrmann, 1999; Hemsley & Code, 1996; LaPointe, 2001; Shadden, 2005; Shadden & Agen, 2004) which are often worked through, in other conditions, via language. While clinicians attempt to address such issues with their clients through diﬀerent forms of counselling, the role of language is often underplayed in this context. Little is known up to this point about how individuals with aphasia talk about their feelings, how their language impairment may compromise this expression, or what resources they employ to work through and assert their “new” identity post stroke. How does their language reﬂect their psychological state? And how can the clinician access such communication? While studies have reported on attitudes, feelings, and identity issues of people with aphasia (e.g., Kagan & Duchan, 2004; LaPointe, 2001; Moss, Parr, Byng, & Petheram, 2004; Parr, Byng, Gilpin, & Ireland, 1997), the focus of these studies was to elucidate the aphasic experience, rather than to explore the linguistic style or devices employed by the aphasic speakers to convey evaluation. Of the few studies that have speciﬁcally used emotive topics to explore the narratives of aphasic speakers, the primary purposes have involved investigation of such cognitive and linguistic abilities of aphasic speakers as their ability to organize and maintain coherence across their discourse (Ulatowska & Olness, 2001), or their ability to convey emotionality as determined by listeners (Borod et al., 1996; 2000). The focus of these studies again, however, has not been on examining the lexical or grammatical resources used to convey the speciﬁc emotive content of the narratives or on evaluative language speciﬁcally. Nonetheless, it is of interest that speakers with left hemisphere damage have been reported to produce “better” discourse (in terms of overall coherence) when discussing emotional rather than non-emotional topics (Borod et al., 2000), suggesting that the element of emotion may well be a facilitating and hence signiﬁcant factor for speakers with aphasia. Individuals with aphasia have also been noted to use evaluative language as part of overall text organizing devices (Ulatowska & Olness, 2001). Results from one study to date (Armstrong, 2005) that has undertaken a speciﬁc lexicogrammatical analysis of evaluative language in personal accounts of aphasic speakers, suggests that the aphasic speakers involved used fewer evaluative resources than non-brain-damaged speakers. However, this study focused on verb usage in particular, which is only one of numerous resources involved in evaluation.

Aphasic narratives Due to the multi-faceted processes involved in conveying attitudes, feelings, and opinions, including non-verbal and prosodic means, the description

Stroke stories 199 involved in this chapter is obviously not comprehensive or all-encompassing. Rather, the purpose of the discussion is to begin to explore the evaluative language resources available to aphasic speakers, and to suggest potential taxonomies both for describing these resources and for using them in a clinical context. For clinical purposes, such descriptors can provide information on the speaker’s linguistic abilities, supplementing formal test results and other analyses of more structured discourse samples. They can also provide a window into the individual’s psychological state with regard to their perceptions of identity, and ways of viewing the world – vital insights when planning and monitoring therapy goals and treatments. The discourse samples on which the present discussion is based were obtained from corpora collected in Australia by Armstrong and in the US by Ulatowska, Olness, and colleagues, and consisted of people with aphasia discussing what happened when they had their strokes. They varied in time post onset (a factor that will be discussed), and their aphasias ranged from mild to moderate degrees of severity. Amount and intensity of evaluation What is immediately obvious when scanning diﬀerent narratives is the varying amounts of evaluative language used in each – speciﬁc evaluative devices to be described below. People vary in their motivation to evaluate and provide personal and/or emotional aspects of accounts, as noted by previous researchers (e.g., McKevitt, 2000; Moss et al., 2004). Potential factors inﬂuencing evaluation include cultural background, personality, gender (although still a controversial issue), as well as, of course, motivation to participate in the study at hand (see McKevitt, 2000, for an overview of these issues). In the case of aphasic individuals, severity of aphasia as well as the amount of time that has elapsed since the onset of the language disorder (potentially aﬀecting memory of the event, or perhaps their cognitive ability to reﬂect on past events) may inﬂuence the kinds of language the speakers are able to use, as well as want to use. It appears that such language occurs on a continuum within speakers’ discourse. At the more emotive end of the continuum is the discourse of a 55-year-old African American woman, SL, who had suﬀered a stroke 5 years previously. SL provided a narrative rich in evaluation, as she explored her feelings at the time of her stroke. She drew on numerous images throughout, using much metaphoric language to convey her feelings. In the setting stage of her narrative, she recounted the following: Example 1 At that time, in my mind, I could see the picture of the old lady. When I say old, I mean a hundred, a hundred and two or a hundred and ﬁve and she was sitting in a wheelchair and she was leaning forward like (speaker leans forward). She was leaning forward and she had nothing

200

Armstrong and Ulatowska

in her arms, nothing in her arms. And she was dressed and she had a robe on and she was turned to the side or something like this (speaker twists her body). And there was a nurse prancing prancing around in front of her and made a a attempt to feed this lady in her mouth and I pictured that as being me. And I said no no God this can’t be me . . . Such depiction of SL’s mental state at the time provides a detailed example of what Labov would note as external evaluation, where the narrator quotes her feelings at the time, and also her talking to God. There is a suspension of the actual chain of events in the physical realm, while the narrator elaborates on particular feelings occurring to her at the time. Accompanying each such “section” of the record of events, however, is emotive language conveyed with the immediacy of the present tense and said as if the narrator was still in the situation. A diﬀerent type of evaluation is evident in the discourse of the following speaker, CP (aged 68, 3 months post onset of her aphasia), who provides more detail of actual action related to the onset of the stroke, but who also provides evaluation as the narrative progresses, yet less ﬂoridly than the previous example. Interestingly it is embedded in the action in the form of conversational dialogue: Example 2 Well I was scared when I had my surgery and when I had my stroke. I was scared because I didn’t know what had happened to me. And ah, I got up, I tried to get up. But I fell back down and then my daughter em said what’s wrong with you momma. I said, I don’t know what’s wrong. And they said sit down before you fall again. I said, shoot it’s something wrong with me. And they looked at me and said it sho’ is. In contrast to the above, an example of a text containing little evaluation at all is the following from a 70-year-old male, FP, in which he recounts getting to hospital and what happened on arrival. At this point, it was only 1 month since FP had suﬀered his stroke: Example 3 On the day it happened I got on the Friday morning and just collapsed on a belt at the uh hospital . . . swell . . . (–) – the one . . . Clinician: Westmead? Westmead . . . Westmead. And just waited there until oh well 4 o’clock in the afternoon. And said oh you’ll have just have to wait. And so they waited there and waited. They put it on the bed and keep me there for Saturday, the Friday, the Saturday, the Sunday, Monday and didn’t food me anything. They just more or less . . . give me . . . (–) food no food and that was it.

Stroke stories 201 In this account, there is minimal evaluation. While it must be noted that males in the samples examined tended to use less evaluative language overall than females, similar to other reports (e.g., Holmes, 1998; Page, 2003), further discussion below reveals how FP’s discourse changed over time, although was never as emotive as the females’ discourse. However, a more detailed examination over a larger number of samples would obviously have to be undertaken before any statements regarding the eﬀect of gender could be made. Functions of evaluation Speaker’s attitudes and maintaining social relations between speaker and listener As Hunston and Thompson (2003) note, it is diﬃcult to separate out the diﬀerent functions of evaluative language, and for the purposes of this discussion and the data being presented, the ﬁrst two functions as described by these two authors will be discussed concurrently. As noted particularly in the ﬁrst two examples above, the speaker fulﬁls the two functions of conveying stance and engaging the listener simultaneously. Other examples expressing the commonly cited fear and the feeling of not knowing what was happening, experienced in the early stages post stroke, also convey the narrator’s feelings, while capturing the listener’s interest by highlighting that this incident was something out of the ordinary, emotional, and signiﬁcant (“that was a scariery moment; I was terriﬁed; that was the most frightening thing; I didn’t know what had happened to me; what’s the matter?”). In terms of the language conveying the speaker’s psychological state at the time, Frank’s (1995) major stages of illness provide a framework within which to view such examples. Frank suggests that there is a chaos stage in which the individual is in a state of confusion, with things happening around him or her over which he or she has no control; a restitution stage, where the person aspires to return to “wellness” and a previous state of normality; and a quest stage, in which individuals see purpose in their illness and their struggle through the barriers encountered along the way, and see a way forward based on their experience. The above examples of fear and confusion ﬁt appropriately with the chaos stage, while an example of a restitution theme is the following, although it must be noted that the prior text for this speaker involved chaos narrative as well: Example 4 I said I’m handicapped but I will not be but at that moment I saw that picture “I said no.” If it was the devil showing me the way that I was going to be he is a LIAR. HE IS A LIAR. HE’S A LIAR. Because I’m not down yet. But girl that was a scariery moment. I had to make sure I could talk. I was lying in a position ﬂat on the ﬂoor. Thankyou Jesus Thankyou Jesus.

202

Armstrong and Ulatowska

In this part of her narrative, SL resolves not to be handicapped, and shows a ﬁghting spirit, using the religious imagery, as well as imagery of herself not being down yet as if in a ﬁghting context. Another speaker, JB (68 years old, 15 years post onset) said, “Only thing I was thinking about was getting myself together so I could do for myself.” It is of interest, that JB later became a volunteer at the local hospital, working with people with aphasia. Her “narrative” at that time hence became that of quest, as she saw a role for herself in assisting others through the experience and seeing meaning/ purpose in her own experience. Another common theme to aphasic narratives also involved thinking of premorbid status as an independent capable person who is now unable to do the simplest things, and also of the fear of becoming dependent on others: Example 5 I’ve got a college degree . . . two years in the running I was on the dean’s honours list and now I’m back learning ﬁrst grad math, second grade math. And it’s like my life is just like a wiped oﬀ blackboard. (PC, aged 57, 2 years 3 months post onset) Example 6 When I went to hospital I went by myself ah ah I was very independent cause after twenty years you have to be inde you know in ah a displaced housewife you have to be independent and strong and I went to hospital by myself . . . and now I was scare because I was the mother I’m the child and I have you know there’s no one else and my kids and I was their mother like my father was my father you know . . . you were the strong ﬁgure . . . and I and I was get caught I would be somebody daughter again I didn’t want to be somebody’s kid because I was so scared. (AS, aged 55, 4 years 7 months post onset) In these examples, again strong feelings are expressed in such a way as to engage the listener beyond the factual account. The juxtaposition of the college degree and learning ﬁrst grade maths is potent in Example 5, as is the discussion of independence and strength related to being a child again in Example 6. Organization of the text The third function of evaluation, as noted above, is to organize the text in a coherent manner. While numerous other organizing forces exist within discourse, such as cohesive devices, logical connections, and chronological continuity, evaluation is important in maintaining the “point” of the story, and linking relevant points together. The positioning of the evaluation within the narratives is thus of signiﬁcance in understanding both the nature and the degree of resources retained by the aphasic speaker. For the

Stroke stories 203 non-brain-damaged speaker, evaluation can occur at almost any point in the narrative. For example, Labov (1972) suggests that it can occur towards the end of the narrative, as the speaker provides a summary of the “point” of the story. However, it can also actually interrupt the “action” itself in order for the speaker to talk to the listener more directly, or even for the narrator to engage in reported self-talk (external evaluation). Longacre (1996) notes that evaluation is also eﬀective when associated with the climax of the story. As noted above, the evaluation can also be embedded throughout the narrative via lexical choices that convey certain emotive/attitudinal meanings and/or by propositions that form part of the narrative itself. Organization of these types can depend on linguistic skills (although little has been written on cognitive/syntactic capacity required of each type). The aphasic data discussed here revealed evaluation at various points throughout the speakers’ narratives. Evaluation was noted in some as being part of all aspects of the narrative; that is, the setting, complicating action, resolution, coda, all in the external evaluation mode discussed by Labov, where the speaker temporarily postpones the sequence of events to reﬂect in some way. Consider the following example involved in the setting (evaluation in italics): Example 7 Um um when I went to the hospital I went by myself ah ah I was very independent cause after twenty years you have to be inde you know in ah a displaced housewife you have to be independent and strong and I went to the hospital by myself and I wanted to ﬁnd out what I had ﬁrst . . . (AS) For other speakers, the evaluation was embedded throughout the sequence of events: Example 8 I tried to get up. But I fell back down and then my daughter em said what’s wrong with you momma. I said “I don’t know what’s wrong.” And they said sit down before you fall again. I said shoot it’s something wrong with me. And they looked at me and said it sho’ is. And I tried to write and I couldn’t write and that scared me. (CP) Linguistic devices As can be seen in the examples above, a variety of linguistic devices are employed by speakers to realize evaluative meanings. As complexity can vary within the use of any of the realms of devices described below, it is diﬃcult to defend a sequencing of them in this regard. For this reason, the reader should be aware that the following order of description has no particular signiﬁcance, and that each of the devices is capable of being used in both simple and complex forms.

204

Armstrong and Ulatowska

Evaluative words/phrases Explicit evaluative meanings are conveyed in a number of ways in the lexicogrammar, examples of which are found in many of the above quotations. Mental clauses involving mental verbs such as “felt”, “worried”, were used in the aphasic texts, realizing the speaker’s perspective on a particular proposition, person or thing, while descriptive clauses (e.g., “I was scared, something was wrong”) (described further in Armstrong, 2005) also provided evaluation. Word level evaluative meanings were also conveyed through evaluative verbs (e.g., “saddled with”, “ﬂopping”), evaluative nouns (e.g. “a burden”), adjectives (e.g., “funny”, “scared”, “numb”), and adverbs (e.g., “naturally”). In addition, intensiﬁers (e.g., “most frightening”, “really wanted”) and modal adjuncts (e.g., “unfortunately”) were further resources (for a full account of potential lexical resources, the reader is directed to Martin, 2003). Hence, it is clear that at least at the mild to moderate level of severity, aphasic speakers do retain the evaluative function at the lexicogrammatical level. Even in the presence of clauses that are not syntactically or semantically “correct”, evaluation is obviously present. Consider the following extract from the narrative of a man, MD, aged 60, with a moderate degree of aphasia: Example 9 I know I was gonna be sick some day. I know it. Maybe it was for dreams I did have . . . Anyway I did do cripple. Yeah I did sick it was my head. Ha. I guess I had it for sixty years but I had some fun . . . It is to laugh. I have I am still for fun . . . It is to laugh. I have I am still for fun because I am still alive . . . In this example, lexicogrammatical breakdown is obvious, however the evaluative meanings are clear through both the use of individual words such as sick, cripple, fun, as well as the whole process involved, for example it was for dreams, I did do cripple, I am still for fun. It is obvious, however, that range of wording, when compared with nonbrain-damaged speakers is potentially restricted in the narratives of aphasic speakers (as found by Armstrong, 2001, 2005), depending on both severity and type of aphasia. While aphasic speakers may retain emotive words, they may be of a general/high frequency nature rather than as broad an array as non-aphasic speakers might use. In addition, the more sophisticated devices such as modal adjuncts, adverbs, and intensiﬁers may indeed be less available to aphasic speakers, as evidenced in the data examined. Repetition Repetition is a frequent and important evaluative device in discourse, performing an emphasizing function. It can occur along a continuum from

Stroke stories 205 the simplest form, where a word or complete proposition is repeated, to the most sophisticated form, in which a proposition is re-phrased either in a literal or metaphorical form throughout the discourse. Repetition is well recognized as a feature of aphasic discourse (Armstrong, 1997; Ulatowska & Olness, 2001). While it can be pathological in the form of perseveration, it may also be a strategic evaluative resource used by an aphasic speaker for the purpose of emphasis. Consider the following example of repetition at the word level: Example 10 In my right hand it really tried to scare me because I couldn’t write. And that was one time I was really scared. And I was scared then to ﬁrst when they told me I had to have my heart surgery and that really scared me. (CP) The following provides an example of repetition at the phrase and clause level, emphasizing the deep emotion felt by the speaker: Example 11 I thought about killing myself. That was the most frightening thing that ever happened to me. Because I told my supervisor about killing myself. I really wanted to kill myself. (PC) Direct speech As mentioned, one of the devices used by several of the speakers was direct quotes during the narrative, involving dialogue between the narrator and others in the story, and other participants’ dialogues, as well as the narrator’s self-talk. Labov (1972) considered direct speech as being one of the highest forms of evaluation in that it “translates our personal narrative into dramatic form” (p. 396). Ulatowska, Streit-Olness, Samson, Keebler, and Goins (2004) found large amounts of direct speech in personal narratives of good storytellers in African American adults. Interestingly, Ulatowska and Olness (2001) also reported on its use in African American aphasic narratives, where it was used eﬀectively as a means of engaging the listener in a highly emotive and immediate way. While in the examples above, direct speech was used by relatively mildly aphasic speakers, the following example from a more severely aﬀected speaker, GB (aged 47, and 4 years 2 months post stroke) indicates that it is still possible to use this sophisticated device even in the presence of relatively severe aphasia. GB’s language was aﬀected in terms of lack of grammatical complexity and lexical variety (Broca’s type aphasia), with the use of direct speech achieved without completeness of clauses or projection:

206

Armstrong and Ulatowska

Example 12 “Help me, help me,” I don’t speak. I I am rushed to Memorial, only to Memorial. Um um six o’clock. Tests won’t though. Um thought I was getting better, but no speak. “Help me, help me” no, no I don’t have words. Noon. “Help me please,” I don’t see, I don’t mmmm no sounds. Five o’clock, um, my little brother and, um, Pat, my lifelong friends, okay. And “it’s okay, we’ll we’ll, we’ll get out of your way” and um, “take me home please.” This evocative section reveals restricted lexicogrammatical form, and yet much emotion. The primary way in which this speaker engages the listener here is through the juxtaposition of time elements and direct speech. The direct speech was not projected by a clause stating who said what and yet the meaning is clear. Metaphoric language Metaphoric language is used in a number of contexts (e.g., literature, casual conversation) to engage the listener/reader through imagery. Some but not all of the aphasic narratives included such language. One might hypothesize that individuals whose language was more severely impaired would have greater diﬃculty with metaphoric language, as it is considered “inherently complex” from both semantic and syntactic perspectives (Halliday, 1994). And indeed, the narratives produced by some of the milder aphasic speakers contained rich imagery. Consider the following examples: Example 13 It was this wrestler or it was like something was pushing down on me . . . and ﬁnally I got up enough strength and I gained on him. (SL) Example 14 It’s like my life is just like a wiped oﬀ blackboard. (PC) A more severely impaired speaker in our corpus also used a degree of imagery, although the following excerpt is obviously less explicit than the ﬁrst examples due to word-ﬁnding diﬃculties: Example 15 And a little bandage of brain or something or other went sss and went up in the air. And went down there and went out . . . for keeps. That’s what’s been building back ever since. That’s building up this brain uh . . . up. (FP) Further studies would have to explore the degree to which metaphoric language is impaired in severely aphasic individuals, and whether or not it is

Stroke stories 207 possible to produce at a phrase or even single word level (e.g., using the above example, wrestler . . . pushing down). Change in evaluation over time While it is noted that identity reconstruction is an ongoing process and that narratives can change over time, in the case of the aphasic speaker, time also provides potential recovery of language function and cognitive function, as well as the time to reﬂect on what has happened. On the other hand, the farther we are from an event, our memory for factual details may deteriorate somewhat. From our corpora, the narrative of one aphasic individual, FP, was examined over a 12-month period at 3-month intervals, in order explore the potential eﬀects of time on aphasic narratives. At the ﬁrst interview, the speaker FP provided the factual account given above in Example 3. At 3 months post onset, a similar narrative was elicited. In the following months, however, more detail emerged, as well as reﬂections on his impairments, followed by his progress: Example 16 And uh I just lay there and said very little to anybody. Didn’t say a word and didn’t want to say anything cos I had . . . I couldn’t even speak to anybody. Example 17 I can almost write now . . . normally . . . and speak and I can speak properly. And uh while I’m writing I I get a bit tired in the arms . . . and the hand writing. But uh . . . allright otherwise OK. It must be noted that this speaker’s linguistic resources improved over time in all respects, as well as evaluation. Hence, in this regard, it would appear that FP’s aphasia certainly inhibited his expression of evaluation in the early stages post onset.

Implications From this preliminary exploration, it is clear that while individual variation exists, mildly to moderately aphasic speakers are able to make use of evaluative language to convey their attitudes and feelings, and to use evaluative language in a way that helps to organize their discourse coherently. In this way, they are capable of bonding with, and engaging the listener, as well as using language to express their identity, and to some extent, construct and conﬁrm their own view of reality in their post-stroke context. Severity, as well as factors related to premorbid style, may aﬀect type of evaluation used, although both external and embedded evaluation were evidenced, as well as evaluation as dialogue – all seen in non-brain-damaged discourse. The fact

208

Armstrong and Ulatowska

that evaluation could be ascertained from incomplete utterances through use of evaluative words and phrases supports the notion that aphasic speakers do not have to be syntactically correct or even semantically accurate in order to convey meaning. However, the samples used for discussion here were limited to mildly and moderately aphasic speakers. Aphasia obviously has the potential to impact on evaluative language use in terms of quality and also the kinds of devices used. The extent to which diﬀerent severities of aphasia aﬀect/ restrict expression of evaluation will form the basis of future investigations. In terms of the experience of suﬀering a stroke and being aphasic, it appears that the aphasic speakers in the samples examined conveyed the chaos and, to a lesser extent, the restitutive stages of their illness, as reported in narratives of other populations suﬀering from chronic illness. The fear, uncertainty and disruption caused by the stroke was obvious in all the accounts, related to both the initial life-threatening situation and potential changes to future independence, as well as ongoing chaos. The importance of verbalizing such emotions has been reiterated throughout the narrative literature, including the signiﬁcance to the individual in terms of managing life experiences and relationships. Hence, given the strengths noted above, it may well be that the illness narrative, as well as other potentially emotive narratives, may be powerful contexts to be used in clinical and external situations for providing aphasic individuals with the opportunity to express important issues of identity changes experienced post stroke. The narrative may well provide an opportunity for clinicians to engage with the aphasic person in dealing with these ongoing emotions. Concurrently, the emotive narrative provides a meaningful communication experience for aphasic speakers to practise their verbal expression in the clinical situation. In so doing, they gain stimulation for language other than factual expressions involved in typical therapy activities such as naming, or discourse tasks focused on picture description. While the eﬀects of severity and type of aphasia on amount and type of evaluative language used may constitute further studies, non-verbal means of conveying evaluation could also be explored. Longitudinal studies documenting recovery of language function could address some of the issues that complicate the picture in aphasia, such as the impact of the speaker’s psychological state in the early stages post stroke, as well as level of cognitive impairment, aﬀecting such aspects as memory, and ability to reﬂect. In addition, co-construction of evaluation in dialogue would be an important area to explore in order to further address the social nature of stance and attitude. Such explorations should further elucidate the issues involved in evaluation and its signiﬁcance for aphasic individuals.

Acknowledgments This project was supported by grants from the following: Department of Veterans Aﬀairs Rehabilitation Research and Development Program,

Stroke stories 209 National Institute on Deafness and Other Communication Disorders, Callier Center for Communication Disorders at the University of Texas at Dallas, Community Partners Program (a collaborative program of the University of Texas at Dallas and Baylor Institute for Rehabilitation). Our thanks to both the institutions and participants involved

References Armstrong, E. M. (1997). A grammatical analysis of aphasic discourse: Changes in meaning-making over time. PhD thesis, Macquarie University, Sydney, Australia. Armstrong, E. M. (2001). Connecting lexical patterns of verb usage with discourse meanings in aphasia. Aphasiology, 15, 1029–1046. Armstrong, E. (2005). Expressing opinions and feelings in aphasia: Linguistic options. Aphasiology, 19 (3/5), 285–296. Becker, G., & Kaufman, S. (1995). Managing an uncertain illness trajectory in old age: Patients’ and physicians’ views of stroke. Medical Anthropology, 9, 175–187. Biber, D., & Finegan, E. (1989). Styles of stance in English: Lexical and grammatical marking of evidentiality and aﬀect. Text, 9, 93–124. Borod, J. C., Pick, L. H., Andelman, F., Obler, L. K., Welkowitz, J., Rorie, K. D., et al. (2000). Verbal pragmatics following unilateral stroke: Emotional content and valence. Neuropsychology, 14 (1), 112–124. Borod, J., Rorie, K. D., Haywood, C. S., Andelman, F., Obler, L. K., Welkowitz, J., et al. (1996). Hemispheric specialization for discourse reports of emotional experiences: Relationships to demographic, neurological, and perceptual variables. Neurospychologia, 34 (5), 351–359. Bury, M. (1982). Chronic illness as biographical disruption. Sociology of Health and Illness, 4, 167–182. Carter, R., & Nash, W. (1990). Seeing through language. Oxford, UK: Blackwell. Code, C., Hemsley, G., & Herrmann M. (1999). The emotional impact of aphasia. Seminars in Speech and Language, 20 (1), 19–31. Cortazzi, M., & Jin, L. (2003). Evaluating evaluation in narrative. In G. Thompson & S. Hunston (Eds.), Evaluation in text: Authorial stance and the construction of discourse (pp. 102–120). Oxford, UK: Oxford University Press. Faircloth, C. A., Boylstein, C., Rittman, M., Young, M. E., & Gubrium, J. (2005). Sudden illness and biographical ﬂow in narratives of stroke recovery. Sociology of Health and Illness, 26, 242–261. Frank, A. (1995). The wounded storyteller. Chicago: University of Chicago Press. Halliday, M. A. K. (1994). Introduction to functional grammar. London: Longman. Hemsley, G., & Code, C. (1996). Interactions between recovery in aphasia: Emotional and psychosocial factors in subjects with aphasia, their signiﬁcant others and speech pathologists. Disability and Rehabilitation, 18, 567–584. Holmes, J. (1998). Women’s talk: The question of sociolinguistic universals. In J. Coates (Ed.), Language and gender: A reader (pp. 461–483). Oxford, UK: Blackwell. Hunston, S., & Thompson, G. (2003). Evaluation: An introduction. In S. Hunston & G. Thompson (Eds.), Evaluation in text: Authorial stance and the construction of discourse (pp. 1–27). Oxford, UK: Oxford University Press. Hydén, L.-C. (1997). Illness and narrative. Sociology of Health and Illness, 19, 48–69.

210

Armstrong and Ulatowska

Jordens, C. F. C., Little, M., Paul, K., & Sayers, E. J. (2001). Life disruption and generic complexity: A social linguistic analysis of narratives of cancer illness. Social Science and Medicine, 53, 1227–1236. Kagan, A., & Duchan, J. F. (2004). Consumers’ views of what makes therapy worthwhile. In J. F. Duchan & S. Byng (Eds.), Challenging aphasia therapies: Broadening the discourse and extending the boundaries (pp. 158–172). Hove, UK: Psychology Press. Labov, W. (1972). Language in the inner city. Philadelphia: University of Pennsylvania. Labov, W., & Waletsky, J. (1967). Narrative analysis. In J. Helm (Ed.), Essays on the verbal and visual arts (pp. 12–44). Seattle, WA: University of Washington Press. LaPointe, L. L. (2001). Darley and the psychosocial side. Aphasiology, 15 (3), 249–260. Longacre, R. E. (1996). The grammar of discourse (2nd ed.). New York: Plenum Press. Martin, J. R. (1995). Interpersonal meaning, persuasion, and public discourse: Packing semiotic punch. Australian Journal of Linguistics, 15, 3–67. Martin, J. R. (2003). Beyond exchange: APPRAISAL systems in English. In S. Hunston & G. Thompson (Eds.), Evaluation in text: Authorial stance and the construction of discourse (pp. 142–175). Oxford, UK: Oxford University Press. McKevitt, C. (2000). Short stories about stroke: Interviews and narrative production. Anthropology and Medicine, 7, 79–96. Moss, B., Parr, S., Byng, S., & Petheram, B. (2004). “Pick me up and not a down down, up up”: How are the identities of people with aphasia represented in aphasia, stroke, and disability websites? Disability and Society, 19, 753–769. Ochberg, R. L. (1988). Life stories and the psychosocial construction of careers. Journal of Personality, 56, 173–204. Page, R. E. (2003). An analysis of appraisal in childbirth narratives with special consideration of gender and storytelling style. Text, 23 (2), 211–237. Parr, S., Byng, S., Gilpin, S., & Ireland, C. (1997). Talking about aphasia: Living with loss of language after stroke. Buckingham, UK: Open University Press. Peterson, C., & McCabe, A. (1983). Developmental psycholinguistics: Three ways of looking at a child’s narrative. New York: Plenum Press. Sacks, O. (2005). A neurologist’s notebook: Recalled to life. The New Yorker, October. Shadden, B. (2005). Aphasia as identity theft: Theory and practice. Aphasiology, 19, 211–223. Shadden, B., & Agan, J. (2004). Renegotiation of identity: The social context of aphasia support groups. Topics in Language Disorders, 3, 174–186. Smyth, J., & Pennebaker, J. (1999). Sharing one’s story: Translating emotional experience into words as a coping tool. In C. R. Snyder (Ed.), Coping: The psychology of what works (pp. 70–89). Oxford, UK: Oxford University Press. Stubbs, M. (1986). A matter of prolonged ﬁeldwork: Towards a modal grammar of English. Applied Linguistics, 7 (1), 1–25. Ulatowska, H. K., & Olness, G. (2001). Dialectal variants of verbs in narratives of African Americans with aphasia: Some methodological considerations. In M. Paradis (Ed.), Manifestations of aphasia symptoms in diﬀerent languages (pp. 9–26). Amsterdam: Pergamon. Ulatowska, H. K., Streit-Olness, G., Samson, A. M., Keebler, M. W., & Goins, K. E. (2004). On the nature of personal narratives of high quality. Advances in SpeechLanguage Pathology, 6 (1), 3–14.

Part III

Clinical considerations

14 Counseling families and adults with speech and language disorders The view from a wellness perspective Audrey L. Holland Introduction The scope of Chris Code’s contributions to neurolinguistics, and especially aphasiology, has been vast. Both as a scientist and as an enabler, through the journal Aphasiology, he has enhanced what we know about both right and left hemisphere language processing, and how to inﬂuence it through treatment. He has also been very open to the importance of the so called “softer sides,” that is our understanding of discourse and pragmatics and, ﬁnally, the psychosocial issues that surround negative changes in normal language functioning. This chapter has been written to honor that part of his enormous inﬂuence on the ﬁeld. According to the American Speech-Language-Hearing Association (ASHA) Scope of practice (2001) counseling families of children with speech, language, and hearing disorders, as well as adults who have such disorders, is an integral part of clinical responsibility. Counseling is perhaps the most important way we have to help our clients, yet it is likely to be that aspect of practice that most Speech-Language Pathologists and Audiologists feel most uncomfortable about, and are most likely to avoid. There are probably many reasons for this. Our reluctance might be explained by a lack of explicit training. Although we are given a wealth of information concerning potential counseling problems faced by individuals and families with communication disorders, we are not instructed in how to manage them. Counseling is often just tagged on to the end of disorderspeciﬁc courses, rather than having a focus as a special art, and a skill that can be learned in a general way, and then burnished by the speciﬁc problems evidenced by say, an adult and his family who face the realities of living with aphasia following a stroke. But I suspect there is an additional, probably bigger, reason. Why are we experts in communication so nervous about assuming our counseling role? Most counseling approaches used with communication disorders have been borrowed from a clinical psychology that emphasizes psychopathology and its eﬀects on behavior. This, despite the fact that the counseling problems faced

214

Holland

by experts in communication disorders do not stem from psychopathology per se, but from some form of catastrophe imposed on individuals who for the most part (even those most likely to be victims of traumatic brain injury) were at least coping with life in a fairly normal way. To my knowledge, our discipline’s reliance on abnormal psychology has seldom been examined, although it might explain why many practitioners feel uneasy with their counseling roles. Most families and individuals who experience communication disorders don’t ﬁt easily into a psychopathological model. Much of what follows stems from my conviction that a more appropriate model for our counseling lies elsewhere; not in what we know about illness and psychopathology, but rather in models that are grounded in wellness. The recent explosion of information and interest in Positive Psychology provides the best example, particularly as it is illuminated by the work of Seligman and his colleagues (e.g., Seligman, 1991, 2002; see also Reivich & Shatté, 2002). In fact, although I have used the word “counseling” in this chapter, I believe the notion of “coaching” as is reﬂected in the growth of contemporary interest in the phenomenon of Life Coaching, is probably a more appropriate description of our counseling activities. From the vantage point of Speech-Language Pathology (hereafter simply referred to as SLP), it seems to me one of the most appealing aspects of a focus on wellness and positive psychology as a model for counseling is that it ﬁts squarely and comfortably with that aspect of counseling with which we are most comfortable, namely our educational role. In my understanding of Seligman and his colleagues’ work, positive psychology attempts to teach individuals a number of exercises and very speciﬁc approaches that they can learn to use daily (or thereabouts) to increase their resilience and optimism (among other things) and that can contribute meaningfully to their leading happier and more fulﬁlling lives. Our discipline produces good teachers – from helping children to move lateral lisping into more acceptable /s/ production, to re-establishing semantic skills in aphasic adults. To the extent that our counseling can capitalize on our teaching skills, we should be more comfortable with our counseling roles.

What is counseling in SLP? These remarks are limited to working with adults who have communication disorders resulting from catastrophic events and their families; nevertheless, almost all of the ideas I will be discussing also have a place in work with the children and families who seek our help. In what follows, I ﬁrst deﬁne counseling, then I enumerate the disorders that I believe would fall under the rubric of “catastrophic” and provide a very cursory glance at the general problems each presents. I then outline a tentative model for counseling in adult catastrophic disorders. Next, I provide information concerning some basic characteristics of good clinicians, and then brieﬂy digress into a discussion of group versus individual counseling. Then, I ﬁnally get back to the initial

Counseling families and adults with speech and language disorders

215

question I raised concerning our professional anxieties about the counseling role. What is counseling? Brieﬂy, counseling is a listening process that is geared to understanding how the world looks to the person being counseled. Once careful listening has increased the clinician’s understanding, counseling moves on to guide the counseled person to express feelings, concerns, anxieties, and so forth. The third aspect of the counseling process involves advising, that is, providing the information people need to hear to help them understand what is happening to them, how to get on with their lives, and to live in a realistic, yet optimistic and resilient fashion. Then comes the most diﬃcult step; helping individuals to translate the information into action that is helpful, satisfying and successful. That is, the goal of counseling is to help individuals and families to live as successfully as they possibly can, despite the intrusion of the unexpected stroke, the unanticipated dementia, the communicationcompromising disorder such as laryngeal cancer, or the sudden and dramatic traumatic brain injury. The major aspects of communication counseling have been well summarized by Webster (1977) as follows: 1 2 3 4

To receive information that the individual and his or her family wish to share with you. To give information. To help individuals clarify their ideas, attitudes, emotions and beliefs. To provide options for changing behaviors.

The intent of counseling in situations such as those encountered with communicatively impaired individuals and their families is to help them: 1 2 3 4 5 6 7

to grieve for what has been lost to understand it as fully as possible to develop coping strategies and increase resilience to make peace with the disorder to make sensible adaptations to it to capitalize on strengths to minimize weaknesses, and to live as fully as possible, despite impairment.

We need to be reminded that, for those of us in this profession, counseling is seldom the general focus. Rather, counseling occurs “around the edges” of more direct treatment. This in no way denigrates its importance. Far from it, it accentuates the responsibility of clinicians to be on their counseling toes at all times.

216

Holland

Who has these catastrophic conditions? Although individuals who stutter (or their families), or families and individuals who as adults are continuing to cope with autism-spectrum disorders or other developmental disabilities, may have signiﬁcant counseling needs, this is too big a topic for a brief chapter. It seems sensible, therefore, to focus here on those who have previously been coping somewhat successfully, and whose problems come without warning, creating a crisis. The point here is that before the onset of these conditions, most individuals have been living in relative wellness (even a majority of individuals with TBI). Their problems also have unique, signiﬁcant, and reverberating eﬀects on families, who are, in the main, largely as unprepared for their unwelcome intrusion as are those who incur the problems in the ﬁrst place. The most important way to diﬀerentiate these disorders and their distinctive needs is based largely on their typical progression and time course. That is, there are diﬀerent counseling agendas for those who will improve and those who will deteriorate. Make no mistake; all of these disorders are to some degree chronic. However, in large measure, (although not without exception) these two types of catastrophic problems have diﬀerent implications for the nature of the counseling challenges they provide. The ﬁrst type of disorder involves chronic conditions that tend to improve, to experience some recovery spontaneously over time, or that change in a positive direction substantially with clinical intervention. These include conditions such as aphasia and right hemisphere cognitive disorders following stroke, laryngeal cancer, operable and non-metastatic brain tumors, some forms of encephalitis, traumatic brain injury and the like. For such disorders, after the initial listening and the information-providing is done, the counseling focus should be on measured and graceful acceptance, on building realistic optimism and resilience, and on coping in a balanced positive way toward living successfully with the disorder. The second type of disorders includes conditions such as dementia, primary progressive aphasia, Parkinsonism, multiple sclerosis, and the particularly challenging disorders of amyotrophic lateral sclerosis and brain tumors such as glioblastoma multiformae, which have an unrelentingly grim prognosis. For these disorders, listening and providing information of course must happen, but the truly challenging counseling responsibility is mutually to work toward acceptance, learning to live the best of what is left of one’s life, and even possibly to deal with some end-of-life issues such as making peace. It is important to add a few words about depression and learned helplessness. Without exception, the problems mentioned above all have the potential for resulting in reactive depression. For disorders that involve brain damage, there is the additional possibility that a concomitant depression, brought about by faulty or disturbed patterns of normal neural transmission, may also occur. Finally, individuals may have come to their present disorder already carrying a suitcase full of depression. Counselors in communication

Counseling families and adults with speech and language disorders

217

disorders lack the technical skills to treat depression, both behaviorally and pharmacologically. But because depression is so likely to co-occur in some form with the catastrophic problems we deal with, it is extremely important for us to be highly sensitive to the problems that forecast it. According to DSM-IV, depression includes mood disorders, lack of zest, unexplained weight loss, sleeping problems, psychomotor problems, excessive fatigue, feelings of worthlessness, statements of futility, and such. When these problems persist, our ethical responsibility is to state our concerns directly and to make appropriate referrals. A useful model Although it has signiﬁcant shortcomings, a crisis model, particularly as Webster and Newhoﬀ adapted it (1981), can be useful for understanding the process whereby individuals can learn to deal with catastrophic events. First developed by Elisabeth Kubler-Ross for dealing with grief, death and dying (1969) it has been useful with many chronic health issues as well. Webster and Newhoﬀ discuss the relevance of crisis to families and individuals following stroke. Speciﬁcally, four stages are postulated to occur as individuals progress toward healthy resolution. They are, in order, Shock, Realization, Retreat, and Acknowledgment. Not all individuals go through all stages, and not all individuals actually reach satisfactory acknowledgment (more on this below). Nevertheless these stages set the tone for what are the important counseling parameters for SLPs to keep in mind as they conduct counseling related to communication. Following are some examples. Soon after an aphasia-producing stroke, neither families nor aphasic individuals are in a particularly good position to take advantage of the information we might have to oﬀer them concerning aphasia and its aftermath. I am aware that good clinicians almost without exception provide such information. Nevertheless, someone like me (who is unlikely to see aphasic individuals until they complete their course of formal rehabilitation) almost always hears that things weren’t explained, that individuals and their families had no idea what to expect, and so forth. This happens because early shock pretty much precludes the ability to absorb new information. This does NOT mean that we should stop providing it in the most acute stages, probably in writing and for placement on fridge magnets and the like, to be consulted later. But it DOES mean that the ﬁrst of Webster’s (1977) counseling functions probably should be primary. Listening to what people wish to share, to their fears about the future and such, and simply holding hands and being there is what matters then. And only after some realization about what this problem might actually be, can information be productively used. (For a detailed look at an approach to aphasia management in the acute stage, readers are referred to Holland & Fridriksson, 2001.) Although retreat seems to me to be the least universal of these crisis stages, we must be aware of the delicate nature of denial, and the need to deal with it

218 Holland clinically should it occur in the individuals we work with. A common ﬁnding in our clinic for individuals with chronic aphasia is that when families of those who are newly discharged from rehabilitation complete the required Communication Eﬀectiveness Index (CETI) (Lomas, Pickard, Bester, Elbard, Findlayson, & Zoghabib, 1989), their scores are substantially better than they will be the next time they do the CETI, after they have lived with the disorder for a longer period of time. This is an issue for gentle and careful family counseling. Acknowledgment is not a synonym for “giving up.” It is recognizing where one is, making room for one’s changed condition, and ideally moving on with life. Ram Dass, who ﬁnished his book Still here, after a stroke resulted in aphasia and hemiplegia, eloquently described his experiences, and the good that resulted from them. He notes (2000, p. 185): The stroke was like a samurai sword, cutting apart the two halves of my life. It was a demarcation between the two stages. In a way, it’s been like having two incarnations in one; this is me that was “him.” Seeing it that way saves me from the suﬀering of making comparisons, of thinking about the things I used to do but can’t do any more because of the paralysis in my hand. In the “past incarnation” I had an MG with a stick shift, I had golf clubs, I had a cello. Now I don’t have any use for those things! New incarnation! Mezirow (1991) has written extensively about the role of transformative learning in adults, producing evidence that many individuals go through what he terms “disorienting dilemmas” that cause them to re-evaluate, reﬂect critically, ﬁnd out that they are not alone, and for many, restructure the meaning of our lives. This is the sense of acknowledgment that counseling should strive toward, if not always achieve. What are the characteristics of a good SLP counselor? Robert Crum, a child psychologist with extensive experience in working with children and families with communication disorders remarked to me recently (personal communication, October 2004) that in his view, SLPs were masters at presenting relevant information, but that their other counseling skills were not nearly as highly developed. I agree. In our training curricula, counseling and interviewing often are approached together. This makes it almost a given that we should see their respective roles as more overlapping than they actually are. In addition, we learn early on that we must communicate as much of our expertise as possible to our clients. Along the way, we forget that we are only one of the “experts.” Along with the individual whose expertise is living inside the problem, and those whose expertise is living beside the problem (i.e., the family), we bring the expertise of “the one who has seen many such.”

Counseling families and adults with speech and language disorders

219

But we have not lived it. Exquisite awareness of the three sources of expertise is one characteristic of the successful counselor. There are others, of course. I believe that the next most important clinical skill is the ability to be a good listener. (Luckily, listening well is a learnable skill.) Good listening comes in many forms, including aﬃrmative and supportive listening, reﬂective listening, and critical listening. It involves sensitivity to both a message’s manifest (surface) content and its latent (deeper emotional) content, and whether or not these two message levels are in agreement. Often, insights result from our ability to listen, not only with our ears, but with our eyes as well to non-verbal features of communication including prosody, intonation and body language. Counseling skills also include our own words and body language. Some technical skills consist of a variety of learnable techniques, such as how to reﬂect what someone is saying, knowing how to ask appropriate questions, communicating support and aﬃrmation verbally. Because I am an active and involved counselor, as opposed to a neutral and passive one, I also come down on the side of providing advice, but giving it tentatively and from my outsider position, as noted above. And we also must capitalize on our information giving skills. As Crum (personal communication, October 2004) suggests, we need to know what is relevant and what is acceptable to a given client about issues ranging from what can be expected over the next few years concerning a disorder, to how to get the most from services available in the community. As a counselor, I try very hard to communicate in every way that I am consistently “being there,” as a helper, an advocate, and as, simply, a listener. Next, I believe that competent SLP counselors know who they are.1 They know their strengths, and what things are not within their basic competencies. This puts them in a position to work with clients from their own strengths and capabilities. I ﬁrmly believe that a major reason for my being a good counselor is that I know pretty well who I am, and how to capitalize on it when I counsel. Finally, in an overarching way, good counselors must be optimists who like people, enjoy challenges, know and accept themselves, and communicate their positivity. Group vs. individual counseling A few words about the manner in which counseling is conducted seem to be in order. Whether to choose a group or an individual format seems to me to largely be a matter of mutual choice, agreed on by the counseling clinician and those being counseled. I personally gravitate toward group work for a number of reasons. First, given my earlier comments about who are experts, it seems likely that when there is more than one of those other experts around, there should be a lot to share, thereby greatly increasing the extent of expertise in the room. Second, as Mezirow (1991) points out, social interaction greatly enhances the likelihood of transformative learning. Third it is

220

Holland

cheaper and more practical, often bringing the group within the reach of individuals who otherwise would not be able to aﬀord counseling. But should individual counseling be the order of the day, then I think the clinician has increased responsibility for sharing what has been learned from working with others and being a surrogate expert. And, it must be added, frequently our counseling of individual clients occurs “around the edges” of more direct therapy. I also prefer family groups and groups for individuals who have the disorders to meet separately. I have learned the value of this over the years, mostly from the people I have worked with. The focus of combined groups almost invariably settles on the individual with the problem, with family needs going by the wayside. And this seems to occur despite the fact that family members dominate the talking time.

Concluding comments This has been a cursory review of counseling issues for clinicians dealing with adults and families who have neurogenic communication disorders. It is not a clinical roadmap; rather it attempts to point out the major counseling issues for these people, and to provide a rationale for treating them. The most important underlying message (the latent one) is that professionals in this ﬁeld must take their counseling responsibilities seriously, and that counseling individuals with neurogenic communication disorders is among the most important things we do to inﬂuence individuals in their return to their everyday lives.

Acknowledgment A version of this chapter appeared in the newsletter of the California Speech and Hearing Association in Autumn, 2005. I am grateful for CSHA’s permission to expand on and modify it here in honor of Chris Code.

Note 1 A number of self-inventories are useful to clinicians. These include the MyersBriggs and the Values in Action (VIA). A form of the Myers Briggs can be taken on the Internet at www.Humanmetrics.com and the VIA can be taken at www.Authentichappiness.org

References American Speech-Language-Hearing Association (2001). Scope of practice in speechlanguage pathology. Available as pdf ﬁle at www.asha.org Holland, A., & Fridriksson, J. (2001). Management for aphasia in the acute phases post stroke. American Journal of Speech-Language Pathology, 10 (1), 19–28. Kubler-Ross, E. (1969). On death and dying. New York: Macmillan.

Counseling families and adults with speech and language disorders

221

Lomas, J., Pickard, L., Bester, S., Elbard, H. Findlayson, A., & Zoghabib, C. (1989). The Communicative Eﬀectiveness Index: Development and psychometric evaluation of functional communication measure for adult aphasia. Journal of Speech and Hearing Disorders, 54, 113–124. Mezirow, J. (1991). Transformative dimensions of adult learning. New York: Wiley. Ram Dass (2000). Still here. New York: Riverhead. Reivich, K., & Shatté, A. (2002). The resilience factor. New York: Broadway Books. Seligman, M. (1991). Learned optimism. New York: Knopf. Seligman, M. (2002). Authentic happiness. New York: Free Press. Webster, E. (1977). Counseling with parents of handicapped children: Guidelines for improving communication. New York: Grune & Stratton. Webster, E., & Newhoﬀ, M. (1981). Intervention with families of communicatively impaired adults. In D. S. Beasley & G. A. Davis (Eds.), Aging: Communication processes and disorders. Orlando, FL: Grune & Stratton.

15 Cultural dimensions of aphasia Adding diversity and ﬂexibility to the equation Claire Penn

The cultural context in which assessment and therapy take place provides probably the most powerful explanation for many of the features of aphasia the clinician encounters and is the key to most aspects of therapy and longterm outcome. Certain sociocultural contexts provide a unique opportunity to examine recovery in aphasia. This chapter presents some evidence and some insights regarding the cultural dimension of aphasia, and proposes some implications for assessment and intervention. Though the evidence I draw on is based on my experience in South Africa, I believe that in the context of globalization and with increasing diversity in every clinician’s caseload, there are some clear universal principles that emerge. I argue that: 1 2

3

Multilingual persons with aphasia use the tools in their linguistic repertoire diﬀerently and respond to aphasia in diﬀerent ways. There tends to be a very ﬁne, often indiscernible, line to be drawn between pathological and normal language in the context of natural language use. Narrative discourse provides at the same time a culturally relevant assessment tool and an opportunity to explore the complexity of language and its use, a window onto cognitive and pragmatic processes and an genre for meaningful intervention.

The context of practice that I draw from is South Africa, in which 11 oﬃcial languages are acknowledged but in which many more languages and regional variations exist, where practically every inhabitant is bi- or multilingual, where there is daily interface of languages, and where language use is coupled strongly with sociopolitical identity. This situation has necessitated the development of methods of assessment and intervention for individuals with speech language pathology that are not based on the western model. It is not appropriate for example to approach a rural illiterate Zulu-speaking aphasic patient with an item from one of the well-known aphasia tests: “Roses are red and violets are. . .”. Neither is it

Cultural dimensions of aphasia

223

appropriate to assume that a traditional one-to-one model of aphasia therapy will work in a situation characterized for the most part by lack of resources, lack of access, and poverty. However I argue that being aphasic in a multilingual context such as South Africa may not be altogether bad. In fact the nature of language use in that society may well provide a scaﬀolding framework for compensatory strengths to emerge in the presence of language pathology. It would seem that certain tasks and certain analysis frameworks allow highly signiﬁcant cultural features to emerge, which have strong implications for the clinician and shed light on language processing in general. This chapter proposes that a number of the stylistic and syntactic aspects to be seen in the discourse of such aphasic persons reﬂect the compensatory eﬀorts of a group whose sociolinguistic status (marked by diverse daily interface/contact) provides well-rehearsed shift strategies. Those individuals with aphasia therefore have a particularly well-stocked armamentarium of strategies for deployment during conversational interchange. Underlying much of my work is the basic premise that aphasic language is about compensation. It has long been recognized that many of the behaviours we see in aphasia are not necessarily aphasic symptoms, but the adaptation of the organism to the primary deﬁcit. Goldstein for example in 1948 said: “The aphasic patient has to achieve a condition which allows him to react as well as possible to the tasks arising from the environment” (p. 21). Such compensatory explanations of aphasia are frequent in explaining aphasic symptoms, and in bilingual patients and in speciﬁed sociocultural contexts these compensatory behaviours may play out in a very speciﬁc and interesting way. The prime evidence that I will draw from in this chapter is Afrikaans. This is one of the languages unique to South Africa that has a relatively short history, yet ironically is one of the most studied and documented. It existed much in today’s form from about 1850, and was given legal recognition in 1925 when it became the language of the church and government. It is a language that is diverse in terms of region, dialect and social class, originating not only from the Dutch used by the seventeenth-century settlers in South Africa, but also having features of Malay, Portuguese, Khoin, French and German as well as English (Combrink, 1978; Roberge, 1995). This is the home language of a large number of people in South Africa (7 million) and until recently was the medium of education for a number of non-ﬁrst-language speakers (Kroes, 1978). Viewed as the language of the oppressor for many years, it has been the topic of extensive debate among politicians and educationalists and in the formulation of the language policy of the new South African government. There is distinct dialectal version of Afrikaans that has developed in a group of mixed racial heritage, largely resident in the Cape Province. This community developed through events of Dutch colonization in the seventeenth century and the interaction between the settlers and the indigenous people of the Cape. There are estimated to be more than 3 million users of

224

Penn

Cape Afrikaans, which diﬀers from the language of standard Afrikaans speakers in a number of diﬀerent ways. These have been highlighted by van Rensburg (1997), McCormick (1989, 1995) and others, and include diﬀerences in phonology, lexicon, syntax and stylistic variables. The codeswitching and code-mixing1 that have been documented extensively in this dialect reﬂect important sociocultural factors. The strong oral tradition of this group, as well as its unique dynamic position in society, account for some of these aspects, including “intensive linguistic exchange” (McCormick, 1995, p. 204) and language contact factors with a very strong eﬀect of English, often spoken to children in the home and at school by second language speakers. Little work has been done on aphasia in Afrikaans, but given what we know about the structure of Afrikaans and its origins, areas particularly susceptible to aphasic breakdown for agrammatic patients at least are the verb and operations surrounding the verb movement. Extrapolating from the extensive and explicit work of Kolk, Heling, and Keyser (1990) and Batsiaanse and colleagues on Dutch aphasia, verb movement and retrieval diﬃculties as well as problems with prepositions and articles and sentence embedding would be anticipated (e.g., Bastiaanse & Jonkers, 1998; Bastiaanse & van Zonneveld, 1998; Edwards & Bastiaanse, 1998; Vermeulen, Bastiaanse, & van Wageningen, 1989). Much of the cross-linguistic work that has been done has been based on tasks that are sentence or clause based, including picture and sentence matching, sentence completion and anagrams. However the impact of the task strongly inﬂuences the accuracy and nature of the language obtained, and there remains a scarcity of studies at a discourse level, especially for the person with mild aphasia. This genre is a particularly fruitful one in any group (such as those in South Africa) where literacy is limited, especially in older members of society for whom oral narrative is a strong tradition. This chapter thus focuses on some speciﬁc linguistic structures that are particularly prevalent in the discourse genre. Selecting these aspects serves to illustrate the close connection between linguistic and pragmatic factors in aphasic breakdown. Studying them in the two languages of bilingual subjects and in aphasic and control subjects provides the opportunity to separate out normal from compromised processes, and to examine compensatory strategies operating that are independent of or dependent on speciﬁc linguistic factors in discourse. Some pragmatic and syntactic ﬁndings provide interesting insights not just for the bilingual patient, but for, I hope, aphasia in general.

The evidence A series of studies have been undertaken on the narrative discourse of bilingual persons with aphasia in South Africa and matched controls (Archer, 2006; Kalmek, 2001; Nabeemeah, 2002; Venter, 2000; von Bentheim, 2001). The goal of the research has been to examine the connected language of

Cultural dimensions of aphasia

225

bilingual persons living in a multilingual context in order to better understand the cultural inﬂuences on aphasia, and to determine ecologically valid assessment and therapy approaches. Participants We now have data from 62 bilingual participants, 31 people with aphasia and 31 matched controls. All aphasic participants were right handed and developed aphasia as a result of a single CVA. They had to be a least 3 months post onset of stroke and were rated as having a mild to moderate degree of aphasia on the Western Aphasia Battery (WAB) (Kertesz, 1982; adapted for language and culture). Participants with severe aphasia were excluded from the study, as the task involved connected language. Participants were also required to be under the age of 69 years with at least 7 years education. Control participants who had no history of neurological or psychiatric problems were matched for age, gender, language, cultural group, education and occupation. An adapted version of Paradis’ bilingualism questionnaire was administered to each participant (Paradis, 1987) to ensure the language status of this group and to document patterns of language exposure, current contexts of language use, patterns of acquisition, family and educational language patterns, and diﬀerential recovery patterns. The participants were tested in both their languages on the same tasks by linguistically and culturally matched individuals on separate days. Tasks and analysis framework A range of narrative tasks were employed, following the protocol of Ulatowska and her colleagues (1993, 1998; Olness, Ulatowska, Carpenter, Williams-Hubbard, & Dykes, 2005). We used picture description, picture sequence, the narrative of personal experience and a fable task. In line with the framework of Ulatowska et al., our analysis included a range of measurements. Productivity measures included calculation of narrative length, proposition analysis, T-units, words per T-unit, and error analyses. A number of lexical and syntactic aspects were also examined, including verb and word order aspects which will be considered here. Quality of narrative was measured using a 5-point rating scale. This was based on the work of Labov (1972, 1984) and included the dimensions of Relevance, Character, Supporting description and Ending. The ratings were conducted by culturally matched speech-language pathologists from the Cape community. Three raters reached acceptable agreement on these measures. The analysis also examined speciﬁcally the presence of “ethnic discourse markers” described as features particular to a certain cultural group, as well as a range of stylistic and pragmatic devices including code-switching, repetition and evaluation.

226

Penn

Results The ﬁndings of some of this research have been published in detail elsewhere (Ogilvy, von Bentheim, Venter, Ulatowska, & Penn, 2000; Penn, Venter, & Ogilvy, 2001). In this chapter I focus primarily on the narratives of personal experience from the bilingual Cape Afrikaans group (with 14 participants), as the particular nature of their data seems to highlight particularly well the essential challenge of diﬀerentiating normal features of discourse, cultural markers and stylistic markers from frank aphasic errors. A summary of the main ﬁndings appears in Table 15.1. Productivity measures The productivity measures for the aphasic participants and the controls for their narratives of personal experience in Cape Afrikaans are summarized in Table 15.2. These results reﬂect group means but exclude, where relevant, A2 whose very lengthy sample (1288 words) rendered him an outlier. In general the control subjects produced longer narratives with a greater number of T-units. The mean length of the narrative for the aphasic sample was 167 words (range 83–285), indicating generally a shorter and more diverse sample size for the aphasic group than for the controls, whose range was 226 to 512 words. This diﬀerence was found to be statistically signiﬁcant (Mann Whitney U test, U = 5.0, p = .22). The numbers of T-units and propositions were comparable when the sample of A2 was included in the tally of the means, but were signiﬁcantly fewer for aphasic subjects when S2’s sample was excluded. This is similar to the ﬁndings of Olness, Ulatowska, Wertz, Thompson, and Auther (2002) who found a lower number of propositions in their aphasic African American group. Table 15.1 Summary of narrative ﬁndings in a group of bilingual Cape Afrikaans speakers with and without aphasia • Control samples longer than the aphasic samples in both languages tested • Fewer complex or non-canonical sentence forms in aphasic samples in both languages • Evidence of wider verb variety and complexity in control than aphasic samples • More evidence of verb errors (aux omission) in aphasic samples, and incomplete sentences • Some tense shift patterns distinctive in aphasia • Equivalent evidence of dialectic features and ethnic markers in aphasic and in normal samples (in both English and Afrikaans) • Some marked qualitative/coherence rating diﬀerences between aphasic and control samples in temporal sequencing • Qualitative diﬀerences in evaluative elements • More language alternation in aphasic than control narratives • Less language alternation in English than in Afrikaans narratives

Cultural dimensions of aphasia

227

Table 15.2 Group data for productivity measures in Cape Afrikaans (means) Variable

Aphasic participants (n = 7)

Controls (n = 7)

Number of words*

167 SD = 122.31 28 SD = 14.81 9.16 25.3 SD = 11.7 2.0 SD = 0.37 0.52 SD = 0.27 0.44 SD = 0.17 0.3 SD = 0.11 27.5 SD = 10.58 16.7 SD = 5.82 0.53 SD = 0.22 0.86 SD = 0.23 0.12 SD = 0.076 24.71 SD = 37.69 38.33 SD = 17.9295

316.57 SD = 111.98 38.26 SD = 12.57 10.23 31.7 SD = 11.6 2.24 SD = 0.28 0.47 SD = 0.27 0.4 SD = 0.14 0.2 SD = 0.11 50.86 SD = 21.42 26.6 SD = 8.66 0.54 SD = 0.13 0.88 SD = 0.19 0.18 SD = 0.09 18.57 SD = 6.425 69.42 SD = 25.178

Number of propositions* Words per T-unit Number of T-units* Verbs per T-unit Auxiliaries per T-unit Tense shift per T-unit Copulas per T-unit Tokens* Types* TTR Tokens/T-unit Subordinates/T-unit* Verbs–verb tokens Number of verbs*

Note: * indicates signiﬁcance without outlier.

Because of the wide variation in sample size, direct comparisons of other productivity measures were possible only through ratios expressed in relation to the T-unit. The mean length of the T-units was 9.16 words for the aphasic subjects (range 7.5–12) and 10.23 for the control subjects (range 8.3–14). This was not statistically signiﬁcant. The mean number of verbs per T-unit was also found not to diﬀerentiate groups. However, the total number of verbs, the number of verb types and tokens, and the number of subordinations per T-unit were signiﬁcantly higher in the control sample and this is discussed in more detail in the following section.

228

Penn

Syntactic features In general there were more frank errors and a higher presence of incomplete and minor utterances in the aphasic samples. There were fewer complex or non-canonical sentence forms in aphasic samples in both languages, and there was evidence of wider verb variety and complexity in control than in aphasic samples. There was lower diversity of verbs and more evidence of verb errors (auxiliary, shown as “Aux” omission) in aphasic samples, as well as of incomplete sentences. Disrupted auxiliaries were found in aphasic samples only and took various patterns. Auxiliary doubling was found as in the following instance: Maar ek het nog altyd gebid het But I always prayed Other examples show Aux omission, for example: Ek veld loop I walk ﬁeld Ek op die plaas gebly I lived on the farm Ek gele in die bed I lie on the bed The sample of one participant with a moderate (rather than mild aphasia) was interesting as she had more frank syntactic problems. Interestingly her diﬃculties with the auxiliary are manifested in each attempt at use. In her narrative of personal experience, for instance she produced 12 T-units, 9 of which were complete and 3 of which were inaccurate or abandoned attempts. All these false starts related to the management of the past tense auxiliary: Aux omission:

Ek ge- gedink hy gaat my klap (omission of het) I thought he would hit me

Incomplete Aux: Ek het ged gedink (incomplete) . . . Ek was baie bang I thought . . . I was very scared (arguably changed from Aux to copula form) Abandoned Aux: Ek het die man wat vir my geslaat het so — I (past tense Aux) the man who hit me so — (abandoned, presumably because of processing demands induced by syntactic complexity/embedding)

Cultural dimensions of aphasia

229

The rest of her verb use consists of copulas and the use of historical present tense. Other errors noted in the aphasic sample included (1) omission of aux “het” and marker “ge” but maintenance of the past tense word order: A2

Ek veld loop (Target Ek het in die veld geloop) I walk in the veld Ek op die plaas gebly (Target Ek het op die plaas gebly) I lived on the farm Ek het hospital twee jaar agt maande (Target Ek het ?in die hospital twee jaar agt maande gewees) I was in hospital for 2 years and 8 months

(2) Using the past tense marker ge- (rather than the auxiliary plus -ge) to denote past: Ek gelê in die bed (Target Ek het in die bed gelê) I lay in the bed Other syntactic aspects were common to both aphasic and control samples in Afrikaans. Those common to both have been described as “syntactic convergence features” and are a documented feature of Cape Afrikaans (McCormick, 1995). Word order changes/verb movement Afrikaans samples were examined for the presence of English word order. This optional change to subject–verb–object (SVO) from subject–object–verb (SOV) in Afrikaans is often triggered by a speciﬁc main clause verb type (I know, I think, I see) and by the use of the copula in the subordinate clause. Also, following the verb complementizer wat (what/which) in Standard Afrikaans will require verb to be in clause ﬁnal position. In Cape Afrikaans an optional rule allows the verb to precede the object; for example: A2

En ek sien hier staan ’n ry trokke And I see here stands a row of trucks Dink ek iets is darem nie reg hier nie is I think something is really not right here

Versus the following examples where verb ﬁnal position is kept: Ek dink ek gaan darem nie so na aan hom draai nie I think I will really not turn so close to him

230

Penn Ek het gedink ek gaan nou nooit weer uit die hospitaal uit kom nie I thought I would never again get out of hospital Ek dink toe en ek wil gaat na haar toe met ’n bos blomme I then thought and I wanted to go to her with a bunch of ﬂowers A6

Miskien my spraak gaan weg Perhaps my speech would go away

Such examples were found in both aphasic and control subjects, and variation was found within subjects, so reinforcing the dialectal nature of this shift. The presence of English word order in the Afrikaans sample, while not exclusive to the aphasic samples, seemed more prominent among these, and has some important clinical implications. A large body of literature has demonstrated that aphasic patients have problems processing sentences in which the order deviates from the canonical one (Thompson, Lange, Schneider, & Shapiro, 1997). There are interesting therapeutic implications arising from this, suggesting that SVO therapy may be more eﬀective than SOV therapy, or that when there are optional contexts (seen in normal production), these should be identiﬁed and reinforced in therapy (using for a starter, I know, I think, I see verbs). Post-verbal expansion frames should also be supported. There are some very promising results from therapy programmes that are verb focused and are sensitive to the processing demands imposed by certain syntactic operations (Mitchum & Berndt, 1994). An examination of tense-shifting in the samples proved this to be an interesting and related phenomenon. Tense-shift occurred regularly in the narrative samples in both aphasic and control samples. The aphasic samples showed errors in the verb speciﬁcally at these junctures, suggesting that this is a “danger point”, and possibly a focus of therapy. None of these errors were observed in the narratives of the control participants. Shifting to the present tense in Afrikaans reduces verb complexity, and avoids word order and morphological changes. It is associated in narrative with the use of the historical present as well as direct speech. The conversational historical present is a stylistic device that adds a theatrical component to a narrative (Wolfson, 1978). It also conveniently obviates the necessity for past tense which, as the above examples demonstrate, has processing costs particularly in Afrikaans. The fact that it was found more frequently in the aphasic than the control subjects suggests that verb variety and complexity was a choice for the controls but not always a possibility for the aphasic speakers. One of the participants showed a unique eﬀect: use of present tense for the entire narrative in Afrikaans and the past tense for the same story in English. This is perhaps a reﬂection of complexity of past tense in Afrikaans. While this device occurred in the English samples it was less frequent. An example of both of these aspects is provided from an English narrative:

Cultural dimensions of aphasia C1

231

And on my way back, well I was on foot, I have to walk home. And suddenly I hear something behind me and I know things is not good for me because we live in crime, we live in lots of things. And I said to myself “Wow terrible things is going to happen!” Then I start walking faster but my heart was start doing this and I was feeling real ice. I was real scared and I said to myself “If home can just be very near me now.”

Quality aspects of discourse Coherence A coherence rating was undertaken for all the transcripts using a 5-point rating scale for Temporal organization, Relevance, Character, Supporting description and Ending. As Figure 15.1 suggests, a marked diﬀerence was found between the coherence of the narratives of the aphasic subjects and that of the controls in clarity and temporal sequencing. The clear diﬀerence between the coherence of the aphasic and the control narratives is markedly in contrast to some of the productivity and complexity measures utilized in which often no marked diﬀerences could be found. This ﬁnding has important implications both for assessment and for therapy and seems to reﬂect the sensitivity of narrative discourse not solely to linguistic factors but to cognitive and social aspects as well. Ethnic markers In the transcripts there were some examples of lexical items typifying this dialect and the retention of some old forms of Afrikaans (probably reﬂecting the age group). These included words such as Kooi (bed), daai (the demonstrative “that”), gaat (for gaan (go)) and Slaat (for slaan (hit)).

Figure 15.1 Coherence ratings for narratives of aphasic and control participants.

232

Penn

There are many examples of loan words in the samples, mostly from English, reﬂecting the high contact patterns between languages in the Western Cape region of South Africa. Examples of loan words were found in most word classes including nouns, conjunctions, adjectives, verbs and adverbials (see Appendix 15.1) (Branford & Claughton, 1995). Dialectal aspects were also features in both aphasic and control samples, which included, in Afrikaans, regularizing of irregular past tense, shift from SOV to SVO triggered by speciﬁc verbs, topicalization, and reduplication. In the English transcripts, ethnic markers included deletion of contractible forms of “be” and “have”, changes in number concord, deletion of past tense marker “-ed”, deletion of adverbial suﬃx and preposition substitution, conﬁrming features of the dialect documented by McCormick (1995) and others. Stylistic and pragmatic factors Certain stylistic features have been identiﬁed as enhancing the properties of narrative, and the narrative genre has been found to yield a high number of such elements (known as evaluative elements) that help to dramatize a story and provide it with a speaker’s particular structure and “ﬂair”. Also known as “intensiﬁer elements” of the narrative, they convey the narrator’s feelings about characters and events and include ritual utterances, phonological intensiﬁers, lexical items, repetition and gesture, comparatives, syntactic devices such as ellipsis and topicalization, as well as direct quotations, asides and sound eﬀects (Chafe, 1982; Dorian, 1997; McCormick, 1995; Wolfson, 1978). Labov (1984) suggests that evaluative devices are used to direct discourse to the intended audience. Those with well-developed discourse competence will be able to select a level of detail within which to cast ideas, highlight certain aspects to make the story understandable or exciting, and alter sequences and shift perspectives to portray feelings of other participants. They are closely linked to the ethnic markers identiﬁed and it is probably not appropriate or feasible to diﬀerentiate them, especially in Cape Afrikaans. Though evaluative features were present in both aphasic and control samples, there were diﬀerences between the control and aphasic groups in this regard, with more frequency and diversity of such narrative elements occurring in the control group. In the data we found rich examples of such devices including ellipsis and topicalization, the use of ritual utterances, comment clauses, expressive phonology, direct speech, repetition and enactment. Examples of these are provided in Appendix 15.1. Direct reported speech is a fascinating feature of narrative that occurred frequently in the samples. It has a strong pragmatic function serving as a stylistic device that enriches a narrative but can also be regarded as a well-documented simpliﬁcation strategy mechanism to avoid tense shift and embedding, exploited fairly frequently by aphasic persons (Hengst, Frame, NeumanStritzel, & Gannaway, 2005; Penn, 1987). Further it has been considered as a

Cultural dimensions of aphasia

233

powerful measure of the degree of bilingualism and is often foregrounded by a language switch (Dorian, 1997). Many examples of reported speech were found in both aphasic and control samples, and in both of the languages tested. One of the most delightful is the following, which also illustrates the relationship between direct speech and code-switching: En ek se vir hom “Ek wil Kaap toe gaan” Hy se. “Eish but you’ve just missed the train”. “Ah uh”. Hy se vir my “But you are not alone”. Maar ek is alone. Ek se vir hom “Of course I’m alone. Daar’s niemand by my nie. I’m not alone!” Wilkinson, Beeke, and Maxim (2003) and Goodwin (2003) comment on the pragmatic function of enactment, which is used to describe and report events: a demonstration of what participants did or said rather than a description of the event. This typically involves using direct reported speech as an index of change of voice/footing shift as in the example above. These authors demonstrate the evidence from aphasic conversational samples of how persons with aphasia use such enactment in a distinctive way to deal with the contextual demands of conversation – to describe events and actions and enabling the presentation of the past and future in the here and now. Direct speech used in combination with intensiﬁers (as discussed above) including expressive phonology, repetition, gestures, quantiﬁers and proforms (which only derive meaning in context), enables such enactment to occur. Given the strong cultural correlations of such enactment, this suggests a powerful medium of therapy especially for more moderate to severe cases of aphasia. Repetition Repetition has been identiﬁed as an ethnic stylistic feature (e.g., in the discourses of African American individuals) but also as an aphasic strategy (Ulatowska, Streit-Olness, Hill, Roberts, & Keebler, 2000). One might predict that repetition/reduplication might appear more frequently in Afrikaans aphasic samples, ﬁrst because reduplication is a feature of the dialect, and second, because it is well documented as a compensatory and stylistic device Repetition was found in all samples (English and Afrikaans) and as the examples illustrate, has an obvious stylistic function. However repetition seemed to occur more frequently in the aphasic groups and is probably serving the role of emphasis in the face of restricted linguistic competence. Language alternation patterns were interesting and correlated closely within individual language history proﬁles. Not unexpectedly such language alternation/code-switching occurred more in aphasic than in control samples. An impoverished linguistic system may well account for the presence of

234

Penn

such code-switching in aphasic samples, but the fact that language alternation occurred more in Afrikaans than in English samples and was used by the control group only in Afrikaans points to more subtle contextual inﬂuences reﬂecting changing patterns of language use in South Africa and political variables.

Discussion The ﬁndings presented above suggest that while some aspects of the analysis diﬀerentiated aphasic from non-aphasic bilingual persons, there are a number of apparently non-standard features of language common to the two groups. Some may be a function of the genre of elicitation and some a function of the speciﬁc language and the context in which the data were collected. The point made by Ulatowska and Olness (2001, p. 107) that “the key question in any attempt to look at the interaction between dialect and aphasia is discerning which diﬀerences are attributable to the dialect and which are attributable to the pathological processes” needs to addressed. In the sample of ﬂuent bilingual aphasic participants studied, we found a range of linguistic and stylistic features in their narratives, reﬂecting aspects that can be hypothesized to be aphasic in origin, but also unique aspects of the languages in their regional form. It is argued that the “default mode” of natural language in this context, which includes patterns of code-switching, ﬂexible word order and stylistic intensiﬁcation, provides a robust compensatory and scaﬀolding structure for some of the primary aphasic deﬁcits and that the genre of narrative provides a strong basis for such pragmatic strengths to emerge. Aspects such as enactment and language alternation may in fact reﬂect attempts to compensate for a reduction in processing capacity in the on-line task of narrative. There are some aspects of the data that seem to be features of the narrative genre (across cultures and languages); there are some aspects that have features that are speciﬁc to Afrikaans (and the non-standard variety in particular); ﬁnally there are features that have been identiﬁed as possible aphasic compensatory features which reﬂect preserved pragmatic competence in the face of linguistic erosion. This study suggests that, at least in this population, it may be impossible/ unrealistic to attempt to single out explanations for the appearance in the samples of each of the above three aspects. Indeed this would probably be an oversimpliﬁcation of dynamic and complex data. What might be possible however is to suggest that some of the features are common to all three dimensions, whereas some are more likely to emerge in certain genres, in certain ethnic groups, or in the presence of aphasia. Figure 15.2 presents this interaction. Many of the dimensions examined (e.g., repetition, word order changes, historic present tense, repetition and code-switching) have been commented on in the literature relating to all three.

Cultural dimensions of aphasia

235

For example, spontaneous verbal repetition in aphasia has been identiﬁed as a compensatory strategy (Leiwo & Klippi, 2000; Oelschager & Damico, 1998; Penn, 1987) but also as an ethnic marker (Labov, 1972; Ulatowska et al., 2000). Word order changes similarly may be viewed as a compensation device in aphasia (Menn, Reilly, Hayashi, Kamio, Fujita, & Sasanuma, 1998; Saﬀran, 1980; Schnitzer, 1974), a reﬂection of syntactic convergence (McCormick, 1995) or as having a stylistic purpose (Labov, 1972). Examples of all three appeared in the narratives of the aphasic and control subjects. Code-switching (or language alternation) is a particularly challenging and paradoxical behaviour. This is a highly complex phenomenon depending on factors such as age, internal state and experience in bilingual speakers. It may be used to emphasize a point, to replace an unknown word, for clariﬁcation, to express group identity, to cross social and ethnic boundaries, or for conversational purposes (Auer, 1999). Factors that inﬂuence type and amount of code-switching include the genre, the purpose, the topic, the interlocutors and their relationship, their relative level of bilingualism and the structure of the languages (including the phonetic structure). There are apparent examples in the data at all points along a continuum. Some language alternation is conversational, some is participant related, some seems linked to linguistic diﬃculty, and some is obviously dialectal and probably more linked to the notion of fused lect which McCormick (1995) suggests characterizes Western Cape dialect. In traditional formulations of code-switching in bilingual aphasia, it has been suggested that this feature may be a pathological phenomenon and a reﬂection of an unstable language system. Research suggests that bilingual individuals with neurogenic communication disorders may not exhibit normal linguistic ﬂexibility (Fabbro, Skrap, & Agliotti, 2000), ranging from rare documented cases of pathological code-switching to more subtle diﬃculties. For example, in a comparative study on Spanish-English bilingual speakers with aphasia and neurologically normal speakers, Munoz, Marquardt, and Copeland (1999) found that aphasic speakers demonstrated greater frequency of

Figure 15.2 Discourse model indicating interaction between variables.

236

Penn

code-switching patterns and concluded that their subjects demonstrated an increased dependence on both languages for communication. These authors viewed this greater frequency of code-switching patterns as an inability to separately access languages. Fabbro et al. (2000) suggest that any lesion in the brain may aﬀect ﬂexibility of language use in bilingual speakers, and that frontal lobe lesions in particular (where the primary deﬁcit is a diﬃculty in shifting set) may lead to reduced ﬂexibility. Other explanations of code-switching in normal and child language studies similarly point to the possible processing costs of code-switching. However, contextual aspects seem to play as important a role. In an electrophysiological study of code-switching by Moreno, Federmeier, and Kutas (2002) who used event-related potentials to compare switches between two languages in bilingual speakers, it was found that for some speakers in some contexts the processing of a code switch was less costly than the processing of an unexpected within-language item. This ﬁnding suggests that the ease of switch is determined by context and task, and that the process of codeswitching per se does not necessarily use up additional resources. In fact it suggests that language switching may provide the bilingual person with aphasia additional options to those of the monolingual aphasic speaker, and that at least under conditions of conscious control, code-switching may provide an extra mechanism for the bilingual person to cope with the challenges of aphasia. Thus, paradoxically, while language alternation may reﬂect disruption in access to either language in aphasia, it may also reﬂect an attuned and sophisticated appreciation of contextual factors and it is therefore likely that the natural context may “prime” such strategies in the bilingual speaker. Explanatory paradigms for code-switching in aphasia thus should go further than pathological explanations and should incorporate both sociocultural and pragmatic factors.

Conclusions The data described above suggest that any explanations of pathological language must be context-bound and that certain sociocultural contexts provide a unique opportunity to examine recovery in aphasia. It should be remembered that each participant in the study showed a unique proﬁle, masked by group results, but providing a fascinating explanatory basis for the language proﬁle and compensatory choices. Persons living in a society with diverse cultures and languages may well have linguistic and cognitive ﬂexibility that will serve them well in the event of aphasia. Further the realities of the natural context may serve as a prime for the emergence of positive strategies in recovery. The challenge for the clinician is to have an understanding of these aspects and to harness them meaningfully in therapy.

Cultural dimensions of aphasia

237

Working with the multilingual patient implies some modiﬁcation of assessment procedures to include the examination of interaction with varying interlocutors, making a detailed sociocultural analysis of a speaker’s language history, language context, attitudes towards language use and in situ observation of the eﬀectiveness of mechanisms such as code-switching and its processing demands on both the speaker and the listener. These are probably more useful than structured or adapted language tests. In short our evaluation should be geared at unearthing the well-practised adaptation patterns that the individual has already developed and that may be drawn on in the presence of aphasia. Perhaps, as the literature suggests, bilingual people are more adept at reading the interlocutor’s home language, communication style and modality preferences and applying metalinguistic strategies. How well that capacity is retained may depend both on the neurological limitations of the individual and on premorbid sociolinguistic strategies. Similarly, the results suggest that we may have to be less precise about which language to remediate. Indeed if the context is one in which languages are mixed and the strategies adopted result in ease of communication, perhaps this could work, particularly if a partner-based approach to therapy is adopted. Finally, some of the implicit features of multilingualism may be harnessed eﬀectively in therapy. I would suggest too that the cognitive demands of translation and their potential as a therapy tool should be explored. In line with other therapy techniques that are thought rather than language centred, the operation of translation, accessing as it does possibly shared and discrete memories, may well facilitate language recovery. Given the increased diversity of clinical caseloads, monocultural models of service delivery are no longer appropriate. I predict that cultural speechlanguage pathology is an emerging necessity of the twenty-ﬁrst century and clinicians should be expanding their understanding of the inﬂuence of cultural variables on language behaviours as well as the repertoire of assessment and therapy activities (Penn, 2002). Taking culture into account undoubtedly makes things more complex, but may lead to explanations for some unresolved phenomena. This dimension builds strongly on the work of aphasiologists like Chris Code, who even when it was unfashionable, has always placed emphasis on the critical psychosocial dimensions of aphasia. Indeed, diversity and ﬂexibility are the essence of the human condition and are probably nowhere better expressed than in the phenomenon of aphasia.

Acknowledgments Earlier sections of this chapter were presented at the 10th Congress of the International Association of Clinical Linguistics and Phonetics held in Louisiana, USA, in 2004 and in a presentation entitled Cultural inﬂuences in

238

Penn

bilingual ageing presented at the American Speech and Hearing Convention in Philadelphia in the same year. I am deeply indebted to Brent Archer for his help with analysis of this material; and to Dale Ogilvy, Analou Venter, Ingrid von Bentheim, Kauthar Nabeemeah and Lisa Kalmek who were involved in various phases of the larger project.

Note 1 The terminology surrounding language alternation is confusing. For the purposes of this chapter I will use code-switching to reﬂect alternating of units from two language across sentence boundaries; alternation of elements longer than one word within a sentence as code-mixing; and lexical borrowing to describe inclusion of single foreign words into a language.

References Archer, B. (2006). Afrikaans aphasia: Some generational diﬀerences. Undergraduate research project, University of the Witwatersrand. Auer, P. (1999). From codeswitching via language mixing to fused lects: Towards a dynamic typology of bilingual speech. International Journal of Bilingualism, 3 (4), 309–332. Bastiaanse, R., & Jonkers, R. (1998). Verb retrieval in action naming and spontaneous speech in agrammatic and anomic aphasia. Aphasiology, 12, 951–969. Bastiaanse, R., & van Zonneveld, R. (1998). On the relation between verb inﬂection and verb position in Dutch agrammatic aphasics. Brain and Language, 64, 165–181. Branford, W., & Claughton, J. S. (1995). Mutual lexical borrowings among some languages of Southern African: Xhosa, Afrikaans and English. In R. Mesthrie (Ed.), Language and social history. Cape Town: David Philip. Chafe, W. L. (1982). Integration and involvement in speaking, writing, and oral literature. In D. Tannen (Ed.), Spoken and written language: Exploring orality and literacy (pp. 35–54). Norwood, NJ: Able. Combrink, J. G. H. (1978). Afrikaans: Its origins and development. In L. W. Lanham & K. P. Prinsloo (Eds.), Language and communication studies in South Africa (pp. 69–95). Cape Town: Oxford University Press. Dorian, N. C. (1997). Telling the monolinguals from the bilinguals: Unrealistic code choices in direct quotations within Scottish Gaelic narratives. International Journal of Bilingualism, 1 (1), 41–54. Edwards, S., & Bastiaanse, R. (1998). Diversity in the lexical and syntactic abilities of ﬂuent aphasic speakers. Aphasiology, 12, 99–117. Fabbro, F., Skrap, M., & Agliotti, S. (2000). Pathological switching between languages after frontal lesions in a bilingual patient. Journal of Neurology, Neurosurgery and Psychiatry, 68, 650–652. Goldstein, K. (1948). Language and language disturbances: Aphasic symptom complexes and their signiﬁcance for medicine and theory of language. New York: Grune & Stratton. Goodwin, C. (2003). Conversation and brain damage. New York: Oxford University Press.

Cultural dimensions of aphasia

239

Hengst, J. A., Frame, S. R., Neuman-Stritzel, T., & Gannaway, R. (2005). Using others’ words: Conversational use of reported speech by individuals with aphasia and their partners. Journal of Speech, Language and Hearing Research, 48, 137– 156. Kalmek, L. (2001). Narrative strategies in bilingual aphasia. Masters dissertation, University of the Witwatersrand. Kertesz, A. (1982). Western Aphasia Battery. San Diego, CA: The Psychological Corporation & Harcourt Brace Jovanovich. Kolk, H., Heling, G., & Keyser, A. (1990). Agrammatism in Dutch. In L. Menn & L. K. Obler (Eds.), Agrammatic aphasia: A cross-language narrative source book. Amsterdam: John Benjamins. Kroes, H. (1978). Afrikaans in education. In L. W. Lanham & K. P. Prinsloo (Eds.), Language and communication studies in South Africa. Cape Town: Oxford University Press. Labov, W. (1972). Language in the inner city: Studies in the black English vernacular. Philadelphia: University of Pennsylvania Press. Labov, W. (1984). Intensity. In D. Schiﬀrin (Ed.), Meaning, form and use in context: Linguistic applications. Washington, DC: Georgetown University Press. Leiwo, M., & Klippi, A. (2000). Lexical repetition as a communicative strategy in Broca’s aphasia. Aphasiology, 14, 203–224. McCormick, K. (1989). A sociolinguistic study of English and Afrikaans in District 6. Unpublished PhD thesis, University of Cape Town. McCormick, K. (1995). Code-switching, code-mixing and convergence in Cape Town. In R. Mesthrie (Ed.), Language and social history. Cape Town: David Philips. Menn, L., Reilly, K. F., Hayashi, M., Kamio, A, Fujita, I., & Sasanuma, S. (1998). The interaction of preserved pragmatics and impaired syntax in Japanese and English aphasic speech. Brain and Language, 61, 183–225. Mitchum, C. C., & Berndt, R. S. (1994). Verb retrieval and sentence construction: Eﬀects of targeted intervention. In G. W. Humphrey & J. M. Riddoch (Eds.), Cognitive neuropsychology and cognitive rehabilitation (pp. 317–348). Hove, UK: Lawrence Erlbaum Associates Ltd. Moreno, E. M., Federmeier, K. D., & Kutas, M. (2002). Switching languages, switching palabras (words): An electrophysiological study of code-switching. Brain and Language, 80, 188–207. Munoz, M. L., Marquardt, T. P., & Copeland, G. (1999). A comparison of the codeswitching patterns of aphasic and neurologically normal bilingual speakers of English and Spanish. Brain and Language, 66, 249–274. Nabeemeah, K. (2002). Narrative discourse in Mauritian Creole. Masters research report, University of Cape Town. Oelschager, M. L., & Damico, J. S. (1998). Spontaneous verbal repetition: A social strategy in aphasic conversation. Aphasiology, 12 (11), 971–988. Ogilvy, D., von Bentheim, I., Venter, A., Ulatowska, H., & Penn, C. (2000). Discourse, dialect and aphasia in the Western Cape. South African Journal of Communication Disorders: Special Issue on Communication Disorders in Multilingual Populations, 47, 111–118. Olness, G. S., Ulatowska, H. K., Carpenter, C. M., Williams-Hubbard, L. J., & Dykes, J. C. (2005). Holistic assessment of narrative quality: A social validation study. Aphasiology, 19 (3/4/5), 251–262. Olness, G. S., Ulatowska, H. K., Wertz, R. T., Thompson, J. L., & Auther, L. L.

240

Penn

(2002). Discourse elicitation with pictorial stimuli in African Americans and Caucasians with and without aphasia. Aphasiology, 16 (4–6), 623–633. Paradis, M. (1987). The assessment of bilingual aphasia. Hillsdale, NJ: Lawrence Erlbaum Associates, Inc. Penn, C. (1987). Compensatory strategies in the chronic aphasic patient. Aphasiology, 1 (3), 235–245. Penn, C. (2002). Cultural narratives. Folia Phoniatrica et Logopedica, 54 (2), 95–99. Penn, C., Venter, A., & Ogilvy, D. (2001). Aphasia in Afrikaans: A preliminary analysis. In M. Paradis (Ed.), Manifestations of aphasic symptoms in diﬀerent languages. Oxford, UK: Pergamon Press. Roberge, P. T. (1995). The formation of Afrikaans. In R. Mesthrie (Ed.), Language and social history. Cape Town: David Philip. Saﬀran, E. M. (1980). The word order problem in agrammatism. Brain and Language, 10, 163–280. Schnitzer, M. L. (1974). Aphasiological evidence for ﬁve linguistic hypotheses. Language, 50, 300–315. Thompson, C. K., Lange, K. L., Schneider, S. L., & Shapiro, L. P. (1997). Agrammatic and non-brain-injured subjects’ verb and verb argument structure production. Aphasiology, 11 (4), 473–490. Ulatowska, H. K. (1998). Narrative discourse battery. Callier Communication Centre: University of Texas. Ulatowska, H. K., Freedman-Stern, R., Weiss Doyle, A., & Macaluso-Hayes, S. (1983). Production of narrative discourse in aphasia. Brain and Language, 19, 317–334. Ulatowska, H. K., & Olness, G. S. (2001). Dialectal variants of verbs in narratives of African Americans with aphasia: Some methodological considerations. Journal of Neurolinguistics, 14, 93–110. Ulatowska, H., Streit-Olness, G., Hill, C. L., Roberts, J., & Keebler, M. W. (2000). Repetition in narratives of African Americans: The eﬀects of aphasia. Discourse Processes, 30, 265–283. Van Rensburg, C. (1997). Afrikaans in Afrika. Pretoria: J. L. van Schaik. Venter, A. (2000). Narrative discourse of Afrikaans speaking coloured aphasics in the Western Cape. Masters research report, University of Cape Town. Vermeulen, J., Bastiaanse, R., & van Wageningen, B. (1989). Spontaneous speech in aphasia: Correlational study. Brain and Language, 36, 252–274. von Bentheim, I. (2001). Narrative discourse in English speaking aphasics in the Western Cape. Masters research report, University of Cape Town. Wilkinson, R., Beeke, S., & Maxim, J. (2003). Combining language and functional abilities: The use of enactment by speakers with aphasia in conversation. Paper presented at British Aphasiology Congress, Newcastle. Wolfson. N. (1978). A feature of performed narrative: The conversational historical present. Language in Society, 7, 215–237.

Cultural dimensions of aphasia

241

Appendix 15.1: Sample examples of evaluative devices used in the narratives of bilingual aphasic and control participants (translations in italics) (Extracts from the samples are identiﬁed as A for aphasic samples, C for control samples, and Afr and Eng for Afrikaans and English.) Ellipsis and topicalization A3 Eng: All of a sudden from nowhere . . . There it was A4 Eng: Bearing in mind that I was eighteen . . . I decided to argue C1 Afr: Hoe hy die een aan die arm gryp . . . weet ek nie How he grabbed one by the arm, I don’t know C3 Eng: The size of the snake . . . I was mesmerized A9 Afr: Maar ongelukking is ek daai dag. But unlucky I was that day A9 Afr: Hoe het ek deur die drade gaan, weet ek nie How I got through the wires, I don’t know Ritual utterances A4 Afr: Het ek vir hom gesê “wo!” I said “hey” what is happening to me now C1 Afr: Dis net soos in die movies sien It’s just as (you) see in the movies C1 Eng: You can’t see your hand in front of you And I’m thinking “maybe there’s absolutely nothing” C4 Eng: I was really showing oﬀ C5 Afr: Maar ek gaan iets probeer hier But I will try something here Ongelukkig is ek daai dag Unlucky I was that day C5 Eng: I don’t even want to listen to this Do you know what that cost us eventually? So we couldn’t argue

242

Penn

Comment clauses A1 U sal seker nie weet vam n tiekie nie You probably don’t know about a ticky Dis nou n ware storie, ne? It’s a true story now, okay? Expressive phonology A1 Afr: Oooo ek was bang A4 Eng: It happened maaany years ago C1 Afr: Ons is veeeer van alle plekke af C3 Afr: ’n Groooot boom Quantiﬁers A3 Eng: All of a sudden That was the worst experience of my life A4 Afr: Hy het alle reg die pad te gebruik He had every right to use the path C2 Afr: ’n Hele klomp mense Daar was baie van hulle C3 Eng: It was the biggest snake I have ever seen C4 Eng: I took all my clothes oﬀ C5 Eng: We were just married And I’m thinking “maybe there’s absolutely nothing” C4 Eng: I was really showing oﬀ Repetition A1:

Ek is bang. Ek is baie bang I am scared. I am very scared A2 Afr: Hy kom kom die slang gryp He comes comes to grip the snake A3: That was the worst experience of my life . . . It was the most terrible experience of my life A5: Ek het gelê en gelê I lay and lay A4: Maar ex sal nooit vergeet nie. Ek is nou . . . Ek sal dit nooit vergeet nie But I shall never forget it. I am now I shall never forget it.

Cultural dimensions of aphasia C3: C5: C7:

243

I can actually, I can actually see it Most beautiful beautiful paw paws All we see is farms and farms and farms En ons wag en wag en wag And we wait and wait and wait

Direct reported speech A1: A3: S8:

“Die water is; Oe Vader jy moet my nou help” The water is . . . “Oh Father you must help me” Maar die doktor . . . sê die Doktor “Nee man” But the doctor . . . the doctor said “no man” “and she just walked past and said “Kom sluit die deur toe” (Come close the door)

Language alternation (code mixing and lexical borrowing) From English into Afrikaans: Aphasic We went to hand out those eh um dinges And sy s grapes is the treasure and sy moet verstaan Hy het ’n groot, ’n groot a big crop gekry He got a big crop I just gave him one tramp to the head (Eng: thump) Sitting with a whole klomp newspapers (Eng: clump) Why must I sukkel (Eng: struggle) Those big ouens came and arrested us (fellows)

244

Penn

From Afrikaans into English: Aphasic Dit was die grootest in my lewe This was the biggest in my life Iemand het hom geld gegive Someone gave him money Ek het nie gepanic nie I did not panic (Note the adoption of English morphological endings in some cases, as well as retention of Afrikaans morphology on loanwords.) Dit was nie ’n nice ondervinding nie That was not a nice experience Ek was bang dat n stray bullet deur die venster sou kom I was scared a stray bullet would come through the window En die kerels, ons is groot pals And the fellows, we are big pals (Note the noun characteristically has retained the English number marking.) One two three is hy dood 1 2 3 he’s dead As jy werk sal jy geld vat, as jy sit by die huis op jou bum sal jy niks vat. If you work you will get money if you sit on your bum at home you’ll get nothing. (Note this example of the dropping of the second negative is a common feature reﬂecting instability of this structure in modern Afrikaans.)

16 Assessment of aphasia in a multi-lingual world Susan Edwards and Roelien Bastiaanse

Introduction Many disciplines engage in the assessment of aphasia, which is conducted in various languages, in various forms, across many countries and for diﬀerent purposes. In this chapter we consider the use of assessments, brieﬂy review the development of aphasia assessments and describe some types of assessments. The need for procedures and materials for testing bi-lingual speakers with aphasia has been recognized for some time (Paradis, 1987), and there are a growing number of tests that are used across diﬀerent languages. Some of these are translations and some are specially adapted for each new language. In this chapter, we consider why it is necessary to make adaptations rather than translate tests to use in diﬀerent languages. By way of illustration, a brief description is given of the development of two tests that are used across two languages: the PALPA (originally written in English and then adapted for Dutch) and the Verb and Sentence Test (VAST: originally written in Dutch and then adapted for English). However, it is sometimes necessary to assess people in a language other than their primary language, a contemporary problem we discuss.

Background The assessment of aphasia has developed over the past hundred years from meticulous, if idiosyncratic, clinical examinations, through the development of batteries based on psychometric testing, batteries inﬂuenced by cognitive neuropsychology, and those motivated by linguistic investigation of aphasia. No assessment is theory free, although the underlying theoretical motivation behind the development of an aphasia assessment may not be explicit or may have got lost over time. In the early stages of assessment, neurologists such as Hughlings Jackson (1932), Freud (1891) and Henry Head (1926) carefully recorded symptoms that they observed in their clinics and related these symptoms to presumed sites of cerebral lesions. Jackson (1932) developed clinical tests comprising tasks that are still used today by some neurologists in their clinical examinations, such as naming the doctor’s pen and watch, and

246

Edwards and Bastiaanse

counting. The neurologists searched for evidence of the major clinical signs of aphasia; problems with word retrieval, sentence construction and understanding commands. Highly learnt serial speech such as counting or reciting the days of the week was tested to establish if non-propositional speech had been retained (Jackson, 1932). Many similar tasks are found today both in clinical examinations and in some published aphasia tests, although the motivation for inclusion is far from clear. The early aphasiologists were spurred on with their work because of the number of young men they encountered who had language problems. These were young men returning from the “great” war who, through warinduced brain injury, faced years ahead with aphasia. The purpose of these early aphasiologists was to document symptoms and there was no attempt, at least no systematic attempt, to suggest treatment. Following the Second World War, a new impetus arose in the UK, the USA and the USSR to formulate a means of documenting aphasic symptoms, but now there were also some parallel eﬀorts to think about treatment following assessment (Wepman, 1951). During the war, psychometric testing had been developed and the new tests of aphasia used these developments, mimicking the rubric of the psychiatric assessment by using an array of tasks for this purpose, probing skills in reading, writing, speaking and comprehension of spoken language. The familiar tasks (used by the early twentieth-century neurologists) of serial speech and repetition of language were included by clinicians and survive today. These tests were based on the classical view of aphasia, which was that the condition aﬀects primarily expression or understanding of language, and is termed expressive or receptive aphasia (Eisenson, 1973). This view seriously under-rates the complexity of aphasia and was overtaken by a more detailed and sophisticated understanding of the nature of aphasia during the latter half of the twentieth century and beyond. A very diﬀerent view of aphasia was held by Wepman (1951), developed by Schuell and published as The Minnesota Test of Aphasia (Schuell, 1965). Hildred Schuell’s view of aphasia was based on Pierre Marie’s (1926) idea that aphasia was a unitary syndrome. This diverged from what had been the mainstream view since the classic descriptions of Broca (1865), Wernicke (1874), and Lichtheim (1885). Marie abandoned the idea that there were diﬀerent aphasia symptoms and conceived aphasia as a unitary phenomenon. This view held that aphasia is a condition in which language is aﬀected, and which diﬀered from person to person not by syndrome but by severity and by the presence or absence of deﬁcits involving written language and articulation. Schuell was one of the last followers of this theory. It may surprise some readers to learn that her assessment (and presumably the theory behind it) was used extensively not only in regular clinical assessments but also in research in the latter half of the twentieth century (David, Enderby, & Bainton, 1982; Edwards, Ellams, & Thompson, 1976). The early death of Schuell curtailed the development of this idea and the publication of the

Assessment of aphasia in a multi-lingual world

247

Boston Diagnostic Aphasia Examination (BDAE) by Goodglass and Kaplan in 1972 re-established the neo-classic view of aphasia. Another important assessment tool, inspired by and similar to the BDAE was published in 1982: the Western Aphasia Battery (WAB; Kertesz, 1982). These two assessments of aphasia set out to categorize participants/patients by classical aphasic syndromes, and despite the low proportion of the clinical population that can be successfully categorized (Goodglass & Kaplan, 1972; Kertesz, 1982) the BDAE and the WAB are the most widely used assessment tools in North America and Western Europe. The BDAE has proved to be very robust, with the third edition published in 2000 (Goodglass, Kaplan, & Baresi, 2000), almost 30 years since the ﬁrst edition, and versions of this test have appeared in a number of languages other than English. Slightly earlier than the publication of these two tests, Alexander Romanovich Luria (1966, 1970) was developing similar ideas on clinical assessment in the USSR, although his work took some time to reach Western Europe in translation. His concept of clinical aphasia types was slightly different from those in Western Europe and has been, and remains, very inﬂuential in Russia and the Nordic countries. Another test that aims for diagnosis of type of aphasia is the Aachen Aphasia Test (Huber, Poeck, Weniger, & Willmes, 1983). This has been widely used in Western Europe and has been adapted from the original German to Dutch, Italian and English and is considered the principal test in Germany, Switzerland, Austria, The Netherlands, Italy and Belgium. In summary, since 1970, four main aphasia assessment tools have been developed that are still widely used around the world. The main goals of these tools were: • •

to assess the severity of aphasia in the four language modalities (comprehension and production of spoken language, reading and writing) to classify the patients in one of the classical aphasia types.

Before moving on to discuss more recent assessments that focus on features of aphasia, it is interesting to note the relatively new publication of an assessment that has followed a classical design in terms of modalities, production and understanding of written and spoken language, and in test items. This test, the Comprehensive Aphasia Test (CAT; Swinburn, Porter, & Howard, 2004) includes many classic items such as naming, word ﬂuency and repetition, but has additional tests for cognitive functions that may impact on aphasia, and a means of exploring the “disability and emotional sequelae of acquiring aphasia” (p. 5). The CAT is a collection of tests developed for diagnosis of impairment; to provide guidance for further assessment and motivation for treatment. It can be used for predicting and tracking changes in language behaviour over time. It is comprehensive in the areas covered but, as it is designed to be administered within two sessions, exploration is brief. Extensive guidance is given on administration, including assessing “grammatical well-formedness” (although some of the analysis is debatable), and on

248

Edwards and Bastiaanse

the development of the test. Test data collected from aphasic and nonaphasic subjects are given for each section, providing a really useful clinical reference. The structure of this test while closely resembling the classic tests discussed above, has additional features that reﬂect research in the ﬁeld as well as the “broad church” approach current in clinical practice. Further, an explicit aim of the test is to provide guidance for intervention. It is currently only available in English.

Single words and grammar: Tests and connected speech data Although the classic assessments have been successfully used in clinical practice in many countries, their contribution to planning treatment and setting goals for aphasia therapy has been limited. There are two reasons for this. First, changes in aphasic language behaviour are often slow and/or limited and may be restricted to part of the language system. These tests are not sensitive enough to measure such changes. Second, they focus on the severity of aphasia across diﬀerent modalities and not on the nature of the underlying language deﬁcits. They are therefore limited in providing guidance for treatment. Areas of relative weakness can be identiﬁed from the results and general goals set, but the results do not readily lead to detailed planning for either deﬁcit based or so-called “functional” aphasia therapy. While the relative impairments in diﬀerent modalities can be identiﬁed, these tests do not set out to identify the assumed underlying nature of language deﬁcits. Towards the end of the twentieth century, a diﬀerent type of assessment was developed that sought to address this matter. In seeking to reveal something about the nature of the aphasic deﬁcits, authors of these tests were obliged to make at least something about their theoretical assumptions explicit. As a result, we ﬁnd a divergence in the type of tests that started to be published. We now brieﬂy review some of these. Single word battery Towards the end of the twentieth century, a new and diﬀerent way of assessing aphasia was developed, based on neuropsychological and neurolinguistic theories. In many laboratories people were working on experimental tasks within modular, word processing models (e.g., Ellis & Young, 1988). A major development was the publication of an extensive clinical test battery, the Psycholinguistic Assessment of Language Processing in Aphasia (PALPA), a battery of tests for the assessment of production and processing/comprehension of spoken and written words and sentences (Kay, Lesser, & Coltheart, 1992). This battery of tests was based on ideas from neuropsychology and especially from work with developmental and acquired dyslexia. Rather than testing for an array of aphasic symptoms, as tests up to that date had done, the new way of assessing aphasia was based on notions of modules and

Assessment of aphasia in a multi-lingual world

249

connections between modules. Tasks were developed to test the functioning of the assumed modules (and inter-modular connections) such as the auditory analyser, and phonological assembly. This concept eschewed the pursuit of a relationship between lesion site and symptoms that had been paramount in the neo-classical view. In this test, performance is interpreted within a deﬁned modular, serial model of single word processing, which the authors have conceded was “under-developed”. Instead of sites of lesion, language deﬁcits are located within modules or in the connections between modules. In addition to locating the source of the diﬃculties within this box and arrow plan, some control of certain psycholinguistic variables was built into most of the tests. The selection of these variables was based on experimental evidence that they inﬂuenced spoken or written word processing. References to this evidence are given throughout the battery. The variables included word frequency, imageability, length, and regularity of spelling. The PALPA, although largely concerned with investigating single word processing and production, also included two tests of sentence comprehension in the English version. Both tests investigate the same array of syntactic variables; one has spoken stimuli and the other written. A further test investigates “locative relations” using eight locatives within 24 NP + PP constructions. Versions of the PALPA are available in a number of languages (e.g., Spanish, Dutch, German and, recently, Russian). The PALPA is strong on investigating noun production and understanding, but verbs are largely ignored. However, from the late 1980s on, it became clear, that word class is an inﬂuential factor in word and sentence processing in aphasia. Several studies found that aphasic patients treat verbs and nouns diﬀerently (e.g., Jonkers & Bastiaanse, 1998; Kohn, Lorch, & Pearson, 1989; Miceli, Silveri, Villa, & Caramazza, 1984). Further, within the class of verbs, various factors seem to play a role: instrumentality (Jonkers, 1998; Jonkers & Bastiaanse, 2006), argument structure (Kiss, 2000; Thompson, Lange, Schneider, & Shapiro, 1997), morphology (Bastiaanse & van Zonneveld, 1998; Friedmann, 2000). It would seem that the variables that inﬂuence noun and verb processing are diﬀerent. For example, the eﬀect of frequency may play a role in noun retrieval, although there is much individual variation (Kay & Ellis, 1987; Zingeser & Berndt, 1988), but has not been found in verb production (e.g., Kemmerer & Tranel, 2000, McCann, 2005). Some experimental materials used to investigate aphasia have been adapted for clinical practice, for example An Object and Action Naming Battery (Druks & Masterson, 2000), the Thematic Roles in Production (TRIP; Whitworth, 1996) and parts of the Verb and Sentence Test (VAST; Bastiaanse, Edwards, & Rispens, 2002). Batteries focused on grammatical abilities There is an extensive amount of literature and a relatively large number of theories on sentence comprehension impairment. Many laboratories have

250

Edwards and Bastiaanse

developed their own tests, suitable for exploring their theories of language comprehension, but there has not been a systematic adaptation of these procedures for clinical practice, although many ideas are used in clinical practice, at least in the UK. An exception is a relatively new test, the Verb and Sentence Test (VAST; Bastiaanse et al., 2002), a test that has been motivated by neurolinguistic theories, but developed for clinical practice as well as for use in research laboratories. A unique feature of this assessment is that for all the aphasic features that are tested, there are published treatment protocols or ideas. We will come back to this test later. Spontaneous speech During the latter half of the twentieth century, the application of linguistic theory to aphasia started to seep into clinical practice and noticeably into clinical assessment of aphasia. Not only did some linguistically motivated assessments begin to appear but there was also a move to a completely diﬀerent methodology. One major methodological development was the use of samples of connected or spontaneous speech data to investigate phonology, lexis and grammar. In these studies, aphasic speech samples were compared with non-aphasic samples collected in the same conditions. These studies provided insights into how aphasic language sounded when the speaker was permitted to produce chunks of speech, rather than answering questions or naming pictures. The picture that emerged was one that supported the subtraction notion: it was possible to see the extent to which the language system had been preserved, and the extent to which it deviated from non-aphasic, normal language. So, for example, for Dutch, Wagenaar, Snow, and Prins (1975) and Vermeulen, Bastiaanse, and van Wageningen (1989) found that there were certain linguistic dimensions distinguishable, on which aphasic speakers could be independently impaired. In English, comparisons of aphasic and non-aphasic speech were made using matched speech samples (Edwards, 1995; Edwards & Garman, 1992; Edwards & Knott, 1994, Garman & Edwards, 1995). The Dutch and English work was brought together applying the framework developed for the English studies to data from both languages. Edwards and Bastiaanse (1998) examined grammatical and lexical features in Dutch and English ﬂuent aphasic speakers and found a reduction in the proportion of complex sentences and verb diversity in the English aphasic speakers compared with the control data. The use of connected speech data now plays an important part in evaluating eﬀectiveness of treatment. Researchers are interested in whether improvements found in test performances extend to connected speech (Bastiaanse, Hurkmans, & Links, 2006; Edwards & Tucker, 2006; Webster, Morris, & Franklin, 2005). However, the assessment of connected speech data is not straightforward. There are issues concerning segmentation and reliability, and features to be noted and scored. See Edwards (2005) for a discussion on the use of connected speech data in assessment. These same issues also impact

Assessment of aphasia in a multi-lingual world

251

on what, on the face of it, looks like an easier task, the investigation of lexis within connected speech samples. Given that lexical retrieval is a pervasive problem in aphasia, it is not surprising that there are a myriad of studies investigating word retrieval. If one wishes to employ range of vocabulary as a measure of improvement over time, or as a measure to separate types of aphasia, then there are various methodologies. Wright, Silverman, and Newhoﬀ (2003) have compared the use of three diﬀerent measures of vocabulary; type–token ratio (TTR); number of diﬀerent words (NDW) and a D(iversity) measure developed by Malvern, Richards and colleagues (Malvern, Richards, Chipere, & Durán, 2004; Richards & Malvern, 1997). The D measure, a measure of lexical diversity, is obtained via special software. It is calculated by ﬁrst randomly sampling words from a transcript to produce a TTR against tokens for the empirical data. The software then ﬁnds the best ﬁt between this empirical curve and the theoretical curves generated by the model by adjusting the value of D. Higher values of D represent greater lexical diversity. The authors claim that this procedure is suitable to use with small samples and ensures that all researchers carry out measurement in the same way (p. 60). In the aphasia study, Wright et al. (2003) found that TTR and NDW correlated when the sample size was held constant, although this entailed ignoring some of the data. The D measure correlated with the two other measures only when sample size was held constant, thus illustrating the complexity of computing lexical diversity in connected speech. Other spontaneous speech analysis systems have speciﬁcally been developed to analyse the grammatical aspects of Broca’s aphasia (Saﬀran, Berndt, & Schwartz, 1989; Thompson et al., 1997). The only system that has been published to date as a clinical tool and is therefore accessible to clinicians is the Quantitative Production Analysis (Berndt, Wayland, Rochon, Saﬀran, & Schwartz, 2000; Saﬀran et al., 1989). Of course, some highly motivated therapists do use procedures that are still experimental. An overview and critical analysis of spontaneous speech analysis methods can be found in Prins and Bastiaanse (2004). They claim that only a few methods are valid and reliable and not all are suitable to measure improvement. Nevertheless we remain committed to the importance of examining samples of spontaneous speech when trying to measure the eﬀectiveness of treatment. After all, as the main goal of treatment of speech production is improving language use in daily life, we need to continue to try to monitor and measure relevant features of connected speech very carefully.

Translating tests: Clinical imperatives and empirical pitfalls There is a reasonably widespread understanding that a straightforward translation of the vocabulary of tests is not suﬃcient when trying to produce a version of a test in a language other than the original. Cultural issues need to be taken into account, such as choice of vocabulary items, illustrations and the topics utilized, but the issue of translation is broader. There is also a

252

Edwards and Bastiaanse

growing awareness that the psychometric variables that may be controlled for in the original test, such as frequency, age of acquisition and imageability, may only hold for the original language of the test. At a very simple level, clinicians working in the UK know that most of their clients/patients will not be able to name the bagel or wreath in the Boston Naming Test (Kaplan, Goodglass, & Weintraub 1983). However, the problems are wider than lack of knowledge of certain objects or foods. There is not always a one-to-one translation across verbs. For example, Dutch has one word badmintonnen for to play badminton and one word schaken for to play chess so a verb to verb translation is not always possible. Further, sentence constituents such as adverbs, that are free morphemes in English and Dutch, may be bound morphemes in some languages, Finnish and Hungarian, for example. We cannot be sure that the verbs take the same argument structure in the language into which the test is being translated. Some will but others will not. If the test includes production and comprehension of sentence structure, then the problems are even greater as we will see below. There is a large amount of linguistic data on English and a number of European languages on which to draw conclusions but this is not the case for many other languages. In addition, the linguistic tradition diﬀers across the world and the information available about a language may be incompatible with the theoretical motivation of the original test.

Translating tests: Two examples In this section, two tests that have been translated and adapted to another language will be discussed. First the PALPA, which was developed in English and has been made available for Dutch. Second, the VAST, a test that was developed for Dutch and has been adapted to English. Some problems that were encountered in the adaptation of these tests are discussed here. Translation and adaptation of the PALPA to Dutch The English PALPA is a test battery that consists of more than 50 subtests, divided into four parts: auditory processing, reading and spelling, picture and word semantics and sentence comprehension. The items in most subtests are controlled for word frequency, length, regularity of spelling and other factors, which make a word-to-word translation into another language impossible. Thus only the principles of the PALPA could be preserved in adapting the test for Dutch, although new words that were included in the test were matched on the same variables and new pictures were necessary. Although many high-frequency English words have high frequency in Dutch, word length is not always the same. In addition, there are problems with trying to assemble irregularly spelled words as there are fewer irregularly spelled Dutch words compared to English. Although Dutch has a considerable number of loanwords that are irregularly spelled, it was not possible to

Assessment of aphasia in a multi-lingual world

253

obtain the same distribution of regularly and irregularly spelled words in the Dutch version of the PALPA Not only did new pictures need to be drawn for words that were not included in the English version, but some pictures had to be changed to account for cultural diﬀerence. For example, the picture of a stamp in the word comprehension subtest in the English version needed to be replaced as it has a picture of Queen Elizabeth II on it. Naturally, the subtests for low imageability words, synonym judgement and word semantic association, could not be translated literally. All these adaptations were quite easy to implement, but a real problem arose when the subtests at the sentence level were considered. The theoretical motivation of this part of the PALPA is quite weak compared to that underlying the tests focused on single word processing. It was decided to omit this part in the Dutch PALPA and to develop a new, well-motivated test for comprehension and production of verbs and sentences, which we called the Verb and Sentence Test (VAST). This was subsequently translated and adapted to English. Translation and adaptation of the VAST to English The Verb and Sentence Test was originally developed for use in Dutch. When the translation and adaptation of the PALPA was ﬁnished, the need was felt for a test that could assess comprehension and production of verbs. The subsection of PALPA that tests sentence comprehension was not adapted in the Dutch version and thus there was a need for a new test of sentence comprehension and production. The type of sentence structures to be included for assessment was carefully considered: sentences that had the basic word order for Dutch plus sentences with “moved” NPs and verbs were selected for testing. One of the principles guiding the development of the VAST was that only linguistic variables that have been shown to be aﬀected in aphasia would be included. So verbs were controlled for frequency, name relation with a noun and transitivity. For sentences the main variable was word order, thus in testing Dutch sentences, it was necessary to include sentences that had the basic word order, so sentences with “moved” NPs (passives, wh-questions) and “moved” (embedded vs. matrix vs. question order) verbs were included. The second principle was that the VAST should be a tool that could be used with a broad range of aphasia types. Finally, the VAST should be “treatmentoriented”: for each tested variable a treatment programme or method should be available that shows that this variable can be successfully trained. This resulted in 10 subtasks. The VAST has been translated into and adapted for a number of languages: English (Bastiaanse et al., 2002), Norwegian (Bastiaanse, Lind, Moen, & Simonsen, 2006), French and German. The tests in the latter two languages are not yet standardized. When translated into English, a number of problems were encountered. First, a main variable in the Dutch version was “position of the verb”. In

254

Edwards and Bastiaanse

Dutch the verb can take diﬀerent positions in the sentence, whereas in English it always precedes the object. So “verb movement” could not be included in the English version. It was decided to add two extra sentence types: subject clefts and object clefts. These structures are not in the Dutch version because they are ambiguous in Dutch. In the ﬁrst version of the Dutch VAST, one test was included which entailed the selection of the correct wh-word (who, what, when and where). While Dutch non-brain-damaged speakers were able to perform this test, none of the ﬁrst 10 aphasic patients who were tested with these materials could to do the task because they did not understand what they were supposed to do. It was then decided to remove the task. Because we suspected that the task could be valuable, an adapted version was made for the trial English version of the VAST. This proved to be as problematic in English as it had been in Dutch and so was not included in the ﬁnal version. The English VAST is similar to the Dutch version in terms of structure, but many lexical items as well as the sentences needed to be changed. Some changes were made because the variables they were controlled for did not translate, for example there were diﬀerent frequency ratings across the two languages. The verb “to skate” is much more frequent in Dutch than in British English (and has a zero frequency in Australian English). Other actions are expressed by a verb in Dutch, but by a verb phrase in English: for example, to play badminton is one word in Dutch, badmintonnen, as mentioned above. The same problems arose with the verbs that have a name relation to a noun in Dutch, but not in English, or the other way around. Thus the list of verbs was adapted. The phrasal verbs were removed and those that did not achieve a high name agreement score were omitted. A number of new verbs were added and all variables checked. All items in all subtests were trialled on non-aphasic English speakers.

Assessment when it is not possible to use standardized tests We have seen above that there are tests being developed for use in a range of languages, yet in many European countries there are now an increasing number of people whose ﬁrst language is not that of the host country. The increase in demand on speech and language therapy services has arrived before we have the necessary range of standardized tests for clinical practice despite a longstanding awareness of the need for assessments designed for bilingual speakers (Paradis, 1987). Unfortunately, some clinicians do try to use direct translation but, as we have illustrated above, this is far from satisfactory. As the new migrants age within their new countries, there are an increasing number of people who have acquired aphasia but do not have native competence of the language of their adopted country, and clinicians are in the position of having to do the best they can. The development of language assessments needs to be within a context of knowledge of the language of the assessment, and we have endeavoured to demonstrate why straightforward translation of a

Assessment of aphasia in a multi-lingual world

255

test into another language will not provide an assessment tool that can be of any use. Unfortunately, a detailed knowledge of the languages we need is just not available. There is some work underway in the UK by Bryan and her colleagues investigating the comparative inﬂuences on test scores of age and having English as an additional language, but to date resources are pitifully small. This then creates a real practical dilemma for the clinician. In striving to provide equality of medical provision, the clinician needs some way of assessing the presenting disorder if only to advise the patient, his or her family and the other medical staﬀ involved in the care of the patient/client. Practically, a clinician still needs to make some kind of assessment in order to oﬀer advice, as a minimum of care. The clinician can choose to work through a translator, selecting parts of tests that can most easily be translated. As we have argued above, this is less than satisfactory because in changing tests, standardization is lost and so the results can only be used for guidance and must be interpreted with extreme caution. They can, however, be used to demonstrate to other professionals how aphasia has aﬀected the patient’s/ client’s language. The alternative is to oﬀer no help, clearly an unacceptable position. It may be that there will be suﬃcient academic interest or political pressure to create assessment batteries in a much wider range of languages. Despite more than a hundred years of aphasia investigations by talented researchers (such as Chris Code), public awareness of aphasia in monolingual contexts is minimal, as Chris and his colleagues have demonstrated (Simmons-Mackie, Code, Armstrong, Stiegler, & Elman, 2002), and our knowledge of how to assess aphasia in a multi-lingual world is equally limited. We are beginning to explore how to create assessments that are applicable in cross-language research and how best to assess people who are aphasic in a multi-lingual world. There is much work still to be done.

References Bastiaanse, R., Edwards, S., & Rispens, J. (2002). Verb and Sentence Test (VAST). Bury St Edmunds, UK: Thames Valley Test Company. Bastiaanse, R., Hurkmans, J., & Links, P. (2006). The training of verb production in Broca’s aphasia: A multiple baseline across behaviours study. Aphasiology, 20, 298–311. Bastiaanse, R., Lind, M., Moen, I., & Simonsen H. G. (2006). Verb- og Setningstesten (VOST). Oslo: Novus. Bastiaanse, R., & van Zonneveld, R. (1998). On the relation between verb inﬂection and verb position in Dutch agrammatic aphasics. Brain and Language, 64, 165–181. Berndt, R. S., Wayland, S., Rochon, E., Saﬀran, E., & Schwartz, M. (2000). Quantitative production analysis. Hove, UK: Psychology Press. Broca, P. (1865). Du siège de la faculté du langage articulé. Bulletin de la Societé d’Anthropologie, 6, 377–393. David, R., Enderby, P., & Bainton, D. (1982). Treatment of acquired dysphasia: Speech therapists and volunteers compared. Journal of Neurology, Neurosurgery, and Psychiatry, 45, 957–961.

256

Edwards and Bastiaanse

Druks, J., & Masterson, J. (2000). An object and action naming battery. Hove, UK: Psychology Press. Edwards, S. (1995). Proﬁling ﬂuent aphasic spontaneous speech: A comparison of two methodologies. European Journal of Disorders of Communication, 30, 333–345. Edwards, S. (2005). Fluent aphasia. Cambridge, UK: Cambridge University Press. Edwards, S., & Bastiaanse, R. (1998). Diversity in the lexical and syntactic abilities of ﬂuent aphasic speakers. Aphasiology, 12, 99–117. Edwards, S., Ellams, J., & Thompson, J. (1976). Language and intelligence in dysphasia: Are they related? British Journal of Disorders of Communication, 11, 83–94. Edwards, S., & Garman, M. (1992). Project report: The grammatical analysis of aphasic speech. Clinical Linguistics and Phonetics, 6, 161–164. Edwards, S., & Knott, R. (1994). Assessing spontaneous language abilities of aphasic speakers. Testing, 11, 49–64. Edwards, S., & Tucker, K. (2006). Verb retrieval in ﬂuent aphasia: A clinical study. Aphasiology, 20, 644–675. Eisenson, J. (1973). Adult aphasia: Assessment and treatment. New York: Appleton Century Croft. Ellis, A. W., & Young, A. W. (1988). Human cognitive neuropsychology. Hove, UK: Lawrence Erlbaum Associates Ltd. Freud, S. (1891). Zur Auﬀassung der Aphasien. Leipzig & Vienna: Deuticke. English translation (On aphasia: A critical study) London: Imago Publishing Co, 1953. Friedmann, N. (2000). Moving verbs in agrammatic production. In R. Bastiaanse, & Y. Grodzinsky, (Eds.) Grammatical disorders in aphasia. London: Whurr. Garman, M., & Edwards, S. (1995). Syntactic assessment of expressive language. In K. Grundy (Ed.), Linguistics in clinical practice (2nd ed., pp. 134–166.). London: Taylor & Francis. Goodglass, H., & Kaplan, E. (1972). The assessment of aphasia and related disorders. Philadelphia: Lea & Febiger. Goodglass, H., Kaplan, E., & Baresi (2000). The assessment of aphasia and related disorders (3rd ed.). Philadelphia: Lippincott, Williams, & Wilkins. Head, H. (1926). Aphasia and kindred disorders of speech. London: Cambridge University Press. Huber, W., Poeck, K., Weniger, D., & Willmes, K. (1983). Aachener Aphasie Test. Göttingen: Hogrefe. Jackson, J. H. (1932). Selected writings. London: Hodder & Stoughton. Jonkers, R. (1998). Comprehension and production in aphasic speakers. Diss: University of Groningen. Jonkers, R., & Bastiaanse, R. (1998). How selective are selective word class deﬁcits? Two case studies of action and object naming. Aphasiology, 12, 245–256. Jonkers, R., & Bastiaanse, R. (2006). The inﬂuence of instrumentality and namerelation to a noun on verb comprehension in Dutch aphasic speakers. Aphasiology, 20, 3–16 Kaplan, E., Goodglass, H., & Weintraub, S. (1983). Boston Naming Test. Philadelphia: Lea & Febiger. Kay, J., & Ellis, A. (1987). A cognitive neuropsychological case study of anomia: Implication for neuropsychological models of word retrieval. Brain, 110, 613–629. Kay, J., Lesser, R., & Coltheart, M. (1992). Psycholinguistic assessements of language processing in aphasia. Hove, UK: Lawrence Erlbaum Associates Ltd. Kemmerer, D., & Tranel, D. (2000). Verb retrieval in brain-damaged subjects:

Assessment of aphasia in a multi-lingual world

257

1. Analysis of stimulus, lexical, and conceptual factors. Brain and Language, 73, 347–392. Kertesz, A. (1982). Western aphasia battery. New York: Grune & Stratton. Kiss, K. (2000). Eﬀect of verb complexity on agrammatic aphasics’ sentence production. In R. Bastiaanse, & Y. Grodzinsky (Eds.), Grammatical disorders in aphasia. London: Whurr. Kohn, S. E., Lorch, M. P., & Pearson, D. M. (1989). Verb ﬁnding in aphasia. Cortex, 25, 57–69. Lichtheim, L. (1885). Über Aphasie. Deutsches Archiv für klinische Medizin, 36, 204–268. Luria, A. R. (1966). Higher cortical functions in men. London: Tavistock Publications. Luria, A. R. (1970). Traumatic aphasia: Its syndromes, psychology and treatment. The Hague: Mouton. Malvern, D., Richards, B., Chipere, N. and Durán, P. (2004). Lexical diversity and language development. Basingstoke, UK: Palgrave Macmillan. Marie, P. (1926). Travaux et Mémoires. Tome 1. Paris: Masson et Cie. McCann, C. (2005). Verb production in ﬂuent aphasia: An analysis of argument structure and event structure. Unpublished doctoral dissertation, University of Reading, UK. Miceli, G., Silveri, M. C., Villa, G., & Caramazza, A. (1984). On the basis of the agrammatics’ diﬃculty in producing main verbs. Cortex, 20, 207–220. Paradis, M. (1987). The assessment of bilingual aphasia. Hillsdale, NJ: Lawrence Erlbaum Associates, Inc. Prins, R. S., & Bastiaanse, R. (2004). Analysing the spontaneous speech of aphasic speakers. Aphasiology, 18, 1075–1091. Richards, B. J., & Malvern, D. D. (1997). Quantifying lexical diversity in the study of language development. Reading, UK: University of Reading, The New Bulmershe Papers. Saﬀran, E., Berndt, R. S., & Schwartz, M. (1989). The quantitative analysis of agrammatic production: Procedure and data. Brain and Language, 37, 440–479. Schuell, H. M. (1965). The Minnesota test for diﬀerential diagnosis of aphasia. Minneapolis MN: University of Minnesota. Simmons-Mackie, N., Code, C., Armstrong, E., Stiegler, L., & Elman, R. (2002). What is aphasia? Results of an international survey. Aphasiology, 12, 837–848. Swinburn, K., Porter, G., & Howard, D. (2004). The comprehensive aphasia test (CAT). Hove, UK: Psychology Press. Thompson, C. K., Lange, K. L., Schneider, S. L., & Shapiro, L. P. (1997). Agrammatic and non-brain-damaged subjects’ verb and verb argument structure production. Aphasiology, 11, 473–490. Vermeulen, J., Bastiaanse, R., & van Wageningen, B. (1989). Spontaneous speech in aphasia: A correlational study. Brain and Language, 36, 252–274. Wagenaar, E., Snow, C., & Prins, R. (1975). Spontaneous speech of aphasic patients: A psycholinguistic analysis. Brain and Language, 2, 281–303. Webster, J., Morris, J., & Franklin, S. (2005). Eﬀects of therapy targeted at verb retrieval and the realisation of the predicate argument structure: A case study. Aphasiology, 19, 748–764. Wepman, J. M. (1951). Recovery from aphasia. New York: Ronald Press. Wernicke, C. (1874). Der aphasische Symptomencomplex. Eine psychologische Studie auf anatomischer Basis. Breslau: Cohn & Weigert.

258

Edwards and Bastiaanse

Whitworth, A. (1996). Thematic roles in production (TRIP). London: Whurr. Wright, H. H., Silverman, S., & Newhoﬀ, M. (2003). Measures of lexical diversity in aphasia. Aphasiology, 17, 443–452. Zingeser, L., & Berndt, R. (1988). Grammatical class and context eﬀects in a case of pure anomia: Implications for models of language production. Cognitive Neuropsychology, 5, 473–516.

17 Computerized aphasia treatment outcomes research The past and a proposal Richard C. Katz and Robert T. Wertz

Almost 20 years ago, we were in the ﬁnal stages of our 5-year Phase III study testing the eﬃcacy of our computerized aphasia treatment protocol. At that time, I was approached by one of the two editors of a new, soon-to-bereleased, journal, called Aphasiology. Dr. Code asked if I would write a “lead article for a forum” on the use of computers in aphasia therapy. The Aphasiology forum became not only a staple of that journal, but a model for others as well, and as the role of computers in rehabilitation grew, the 1986 forum articles, and the many subsequent articles on computerized treatment published in Aphasiology, helped to propel this aspect of treatment forward by oﬀering an international platform to ask questions and discuss and debate ﬁndings. We will always be grateful to Chris for providing, at that critical time, the opportunity to discuss with our colleagues from all over the world our work and the works of others. Determining the value of aphasia treatment software is complicated by the changing perspectives of clinicians as to what the primary objective of therapy is – to improve language skills, functional communication, or quality of life. Similarly, continual advances in computer hardware and system software provide new opportunities and just as quickly condemn last year’s programs to obsolescence. The purpose of this chapter is to review selected computerized aphasia treatment studies; place them in the ﬁve-phase outcome research model (Robey & Schultz, 1998); and suggest additional research necessary to test the eﬃcacy, eﬀectiveness, and eﬃciency of computerized treatment for aphasia.

Phase I, Phase II, and Phase III studies Phase I and Phase II studies are brief, employ small samples, and do not require external controls. Phase I objectives are to develop the hypothesis about the treatment that will be tested in later phases in the ﬁve-phase model; establish the treatment’s safety; and detect whether the treatment is “active,” essentially, whether aphasic people who receive it improve. Phase II research builds on the results of Phase I studies. The hypothesis is reﬁned, an explanation for the outcome is developed, the target population is speciﬁed, the

260

Katz and Wertz

treatment protocol is standardized, the validity and reliability of the outcome measures are demonstrated, and the treatment dosage is adjusted to maximize outcome. Phase III eﬃcacy studies are long, complex, and expensive. Large sample size is required to obtain acceptable statistical power, and, usually, the means for obtaining the large sample size requires a multi-center eﬀort in which several institutions contribute participants to obtain an adequate sample. The required study design is a randomized controlled clinical trial in which participants who meet selection criteria are assigned randomly to treatment and no-treatment groups. Randomization controls for treatment selection bias and other potential biases, and the treatment versus no-treatment comparison constitutes a true test of the treatment’s eﬃcacy. Of course, explicit protocols and rigid controls across participating centers are essential to ensure program ﬁdelity and that the trial is truly cooperative – everyone is doing the same thing. For almost 30 years, researchers have been creating and testing aphasia treatment software. Early single-subject and small group outcome studies, now designated as Phase I and Phase II computer studies (Wertz & Katz, 2004), demonstrated that independent use of the computer in treatment of aphasia was feasible and that treatment was “active,” but they did not establish whether improvements in outcome measures were of suﬃcient magnitude to justify use of the computer, or resulted from the speciﬁc intervention provided. Moreover, these Phase I and II studies did not demonstrate whether the treatments provided were eﬃcacious, eﬀective, or eﬃcient. Computerized writing treatment Seron, Deloche, Moulard, and Rousselle (1980) reported perhaps the ﬁrst Phase I study to use a computer (a Digital Equipment model PDP–10 minicomputer, time-shared) to provide a multi-step cognitive intervention for written spelling errors of adults with aphasia. Ninety words divided into three groups (depending on number of syllables and complexity) served as stimuli. An experimenter read aloud the stimulus word and the subject attempted to type the word on the computer terminal. Intervention consisted of three levels of feedback: the number of letters in the target word (indicated by square “boxes” displayed on the screen); whether the letter typed was in the word; and, when the correct letter was typed, whether that letter was in the correct position. Five subjects completed the program in 7 to 30 sessions. Pre- and post-treatment tests required the subjects to write by hand a generalization set of single words from dictation. Performance varied among subjects, but all decreased signiﬁcantly (p <. 05); the number of misspelled words by an average of 10 words, and the total number of misspelled letters by an average of 39 letters, on the post-treatment test. These results suggested that typing in response to the computer program improved the subjects’ written spelling of words. Four of the ﬁve subjects maintained improved performance on a second post-treatment test administered 6 weeks later.

Computerized aphasia treatment outcomes research 261 Building on the Phase I Seron et al. study, Katz and Nagy (1984) reported using a computer to provide a diﬀerent multi-step writing (typing/spelling) intervention for adults with aphasia that was error-speciﬁc and linguistically relevant. The program incorporated complex branching algorithms to present six diﬀerent levels of cuing, depending on the number of times a stimulus was incorrectly typed. Single and multiple cues, from a hierarchy of six, were selected by the program automatically in response to the number of attempts made by the patient. Speciﬁc cues included anagrams, multiple-choices, copying from a model, and copying from memory. A 7-point scoring system was used to describe performance and track the eﬀect of each cue. Additional feedback included repetition of the successful stimuli and the most recently successful cues. Additional changes automated every aspect of the program and eliminated the need for a clinician to start the program (a “personal computer,” the Apple II Plus, was used instead of a time-shared minicomputer) and present stimuli (line drawings served as stimuli instead of words presented verbally). The use of pictures as stimuli also reduced task requirements, avoiding complicating the task for patients with auditory comprehension problems. Finally, copying practice was generated by a printer as homework to strengthen generalization to writing. Comparison of pre- and post-writing outcome measures showed signiﬁcant improvement (p < .01) in spelling of the target words for seven of the eight aphasic subjects, demonstrating that multi-level computerized intervention (in this case, the treatment hierarchy and copying assignment) was active. While the Phase I and Phase II studies described above provide the foundation for development of a Phase III eﬃcacy study of multi-step writing treatment, none has been reported. As the treatment in both studies was demonstrated to be “active,” either might be used in a Phase III study. In addition, the treatment program could combine visual and linguistics cues from both studies. For example, the program might employ an algorithm that would select cues (number of letters in the word, position of the letter in the word, anagrams, copying from memory, etc.) in response to errors, randomly at ﬁrst and later based on the prior success of an individual cue or a combination of cues. Like Seron et al., a large number of stimulus words would be used, and, like Katz and Nagy, the program would be fully automated and stimuli presented visually to minimize task requirements. Copying homework would not be generated so that outcomes could be attributed to the computer intervention alone. As in all Phase III studies, a sample size of patients that was suﬃcient to attain acceptable statistical power, and random assignment to treatment and non-treatment groups, would be required. Computerized auditory comprehension treatment An early example of a Phase I computerized aphasia treatment study is Mills’ (1982) report that used a computer (an Apple II Plus with 48 kilobytes of RAM) to present an auditory comprehension task to an adult with aphasia.

262

Katz and Wertz

Because oﬀ-the-shelf “microcomputers” at that time did not have the ability to time responses or reproduce speech, Mills installed two internal cards in the ﬂedgling computer: an internal clock and a speech digitizer. He also added a color television monitor to incorporate colored drawings of objects into the task. A printer (to display performance) and a graphics tablet (to create the color drawings) were also included. The system cost around $4500, a considerable investment in 1982. Mills’ computerized task was a simple auditory comprehension drill that consisted of three levels of diﬃculty incorporating one, two, or three critical elements per level. Four color drawings of objects, numbered “1” through “4,” were displayed on the monitor to serve as multiple choice items. Then, depending on the intended level of task diﬃculty, the speech digitizer presented one-, two-, or three-part verbal “pointing” commands, ampliﬁed through an external speaker. The command consisted of a carrier phrase (“Find the . . .”) and the name or names of the target object or objects. Because a computer mouse was not available as a pointing device in those days, the patient responded by pressing the numbered key or keys on the keyboard that corresponded to the numbered picture or pictures associated with the spoken word or words. Intervention was limited to repetitions of the auditory stimulus, elicited when the patient pressed the Return (Enter) key. If the response was correct, the computer responded with a verbal “Good” or “Right” and displayed a ﬂashing square around the correct choice(s). If the ﬁrst response was not correct, a verbal “Wrong, try again” was presented, and the stimulus was repeated. A second error resulted in a ﬂashing square around the correct choice(s). Twelve items per level were presented. Results were stored on disk. A specially written analysis program was used to show performance on either the monitor or the printer. Mills’ patient was a 39-year-old computer programmer who suﬀered an occlusive stroke 16 months prior to beginning the computerized treatment program. He was described as being “severely involved in all modalities” at the beginning of the 13-month study. Outcomes were determined by measuring accuracy of task performance on the three task levels (gains of 8%, 42%, and 73%, respectively) and periodic administrations of the Porch Index of Communicative Ability (PICA; Porch, 1981) auditory comprehension subtests VI and X (gains of +4.8 and +1.5 points, respectively) and an unspeciﬁed version of the Token Test (gain of 23 percentile points). The inﬂuence of other factors (e.g., placebo eﬀect) cannot be discounted because no withdrawal or multiple baseline single subject research strategies were used. Nevertheless, the study was a ﬁrst step in adapting auditory comprehension activities to the computer and demonstrating that the auditory comprehension of aphasic patients may improve after using a computer program. Mills’ (1982) report was not followed by a Phase II investigation. Possible follow-up studies might administer more comprehensive auditory and functional tests and investigate treatment dosage (intensity and duration). Limiting the duration of treatment (e.g., 3 months as opposed to 13 months) would be

Computerized aphasia treatment outcomes research 263 more in line with current clinical practices. In addition, a treatment model should be speciﬁed. The computerized treatment described by Mills (1982) most closely approximates auditory stimulation treatment. The most widely used approach for treating aphasia (Duﬀy & Coelho, 2001) is clinicianprovided stimulation treatment, which uses controlled and intensive auditory stimulation to facilitate and maximize the patient’s reorganization and recovery of language (Schuell, 1974; Schuell, Jenkins, & Jiménez-Pabón, 1964). Treatment is designed so that patients respond frequently, to many diﬀerent stimuli, and at a high rate of accuracy. Phase II research utilizing an auditory stimulation model might increase the number of stimuli from the original dozen and, at the same time, increase the rate of response (number of responses per session). Should outcomes continue to improve in Phase II studies, a Phase III auditory comprehension study would be in order. The study could manipulate stimulus parameters (part of speech, word length, word frequency, etc.) and task parameters (number of multiple choices, auditory/semantic confusion among multiple choices, delays, distractions, etc.). A complex branching algorithm could advance subjects through a hierarchy of stimulus parameters, from easy to diﬃcult, with the goal of maximizing rate of presentation (number of stimuli per session) while maintaining high accuracy. Like Mills (1982), the program would be fully automated and designed to minimize response requirements. Again, as in all Phase III studies, adequate sample size and random assignment to treatment and no-treatment groups would be required. Computerized reading comprehension treatment Phase I studies by Katz and Nagy (1982, 1983, 1985) demonstrated various functions computers could provide for treating reading problems in patients with aphasia, although like all Phase I studies, interpretation of outcomes is limited due to small sample sizes and research designs. Katz and Nagy (1982) described a program containing ﬁve reading tasks designed to provide reading stimulation for aphasic patients. (The program also contained a task to improve simple math, and a testing module.) Five aphasic subjects ran the computer programs two to four times per week for 8 to 12 weeks. Only corrective feedback was provided. Although several subjects demonstrated improved accuracy, decreased response latency, and increased number of attempted items on some computer tasks, changes in pre- and post-treatment test performance were minimal. The following year, Katz and Nagy (1983) reported a drill and practice computer program for improving word recognition in chronic aphasic patients. The program simulated tachistoscopic presentation of 65 words that occur frequently in text (“recognition vocabulary”) and incrementally varied the rate of exposure as a function of accuracy of response – stimuli were displayed for shorter durations (down to .01 seconds) as words were matched or typed accurately, and displayed for longer

264

Katz and Wertz

durations as words were matched or typed incorrectly. The goal of the program was to increase and stabilize the subject’s sight vocabulary; however, no changes were observed on pre- and post-treatment measures for the ﬁve chronic aphasic subjects. Katz and Nagy (1985) incorporated concepts from both previous studies in a their Phase II study, where a self-modifying computerized reading program was administered to severely impaired aphasic adults. The objective of the study was to improve functional reading. A program was developed to teach subjects to read single words without clinician involvement. Line drawings of 12 semantically related objects were shown individually on the monitor, under which two to six multiple choices were printed. Multiple choice foils included visually confusing and semantically confusing words. The program also generated, through a printer, homework (writing activities) that corresponded to the subject’s performance. Four of the ﬁve subjects demonstrated pre- to post-treatment changes on the treatment items that ranged from 16% to 54%. Katz and Wertz (1997) conducted the only Phase III study of the eﬃcacy of computerized language treatment and computerized non-language stimulation for improving language test performance for chronic aphasic adults. Fifty-ﬁve chronic aphasic subjects who were no longer receiving speechlanguage therapy were assigned randomly to one of three conditions: 78 hours of computer reading treatment, 78 hours of computer stimulation (“non-language” activities), or no treatment. The computer reading treatment software consisted of 29 activities, each containing eight levels of difﬁculty, totaling 232 diﬀerent tasks. Treatment tasks required visual-matching and reading comprehension skills, displayed only text (no pictures), and used a standard, match-to-sample format with two to ﬁve multiple choices. Treatment software automatically adjusted task diﬃculty in response to subject performance by incorporating traditional treatment procedures, such as hierarchically arranged tasks and measurement of performance on baseline and generalization stimulus sets, in conjunction with complex branching algorithms. Software used in the computer stimulation condition was a combination of cognitive rehabilitation software and computer games that used movement, shape, and/or color to focus on reaction time, attention span, memory, and other skills that did not overtly require language or other communication abilities. Subjects in the two computer conditions worked on the computer for 3 hours per week for 26 weeks with minimal clinician interaction. Subjects from all three conditions were tested using the PICA and Western Aphasia Battery (WAB; Kertesz, 1982) at baseline, 3 months, and 6 months. Statistically signiﬁcant improvement over the 26 weeks occurred on ﬁve language measures for the computer reading treatment group, on one language measure for the computer stimulation group, and on none of the language measures for the no-treatment group. The computer reading treatment group displayed signiﬁcantly more improvement on the PICA overall and verbal modality percentiles and on the WAB aphasia quotient

Computerized aphasia treatment outcomes research 265 and repetition subtest than the other two groups. The results suggest that computerized reading treatment can be administered with minimal assistance from a clinician, improvement on the computerized reading treatment tasks generalized to non-computer language performance, improvement resulted from the language content of the software and not stimulation provided by a computer, and the computerized reading treatment provided to chronic aphasic patients was eﬃcacious.

Potential Phase IV studies If the treatment is demonstrated to work in Phase III eﬃcacy research, it is justiﬁable to continue with Phase IV eﬀectiveness research. The purpose is to test the treatment’s eﬀectiveness under ordinary conditions of clinical practice with typical patients, typically trained clinicians, typical dosage, and typical compliance. Again, a large sample is required, however external control (e.g., a no-treatment control group) is not. Thus the typical eﬀectiveness study design is a large single group where, as in Phase I research, performance is measured pre-treatment, the treatment is administered under ordinary conditions, performance is measured post-treatment, and a pre- versus posttreatment comparison is made to determine change. If the group shows signiﬁcant improvement from pre- to post-treatment, it can be inferred that the treatment is eﬀective; essentially, that it does work under conditions of everyday clinical practice. Additional Phase IV experiments might include examination of variations in the target population; for example, study participants who do not meet the selection criteria employed in the Phase III eﬃcacy study. In addition, Phase IV research might examine variation in the dosage, for example, a diﬀerent intensity and duration of treatment from that employed in the Phase III eﬃcacy research. And one might explore diﬀerences in treatment providers, for example, clinicians with less training than those who participated in the Phase III eﬃcacy research or, perhaps, provision of the treatment by nonprofessional, trained volunteers. While no Phase IV computerized aphasia treatment study has been reported, one could be conducted by using the Internet, where a large number of patients and former patients could be solicited through their clinicians to participate in the study. Referring clinicians could administer all pre- and post-testing, and testing could be validated by videotaping or videoconferencing randomly selected test administrations. Standardized language, functional, and quality of life tests would serve as outcome measures to evaluate the eﬀectiveness of treatment. For example, in a Phase IV study developed from Katz and Wertz (1997) computer reading treatment program, all subjects would receive the computerized treatment and be tested before beginning and after completing treatment. The goal would be to evaluate the treatment of “typical” patients under “real-world” conditions. Exclusion criteria would be minimal to include

266

Katz and Wertz

patients typically found in clinics. Data from subjects unable to maintain the prescribed treatment schedule (i.e., treatment dosage) would not be dropped from the study, as under “optimal” conditions tested in Phase III research. Positive outcomes from Phase IV research would provide clinicians with support to justify funding and resources to provide treatment.

Phase V Additional research is continued in Phase V, initiating studies to test the treatment’s eﬀectiveness and eﬃciency. Continued eﬀectiveness research might examine the cost–beneﬁt, or cost eﬀectiveness, of the treatment. Or, additional outcome measures might be employed to determine the patient’s and family’s satisfaction with the intervention and the inﬂuence of the treatment on the patient’s quality of life. Large group studies and/or single-subject designs with multiple replications across patients are appropriate for Phase V research, and, usually, external control is not required. However, some eﬃciency studies require control through random assignment. For example, comparing the eﬃciency of two treatments that have been demonstrated to be eﬃcacious in Phase III research requires a comparison of treatments design, where study participants who meet selection criteria are assigned randomly to one treatment or the other. Similarly, an eﬃciency study designed to compare one intensity and/or duration with another intensity and/or duration would require random assignment of study participants to the diﬀerent schedules. For example, a Phase V study could compare the two comprehension treatments described above, auditory and reading, and determine whether subjects receiving one treatment or the other report and demonstrate better functional outcomes. Loverso and his colleagues provided examples of Phase I and Phase II research, describing the development and testing of a model-driven, clinicianprovided treatment approach, the “verb as core” (Loverso, 1987; Loverso, Prescott, & Selinger, 1988; Loverso, Selinger, & Prescott., 1979). These led to a comparison study of clinician-provided treatment with a computer-provided and clinician-assisted version of the treatment (Loverso, Prescott, & Selinger, 1992; Loverso, Prescott, Selinger, & Riley, 1988; Loverso, Prescott, Selinger, Wheeler, & Smith, 1985). However, the eﬃcacy of neither treatment had been tested in Phase III eﬃcacy research. Consequently, neither treatment had been demonstrated to be eﬀective in Phase IV research. A comparison of two treatments of unknown eﬃcacy will not demonstrate the eﬃcacy of either treatment (Wertz & Irwin, 2001). In both the clinician-provided and the computer/clinician-assisted versions of “verb as core” treatment protocol, verbs were presented as starting points and paired with diﬀerent wh-question words to provide cues to elicit sentences in an actor–action–object framework. Thirty verbs were used in each of six modules. The hierarchy was divided into two major levels, each consisting of an initial module and two sub-modules that provided additional cuing

Computerized aphasia treatment outcomes research

267

for subjects unable to achieve 60% or better accuracy on the initial module. Level I presented stimulus verbs and the question words “who” or “what” to elicit an actor–action sentence. Level II elicited actor–action–object sentences by presenting stimulus verbs and the question words “who” or “what” for the actor, and the question words “how,” “when,” “where,” and “why” for the object. Subjects responded verbally and graphically. Subjects were scheduled for treatment three to ﬁve times per week. During each session, 30 stimulus verbs were presented for generation of sentences. Loverso et al. (1985) compared the eﬀects of the “verb as core” treatment approach when treatment was provided by a clinician and when it was provided by a computer and speech synthesizer assisted by a clinician. The aphasic subject responded in the clinician-only condition by speaking and writing, and in the clinician–computer condition by speaking and typing. Stimulus presentation and feedback in the clinician–computer condition was normally provided only by the computer. The clinician intervened only if the patient’s typed response was correct but the spoken response was in error. The subject improved on the task under both conditions, but took longer to reach criteria under the computer and clinician-assisted condition. Based on the subject’s improvement, both on the treatment task and on “clinically meaningful” changes on successive administrations of the PICA (p < .01), the authors concluded that their listening, reading, and typing activities under the clinician–computer condition had a positive inﬂuence on the patient’s language performance. They suggested that, although still in the early stages of development, aphasia treatment administered by computers is practical and has the capacity for success. Loverso, Prescott, Selinger, and Riley (1988) replicated the study by Loverso et al. (1985) with ﬁve ﬂuent and ﬁve nonﬂuent aphasic subjects for the purpose of examining whether treatment provided under the computer–clinician condition was as eﬀective as a clinician alone when treating various types and severities of aphasia using their cuing–verb–treatment technique. The 10 subjects required 28% more sessions (p < .05) to reach criteria under the computer–clinician condition than under the clinician-only condition. Fluent subjects required 24% more sessions, and nonﬂuent subjects required 33% more sessions under the computer–clinician conditions than under the clinician-only condition. Of the 10 subjects, 8 showed signiﬁcant improvement (p < .05) on the PICA overall percentile measure, on the verbal modality measure, and on the graphic modality measure. All subjects retained these gains after a maintenance phase of 1 month post-treatment or longer. Similar results were reported following a replication of the study using 20 subjects (Loverso et al., 1992). To our knowledge no additional studies examining the eﬃcacy of computer-provided treatment for aphasia have been conducted. As indicated above, any eﬀectiveness or eﬃciency research would require that the treatments being evaluated have been demonstrated to be eﬃcacious in Phase III research.

268

Katz and Wertz

A proposal Previous computer-provided aphasia treatment outcome research has been plagued by the problem that aﬀects clinician-provided aphasia treatment outcome research. Programmatic research, where a treatment is tested systematically in each phase of the ﬁve-phase treatment outcomes research model, is, if not nonexistent, extremely rare (Wertz & Irwin, 2001). Numerous Phase I computer-provided aphasia treatment studies have been reported. Few Phase II studies, building on Phase I research, exist. Only one Phase III investigation (Katz & Wertz, 1997) has tested the eﬃcacy of a computerprovided intervention, and there have been no Phase IV and V eﬀectiveness investigations. The tendency has been to develop new computer interventions that are prompted by new technology or to adapt clinician-provided treatment into computer applications, rather than to build and expand on previous computer-provided treatment research. There are a number of computer-provided treatments that imply the treatment appears to be “active” in Phase I research. The work to be done is to select the most promising of these and test them in Phase II research. If results are positive, subsequent Phase III eﬃcacy testing, and eventually Phases IV and V eﬀectiveness and eﬃciency testing, is essential. Until we become programmatic and systematic in our evaluation of computerized aphasia treatment, we are not documenting, we are dabbling.

References Duﬀy, R. J., & Coelho, C. A. (2001). Schuell’s stimulation approach to rehabilitation. In R. Chapey (Ed.), Language intervention strategies in aphasia and related neurogenic communication disorders. New York: Lippincott, Williams, & Wilkins. Katz, R. C., & Nagy, V. T. (1982). A computerized treatment system for chronic aphasic adults. In R. H. Brookshire (Ed.), Clinical aphasiology: 1982 conference proceedings (pp. 153–160). Minneapolis, MN: BRK. Katz, R. C., & Nagy, V. T. (1983). A computerized approach for improving word recognition in chronic aphasic patients. In R. H. Brookshire (Ed.), Clinical aphasiology: 1983 conference proceedings (pp. 65–72). Minneapolis, MN: BRK. Katz, R. C., & Nagy, V. T. (1984). An intelligent computer-based task for chronic aphasic patients. In R. H. Brookshire (Ed.), Clinical aphasiology: 1984 conference proceedings (pp. 159–165). Minneapolis, MN: BRK. Katz, R. C., & Nagy, V. T. (1985). A self-modifying computerized reading program for severely-impaired aphasic adults. In R. H. Brookshire (Ed.), Clinical aphasiology: 1985 conference proceedings (pp. 184–188). Minneapolis, MN: BRK. Katz, R. C., & Wertz, R. T. (1997). The eﬃcacy of computer-provided reading treatment for chronic aphasic adults. Journal of Speech, Language and Hearing Research, 40 (3), 493–507 Kertesz, A. (1982). Western aphasia battery. New York: Grune & Stratton. Loverso, F. L. (1987). Unfounded expectations: Computers in rehabilitation. Aphasiology, 1 (2), 157–160. Loverso, F. L., Prescott, T. E., & Selinger, M. (1988). Cueing verbs: A treatment

Computerized aphasia treatment outcomes research 269 strategy for aphasic adults. Journal of Rehabilitation Research and Development, 25, 47–60. Loverso, F. L., Prescott, T. E., & Selinger, M. (1992). Microcomputer treatment applications in aphasiology. Aphasiology, 6 (2), 155–163. Loverso, F. L., Prescott, T. E., Selinger, M., & Riley, L. (1988). Comparison of two modes of aphasia treatment: Clinician and computer-clinician assisted. In T. E. Prescott (Ed.), Clinical aphasiology (Vol. 18, pp. 297–319). Austin, TX: Pro-Ed. Loverso, F. L., Prescott, T. E., Selinger, M., Wheeler, K. M., & Smith, R. D. (1985). The application of microcomputers for the treatment of aphasic adults. In R. H. Brookshire (Ed.), Clinical aphasiology: 1985 conference proceedings (pp. 189–195). Minneapolis, MN: BRK. Loverso, F. L., Selinger, M., & Prescott, T. E. (1979). Application of verbing strategies to aphasia treatment. In R. H. Brookshire (Ed.), Clinical aphasiology: 1979 conference proceedings (pp. 229–238). Minneapolis, MN: BRK. Mills, R. H. (1982). Microcomputerized auditory comprehension training. In R. H. Brookshire (Ed.), Clinical aphasiology: 1982 conference proceedings (pp. 147–152). Minneapolis, MN: BRK. Porch, B. E. (1981). Porch Index of Communicative Ability, Vol. 1: Administration, scoring, and interpretation (3rd ed.). Palo Alto, CA: Consulting Psychologists Press. Robey, R. R., & Schultz, M. C. (1998). A model for conducting clinical-outcome research: Adaptation of the standard protocol for use in aphasiology. Aphasiology, 12, 787–810. Schuell, H. (1974). The treatment of aphasia. In L. F. Sies (Ed.), Aphasia theory and therapy: Selected lectures and papers of Hildred Schuell. Baltimore, MD: University Park Press. Schuell, H., Jenkins, J. J., & Jiménez-Pabón, E. (1964). Aphasia in adults. New York: Harper & Row. Seron, X., Deloche, G., Moulard, G., & Rousselle, M. (1980). A computer-based therapy for the treatment of aphasic subjects with writing disorders. Journal of Speech and Hearing Disorders, 45, 45–58. Wertz, R. T., & Irwin, W. H. (2001). Darley and the eﬃcacy of language rehabilitation in aphasia. Aphasiology, 15, 231–247. Wertz, R. T. & Katz, R. C. (2004). Outcomes for computer-provided treatment for aphasia. Aphasiology, 18, 229–244.

18 Traumatic brain injury rehabilitation Advanced communication training perspectives Leanne Togher This chapter presents part of an ongoing research programme that has been developed with the guidance of Professor Chris Code. Chris’ inﬂuence on my work has been far reaching; he was my PhD supervisor during his stay in Australia as the Foundation Chair of Communication Sciences and Disorders at the University of Sydney, my mentor during my postdoctoral fellowship and we continue to work together on current and new projects. Chris’ breadth of knowledge in the ﬁeld of adult neurological communication disorders has been invaluable in the development of my research ideas and my research career. He has that special talent of being able to improve a research proposal, a grant application or a manuscript in preparation with apparent ease. Chris has taught me a great deal about editing and reviewing journal articles, and has given me an appreciation of the work entailed in managing a specialist journal such as Aphasiology. Perhaps his greatest gift has been teaching me the value of collaboration and communication with colleagues in the development and critique of my ideas. Chris’ contributions to the numerous conferences he attends are always insightful and generous. His extraordinary international network is testament to his keen interest in all approaches to neurological communication disorders and his willingness to explore all ideas. My research focus has been the application of novel methods, such as the use of Systemic Functional Linguistic (SFL) theory (Halliday, 1994) to elucidate the nature of everyday interactions of people with traumatic brain injury (TBI). While TBI and SFL are not Chris’ speciﬁc area of interest, he encouraged me to pursue this area, to publish, to present at international conferences, and to apply for research grants. His guidance, mentorship, wise counsel and encouragement are immeasurable, and I am honoured to be able to pay tribute to him in this Festschrift. Traumatic brain injury is the leading cause of disability in young Australians, and is particularly prevalent in young men. The condition disturbs, inter alia, thinking and problem solving. Ultimately, these problems manifest in impaired verbal communication. Communication problems following TBI can make critical relationships – such as father, husband, and employee – impossible to sustain. Those aﬀected are socially inappropriate

Traumatic brain injury rehabilitation

271

and uncomfortable to be around, which causes a lifetime of lost friendships, unemployability, and social isolation. Minimization of these lifelong eﬀects is of the utmost importance to the health of those aﬀected, and is critical to reducing the economic burden of the condition. Traumatic brain injury (TBI) results from an external insult to the brain, and in severe cases, can lead to life-long devastating disability. Seventy per cent of TBI cases are a result of motor vehicle accidents, with most being in the 15–24 year age range (Tate, McDonald, & Lulham, 1998). With normal life expectancies and the addition of more casualties each year, the social burden of TBI is cumulative. Most people with moderate-severe TBI have chronic communication and cognitive problems that result in a breakdown in family relationships, loss of friends, a failure to return to work, and social isolation. Communication diﬃculties for people with TBI include word ﬁnding problems, excessive talkativeness, poor turn taking and repetitiveness (Snow, Douglas, & Ponsford, 1995). These communication diﬃculties are substantially diﬀerent to the sequelae of aphasia and have been termed cognitivecommunication impairments (Hartley, 1995). While some communication problems after TBI reﬂect disorders of language function, the majority arise from more generic cognitive deﬁcits reﬂecting fronto-temporal pathology and diﬀuse axonal injuries. Slowed information processing, impaired working memory/attention and executive dyscontrol may translate into deﬁciencies (e.g., inertia, rigidity, poor conceptualization and planning) or excesses (such as disinhibition) of cognition and behaviour (Tate, 1999; Tate, Lulham, Broe, Strettles, & Pfaﬀ, 1989). Inertia and rigidity can lead to ﬂat presentation, seeming disinterest in the conversation, and an inability to generate and maintain topics. Alternatively, excesses can interfere due to frequent interruptions, disinhibited responses, swearing and perseveration on topics. These inappropriate and disturbing communicative behaviours are diﬃcult to manage, particularly when in a community setting such as a shopping centre. Overall, loss of communicative competence presents a major obstacle to reintegration into the community because it makes the person more taxing and less rewarding to interact with socially (Bond & Godfrey, 1997). Friends, carers and family begin avoiding them and this generally limits their ability to maintain pre-injury relationships (Elsass & Kinsella, 1987; Tate et al., 1989). In addition, they often misjudge social situations, appearing to be overly familiar with potential acquaintances thus interfering with their ability to establish new relationships. As a result of diminished communication skills, people with TBI become socially isolated, have reduced opportunities for employment and may even require care-givers to help them with everyday tasks such as shopping or pursuing leisure options. But even with care-givers, the poor communication skills of people with TBI are problematic. Caring for people with TBI is stressful, with high levels of care-giver burden and depression (Knight, Devereux, & Godfrey, 1998). The main sources for this

272

Togher

stress have been identiﬁed as problems communicating with the person with TBI (MAA, 1998), behavioural disturbance (Knight et al., 1998; Marsh, Kersel, Havill, & Sleigh, 1998) and the level of cognitive processing diﬃculties of the person with TBI (Wallace, Bogner, Corrigan, Clinchot, Mysiw, & Fugate, 1998). Training programmes to provide communication strategies for care-givers, while needed, are currently non-existent, and are urgently called for (Holland & Shigaki, 1998).

Improving the communication skills of the person with TBI Despite its pivotal role in social reintegration there has been surprisingly little research to examine the eﬀectiveness of remediation of communication disorders after TBI. However, there is reason for optimism in this area. Recent studies suggest that behavioural and cognitive deﬁcits suﬀered by TBI patients, thought to contribute to their loss of communicative competence, are amenable to remediation (Cannizzaro & Coelho, 2002; Cramon & Cramon, 1992, Flanagan, McDonald, & Togher, 1995, Helﬀenstein & Wechsler, 1982, Medd & Tate, 2000, Tate, 1987). Furthermore, a systematic review of treatment outcomes in TBI indicated that the broad area of social skills, which encompasses communication skills, was one of only two areas that proved amenable to treatment (Cicerone et al., 2000). However, properly controlled treatment studies in this area are virtually non-existent. In order to redress the lack of research into social skills remediation, we developed a social skills treatment approach (Flanagan et al., 1995). In this study, we evaluated the eﬀectiveness of a social skills training programme with ﬁve males in the chronic stage following severe TBI. The participants’ performance was judged using the six verbal scales of the Behaviourally Referenced Rating System of Intermediate Social Skills (BRISS; Wallander, Conger, & Cohen Conger, 1985; see also Farrell, Rabinowitz, Wallander, & Curran, 1985) during three naturalistic interactions with an opposite-sex stranger. Ratings from the initial interaction were used to develop individualized intervention plans for each of the ﬁve TBI participants. Following the three assessment interactions and the development of the intervention plans, the TBI patients took part in a group-based social skills training programme that allowed for each individual’s speciﬁc deﬁcits to be addressed. This promoted the incorporation of individual goals into a group treatment process. The training consisted of weekly 2-hour group sessions held over a 3-month period. The instruction methods included modelling, role-play, feedback and homework assignments. As the group was severely cognitively impaired, the sessions were highly structured, with repetition, frequent rest breaks, and a variety of interactive activities. Role plays were frequently videotaped and immediately replayed to facilitate the provision of feedback. In addition to practising speciﬁc social skills, the participants were encouraged to attend to social cues. Following the treatment, the post-assessment tasks were the same procedure as pre-intervention assessment. As expected, there was

Traumatic brain injury rehabilitation

273

signiﬁcant variability across participants on some scales pre-intervention. A signiﬁcant ﬁnding, however, was the improvement shown by one of the participants on three of the BRISS scales, which was socially validated. A further participant also improved on one of the BRISS scales. While this study demonstrated that positive changes can occur in interactions of people with severe chronic TBI, there have been no treatments designed and empirically evaluated to speciﬁcally target communication in everyday situations for people with TBI. There has also been a paucity of communication treatment studies using broader models of disability and social participation. These models are acquiring considerable currency in the ﬁeld of aphasia, but are yet to be applied to the everyday communication for people with TBI. There is recognition that social participation should be an outcome of rehabilitation following TBI (Cicerone, 2004), however there has been no explicit examination of the relationship between community reintegration and communication outcomes. In discussing the communication outcomes necessary for community integration, the question arises as to which communication tasks are necessary for the person with TBI to reintegrate into their own community. In an observational study of 10 individuals with TBI in New Zealand, participants were observed for 5 hours within a 1-week time frame to establish the communication activity range, frequency and domain of interaction (Larkins, Worrall, & Hickson, 1999). The most frequently occurring communication activity was social chat, an interactional communication activity that was deﬁned as “communication interactions that maintain social relationships” (p. 188). Speech pathologists spend much of their clinical energy focusing on the transactional features of communication; that is, getting the message across, rather than helping the person to engage in social chat or small talk. This poses diﬃculty for the clinician in a brain injury unit when working on social chat. The ﬁrst problem is that people with TBI are typically young males of working age, who are usually treated by young women with starkly diﬀerent communication styles and preferences in conversation. A second diﬃculty is the social barrier of clinician–patient power imbalance (Togher, Hand, & Code, 1996). Nonetheless, therapy to improve social chat is imperative given Larkins et al.’s (1999) ﬁndings. One solution to this dilemma is to include other conversational partners in the therapy process.

Training communication partners of people with neurogenic communication disorders A wide range of theoretical perspectives have been used to study the issue of training communication partners of people with neurogenic communication disorders, with the majority being completed in the ﬁeld of aphasia. They include Conversational Analysis (CA) (Booth & Perkins, 1999; Wilkinson et al., 1998), functional perspectives (Lyon et al., 1997; Worrall & Yiu,

274

Togher

2000), pragmatic models of communication (Newhoﬀ, Bugbee, & Ferreira, 1981), behavioural approaches (Simmons, Kearns, & Potechin, 1987) and social models of disability (Byng, Pound, & Parr, 2000; Kagan, Black, Duchan, Simmons-Mackie, & Square, 2001; Simmons-Mackie, 2000). The core principles of these approaches are similar. They all focus on improving conversational interaction by training the communication partner and/or the communication interaction rather than the person with communication problems. Conversational analysis of interactions provides a rich source of information about areas such as the way participants repair communication breakdown, take turns and introduce topics (Schiﬀrin, 1987). Booth and Perkins (1999) presented a single case study where the brother of an aphasic man was trained over a 6-week period in collaborative repair management. This man was part of a larger group who participated in training for carers of people with aphasia (Booth & Swabey, 1999). During this training the potential negative consequences of focusing on the correction of aphasic errors was discussed. One of the clearest outcomes in the post-intervention conversation was the absence of correction. The brother permitted aphasic errors to pass and collaborated to resolve sources of trouble. This study is an important preliminary foray into the value of individualized advice for communication partners in facilitating everyday conversation. With the publication of the SPPARC (Supporting Partners of People with Aphasia in Relationships and Conversation; Lock, Wilkinson, & Bryan, 2001), a therapy resource for clinicians to use with communication partners, this type of intervention is now readily accessible. Functional perspectives have also been used in designing training studies for communication partners of people with aphasia (Lyon et al., 1997; Worrall & Yiu, 2000). The functional approach has developed partly in response to ﬁnancial pressures (Frattali, 1993), a belief within the speech pathology profession that functional outcomes are important (Smith & Parr, 1986) and a recognition of the WHO (2001) guidelines that diﬀerentiate between the dimensions of Impairment, Activity and Participation. Worrall and Yiu (2000) incorporated these underlying tenets into a training programme for volunteers called “Speaking Out”, which focused on 10 general communication domains such as banking and using a telephone. Scripted modules consisted of a “trigger” to raise awareness of participants regarding the topic of the module. For example, in the banking module, participants engaged in a discussion around electronic banking and the possible beneﬁts of this for a person with aphasia. A discussion ensued with the volunteer regarding ways a person with aphasia could remain involved in managing his or her ﬁnances, and a plan was set up for the volunteer to assist the person with aphasia during the following week. This planning was accompanied by practical information handouts, which gave general strategies for the volunteers. The training continued over a 10-week training period. Functional measures showed small changes post-training; however, the authors point out

Traumatic brain injury rehabilitation

275

that these changes were nonetheless clinically signiﬁcant. It was also suggested that a more individualized training approach may have further increased the eﬀects of training. The social approach to disability is a more recent movement in the way intervention is viewed in relation to people with aphasia (Pound, Parr, Lindsay, & Woolf, 2000). This approach takes the broader view that therapy should identify social barriers for people with aphasia, including the way communication partners may interact. The Conversation Partners programme described by Pound et al. (2000) is a relatively new scheme where student speech pathologists and some members of the community commit to spending 2 hours per fortnight for at least 6 months with a person with aphasia. Volunteers attend group training sessions before meeting their aphasic partner. Training is focused on giving information about aphasia, its communicative and social consequences, and basic communication techniques. Although this programme has not been evaluated empirically, Pound et al. (2000) presented a case study demonstrating the value of regular visits by a student speech pathologist with regard to increased communicative opportunities for a person with aphasia. The value of these partner-focused treatment regimes is that communication partners, when suitably skilled, can reveal the inherent competence of the person with brain injury by providing communicative opportunity (Kagan et al., 2001, Ylvisaker, Feeney, & Urbanczyk, 1993). In other words, when provided with the opportunity, people with acquired communication problems can capitalize on their preserved cognitive and social abilities to participate in conversation. Kagan et al. (2001) reported empirical evidence of the positive communication and social outcomes of training communication partners of people with severe aphasia. In a randomized controlled trial, 20 communication partners were trained in how to keep talk as natural as possible, to avoid being patronizing and to explicitly let the person know that his or her competence was not in question. Partners were also trained to improve the exchange of information. Results provided experimental support for the eﬃcacy of communication partner training in improving the communication skills of conversation partners. Their brain-impaired partners also improved signiﬁcantly, even though they did not receive speciﬁc training. Communication partners of a range of participants with communication problems have taken part in training programmes. These include volunteers talking with people with aphasia (Kagan et al., 2001; Lyon et al., 1997), nursing staﬀ who were trained to use memory aids as an augmentative and alternative communication device with people with Alzheimer’s disease (Bourgeois, Dijkstra, Burgio, & Allen-Burge, 2001; Burgio et al., 2000) and caregivers who underwent communication training to facilitate communication with people with Alzheimer’s disease (Ripich, Ziol, Fritsch, & Durand, 1999). The type and amount of training has also varied across studies, ranging from 1-hour in-service training for nursing staﬀ (Bourgeois et al., 2001), a one and a half day workshop format for volunteers (Kagan et al.,

276

Togher

2001), a 4-week training programme for nursing staﬀ on memory book use and general communication skills (Burgio et al., 2000), a small group training format where four carers of adults with aphasia attended 2-hour sessions once a week for 6 consecutive weeks (Booth & Perkins, 1999; Booth & Swabey, 1999), up to a 10-week training programme for volunteers (Worrall & Yiu, 2000). The length of training programmes for communication partners that is required for eﬀective communication modiﬁcation has not been speciﬁcally investigated to date.

Communication partner training in traumatic brain injury In a similar vein to the work done in aphasia, training programmes are now beginning to emerge to help families and other care-givers deal with the ongoing problems that can follow TBI (Carnevale, 1996; Holland & Shigaki, 1998; Ylvisaker et al., 1993). Ylvisaker et al. (1993) describe the importance of providing a positive communication culture within the rehabilitation context. They suggest that role-playing and modelling combined with ongoing coaching and support in vivo are appropriate methods to facilitate communication training for communication partners of people with TBI. Further work is needed, however, to develop such training programmes to address individual communication proﬁles in collaboration with the family and peer network of the person with TBI. Importantly, there has been no description of training programmes that may be appropriate for community groups who interact with people with TBI. Thus, although community reintegration is frequently suggested as the primary objective of TBI rehabilitation (Coelho, DeRuyter, & Stein, 1996; Ylvisaker, 1998), there are few documented cases where community agencies have been assisted to encourage more appropriate participation for these clients, and none where the eﬃcacy of such an approach has been demonstrated. This is despite the fact that there are now a number of studies that have clearly documented the nature of social interaction diﬃculties that commonly occur when people with TBI communicate in everyday settings.

Focus on the conversational partners of people with TBI In any conversation, the person with communication diﬃculties represents only one side of the interaction. The behaviour of their conversational partner is important; facilitating, or diminishing opportunities for the individual with brain injury to continue the conversation in a successful manner. Indeed, it has been found that TBI individuals are often disadvantaged in interactions because of the way their communication partners interact with them. For example, in a study of telephone conversations where TBI participants requested information from a range of communication partners, they were asked for and were given less information than matched control participants (Togher, Hand, & Code, 1996, 1997a, 1997b). Therapists and mothers never

Traumatic brain injury rehabilitation

277

asked people with TBI questions to which they did not already know the answer. Additionally, TBI participants were more frequently questioned regarding the accuracy of their contributions, and contributions were followed up less often than matched control participants. Communication partners used patronizing comments, ﬂat voice tone and slowed speech production when talking to people with TBI. This was in contrast to the control interactions, where participants were asked for unknown information, encouraged to elaborate, did not have their contributions checked frequently, and had their contributions followed up. Importantly, we found that communication can be improved by manipulating the speaking situation for the person with TBI. For example, when people with TBI were placed in a powerful information-giving role, such as a guest speaker talking about the experience of having a serious injury, their communication approximated matched control participants (who had a spinal injury) (Togher, 2000; Togher & Hand, 1998). Thus, when provided with a facilitative context such as an equal communicative opportunity, TBI participants were primed to match the performance of control participants. These results suggest that greater opportunities and increased conversational competence can be created for the person with TBI by speciﬁcally training their communication partner. To examine the eﬀect of training communication partners we developed a training programme for carers, which was piloted with a single case in 2000 (Togher & Grant, 2001). We trained a paid attendant care-giver who supported the daily activities of a 28-year-old man with TBI. The main communication problems reported separately by the care-giver and the person with TBI were keeping conversations going and staying on topic. After identifying target speaking situations (e.g., lunch at the shopping centre), we taught the structure of casual conversation (Ventola, 1979) in combination with the strategies of collaboration and elaboration (Ylvisaker, 1998). Pilot data indicated that the care-giver improved his ability to facilitate communication by using collaborative statements, explicitly acknowledging diﬃculty in the interaction, conﬁrming his partner’s contribution and asking questions in a supportive manner. We expanded this approach by developing and evaluating a communicationtraining programme for police oﬃcers, as members of a service industry who are likely to encounter people with TBI. We trained the police oﬃcers to manage speciﬁc service encounters with people with TBI who they had not previously met. This was evaluated in a randomized controlled trial (Togher & Grant, 2001; Togher, McDonald, Code, & Grant, 2004). The TBI speakers rang the police to ask their advice both before and after the police had been trained. Training resulted in more eﬃcient, focused interactions. In other words, this study conﬁrmed that training communication partners improved the competence of people with TBI. What is unknown is whether this approach is better than, or equal to, the eﬃcacy of direct remediation work with the person with TBI, or whether a combined approach is more eﬀective still.

278

Togher

Measuring the interaction – the value of sociolinguistics One of the problems in examining the interactions of people with TBI has been ﬁnding sensitive measures that reﬂect the two-way nature of interactions. This was one of the driving forces in the early research Chris Code and I completed in the mid-1990s; to ﬁnd an alternative way to examine everyday interactions. This led us to use sociolinguistic analyses to provide new insights into the communication of people with TBI (Togher, 2000; Togher & Hand, 1998; Togher et al., 1997a, 1997b), and became the basis for a successful training programme for communication partners (Togher et al., 2004). This approach has been innovative in that it focuses on not only the speaker with TBI, but also the conversational behaviour of their speaking partner. We have found analytic frameworks based on Systemic Functional Linguistics (Halliday, 1994), speciﬁcally Generic Structure Potential (GSP), to be useful in measuring the interactions of people with TBI (Togher & Hand, 1999; Togher et al., 1997b) and in revealing areas of diﬃculty that can be targeted in remediation. GSP analysis examines oral texts as genre (Hasan, 1985). Genres in literary terms describe typical realizations of particular types of texts. Some examples of genres include letters to the editor, appointment making and service encounters. In each of these, the content varies according to the activity (known as ﬁeld) and the participants involved (known as tenor), however there is a common core of structural elements. There are a number of already established spoken genres, some of which are well known to speech pathologists. These include narrative, recount, procedure, exposition, discussion and casual conversation. All these genres can be used to train communication partners to facilitate the interactions of people with TBI. We chose the service encounter genre to train police oﬃcers in ways of dealing with people with TBI for a number of reasons. This highly structured genre is familiar to most people, and has well-deﬁned parameters. Once communication partners are aware of these parameters, it is easy for them to identify deviations from the regular format and to respond accordingly. The service encounter genre has face and social validity, and was easily applied to the goal of measuring an everyday activity that contributes to community reintegration. In broad terms, the service encounter genre was ﬁrst proposed by Hasan (1985) as shown in the table opposite. This example represents a simple service encounter on the telephone. Telephone inquiries, however, are not always this straightforward. Some elements recur with more than one service request and a number of service inquiries before the interaction is completed (Eggins & Slade, 1997; Hasan, 1985). Other features that may occur include a query by either participant if their communication partner has left the call (e.g., “Are you there?”) as well as a statement of action (e.g., “I’ll just write that down”). The interactions of people with TBI have previously been found to consist of other elements not accounted for in traditional SFL analyses (Togher et al., 1997b). These

Traumatic brain injury rehabilitation

279

Generic structural element

Example

GREETING

A: Hello Optus Australia B: Hello B: Could you tell me what the time is in London? A: Do you mean at the moment? B: Yes A: Yes it’s 10AM B: OK thanks very much, you’ve been very helpful A: No problem A: Bye B: Bye

SERVICE REQUEST SERVICE ENQUIRY SERVICE COMPLIANCE CLOSE

GOODBYE

include the aberrant moves of unrelated elements, incomplete or inappropriate elements, and repetition of elements. This way of examining service encounter interactions has proved to be a sensitive measure of everyday interactions as it diﬀerentiates TBI participants’ interactions from control participants’ interactions. As well as providing direction for the clinician in designing treatment for the person with TBI, we have shown that it can be used successfully in training communication partners. The police oﬃcers who underwent training quickly grasped the notion of an interaction being divided into chunks, and therefore knew the expected structure of their service encounter interactions. In the case of a person with TBI deviating from this, the police oﬃcer could then use a range of conversational strategies to prompt the person with TBI back to the task, and therefore promote a productive, timely interaction.

Conclusion Improving the communication of a person with TBI is neither straightforward nor easy. Similar to treatment approaches for people with aphasia, therapy has traditionally focused on improving the person’s ability to get their message across, usually to a clinician in a clinic room. There are a number of problems with this approach, however, including the fact that the most common communication activity for people with brain injury, and for those who have not had a brain injury, is social chat. This interactional task is diﬃcult to replicate in the clinical setting because of the power imbalance inherent in the clinical interaction, and the probable cultural and gender diﬀerences between the clinician and the patient. A possible solution to this dilemma is to include other communication partners in treatment, and to train them to facilitate the person’s everyday interactions. One proven way to measure this process is generic structure potential analysis. Training communication partners is a relatively novel approach in the ﬁeld of TBI, but oﬀers a great deal of promise in engaging the person with brain injury in a socially valid treatment

280

Togher

process designed to improve social participation, community integration, quality of life and overall satisfaction. There is also potential for this approach to be adapted for use with communication partners of people with aphasia; an avenue that Chris Code and I hope to pursue in the future.

References Bond, F., & Godfrey, H. P. D. (1997). Conversation with traumatically brain-injured individuals: A controlled study of behavioural changes and their impact. Brain Injury, 11 (5), 319–329. Booth, S., & Perkins, L. (1999). The use of conversation analysis to guide individualized advice to carers and evaluate change in aphasia: A case study. Aphasiology, 13 (4–5), 283–303. Booth, S., & Swabey, D. (1999). Group training in communication skills for carers of adults with aphasia. International Journal of Language and Communication Disorders, 34 (3), 291–309. Bourgeois, M., Dijkstra, K., Burgio, L., & Allen-Burge, R. (2001). Memory aids as an alternative and augmentative communication strategy for nursing home residents with dementia. Alternative and Augmentative Communication, 17 (3), 196–210. Burgio, L., Allen-Burge, R., Roth, D., Bourgeois, M., Dijkstra, K., Gerstle, J., et al. (2000). Come talk with me: Improving communication between nursing assistants and nursing home residents during care routines. The Gerontologist, 41 (4), 449–460. Byng, S., Pound, C., & Parr, S. (2000). A framework for therapy interventions. In I. Papathanasiou (Ed.), Acquired neurological communication disorders: A clinical perspective. London: Whurr. Cannizzaro, M. S., & Coelho, C. A. (2002). Treatment of story grammar following traumatic brain injury: A pilot study. Brain Injury, 16 (12), 1065–1073. Carnevale, G. (1996). Natural-setting behavior management for individuals with traumatic brain injury: Results of a three-year caregiver training program. Journal of Head Trauma Rehabilitation, 11 (1), 27–38. Cicerone, K. (2004). Participation as an outcome of traumatic brain injury rehabilitation. Journal of Head Trauma Rehabilitation, 19 (6), 494–501. Cicerone, K., Dahlberg, C., Kalmar, K., Langenbahn, D., Malec, J., Bergquist, T., et al. (2000). Evidence-based cognitive rehabilitation: Recommendations for clinical practice. Archives of Physical Medicine and Rehabilitation, 81, 1596–1615. Coelho, C. A., DeRuyter, F., & Stein, M. (1996). Treatment eﬃcacy: Cognitivecommunicative disorders resulting from traumatic brain injury. Journal of Speech and Hearing Research, 39 (5), S5–S17. Cramon, D., & Cramon, G. M.-v. (1992). Reﬂections on the treatment of brain injured patients suﬀering from problem solving disorders. Neuropsychological Rehabilitation, 2, 207–230. Eggins, S., & Slade, D. (1997). Analysing casual conversation. London: Cassell. Elsass, L., & Kinsella, G. (1987). Social interaction after severe closed head injury. Psychological Medicine, 17, 67–78. Farrell, A. D., Rabinowitz, J. A., Wallander, J. L., & Curran, J. P. (1985). An evaluation of two formats for the intermediate-level assessment of social skills. Behavioural Assessment, 7, 155–171.

Traumatic brain injury rehabilitation

281

Flanagan, S., McDonald, S., & Togher, L. (1995). Evaluating social skills following traumatic brain injury: The BRISS as a clinical tool. Brain Injury, 9 (4), 321–338. Frattali, C. (1993). Perspectives on functional assessment: Its use for policy making. Disability and Rehabilitation, 15, 1–9. Halliday, M. A. K. (1994). An introduction to functional grammar (2nd ed.). London: Edward Arnold. Hartley, L. L. (1995). Cognitive-communicative abilities following brain injury: A functional approach. San Diego, CA: Singular. Hasan, R. (1985). Language, context, and text: Aspects of language in a social-semiotic perspective. Victoria: Deakin University Press. Helﬀenstein, D. A., & Wechsler, F. S. (1982). The use of Interpersonal Process Recall (IPR) in the remediation of interpersonal and communication skill deﬁcits in the newly brain-injured. Clinical Neuropsychology, 4, 139–143. Holland, D., & Shigaki, C. (1998). Educating families and caretakers of traumatically brain injured patients in the new health care environment: A three phase model and bibliography. Brain Injury, 12 (12), 993–1009. Kagan, A., Black, S., Duchan, J., Simmons-Mackie, N., & Square, P. (2001). Training volunteers as conversational partners using “Supported Conversation with Adults with Aphasia” (SCA): A controlled trial. Journal of Speech, Language and Hearing Research, 44, 624–638. Knight, R., Devereux, R., & Godfrey, H. (1998). Caring for a family member with traumatic brain injury. Brain Injury, 12 (6), 467–481. Larkins, B., Worrall, L., & Hickson, L. (1999). Everyday communication activities of individuals with traumatic brain injury. Asia Paciﬁc Journal of Speech Language and Hearing, 4, 183–191. Lock, S., Wilkinson, R., & Bryan, K. (2001). Supporting partners of people with aphasia in relationships and conversation. Oxford, UK: Speechmark. Lyon, J., Cariski, D., Keisler, L., Rosenbek, J., Levine, R., Kumpula, J., et al. (1997). Communication partners: Enhancing participation in life and communication for adults with aphasia in natural settings. Aphasiology, 11, 693–708. MAA (1998). Training needs of attendant carers. Sydney: Motor Accidents Authority. Marsh, N. V., Kersel, D. A., Havill, J. H., & Sleigh, J. W. (1998). Cargiver burden at 1 year following severe traumatic brain injury. Brain Injury, 12 (12), 1045–1059. Medd, J., & Tate, R. (2000). Evaluation of an anger management therapy programme following acquired brain injury: A preliminary study. Neuropsychological rehabilitation, 10 (2), 185–201. Newhoﬀ, M., Bugbee, J. K., & Ferreira, A. (1981). A change of PACE: Spouses as treatment targets. In R. H. Brookshire (Ed.), Clinical aphasiology (Vol. 11, pp. 234–243). Minneapolis, MN: BRK Publishers. Pound, C., Parr, S., Lindsay, J., & Woolf, C. (2000). Beyond aphasia: Therapies for living with communication disability. Oxford, UK: Speechmark. Ripich, D., Ziol, E., Fritsch, T., & Durand, E. (1999). Training Alzheimer’s disease caregivers for successful communication. Clinical Gerontologist, 21 (1), 37–53. Schiﬀrin, D. (1987). Discourse markers. Cambridge, UK: Cambridge University Press. Simmons, N. N., Kearns, K. P., & Potechin, G. (1987). Treatment of aphasia through family member training. In R. H. Brookshire (Ed.), Clinical aphasiology (Vol. 17, pp. 106–116). Minneapolis, MN: BRK Publishers. Simmons-Mackie, N. (2000). Social approaches to the management of aphasia. In

282

Togher

L. Worrall & C. Frattali (Eds.), Neurogenic communication disorders: A functional approach (pp. 162–187). New York: Thieme. Smith, L., & Parr, S. (1986). Therapists’ assessment of functional communication in aphasia. Bulletin of the College of Speech Therapists, 409, 10–11. Snow, P., Douglas, J., & Ponsford, J. (1995). Discourse assessment following traumatic brain injury: A pilot study examining some demographic and methodological issues. Aphasiology, 9 (4), 365–380. Tate, R. (1987). Behaviour management techniques for organic psychosocial deﬁcit incurred by severe head injury. Scandinavian Journal of Rehabilitation Medicine, 19, 19–24. Tate, R. L. (1999). Executive dysfunction and characterological changes after traumatic brain injury: Two sides of the same coin? Cortex, 35 (1), 39–55. Tate, R. L., Lulham, J. M., Broe, G. A., Strettles, B., & Pfaﬀ, A. (1989). Psychosocial outcome for the survivors of severe blunt head injury: The results from a consecutive series of 100 patients. Journal of Neurology, Neurosurgery, and Psychiatry, 52, 1128–1134. Tate, R., McDonald, S., & Lulham, J. (1998). Incidence of hospital-treated traumatic brain injury in an Australian community. Australian and New Zealand Journal of Public Health, 22 (4), 419–423. Togher, L. (2000). Giving information: The importance of context on communicative opportunity for people with traumatic brain injury. Aphasiology, 14 (4), 365–390. Togher, L., & Grant, S. (2001). Communication training program for carers. Sydney, Australia: University of Sydney. Togher, L., & Hand, L. (1998). Use of politeness markers with diﬀerent communication partners: An investigation of ﬁve subjects with traumatic brain injury. Aphasiology, 12 (7/8), 491–504. Togher, L., & Hand, L. (1999). The macrostructure of the interview: Are traumatic brain injury interactions structured diﬀerently to control interactions? Aphasiology, 13 (9–11), 709–723. Togher, L., Hand, L., & Code, C. (1996). A new perspective in the relationship between communication impairment and disempowerment following head injury in information exchanges. Disability and Rehabilitation, 18 (11), 559–566. Togher, L., Hand, L., & Code, C. (1997a). Analysing discourse in the traumatic brain injury population: Telephone interactions with diﬀerent communication partners. Brain Injury, 11 (3), 169–189. Togher, L., Hand, L., & Code, C. (1997b). Measuring service encounters in the traumatic brain injury population. Aphasiology, 11 (4/5), 491–504. Togher, L., McDonald, S., Code, C., & Grant, S. (2004). Training communication partners of people with traumatic brain injury: A randomised controlled trial. Aphasiology, 18 (4), 313–335. Ventola, E. (1979). The structure of casual conversation in English. Journal of Pragmatics, 3, 267–298. Wallace, C., Bogner, J., Corrigan, J., Clinchot, D., Mysiw, W., & Fugate, L. (1998). Primary caregivers of persons with brain injury: Life changes 1 year after injury. Brain Injury, 12 (6), 483–493. Wallander, J. L., Conger, A. J., & Cohen Conger, J. (1985). Development and evaluation of a behaviourally referenced rating system for heterosocial skills. Behavioural Assessment, 7, 137–153.

Traumatic brain injury rehabilitation

283

WHO (2001). The international classiﬁcation of functioning, disability and health – ICF. Geneva: WHO. Wilkinson, R., Bryan, K., Lock, S., Bayley, K., Maxim, J., Bruce, C. et al. (1998). Therapy using conversation analysis: Helping couples adapt to aphasia in conversation. International Journal of Language & Communication Disorders, 33 (Suppl), 144–149. Worrall, L., & Yiu, E. (2000). Eﬀectiveness of functional communication therapy by volunteers for people with aphasia following stroke. Aphasiology, 14 (9), 911–924. Ylvisaker, M. (1998). Traumatic brain injury rehabilitation: Children and adolescents. Boston, MA: Butterworth-Heinemann. Ylvisaker, M., Feeney, T. J., & Urbanczyk, B. (1993). Developing a positive communication culture for rehabilitation: Communication training for staﬀ and family members. In C. J. Durgin, N. D. Schmidt, & L. J. Fryer (Eds.), Staﬀ development and clinical intervention in brain injury rehabilitation (pp. 57–81). Gaithersburg, MD: Aspen.

19 The future of our knowledge about communication impairments following a right-hemisphere lesion Yves Joanette, Maud Champagne-Lavau, Karima Kahlaoui and Bernadette Ska The question of the asymmetrical nature of the neurobiological bases of human communication has been fascinating researchers for more than a century. The initial step in this discovery revealed that, in right-handers, the essence of the cerebral representation of language was conﬁned to the left hemisphere. The second act was to come later in the twentieth century when some clever clinical observations were reported by certain visionaries – such as Eisenson (1962), Weinstein (1964) and Critchley (1962) – who raised the possibility that a lesion to the right hemisphere might also interfere with some aspects of communicative abilities. Since that time, the fact has not been challenged: the right hemisphere undeniably contributes in some way to the ability we have to communicate with others, and when the right hemisphere is lesioned, this ability can be altered in various ways. The ﬁrst book to capture, summarize and critique the diﬀerent observations suggesting that the right hemisphere makes such a contribution to communicative abilities, as well as to a patient’s recovery after aphasia, was written by another visionary, Professor Chris Code. In 1987, Professor Code published a monograph entitled Language, aphasia and the right hemisphere. In that book, he provided a unique overview of the diﬀerent sources of observations addressing the question of the right hemisphere’s participation in language. Although the summary of these observations was in itself a ﬁrst, Professor Code did not content himself with a synthesis of the then available knowledge. This book also makes unique theoretical statements and proposals about the nature of the right hemisphere’s contribution to language and communication, and the future studies needed to address these issues. The goal of this chapter is twofold. First, 20 years after the publication of Professor Code’s monograph, a summary of current knowledge of the contribution the right hemisphere of right-handers makes to communicative abilities is oﬀered. Then, some future research directions are discussed with reference to those delineated by Professor Code in his 1987 monograph.

Communication impairments following a right-hemisphere lesion

285

Current status of our knowledge of communication impairments after a right-hemisphere lesion The occurrence of a right-hemisphere (RH) lesion can interfere with communicative abilities at diﬀerent levels of human communication. Apart from its impact on the processing of emotional prosody and aspects of linguistic prosody that require the processing of large time-scales (e.g., modalities) the impact of an RH lesion is essentially semantic in the broadest sense of the term. This includes the semantic processing of words and discourse, as well as pragmatics. Semantic processing of words The occurrence of an RH lesion can interfere with word production as RH-lesioned individuals may exhibit poorer performance on picture-naming tasks (Joanette & Brownell, 1990) and verbal ﬂuency tasks (Cardebat, Doyon, Puel, Goulet, & Joanette, 1990; Goulet, Joanette, Sabourin, & Giroux, 1997; Joanette & Goulet, 1986; Koivisto & Laine, 1999). Studies have consistently shown that the verbal ﬂuency of RH-lesioned individuals is impaired, mostly when the production criterion was semantic in nature as opposed to literal or orthographic. This result emphasizes the fact that the RH’s contribution to the production of words has to do with word access in semantic memory more than the production of their morphological or phonological form. A number of converging clues – including priming studies (Gagnon, Goulet, & Joanette, 1994) and time-course analyses of verbal ﬂuency tasks (Joanette, Goulet, & Le Dorze, 1988) – suggest that this deﬁcit does not reﬂect primarily an impairment of the semantic representation itself, but rather a deﬁciency aﬀecting access to the semantic representation, as is the case in aphasia. One aspect of verbal ﬂuency impairment that has been suggested to be speciﬁc to RH-lesioned individuals is a certain tendency to produce words that are “unexpected,” that is, less prototypical of their semantic category (LeBlanc & Joanette, 1996). If this is conﬁrmed, it would mean that a lesion to the RH not only interferes with normal access to the lexicon, but also has a speciﬁc impact on the nature of the activation of the semantic network, favoring the activation of less central, more peripheral exemplars of a given semantic category. A larger number of studies have addressed the nature of the impairment RH-lesioned individuals exhibit when processing the meaning of words. Again, the quest for the speciﬁc nature of the semantic impairment following an RH lesion is still ongoing. At this point, a number of potential candidates have been raised: •

Impairments of the ability to process the metaphorical alternative meaning of words (Brownell, Simpson, Bihrle, Potter, & Gardner, 1990; Gagnon, Goulet, Giroux, & Joanette, 2003): this feature was one of the

286

•

Joanette et al. ﬁrst to be mentioned as a putative characteristic of an RH lesion. The question regarding the exact nature of this deﬁcit remains a matter of debate. Future studies should try to explore the impact of RH lesions with reference to the depth/nature of the semantic activation of each hemisphere. According to Beeman (1998) and Chiarello (1998), the right hemisphere sustains more shallow, less focal, coarser semantic dimensions of words. This proposal has direct consequences on the nature of the semantic impairments likely to follow an RH lesion that still need to be investigated. However, a major loophole for the proponents of such a speciﬁc impairment resides in the fact that, most of the time, the polysemic words that appear to be most aﬀected in RH-lesioned individuals are also those that are the most demanding in terms of cognitive resources (Monetta & Joanette, 2001, 2003). Consequently, the speciﬁcity of such impairments still needs to be fully demonstrated in contrast to a more general impact of an RH lesion on the overall pool of cognitive resources or access; in this context, an RH lesion would interfere with language’s most complex dimensions. Other possible candidates for a speciﬁc impairment of word semantics after an RH lesion concern the nature of the semantic relationships to be aﬀected. Inspired by the initial proposal by Drew (1987), Nocentini, Goulet, Roberts, and Joanette (2001) provided only partial support for the idea that an RH lesion may have more of an impact on inter- rather than intra-conceptual relationships. Even if it were conﬁrmed, such a speciﬁc constraint on the nature of the semantic relationships aﬀected might reﬂect a more general characteristic of impairments of semantic relationships after an RH lesion. For example, Burgess and Simpson (1988) and Koivisto (1997) suggest that the activation spreading in the semantic network supported by RH-based neural networks appears to operate over a larger time-scale, in more remote areas of the network, and on a smaller number of nodes/items. If this is the case, then predictions could be made regarding the speciﬁcity of the impact of an RH lesion on the nature of the resulting impairments of semantic relationships.

Semantic processing of discourse Discourse production and comprehension require a set of cognitive contributions that make it possible to extract/encode the important pieces of information in a narrative, for example, and to generate the relevant and necessary links/inferences that make it possible to grasp the gist of a story and its situational model. An RH lesion can interfere with many of these levels. Typically, narrative discourse production after an RH lesion includes impoverished informative content, a tendency to digress, unexpected shifts towards a tangential topic, and some level of incoherence reﬂecting a lack of, or inadequate, relation markers. Discourse comprehension may be aﬀected by the diﬃculties RH-lesioned individuals have with making proper inferences,

Communication impairments following a right-hemisphere lesion

287

extracting the macro-structure of the narrative and, above all, revising the situational model when required by the story (e.g., Delis, Wapner, Gardner, & Moses, 1983; Hough, 1990; Huber & Gleber, 1982; Schneiderman, Murasugi, & Saddy, 1991; Stemmer & Joanette, 1998). Obviously, the RH’s contribution to discourse processing is not exclusive. Such a complex and high-level ability depends on numerous basic cognitive abilities, including inference making, inhibition, cognitive ﬂexibility, verbal working memory, and so on. The reason why RH-lesioned individuals frequently appear to be impaired in their discourse abilities may reﬂect at least two things. First, the presence of discourse impairments in RH-lesioned individuals is not overshadowed by more basic syntactic or phonological impairments, as it is in aphasia. Second, it could be the case that RH-based neural networks are important for sustaining a number of cognitive processes (e.g., inference making) that are particularly critical for discourse processing. This possibility does not preclude the possibility, however, that left-hemisphere-based neural networks are also necessary for some other important cognitive processes. Consequently, both left- and right-hemisphere lesions would interfere with discourse abilities, though isolated discourse impairments would be more frequent following an RH lesion. The cognitive processes that are sustained more by the neural networks present in the right rather than the left hemisphere still need to be identiﬁed. Processing communicative intent: Pragmatics The ability to encode or decode communicative intent is a very important dimension of interpersonal communication. Indeed, in natural communication it is frequently the case that not all the relevant information is provided, a situation referred to as non-literal language. Consequently, interlocutors constantly have to rely on their knowledge of the world, or on the immediate context, to fully process a speaker’s communicative intent. In doing so, human beings seem to stimulate interest in the act of communicating with others, since providing each and every piece of information overtly tends to make communication boring; this is the case when automated devices attempt to oﬀer pseudo-natural communicative environments (e.g., phone answering systems). In any case, ever since the ﬁrst systematic descriptions of communicative impairments following an RH lesion, it has been reported that RH-lesioned individuals display improper and/or unexpected communication behavior when engaged in everyday natural communication (e.g., Gardner, Brownell, Wapner, & Michelow, 1983). These deﬁcits can best be described as aﬀecting the pragmatic dimension of communication. Deﬁcits aﬀecting many aspects of non-literal language have thus been reported, such as indirect speech acts, humor, sarcasm, and the ability to take shared knowledge into account (e.g., Chantraine, Joanette, & Ska, 1998; Foldi, 1987; Gardner, Ling, Flamm, & Silverman, 1975; Kaplan, Brownell, Jacobs, & Gardner, 1990; Stemmer, Giroux, & Joanette, 1994; Vanhalle, Lemieux,

288

Joanette et al.

Joubert, Goulet, Ska, & Joanette, 2000; Wapner, Hamby, & Gardner, 1981; Winner, Brownell, Happe, Blum, & Pincus, 1998). The reasons why such a pragmatic deﬁcit may occur following RH damage are still unclear. It is, however, quite clear that there is no such thing as a speciﬁc “pragmatic cognitive module” that is impaired in those cases. Rather, an impairment of one or more known cognitive processes may result in diﬃculties processing the communicative intent. Thus, Champagne and Joanette (2004) suggest that the pragmatic deﬁcit in RH-lesioned individuals is probably determined by some lack of inhibition, whereas similar pragmatic deﬁcits in schizophrenic individuals reﬂect a lack of mental ﬂexibility. Here again, given the cognitive demand of pragmatic abilities, it might be the case that part of the picture in RH-lesioned individuals is related to a lack of cognitive resources or ability to access them. Cues favoring this possibility have been provided by Monetta and Joanette (2003), who showed that normal young individuals given a pragmatic task in a limited resource context (dual task) exhibited patterns of performance similar to those frequently found in RH-lesioned individuals. Consequently, at this level as at other levels, it is still not known whether an RH lesion has a speciﬁc or a nonspeciﬁc impact on the ability to process the pragmatic aspects of language and communication. The answer will probably reﬂect both possibilities, but the underlying cognitive impairments have still to be identiﬁed (McDonald, 2000).

Clinical management of individuals with communicative impairments following an RH lesion The clinical management of individuals with communicative impairments following an RH lesion is still a new ﬁeld of practice for speech-language pathologists and other members of interdisciplinary teams in acute or rehabilitation-oriented health centers. Though many recent articles on the subject insist on the importance of such clinical management (e.g., Myers, 1999; Tompkins, 1995), there is still a lack of clinical descriptions and of evaluation tools and management strategies. Professor Chris Code himself insisted on the importance of this aspect in his 1987 monograph. Our group’s experience in this respect has further convinced us of the relevance of such clinical management, and the importance of providing those tools and strategies. One very important question has to do with the incidence and clinical proﬁle of communicative impairments among individuals suﬀering from RH lesions. It has to be stressed that, as with left-hemisphere-lesioned individuals, not all RH-lesioned individuals suﬀer from communicative impairments. According to our studies, the proportion of individuals with RH lesions who exhibit communicative impairments is between 50% and 80% (Côté, Payer, Giroux, & Joanette, 2006; Joanette, Goulet, & Daoust, 1991). Moreover, when present, these impairments do not always aﬀect all the possible dimensions of communication described in the ﬁrst part of this chapter. Indeed, not

Communication impairments following a right-hemisphere lesion

289

only do RH-lesioned individuals with communication impairments not all exhibit the same pattern of impairment, but there are double-dissociations whereby diﬀerent individuals exhibit patterns of clinical impairment that are the reverse of each other (Joanette et al., 1991). These pieces of information are crucial for the development of a clinical management strategy. Indeed, it follows that RH-lesioned individuals suspected to exhibit communication impairments must be evaluated in order to describe the nature of the clinical proﬁle in each case, as is the case for left-hemisphere-lesioned individuals suspected of having aphasia. The exact clinical description of the impaired dimensions of communication is extremely important in that it allows for crucial counseling with the aﬀected individual and his or her family members. Indeed, despite the fact that these communication impairments are the cause of a major communicative disability, they are poorly recognized by the family and the individual himself or herself since they aﬀect dimensions of communication that are themselves poorly recognized (e.g., discourse abilities, pragmatic abilities). Since the publication of Professor Code’s book, a number of clinical batteries have been proposed in order to help clinicians to conduct such an evaluation. Most of these batteries, however, focus on the evaluation of cognitive impairments, such as neglect, which may accompany communicative impairments in RH-lesioned individuals. One of the most interesting batteries published in English to date is that of Bryan (1988). The proposed tasks address most of the aspects of communication that can be impaired after an RH lesion. More recently, our group has published such a battery in French (Joanette, Ska, & Côté, 2004), which incorporates the most recent theoretical developments in the ﬁeld. Adaptations are being ﬁnalized in Portuguese, Spanish and Italian; an English version prepared with the collaboration of Leonard LaPointe and his team will soon be available with norms. Although the question of the evaluation of the communication impairments that can follow an RH lesion is starting to penetrate the ﬁeld of speechlanguage pathology, that of rehabilitation strategies is still in its infancy. In a recent review, Moix and Côté (2004) report that only a small proportion of speech-language pathologists in rehabilitation centers in Québec engage in systematic rehabilitation strategies with individuals suﬀering from an RH communication impairment. Among the few who do, dissatisfaction is common as there is no evidence-based practice in this area. Both Tompkins (1995) and Myers (1999) suggest some possible rehabilitation strategies, but the ﬁeld remains to be investigated, and systematic observations are still required.

Future directions, now and then In his 1987 monograph, Chris Code identiﬁed a number of areas in which it was felt that the ﬁeld of RH and language would evolve. Some of these predictions became reality, whereas a number of subsequent developments had not been predicted. The following is a selection of topics largely inspired

290

Joanette et al.

by the conclusion of the 1987 monograph, and discussed with reference to future directions as we currently perceive them. The impact of interindividual diﬀerences The presence of interindividual diﬀerences, which modulate the nature of the RH’s contribution to verbal communication in a given individual, was rightly pointed at by Professor Code in 1987. Since then, it has been demonstrated that a number of factors can impact on the nature of the RH’s contribution. Apart from the classical factors linked to genetics (e.g., familial history of left-handedness) or to the nature of the exposure to language (e.g., characteristics of the spoken or written language), Professor Code already foresaw the importance of aging. Indeed, it is now well known that age represents a factor that signiﬁcantly inﬂuences the nature of interhemispheric cooperation and, hence, the RH’s contribution to communication. Summarizing the literature and his own personal observations, Roberto Cabeza (2002) introduced the HAROLD (Hemispheric Asymmetry Reduction in Older Adults) model, which essentially describes the presence of an age-related functional dedifferentiation in the respective contributions of the left and right hemispheres for abilities such as working memory, episodic memory, and inhibition control. Although Cabeza (2002) did not directly report data involving language behavior, the phenomenology described is presumed to be universal. In other words, the neural network subserving a given ability is more widespread over both hemispheres in older adults. This appears to be true only when behavioral performance is maintained at a good level. Older adults with decreased performance would not exhibit this pattern. If this phenomenon is also found for components of communication with which the RH is involved, it would mean that the impact of an RH lesion could be expected to be proportionally greater in older adults. Recently, our group has provided preliminary data using language tasks that could force a reformulation of the HAROLD phenomenology for the neural bases of language. Indeed, using a word semantic category judgment task, Ouellet-Plamondon, Monchi, Senhadji, and Joanette (2006) have shown that the reorganization of neural activations with age not only follows a hemispheric dediﬀerentiation trend, but also – and most markedly – evolves along an anterior–posterior axis. In other words, in order to maintain performance with age, the neural networks necessary for the semantic processing of words are much more posterior, and somewhat more bilateral. Again, if this is conﬁrmed, it would imply not only that RH lesions would be more frequently associated with word semantic impairments with age, but that posterior lesions would probably have more impact than anterior ones. These predictions must, of course, be validated. However, one fact remains: as Professor Code predicted in 1987, age is a factor that probably inﬂuences the nature and extent of communicative impairments after an RH lesion.

Communication impairments following a right-hemisphere lesion

291

The nature of the right hemisphere’s contribution Another comment in the conclusion of Professor Code’s 1987 monograph has to do with the basic question regarding the association between the right hemisphere and communication. As Professor Code rightly wrote (p. 169), “the question concerns the nature and the extent of that involvement,” and not whether or not the RH does contribute to communication. In 1987, Professor Code stated that there was no satisfying answer to both aspects of the question; since then, the situation has certainly evolved, but not very much. There is still debate as to whether the RH’s contribution to communication is in terms of speciﬁc basic cognitive processes that characterize RH-based neural networks, within an interhemispheric cooperation model, or whether this contribution should be conceived more in terms of a source of possible quantitative addition to the pool of neural networks necessary to process some of the more complex dimensions of communication. As is frequently the case when the human mind tries to polarize the answer to a complex question around two opposite points, the reality probably falls somewhere in the middle; in other words, both mechanisms are probably involved, with diﬀerent representations according to speciﬁc components of communication. For instance, as brieﬂy alluded to earlier, the semantic representations in the brain’s neural networks that appear to be sustained on the right side of the brain tend to be characterized diﬀerently, both quantitatively and qualitatively. There is suﬃcient convergence regarding what is suspected to be the nature of the semantic representations (shallow, less focal, coarse semantic representation; Beeman, 1998; Chiarello, 1998) as well as the speciﬁc types of semantic relationships (e.g., interconceptual relationships; Drew, 1987; Nocentini et al., 2001) and the time-course of activation (Koivisto, 1997), to support the idea that the RH’s neural networks make a speciﬁc contribution to the semantic processing of words, and maybe beyond. At the same time, there is also converging evidence at the word level (e.g., Monetta & Joanette, 2001, 2003) as well as at the pragmatic level (e.g., Champagne & Joanette, 2004) to support the idea that the involvement of the RH’s neural networks could also be viewed as a general contribution to a pool of cognitive resources needed to handle the most complex, demanding components of communication. Consequently, we are still left with the same question that Professor Code raised 20 years ago, although a number of converging lines of evidence suggest that the RH’s contribution is both qualitative and quantitative. The advent of new methodologies and techniques Without taking too much of a risk, Professor Code also predicted in his 1987 work that future methodologies and techniques would contribute to diminishing our uncertainty about the RH’s role in communication. He was, of course, quite right. Over the last two decades, functional neuroimagery has

292

Joanette et al.

revolutionized the ﬁeld of cognitive neuroscience of language. Many innovative techniques are now contributing to our knowledge of the extent and nature of the RH’s contribution to communication. Some of these techniques are especially good at spatial resolution and the identiﬁcation of loci of activation (e.g., PET, fMRI); others contribute essentially to the time-line of processing, given their temporal resolution (e.g., ERPs); while still others appear to be able to contribute to both spatial and temporal resolution (MEG, Near Infrared Spectroscopy optical imaging or NIRS/OI). Each of these techniques has its limitations, and the quest for convergence is important. Functional imaging initially provided converging evidence in favor of a speciﬁc role for RH-based neural networks in the processing of metaphoric utterances (e.g., Bottini, Corcoran, Sterzi, & Schenone, 1994; Seger, Desmond, Glover, & Gabrieli, 2000; St. George, Kutas, Martinez, & Sereno, 1999). Contrary to Bottini and colleagues (1994), who reported right lateral temporal and frontal PET activation during the processing of metaphors, Rapp, Leube, Erb, Grodd, and Kircher (2004) conclude that the RH’s involvement may be neither essential nor speciﬁc for metaphor understanding. Like Lee and Dapretto (2006), Rapp and colleagues (2004) suggested that the RH’s involvement in the processing of metaphorical language might reﬂect primarily the increased complexity of non-literal language rather than an RH specialization in metaphor comprehension. In general, the contribution made by modern neuroimagery has been limited by the fact that many of the components of communication for which the RH is suspected to make a speciﬁc contribution are not particularly easy to study with these techniques. Indeed, discourse processing and pragmatic abilities have been much less studied than the processing of words or other unitary events. Moreover, the setting in which data are acquired (e.g., the noise and spatial constraints of fMRI) does not allow the use of naturalistic contexts. Emerging techniques such as NIRS/OI already appear to be ﬁlling the gap between the spatial and temporal resolution needed, and the ability to allow for a noise-free, quasi physical-constraint-free setting compatible with more naturalistic communication situations. For example, Scherer, Ska, and Joanette (2006) have been able to study narrative discourse abilities, trying to disentangle the nature of interhemispheric cooperation for distinct components such as the micro- and macro-propositional levels and the situational model. Their results indicate that the RH’s contribution is optimal at the macro-propositional level and for the appreciation of a situational model. It can therefore be concluded that current neuroimaging techniques are contributing to identifying the nature and extent of the RH’s contribution to semantic processing. The introduction of new data acquisition techniques should not overshadow the immense change that has already taken place in these techniques, which now allows us to address such fundamental questions as the role of RH-based networks in global cerebral connectivity for a given communicative process or ability. Indeed, functional neuroimaging data can now be

Communication impairments following a right-hemisphere lesion

293

analyzed in such a way as to allow for the exploration of the functional networks associated with a given ability or task. Those networks are referred to as having functional connectivity or eﬀective connectivity, depending on whether or not they include causality indications. The type of complementary information they oﬀer is crucial to our understanding of the integration of RH-based neural networks within a more general brain functional network. For example, although it has been known for some time that RH activation is reported when a subject is engaged in the semantic processing of words, it was only recently that evidence was provided of the integration of the RH activations into a more general cerebral network involving both right- and left-hemisphere-based areas (Walter, Jbabdi, Marrelec, Benali, & Joanette, 2006). In sum, Professor Code (1987) was right in anticipating that new techniques and methodologies would help us understand the nature and the extent of the RH’s contribution to communication. Not only has this occurred over the last two decades, but it has allowed us to situate the question regarding the RH exactly where it should be, namely at the level of a contribution nested within a more general question regarding the nature of interhemispheric cooperation for the diﬀerent components of cognition. The unpredicted changes Although it commands admiration and respect, Professor Code’s 1987 monograph manifestly did not predict all the developments that have occurred since its publication. One of the unpredicted changes has to do with the discussion concerning what constitutes a linguistic component of communication and what is extralinguistic [sic]. Indeed, since the ﬁrst descriptions by pioneers such as Eisenson in 1962, there has been a malaise aﬀecting some of the concepts of language. Eisenson (1959), for example, used the concept of super-ordinary aspects of language to refer to subtle word-processing impairments for which he did not have the appropriate conceptual tools and theoretical background to describe adequately. It should be kept in mind that the early 1960s were also the years when the ﬁrst writings were published on what was to become pragmatics, including the concept of direct and indirect speech acts (e.g., Austin, 1962; Searle, 1969). In the 1960s, language was still considered to be limited to certain speciﬁc components, ranging from articulation to morphosyntactic processes. These components were more or less the same in the 1980s as they had been a century before, when the ﬁrst descriptions of aphasia following a left-hemisphere lesion were introduced and crystallized in a number of classical aphasia syndromes. Professor Code in 1987 was therefore still largely inﬂuenced by this long-standing tradition, as the mutual relationships between components such as pragmatics and language were not yet felt to be reconcilable. This is why he maintained the use of concepts such as linguistic and extralinguistic, since the components of language aﬀected by an RH lesion were not part of the traditional deﬁnition

294

Joanette et al.

of language. The 1990s saw a proliferation of research on pragmatics and its relationship with language. In 1999, a special issue of Brain and Language made it obvious that nontraditional components such as pragmatics were not to be considered as being above, beside or apart from language; for instance, Gibbs (1999) considers pragmatics to be an inherent component of language. Even Noam Chomsky, whose opinion is reported by Stemmer (1999) in the same special issue, states that “pragmatics must be a central component of any theory of language that aims to be comprehensive.” Consequently, it must be acknowledged that the concept of language has evolved somewhat since the birth of aphasiology in the late nineteenth century; it now includes a larger set of cognitive processes that, together, make verbal communication possible. In this context, some of us (e.g., Joanette & Ansaldo, 1999, 2000) think that the evolution of the concept of language, which now encompasses all components typically aﬀected following an RH lesion, requires a logical extension of the concept of aphasia. Indeed, given that the universal deﬁnition of aphasia refers to the notion of an acquired language impairment further to an acquired brain lesion – whatever its etiology, nature or localization – it follows that acquired language impairments further to an RH lesion constitute forms of aphasia that will have to be deﬁned with reference to the components of the revised concept of language. This will give the ﬁeld of speech-language pathology further arguments to convince health service providers to oﬀer clinical management to individuals with such impairments. The challenge of evaluating and identifying adaptive and rehabilitation strategies is not a small one; clinical research will have to address these issues in an evidence-based practice manner. In our view, there are no arguments for maintaining the exclusion of RH-lesion communicative impairments from the concepts of language and aphasia, other than arguments based on an a priori excluding deﬁnition. Thus concepts such as extralinguistic appear to be useless, as would be the introduction of equivalent concepts such as extramagnesic or extra-agnosic to refer to recently introduced cognitive concepts in the ﬁeld of memory or perception. This development was not expected by Professor Code in 1987, but will certainly ﬁnd a receptive ear nowadays.

Conclusion The role of the RH in everyday verbal communication and the impact of RH lesions on such abilities, were expertly summarized and predicted by Professor Code in his 1987 monograph. Professor Code delineated the future of the ﬁeld 20 years ago. His writings will remain an inspiration for a long time. In fact, the future lies partly in his inspired and perspicacious reﬂections and output.

References Austin, J. L. (1962). How to do things with words. Oxford, UK: Oxford University Press.

Communication impairments following a right-hemisphere lesion

295

Beeman, M. (1998). Coarse semantic coding and discourse comprehension. In M. Beeman & C. Chiarello (Eds.), Right hemisphere language comprehension: Perspectives from cognitive neuroscience (pp. 255–284). Mahwah, NJ: Lawrence Erlbaum Associates, Inc. Bottini, G., Corcoran, R., Sterzi, R., & Schenone, P. (1994). The role of the right hemisphere in the interpretation of ﬁgurative aspects of language: A positron emission tomography activation study. Brain, 117, 1241–1258. Brownell, H. H., Simpson, T. L., Bihrle, A. M., Potter, H. H., & Gardner, H. (1990). Appreciation of metaphoric alternative word meanings by left and right brain-damaged patients. Neuropsychologia, 28, 375–383. Bryan, K. L. (1988). Assessment of language disorders after right hemisphere damage. British Journal of Disorders of Communication, 23, 111–125. Burgess, C., & Simpson, G. (1988). Cerebral hemispheric mechanisms in the retrieval of ambiguous word meanings. Brain and Language, 33, 86–103. Cabeza, R. (2002). Hemispheric asymmetry reduction in older adults: The HAROLD model. Psychology and Aging, 17, 85–100. Cardebat, D., Doyon, B., Puel, M., Goulet, P., & Joanette, Y. (1990). Évocation lexicale formelle et sémantique chez des sujets normaux. Performances et dynamiques de production en fonction du sexe, de l’âge et du niveau d’étude. Acta Neurologica Belgica, 90, 207–217. Champagne, M., & Joanette, Y. (2004). Lack of inhibition could contribute to nonliteral language impairments in right-hemisphere-damaged individuals. Brain and Language, 91, 172–174. Chantraine, Y., Joanette, Y., & Ska, B. (1998). Conversational abilities in patients with right hemisphere damage. In M. Paradis (Ed.), Pragmatics in neurogenic communication disorders (pp. 21–32). Tarrytown, NY: Pergamon Press. Chiarello, C. (1998). On codes of meaning and the meaning of codes: Semantic access and retrieval within and between hemispheres. In M. Beeman & C. Chiarello (Eds.), Right hemisphere language comprehension: Perspectives from cognitive neuroscience (pp. 141–160). Mahwah, NJ: Lawrence Erlbaum Associates, Inc. Code, C. (1987). Language, aphasia and the right hemisphere. Chichester, UK: Wiley. Côté, H., Payer, M., Giroux, F., & Joanette, Y. (2006). Towards a description of clinical communication proﬁles following right brain damage. Poster presented at the World Federation of Neurology–Aphasia and Cognitive Disorders Research Group, Buenos Aires (Argentina), March 1–4. Critchley, M. (1962). Speech and speech-loss in relation to duality of the brain. In V. B. Mountcastle (Ed.), Interhemispheric relations and cerebral dominance (pp. 208–213). Baltimore, MD: Johns Hopkins Press. Delis, D. C., Wapner, W., Gardner, H., & Moses, J. A. (1983). The contribution of the right hemisphere to the organisation of paragraphs. Cortex, 19, 43–50. Drew, E. (1987). Qualitatively diﬀerent organizational structures of lexical knowledge in the left and right hemisphere. Neuropsychologia, 25, 419–427. Eisenson, J. (1959). Language dysfunctions associated with right brain damage. American Speech and Hearing Association, 1, 107. Eisenson, J. (1962). Language and intellectual modiﬁcations associated with right cerebral damage. Language and Speech, 5, 49–53. Foldi, N. S. (1987). Appreciation of pragmatic interpretations of indirect commands: Comparison of right and left hemisphere brain-damaged patients. Brain and Language, 31, 88–108.

296

Joanette et al.

Gagnon, J., Goulet, P., Giroux, F., & Joanette, Y. (2003). Processing of metaphoric and non-metaphoric alternative meanings of words after right- and left-hemispheric lesion. Brain and Language, 87, 217–226. Gagnon, J., Goulet, P., & Joanette, Y. (1994). Activation of the lexical-semantic system in right-brain-damaged right-handers. Linguistics and Cognitive Neuroscience, Linguistische Berichte, 6 (Special Issue), 33–48. 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 (pp. 169–191). New York: Academic Press. Gardner, H., Ling, P. K., Flamm, L., & Silverman, J. (1975). Comprehension and appreciation of humor in brain-damaged patients. Brain, 98, 399–412. Gibbs, R. W. (1999). Interpreting what speakers say and implicate. Brain and Language, 68, 466–485. Goulet, P., Joanette, Y., Sabourin L., & Giroux, F. (1997). Word ﬂuency after a right-hemisphere lesion. Neuropsychologia, 35, 1565–1570. Hough, M. S. (1990). Narrative comprehension in adults with right and left hemisphere brain damage: Theme organisation. Brain and Language, 38, 253–277. Huber, W., & Gleber, J. (1982). Linguistic and nonlinguistic. Brain and Language, 16, 1–18. Joanette, Y., & Ansaldo, A. I. (1999). Clinical note: Acquired pragmatic impairments and aphasia. Brain and Language, 68, 529–534. Joanette, Y., & Ansaldo, A. I. (2000). The ineluctable and interdependent evolution of the concepts of language and aphasia. Brain and Language, 71, 106–109. Joanette, Y., & Brownell, H. H. (1990). Discourse ability and brain damage: Theoretical and empirical perspectives. New York: Springer-Verlag. 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., & 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., & Le Dorze, G. (1988). Impaired word naming in right braindamaged right-handers. Error types and time-course analyses. Brain and Language, 34, 1, 54–64. Joanette, Y., Ska, B., & Côté, H. (2004). Protocole Montréal d’Évaluation de la Communication. Isbergues, France: Ortho Édition. Kaplan, J. A, Brownell, H. H, Jacobs, J. R., & Gardner, H. (1990). The eﬀects of right hemisphere damage on the pragmatic interpretation of conversational remarks. Brain and Language, 38, 315–333. Koivisto, M. (1997). Time course of semantic activation in the cerebral hemispheres. Neuropsychologia, 35, 497–504. Koivisto, M., & Laine, M. (1999). Strategies of semantic categorization in the cerebral hemispheres. Brain and Language, 66, 341–357. Le Blanc, B., & Joanette, Y. (1996). Unconstrained oral naming in left- and righthemisphere-damaged patients: An analysis of naturalistic semantic strategies. Brain and Language, 55, 1, 42–45. Lee, S. S., & Dapretto, M. (2006). Metaphorical vs. literal word meanings: FMRI evidence against a selective role of the right hemisphere. NeuroImage, 29, 536–544.

Communication impairments following a right-hemisphere lesion

297

McDonald, S. (2000). Exploring the cognitive basis of right-hemisphere pragmatic language disorders. Brain and Language, 75, 82–107. Moix, V., & Côté, H. (2004). Intervention orthophonique chez les cérébrolésés droits. Rééducation orthophonique, 42, 123–133. Monetta, L., & Joanette, Y. (2001). Word processing impairments among right hemisphere damaged patients: Deﬁcits in cognitive resources? Poster presented at the 25th World IALP Congress, Montreal, August 5–9. Monetta, L., & Joanette, Y. (2003). Speciﬁcity of the right hemisphere’s contribution to verbal communication: The cognitive resources hypothesis. Journal of Medical Speech-Language Pathology, 11, 203–211. Myers, P. S. (1999). Right hemisphere damage: Disorders of communication and cognition. San Diego, CA: Singular Publishing Group. Nocentini, U., Goulet, P., Roberts, P. M., & Joanette, Y. (2001). The eﬀects of left- versus right-hemisphere lesions on the sensitivity to intra- and interconceptual semantic relationships. Neuropsychologia, 39, 443–451. Ouellet-Plamondon, C., Monchi, O., Senhadji, N., & Joanette, Y. (2006). Age-related shift of the fMRI activations for the semantic processing of words: Anterior to posterior more than left to right. Poster presented at the World Federation of Neurology–Aphasia and Cognitive Disorders Research Group, Buenos Aires (Argentina), March 1–4. Rapp, A. M., Leube, D. T., Erb, M., Grodd, W., & Kircher, T. T. J. (2004). Neural correlates of metaphor processing. Cognitive Brain Research, 20, 395–402. St. George, M., Kutas, M., Martinez, A., & Sereno, M. I. (1999). Semantic integration in reading: Engagement of the right hemisphere during discourse processing. Brain, 122, 1317–1325 Scherer, L. C., Ska, B., & Joanette, Y. (2006). The impact of aging and language proﬁciency on the interhemispheric dynamic for discourse processing. Poster presented at the Human Brain Mapping Organization, Firenze (Italy), June 11–15. Schneiderman, E. I., Murasugi, K. G., & Saddy, J. D. (1991). Story arrangement ability in right brain-damaged patients. Brain and Language, 43, 107–120. Searle, J. R. (1969). Speech acts. Cambridge, UK: Cambridge University Press. Seger, C. A., Desmond, J. E., Glover, G. H., & Gabrieli, J. D. E. (2000). FMRI evidence for right-hemisphere involvement in semantic relationships, Neuropsychology, 14, 361–369. Stemmer, B. (1999). An on-line interview with Noam Chomsky: On the nature of pragmatics and related issues. Brain and Language, 68, 393–401. Stemmer, B., Giroux, F., & Joanette, Y. (1994). Production and evaluation of requests by right hemisphere brain-damaged individuals. Brain and Language, 47, 1–31. Stemmer, B., & Joanette, Y. (1998). The interpretation of narrative discourse of brain-damaged individuals within the framework of a multi-level discourse model. In M. Beeman & C. Chiarello (Eds.), Right hemisphere language comprehension: Perspectives from cognitive neuroscience (pp. 329–348). Mahwah, NJ: Lawrence Erlbaum Associates, Inc. Tompkins, C. A. (1995). Right hemisphere communication disorders: Theory and management. San Diego, CA: Singular Publishing Group. Vanhalle, C., Lemieux, S., Joubert, S., Goulet, P., Ska, B., & Joanette, Y. (2000). Processing of speech acts by right hemisphere brain-damaged patients: An ecological approach. Aphasiology, 14, 1127–1141. Walter, N., Jbabdi, S., Marrelec, G., Benali, H., & Joanette, Y. (2006). Carl Wernicke

298

Joanette et al.

was essentially right: FMRI brain interactivity analysis of phonological and semantic processing of isolated words. Communication presented at the World Federation of Neurology – Aphasia and Cognitive Disorders Research Group, Buenos Aires (Argentina), March 1–4. Wapner, W., Hamby, S., & Gardner, H. (1981). The role of the right hemisphere in the apprehension of complex linguistic materials. Brain and Language, 14, 15–33. Weinstein, E. A. (1964). Aﬀections of speech with lesions of the non-dominant hemisphere. Research Publications of the Association for Research in Nervous and Mental Disease, 42, 220–228. Winner, E., Brownell, H. H., Happe, F., Blum, A., & Pincus, D. (1998). Distinguishing lies from jokes: Theory of mind deﬁcits and discourse interpretation in right hemisphere brain-damaged patients. Brain and Language, 62, 89–106.

20 Progressive language and speech disorders in dementia Maria Pa˛chalska

Introduction Disturbances of speech and language, ranging from dysarthria through aphasia to mutism, are a common feature of dementia, though often overshadowed by other symptoms of mental deterioration. The symptoms are so diverse and changeable, however, that very few unqualiﬁed statements can be made. Some patients present symptoms that can be easily classiﬁed as phonological, semantic, or syntactic, while in other cases there are relatively nonspeciﬁc communication breakdowns, perhaps related to other cognitive or behavioral deﬁciencies (Kempler, 1995). The disturbances in verbal communication are sometimes mild, sometimes severe; they may appear late in the course of the disease, or they may be the ﬁrst presenting symptom of dementia. This diversity results from a complex calculus, whose main factors include the pathogenesis of the disease itself, the characteristics of the speech and language behavior of the aﬀected individual prior to onset, and the cognitive reserves available to cope with and compensate for the loss of speech and language functions (Stern, 2002). Moreover, by the end stages, as the disease progresses, these and other distinctions (even the diﬀerences between “cortical” and “subcortical” dementias) are gradually wiped out as the deterioration (both structural and functional) becomes increasingly global. The beginning point and initial course of each dementive illness is relatively speciﬁc, but they all converge to a common end point. For a variety of reasons, speech and language has tended to be at best a second-order concern in the study of dementia, while dementia remained until fairly recently an area of only secondary interest for aphasiology (Harciarek & Jodzio, 2005; Ross, Cummings, & Benson, 1990). Nevertheless, the negative impact of these disturbances on the quality of life of demented individuals is in many cases far greater than might be indicated by the relative paucity of scientiﬁc literature on the topic. Moreover, the complex patterns of speech and language decay in dementia, though often diﬃcult to interpret, provide invaluable insights, not only into the relation between neuronal structures and language, but also into the relationship of language to other domains of cognition and behavior.

300

Pa˛chalska

Regardless of the speciﬁc etiology of dementia in a given case, the cognitive deﬁcits that deﬁne dementia typically result from atrophy of brain tissue and a consequent decline in mental eﬃciency. The course of dementia (i.e., how rapidly this decline occurs, and what cognitive, aﬀective, and behavioral symptoms occur in what order) depends in each case on the nature of the tissue destruction caused by the basic pathomechanism, the point at which the degenerative process begins, and the general direction in which it spreads, not to mention the patient’s premorbid intelligence, habits, and predispositions. At the cellular level, each disease is accompanied by particular, pathognomonic neuropathological signs, but the clinical picture in vivo is seldom clear-cut, especially since neuroimaging techniques rarely give an unequivocal answer to the basic nosological questions. Though the search for noninvasive tests based on biological markers continues (Leszek, Malyszczak, Janicka, Kiejna, & Wiak, 2003), at present a deﬁnitive diagnosis of almost all dementive illnesses is only made possible by neuropathological results showing the characteristic cellular features of a given disease. The clinical diagnosis is always at best a reasonable inference awaiting neuropathological conﬁrmation. There do exist, however, identiﬁable neuropsychological syndromes of dementia that have been found to correlate at least roughly with particular dementive illnesses. For example, “Dementia of the Alzheimer’s type” (DAT) is characterized by the insidious onset of problems with working memory appearing after age 55, often followed by depressive symptoms and confusion, then gradual loss of other memory domains and a general cognitive decline, with language disturbances and other neurological signs appearing relatively late. A diagnosis of DAT gives roughly 75% conﬁdence that the patient actually has Alzheimer’s disease (AD) in the neuropathological sense. Thus the neuropsychological diagnosis describes a clinical syndrome of dementia bearing certain characteristic features, not unrelated to the ultimate neuropathological diagnosis, but in an important sense independent of it. For example, a post mortem neuropathological ﬁnding that the patient did not have the amyloid plaques and neuroﬁbrillary tangles characteristic of AD does not mean that the neuropsychological diagnosis of DAT was in error, but only that the neuropathology underlying the observed symptoms proved to be something other than AD. In order to keep the discussion within reasonable limits, only four dementive syndromes will be described here: • • • •

dementia of the Alzheimer’s type (DAT); fronto-temporal dementia (FTD); Creutzfeldt-Jakob disease (CJD); the MELAS syndrome.

Each of these descriptions will be supported by a brief case study, drawn from the author’s own clinical material.

Progressive language and speech disorders in dementia

301

Alzheimer’s dementia (DAT) Though there are several diﬀerent schemes of staging in DAT, for the present purposes it is most convenient to speak simply of an early phase, a middle phase, and a late phase (Gustafson, Elfgren, & Passant, 2004). The early phase is usually pre-clinical, with loss of short-term memory attended by confusion, which becomes increasingly troublesome until it ﬁnally prompts the patient (or the family) to seek medical attention. The late phase is virtually complete loss of logical contact, accompanied by increasingly severe neurological disorders and terminating in death. What we are calling the “middle phase,” then, is not so much a clearly delineated stage as a series of transitions that lead from the early (pre-clinical) stage to the late (terminal) stage. Aphasia usually appears relatively late in the course of DAT. In the classical presentation, speech remains largely unaﬀected until the transition from the middle stage to the late stage, when aphasia joins other neurological symptoms, including motor problems. However, even in early DAT, although ordinary conversation may seem unaﬀected, patients often have more wordﬁnding problems than do healthy elderly, and typically show below-normal scores in verbal ﬂuency (Cerhan, Ivnik, Smith, Tangalos, Petersen, & Boeve, 2002; Harciarek & Jodzio, 2005). The task of naming as many animals as possible in one minute is usually easier for DAT patients than the task of listing words that begin with a certain letter, and shifting from the one task to the other almost always produces perseveration of the ﬁrst task into the second. The steady cognitive decline of the middle-stage AD patient is accompanied by impoverished vocabulary, leading to increasingly severe word-ﬁnding problems and ending in the organic mutism of the late stage. Automatisms and meta-linguistic comments occupy an increasing amount of the patient’s discourse. At the same, the mental confusion typical of AD at this stage leads to apparently nonsensical utterances that begin to take on the features of aphasic jargon (Mendez & Cummings, 2003). Some authors (Gates, Beiser, Rees, D’Agostino, & Wolf, 2002) have compared the typical picture at this stage to transcortical sensory aphasia. A characteristic feature is logoclonia: that is, the tendency to overuse a particular word, substituting it for a number of diﬀerent target words. Case study: JG This patient, a right-handed Polish female, age 67 at ﬁrst contact, was referred for neuropsychological testing by her family, whose concern was aroused when on several diﬀerent occasions she seemed to become completely lost in her own neighborhood, unable to ﬁnd her way home when she was only a block away from her home of 20 years. Since she had recently experienced the loss of her younger brother, the family at ﬁrst attributed the

302

Pa˛chalska

problems to emotional stress, and indeed the ﬁrst diagnostic task (often a diﬃcult one in early DAT, see Dierckx, Ponjaert-Kristoﬀersen, Verté, & De Raedt, 2004) was to diﬀerentiate between depression and dementia. The possibility that JG was suﬀering from depression rather than a neurodegenerative disease was made more likely by the fact that her score on the Mini Mental State Examination (MMSE) in the ﬁrst test was at the low end of normal. On her ﬁrst attempt to draw a clock face (a widely used screening test for dementia) she drew a circle with marks at 12:00, 3:00, 6:00 and 9:00, but then the examiner noticed that she was looking at a clock on the kitchen counter (she was ﬁrst examined at her home). When the clock test was repeated 30 minutes later and the clock was removed from her line of sight, she drew the clock face correctly, but when asked to show “3:05,” she drew four diﬀerent hands (none in the right place), then expressed frustration that she “couldn’t make it come out right” (see Figure 20.1). Her conversation seemed normal and her mood actually improved considerably during the ﬁrst examination session. The Frenchay Aphasia Screening Test did not indicate aphasia. However, on the Boston Naming Test (BNT; Kaplan, Goodglass, & Weintraub, 1983) she showed a sub-normal score (45/60 items properly named), and prompting (whether semantic or verbal) did not help her recover the names of objects she could not remember. In some cases, she indicated by periphrasis or gesture that she knew what the

Figure 20.1 Clock faces drawn by JG over the course of her illness: (A) ﬁrst examination, May 2005, (B) June 2005, (C) August 2005, (D) September 2005 (one month before her death).

Progressive language and speech disorders in dementia

303

object was but could not think of its name. However, she called many of the animals simply “animal,” and all the vegetables or fruits were “onions” (the ﬁrst vegetable encountered on the Polish version of the BNT). When her attention was called to this after the test, she complained that she could not see (when later examined by an ophthalmologist, no abnormalities were found apart from a mild myopia, corrected by eyeglasses). On the test of verbal ﬂuency, she did not reach norms in either task (category or initial letter), but her performance in the “words that begin with P” task was much worse (see Henry, Crawford, & Phillips, 2004). Signiﬁcantly, she fretted that she could not think of the names of any animals (the ﬁrst, “category” task) that begin with P, and even after being reminded several times that the words did not have to be the names of animals, she clung to this restriction and could think of only two, which she repeated over and over. When re-examined a month later, her mood was generally improved, and she remembered the examiners from the ﬁrst meeting. However, her performance on the MMSE was now much worse (19), and all cognitive parameters were likewise reduced; her clock drawing was noticeably disturbed (see Figure 20.1B). For the present purposes, however, most important is the fact that, although her score on the Frenchay Aphasia Screening Test was still within the normal range, conversation had become more diﬃcult. She often left sentences unﬁnished or expressed herself so vaguely that it was not always possible to ascertain what she meant to say. The family likewise complained that it was becoming increasingly diﬃcult to follow her meaning. When questioned as to her meaning she became ﬂustered and occasionally expressed annoyance, sometime at her own inability to say what she wanted to say, sometimes at the obtuseness of the interlocutor, who in her opinion ought to know what she meant. By the next monthly examination, the score on the Frenchay Aphasia Screening Test was now in the subnormal range (the task of identifying items on the “bridge” picture from that test now seemed entirely beyond her capabilities). There was now slight dysarthria (slurring), as well as logoclonia; during the Boston Naming Test almost half the prompts were now called “onions,” and the word “onion” recurred in her conversation as well. Her mood was generally good, but she was often confused and was unable to stay with even simple tasks, though she tried hard to concentrate and was eager to please. Her writing was more agrammatic than her speech, with letter distortions and a general inability to maintain an even line. Her clock drawing now bore little resemblance to a clock (see Figure 20.1C). By six months after the ﬁrst examination, her speech was nearly incomprehensible (see Ball, Code, Tree, Dawe, & Kay, 2004). Logical contact was ﬂeeting and most standard neuropsychological tests had become diﬃcult or impossible to administer. When asked to draw a clock, she made only a series of strokes, which she did not stop making until the paper was taken from her (see Figure 20.1D). By 8 months she required hospitalization, and after 6 weeks of steady deterioration she died. A post mortem neuropathological

304

Pa˛chalska

examination found the amyloid plaques and neuroﬁbrillary tangles characteristic of Alzheimer’s disease. The relatively rapid progress of the disease in this case, dramatically documented by Figure 20.1, is unusual for AD and requires some comment. Clinicians have long noted that AD tends to have a more severe course in persons of above-average intelligence (JG was a teacher, known before her illness for her wit and tendency to take a lively interest in things). It is now suggested by some authors (Stern, 2002; Stern, Zarahn, Hilton, Flynn, DeLaPaz, & Rakitin, 2003) that the reason for this counterintuitive phenomenon is that these patients, due to their high level of cognitive reserves, often do not show any clinical symptoms of illness until the disease progress is well advanced.

Fronto-temporal dementia In fronto-temporal dementia (FTD), personality changes (consistent with the well-known picture of “frontal syndrome”) usually play a much more important role than speciﬁc cognitive deﬁcits (Borkowska & Sobow, 2005; Mendez & Cummings, 2003; Pasquier & Delacourte, 1998). The diagnosis of FTD is most often based on the Lund and Manchester clinical criteria (Lund and Manchester Groups, 1994), combined with a neuroradiological ﬁnding of frontotemporal atrophy consistent with corticobasal degeneration (Boccardi et al., 2002, 2003; Miller, Boone, Mishkin, Schwartz, Koras, & Kushii, 1998; Varma et al., 2002). Among the most important diagnostic criteria listed by the Lund and Manchester study (Gustafson et al., 2004) are the following: • • • • • • • •

insidious onset with slow progression; early loss of insight; early signs of disinhibition and impulsivity; loss of mental ﬂexibility (inability to adjust to changes of plans or circumstances); stereotyped, perseverative behavior (motor and verbal); utilization behavior (a tendency to pick up and manipulate all objects lying within arm’s reach); hyperorality (frequently manifested in compulsive eating and drinking); diﬃculty in staying focused on the task at hand.

Nevertheless, every one of these criteria has been challenged in the literature, especially since the diﬀerence between the clinical picture of FTD and that of DAT or other dementias may be more the timing (i.e., when the given symptom appears) than the speciﬁc symptomatology (Harciarek & Jodzio, 2005). Thus the disputes between “lumpers” and “splitters” rage on to the present (Kertesz, 2005). For the present purposes, however, it is not essential to sort out the “alphabet soup” of proposed nosological entities that may or may not

Progressive language and speech disorders in dementia

305

fall within the general category of FTD. It is surely safe to say that, since the neuronal loss associated with fronto-temporal lobar degeneration and its many variants causing FTD often occurs in areas critical for speech and language, aphasia symptoms tend to appear earlier in the frontal-temporal dementias than in DAT, and not infrequently constitute the ﬁrst presenting symptom (Knopman, Mastri, Frey, Sung, & Rustan, 1990; Neary, Snowden, Northen, & Goulding, 1998; Snowden & Neary, 1993). Aphasia often begins with the loss of verbal spontaneity (the family complains that the patient has grown taciturn and uncommunicative), which not surprisingly is accompanied by diminished verbal ﬂuency in neuropsychological testing, particularly when the task involves listing words that begin with the same letter (Kertesz, 2003). There are frequent stereotyped comments and a marked tendency to repeat a limited number of stock phrases, not always relevant to the context in which they are used (see Code, 1997 for a comparison to the repetition of stock phrases in popular music). The combination of palilalia (repeating the same word over and over), echolalia (repeating the conversation partner’s last words before beginning one’s own utterance; see Lebrun, 2003), late mutism and amimia (loss of spontaneous mimicry), known as the PEMA syndrome (Guiraud, 1956), is typical of FTD; logoclonia, however, is rare. A particularly salient feature of aphasia in FTD is diﬃculty in understanding sentence structure (Grossman, Rhee, & Moore, 2005). In some such cases, the development of further symptoms of dementia may be delayed, sometimes for many years, in which case we speak of “Primary Progressive Aphasia” (PPA), though the term itself and the relation of this syndrome to FTD remain controversial (Knibb & Hodges, 2005; Selnes & Harciarek, 2005). Already in the nineteenth century Arnold Pick had pointed out that progressive atrophy in the frontal and temporal lobes evoked a constellation of symptoms that included personality change and dysphasia (Kertesz, 1998b; Selnes & Harciarek, 2005), but Mesulam (1982) was the ﬁrst modern author to demonstrate the existence of a syndrome of aphasia developing slowly in the absence of other symptoms of dementia or neurological signs. Luzzatti and Poeck (1991), Kempler (1995), and Mesulam (2001) thus identify the most common clinical features of PPA as follows: • • • •

a non-ﬂuent aphasia with hesitant, dysprosodic speech, phonemic paraphasias, and impaired syntax; poor repetition; generally preserved comprehension; normal or near-normal performance on tests of other cognitive functions.

Another variant of FTD that has a noticeable and early eﬀect on speech and language is semantic dementia. Hodges, Patterson, Oxbury, and Funnell (1992; see Garrard & Hodges, 1999) described the insidious onset and

306

Pa˛chalska

progressive breakdown of semantic knowledge, which aﬀects not only language, but also memory, general knowledge, and object recognition. The result is usually a ﬂuent aphasia, involving anomia with circumlocution and semantic paraphasia, single-word comprehension deﬁcits, and reduced category ﬂuency, typically accompanied by visual agnosia and other symptoms of a generalized inability to abstract conceptual meaning from concrete signs and symbols (Knibb & Hodges, 2005). In recent years the term Pick’s complex (Ioannides, Karacostas, Hatzipantazi, & Ioannis, 2005; Kertesz, 1998a) has come into use to denote the signiﬁcant clinical and pathological overlapping between primary progressive aphasia, frontal lobe dementia and corticobasal degeneration. Kertesz (2005) argues that despite the diversity of the clinical picture, FTD is a clinical syndrome, within which one can further specify variants, including a behavioral variety with features of frontal syndrome, progressive aphasia, semantic dementia, corticobasal degeneration and progressive supranuclear palsy (PNP, also known as Steele-Richardson-Olszewski syndrome). Case study: ZE This patient, a right-handed Polish female, was 72 years old at the moment when the ﬁrst symptoms appeared. ZE was a prominent professor of medicine, a cardiosurgeon of international stature in her ﬁeld of specialization, who spoke several languages ﬂuently enough to lecture around the world. She had always been remarkable not only for her high professional and scientiﬁc qualiﬁcations, but also for her warm and outgoing personality. Her home had always been an international “salon” of sorts, and her dinners for specially invited guests were once legendary in Cracow. She had always enjoyed remarkably good health until the spring of 1999, when she noticed that she was more and more often forgetting daily tasks and leaving personal objects in unlikely places. Since her mother had died of Alzheimer’s disease several years earlier, ZE was alarmed by this and reported it to her family, but no one felt that the problems were suﬃciently severe to merit attention. Later, she began to have sudden, unmotivated (and highly uncharacteristic) outbursts of rage, but again, her friends and family interpreted these incidents as the result of stress and fatigue associated with her busy professional calendar (which despite her nominal retirement would have exhausted someone half her age). She herself attributed her emotional lability to her latent fear of AD. The ﬁrst neurological symptoms appeared in late 2001, when her gait slowed and became ataxic, so that she had several falls (early falls are considered a sign of progressive supranuclear palsy; see Litvan et al., 1996). Since the earlier behavioral symptoms were not taken seriously, and ZE developed, in addition to the motor symptoms, a Parkinsonian “mask,” she was initially diagnosed with Parkinson’s disease. However, dopaminergic treatment proved completely ineﬀective and even counterproductive (another sign of PSP). The ﬁnal piece of the puzzle fell into place in May of 2002, when during

Progressive language and speech disorders in dementia

307

neuropsychological testing the present author observed that EZ was unable to look upward or downward without moving her head (“vertical ophthalmoplegia” is virtually pathognomonic for PSP). Neuropsychological testing showed: • • • • •

progressive subcortical dementia, with diﬃculty in planning activities, reduced criticism, impaired working memory, dysexecutive syndrome, and personality changes; disturbances in spatial orientation; limb apraxia; verbal and motor perseverations; constructional apraxia.

The speech and language disturbances presented by ZE (with the exception of slowed speech tempo and slight, barely noticeable slurring, consistent with hypokinetic dysarthria; see Darley, Aronson, & Brown, 1975), accompanied by dysphagia, appeared considerably later than the motor symptoms. There was also dysgraphia, manifested in distortion of letter shapes and diﬃculty keeping the written text on the lines of the paper. Later she began to make orthographical errors. The progress of dysgraphia is illustrated by Figure 20.2. Until very late in the progress of the disease ZE had no pathological scores on any aphasia tests, though it was noticed that, in comparison to her premorbid speech habits, her lexicon was distinctly impoverished. She became markedly less spontaneous, often smiling and nodding instead of speaking, even in response to a direct question. She seemed at that point to be moving in the direction of Luria’s “dynamic aphasia” (Esmonde, Giles, Xuereb, & Hodges, 1996; Luria, 1977), characterized by markedly diminished verbal output with relatively few patent errors. One of the most salient features of ZE’s speech at this stage was an increasing tendency to fall into various forms of pathological repetition, a common feature of both PSP (Lebrun, Devreux, & Rousseau, 1986) and Parkinson’s disease (Benke, Hohenstein, Poewe, & Butterworth, 2000). Initially, ZE in conversation often repeated the question she had just been asked before answering it, as though wanting to be sure that she had understood it correctly. For example: Examiner: ZE:

What time is it? What time is it? Oh, ten o’clock.

Over time this habit developed into echolalia, and the repetition of the interlocutor’s speech was less and less often motivated or followed by an appropriate response, as follows: Examiner: ZE:

It’s very cold today. It’s very cold today. Yes, it’s very cold.

308

Pa˛chalska

Figure 20.2 Writing samples from patient ZE in October (A), November (B) and December (C) 2002. The prompt text was identical in each case.

Later, she also developed palilalia, ﬁrst involving the repetition of words, then syllables, then single phonemes, rendering it diﬃcult to determine a sharp boundary between palilalia and stuttering (Lebrun, 2003). Unlike typical stuttering, however, she most often repeated the last syllable or phoneme of a word she was trying to use, rather than the ﬁrst. It is of particular interest to note that until a relatively late stage in her illness ZE was not only able to converse in English, but in fact showed less

Progressive language and speech disorders in dementia

309

dysarthria and echolalia in this language than in her native Polish. She enjoyed speaking English and often spontaneously shifted languages during testing. However, as the disease progressed she fell into a global aphasia and ultimately ceased to display any verbal behavior at all.

Creutzfeldt-Jakob disease Although Creutzfeldt-Jakob disease (CJD) was ﬁrst described in the early 1920s (Creutzfeldt, 1920; Jakob, 1921), it was not until the 1990s that Stanley Prusiner discovered the basic pathogen of this disease: a “contagious protein” for which he coined the term “prion.” In the present state of our knowledge, however, the process by which prions lead to spongiform encephalopathy (SE) can only be sketched in outline. Prions originate from the protein known as PrP, genetically coded by the PRNP gene in the human chromosome. Normal PrP molecules (designated PrPC) are distributed primarily in the central nervous system, but their exact function remains unknown (Büeler et al., 1992; Mastrianni & Roos, 2000). When pathogenic prions (designated PrPSc) are introduced into the nervous system, they adhere to healthy PrPC molecules and transform them into pathogenic PrPSc, the accumulation of which in the central nervous system leads to neuron death and spongiform encephalopathy. A phenotypically diverse family of prion diseases is known, among which BSE (bovine spongiform encephalopathy, the famous “mad cow disease”) has attracted much attention in the popular press in recent years. The appearance of BSE in England and the later appearance of a previously unknown variant of CJD among younger patients (the previously known spontaneous variants were not known to appear before age 60) led to the conjecture that the new variant (nvCJD) was simply BSE transmitted to humans through the consumption of prion-contaminated beef products. As is often the case, the popular press has largely forgotten about CJD in recent years, in part due to the eﬀectiveness of the rather dramatic countermeasures taken to prevent the further spread of BSE, since it does not appear that prions can be transmitted from human to human (Mastrianni & Roos, 2000). By far the rarest form of CJD is the Heidenhain variant (HvCJD), in which vision disturbances are the ﬁrst presenting symptoms (Heidenhain, 1929). These patients typically present at an early stage with hemianopsia, not accompanied by pyramidal symptoms or lesion detectable by neuroimaging (Brazis, Lee, Graﬀ-Radford, Desai, & Eggenberger, 2000), followed by progressive metamorphopsia (Kropp et al., 1999), visual hallucinations and diminished visual acuity, culminating in cortical blindness without remarkable ocular pathology. The characteristic feature of dementia in Creutzfeldt-Jakob disease is its rapid progression, with death most often occurring from 6 to 18 months after the ﬁrst clinical symptoms are noticed. Ataxia, myoclonus, and hyperkinesia are common. Ironically enough, this dramatic course may well result from the

310

Pa˛chalska

extremely long incubation period of prion diseases (from 8 to 15 years), since the conformation of normal PrPC to the pathogenic PrPSc begins very slowly but proceeds logarithmically, so that by the time clinical symptoms appear the patient is already well advanced. The transition from a clinical status similar to “early” AD to a status almost identical to “late” AD may take only a few months, or even a few weeks. When the disease process hits the period of acceleration, speech and language may change from normal to organic mutism in a matter of a few weeks (Hillis & Selnes, 1999). This is not a sudden change, however, as in a post-stroke aphasia, but rather a series of accelerating transitions. Various aphasic syndromes may appear for a day or two before they give way to another, more profound syndrome. Case study: JR The patient, a right-handed Polish female, was 68 years old at onset, widowed, with no family history of neurological illnesses and generally in good health. She very seldom ate beef, but as a young woman she had extensive close contact at work with animal byproducts (including bovine) and chemical agents of various kinds. In July of 2000, her writing began to show orthographical errors (rare in Polish), perseveration and disorganization, but JR successfully hid the problem and the family did not notice. Only later, when looking over her papers, a progressive dysgraphia was noticed in her monthly accounts (see Figure 20.3). In mid-September 2000 she sought medical attention when she began to experience vision disorders, ophthalmologically diagnosed as hemianopsia, without pyramidal symptoms. By early October she had lost all sense of visual perspective, and the visual images also began to be seriously distorted, as micropsia and macropsia turned into metamorphopsia. She also manifested hypersensitivity to bright colors, especially red.

Figure 20.3 JR’s monthly budget from October (A) and November (B) 2000 (used by permission of the patient’s family).

Progressive language and speech disorders in dementia

311

Systematic neuropsychological testing began in early October. The patient initially had normal scores on the Western Aphasia Battery–Revised (WABR; Kertesz & Poole, 1974), for both the Cortical Quotient and the Aphasia Quotient; however, she showed a low-normal score on the BNT. She had diﬃculties with simple arithmetical operations and was unable to complete all but the very simplest block pattern tests in the Wechsler Adult Intelligence Scale–Revised (Wechsler, 1981). Delayed verbal and visual recall were below normal for her age group on the Wechsler Memory Scale–Revised (WMS-R; Wechsler, 1986). On selected subtests from the Cracow Right Hemisphere Diagnostic Battery (Pachalska & MacQueen, 1998) her scores were borderline for agnosia, constructive apraxia, and dyspragmatism. There was also slight left-sided hemispatial neglect. In early October she reported seeing black spots before her eyes; by late October she was seeing the black spots as insects climbing the walls. She was still aware, however, that these were hallucinations. In mid-November she was hospitalized in the Department of Neurology at the Ministerial Hospital of the Polish Ministry of Internal Aﬀairs and Administration (MSWiA) in Cracow. She never left the hospital again. Her diﬃculties with naming increased considerably, and in conversation she tended to ramble. An MRI performed after admission showed numerous, dispersed changes characteristic of spongiform encephalopathy (Pa˛chalska, Kurzbauer, MacQueen, Formin´ ska-Kapus´cik, & Herman-Sucharska, 2003). By mid-December JR had ceased to be critical of her hallucinations, and often fell into panic when the “big black bugs” began to crawl over her food and her body. She now showed aphasia on the WAB-R, and verbal contact with the examiners began to be diﬃcult. When actively hallucinating she was disoriented and unresponsive. The tempo of mental and physical deterioration began to accelerate in late December and early January. Neuropsychological testing was possible for the last time in mid-January. By this time her verbal output was scarce and barely audible. She showed severe leftsided neglect in a ﬁgure cancellation task (the test had to be specially adapted to use large ﬁgures entirely in red, the only color to which she still reacted). By this time laboratory tests had conﬁrmed the presence of protein 14–3–3 in JR’s cerebrospinal ﬂuid, a highly sensitive (but unfortunately not highly speciﬁc) test for CJD. By late January 2001 logical and verbal contact was irreversibly lost. Myoclonus and hyperkinesia (common features of CJD) had become very pronounced and nearly constant. An ophthalmological examination conﬁrmed cortical blindness. Although it seemed at this point that death was imminent, she lingered for 16 months, never regaining consciousness. An autopsy conﬁrmed spongiform encephalopathy without any of the neuropathological features characteristic of other dementive illnesses. In view of these results, along with the prominence and early appearance of vision problems, JR was diagnosed with the Heidenhain variant of CJD (Kropp et al., 1999).

312

Pa˛chalska

For the present purposes, the most salient features of this case are the following: • • •

early appearance of agraphia (initially not detected by the family), which may well be related to the speciﬁc features of the Heidenhain variant of CJD; the process by which metaphors (black spots that “look like bugs”) concretized into visual hallucination (“bugs” crawling on the wall; see Pa˛chalska, Kurzbauer, & MacQueen, 2002); the rapid but not sudden deterioration of linguistic competence (Hillis & Selnes, 1999) when the disease progressed to the crisis point.

The MELAS syndrome MELAS (an abbreviation for mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes) is a relatively rare disease, though in reality it may be more common than the available statistics would indicate. Because of the considerable diﬃculties involved in establishing a diagnosis, MELAS is often mistaken for a range of other neurological disorders. The course of this mitochrondrial cytopathy is remarkable for the combination of a steadily progressive dementia punctuated by the sudden appearance and equally sudden disappearance of acute neurological symptoms (caused by the so-called “stroke-like episodes”). It is not at all uncommon for MELAS patients to be admitted to the emergency room with every neurological indication of an ischemic stroke, and then to be discharged a few days later with no apparent deﬁcits. The basic pathomechanism of MELAS is an energy deﬁciency on the cellular level, caused by insuﬃcient output from the mitochondria, which triggers a shift to anaerobic respiration and lactic acidosis. In the brain, the repeated mitochondrial crises over time produce spongiform encephalopathy, which may be concentrated in one or several regions (appearing as a hypodense lesion in neuroradiological testing), or may aﬀect the entire brain more or less evenly (visible in CT scans or MRI as generalized atrophy). Each stroke-like episode produces mostly transient eﬀects, but the cumulative eﬀect is neuron loss and atrophy. Unlike the other dementive illnesses presented here, MELAS is not primarily or even commonly a disease of the elderly. A normal childhood is typical, with the ﬁrst symptoms usually appearing between puberty and young adulthood. The ﬁrst episode is often triggered by psychological stress or an otherwise unrelated illness (e.g., ﬂu) that increases the body’s energy demands, which the ineﬃcient mitochondria cannot meet. The combination of periodic acute episodes against the background of slowly progressive atrophy gives a complex neuropsychological picture, characterized by a combination of “stroke-like” and “dementia-like” features, not always consistent with each other (Pa˛chalska & MacQueen, 2002).

Progressive language and speech disorders in dementia

313

Case study: KS KS, a right-handed Polish female, was born in 1978 without perinatal complications, and her psychomotor development was fully normal to age 15. Her mother is of unusually short stature and suﬀers from migraine headaches, a typical pattern in MELAS families (DiMauro, personal information), since the mutation is likely to have been present over several generations, with earlier and more severe symptoms in each successive generation. She was an outstanding student in secondary school, gregarious and popular. There was no history of substance abuse or promiscuity. At the age of 16, she began to experience an array of apparently inexplicable, continually worsening “attacks”: acute headaches, weakness (exercise intolerance), nausea and vomiting, and periodic fevers without apparent cause reaching 40°C. While preparing for her ﬁnal examinations in her last year of secondary school, she had a neurological episode now recognized as having been a stroke-like episode, resulting in transient hemianopsia, moderate non-ﬂuent aphasia and mild left hemiparesis, followed by vision and hearing disturbances and cognitive dysfunctions. An MRI revealed changes, not of vascular origin, in the right posterior parietal and occipital lobes, and in the left hemisphere of the cerebellum. In 1998, during the ﬁrst of four lengthy stays under the present author’s care at the Cracow Rehabilitation Center, the clinical diagnosis of MELAS was advanced, since the patient exhibited all the clinical signs and symptoms, including lactic acidosis. At the same time, intensive genetic testing was begun at Columbia University, which bore fruit in mid-2000 with the discovery of a novel mutation (C8293T in mitochondrial DNA; see Pa˛chalska & MacQueen, 2001). KS was treated with Neurotop (carbamazepine) to control epileptic seizures, and co-enzyme Q10 combined with L-carnitine to support her energy metabolism. In addition, she received a comprehensive program of neurorehabilitation, which seems to have delayed the progress of the disease (Pa˛chalska & MacQueen, 2001). The number and intensity of the stroke-like episodes diminished considerably after 1999, but dementia progressed steadily. Until her death in June of 2005, KS lived at home with her parents, but required increasing supervision due to paranoid delusions of persecution by her younger brother. The overall course of each mitochondrial crisis experienced by KS was essentially similar. The prodrome consisted of severe headache, protracted spells of nausea and vomiting, followed by epileptic seizures (initially focal, later sometimes generalized), narrowing of the ﬁeld of vision and deteriorating visual acuity, culminating either in a grand mal epileptic seizure (sometimes status epilepticus) or stroke-like neurological symptoms, including serious disturbances of hearing and vision, occasional paresthesia or paresis, and aphasia-like symptoms. Within days or even hours after the onset of the episode, however, most of these symptoms receded, though residual eﬀects were often noted. The eﬀects can be seen in Figure 20.4.

314

Pa˛chalska

Figure 20.4 Speech and language results obtained by KS: (A) the course of a typical stroke-like episode (courses converted to percentages to facilitate comparison), (B) overall decline in language and mentation.

Figure 20.4A shows the results from a battery of selected subtests that were administered to KS on a daily basis when prodromal symptoms appeared, pointing to an imminent stroke-like episode (see Pa˛chalska & MacQueen, 2001). This battery (which had to be kept short due to the patient’s low fatigue threshold) included the following six elements: • • • • • •

naming (BNT); repetition of high probability (i.e., commonly used) words (Cracow Neurolinguistic Aphasia Battery, CNAB; Pa˛chalska, Kaczmarek, & Knapik, 1995); repetition of low probability (i.e., infrequent) words (CNAB); sequential commands (WAB); reading (CNAB); writing (CNAB).

As can be seen, repetition of high probability words, reading, and writing were at normal levels when testing began, while repetition of low probability words, naming, and sequential commands were already showing some pathology at about 80% of normal. Since by 1998 KS never showed 100% results on these three subtests, the examination of September 10, 1998, though prodromal symptoms were already occurring, can safely be taken as baseline. By the afternoon of September 16, KS was nearly mute, with minimal responses (about 20% of normal) on naming and sequential commands, and no response at all on the remaining tests. This state only lasted for 1 day, however, and the recovery was nearly as dramatic as the loss of function. Other

Progressive language and speech disorders in dementia

315

episodes show a very similar proﬁle in terms of the overall shape, but in each case the various parameters are aﬀected in diﬀerent ways (Pa˛chalska & MacQueen, 2001). Figure 20.4B, by contrast, shows the steady decline over the years of KS’s illnesses, independent of the dramatic course of the episodes. By mid– 2004, her language capacity had fallen to the point that further testing was pointless. As her hearing deteriorated, she developed slight dysarthria, but as the disease progressed her speech became more and more diﬃcult to understand (see Ball et al., 2004). In the last year of her life KS spoke only a few mumbled words; on the Boston Naming Test, she identiﬁed the cat but no other pictures (1/60). She spoke of herself (when she could be induced to speak at all) in the third person singular (see Pa˛chalska & MacQueen, 2002), which is a common feature of the speech of the demented in a late stage, when disturbances of consciousness and identity become common.

Discussion In a modular approach to brain work (Jackendoﬀ, 2000), one assumes that, somewhere in the brain, there is a thought module, which is both the origin of data presented to the language module to be transformed into a speech act, and the destination of information decoded by the process of comprehension. In such a view, the language module (whether it is conceived of as a single module or as a set of modules forming a processing unit; see Jackendoﬀ, 2000) receives input in the form of thoughts, concepts, images, or the like, and produces a speech act as output, or, in reverse, receives phonemes or graphemes and transforms them through the application of linguistic rules into thoughts (or cognitions). Its function, then, is one of mediation between self and the world, inner and outer, a center for encoding and decoding information that can be sent and received. Postulating the existence of a “thinking module” at the apex of brain functioning seems reasonable enough, virtually instinctive, but it is attended by some serious problems, not the least of which is the diﬃculty in establishing where in the brain such a “thinking module” would be located. Could thinking be one of the executive functions performed by the frontal lobes, or is it kind of meta-cognition situated in the strategic temporo-parietooccipital (TPO) region? Or are there two thinking modules, one anterior and one posterior? If so, how are they related to each other? The problem becomes more diﬃcult the longer it is pursued. Perhaps it would be more expedient to question the necessity to postulate a distinct thought module, as Luria did (1977). There is really no such thing as “thinking,” one might argue. Mentation would then be reduced to inner speech; that is, a speech act that has not been realized through the motor segment (Brown, 2004), or to imagination, assuming that the “stuﬀ” of thought consists of words and pictures. This alternative has the further advantage of avoiding the

316

Pa˛chalska

“homunculus” fallacy, which necessarily emerges whenever a thought module is postulated. Attempts to tease thought processes away from language-related processes begin by searching for a kind of “pure” aphasia (or dyslexia, or dysgraphia), in which thought processes are intact but speciﬁc language functions are disturbed, so that: • •

on the active side, the content of the intended speech act is normal, but the language module is unable to process this content into a comprehensible and ﬂuent speech act; on the passive side, there is a retained ability to receive the signals that make up another person’s speech act (or written text) as sensory data, but the meaning is not extracted from the signals.

The principle of double dissociation can perhaps be used to argue that in patients with focal lesions there are indeed “purely” cognitive processes and “purely” linguistic processes that are selectively disturbed, but even so this actually requires some mental gymnastics. The incessant disputes in clinical psychology over the problem of deﬁning and measuring intelligence should make us cautious about naively assuming that we know how to assess the quality of thinking in a manner that is not in some way dependent on language. In clinical practice, it is possible to be sure that there is intact thinking with disturbed speech only when the disorder is rather obviously peripheral in nature, sensory or motor, as in a hearing defect or dysarthria; that is, aﬀecting the receptor or eﬀector responsible for receiving sensory signals or executing motor programs. The more central the point of disturbance, however, the more diﬃcult it becomes to disentangle language from thinking. This is diﬃcult to explain in the light of a modular system, in which the language module is conceived of as a center for encoding and decoding, mediating between the inner world of thought and the outer world of behavior. If the language module is content neutral, as much of contemporary linguistics seems to assume, then it is only a messenger between “inner” and “outer” domains of information; if it is not content neutral, then the problem of distinguishing language from mentation becomes much more diﬃcult. This is why dementia-related aphasia is “messy,” enough so that for some time no one was willing to allow the speech and language disturbances occurring in conjunction with dementia to be classiﬁed as “aphasia” (Ross et al., 1990). It seems an obvious conclusion that from the perspective of aphasia the basic speech and language problem in dementia is similar to what occurs in schizophrenia: there is disordered speech because there is disordered thinking. Problems arise, however, when these concepts are tested critically in the clinic. A strictly psychometric approach can sometimes give us the illusion that mentation can collapse while leaving speech and language intact, or vice versa, but a careful observation of the patient’s behavior, in and out of

Progressive language and speech disorders in dementia

317

the clinical setting, very often gives the lie to this conclusion. In what sense can a nonsensical sentence be linguistically correct? For analogous reasons, semantics and syntax may seem to be separate processors within the language module, but when we examine what the brain actually does in real time to take in a sentence (MacQueen, 2003), it turns out to be inordinately diﬃcult to ﬁnd “purely” syntactical or “purely” semantic operations. We seem to be faced with a signiﬁcant conceptual dilemma: •

•

On the one hand, many patients and their families, and a good part of the general public, cannot dissociate disordered speech from disordered thinking. The patient is (or is not) mentally ill, “crazy,” and the test is whether or not speech is coherent. The one who talks “crazy” is “crazy.” Clinicians know the problems faced by the aphasic patient who, on coming into casual verbal contact with strangers, is immediately categorized as inebriated, mentally ill, or mentally retarded, and who often reacts to that perceived stigma simply by avoiding such contacts. As mental health professionals we ﬁght this attitude on a daily basis. On the other hand, currently fashionable modular approaches force us into a dissociation that, as previously mentioned, is much easier to maintain in theory than it is in practice. If, for example, the patient is unable to form a grammatical sentence, is this simply a defect of a speciﬁc function in the language system, perhaps due to the loss of one particular syntactic rule, or is there an underlying loss of the ability to form a logical proposition? Could we ﬁnd a way to test one hypothesis or the other, without making a series of simplifying assumptions regarding either the nature of syntax or the nature of logical thinking?

The problem raised here is far too complex and far-reaching to solve in this chapter, though indeed dementia is a good point at which to begin the discussion, precisely because we are forced to ask the basic question: What is thinking? The very derivation of the word dementia (in past centuries a very general term for mental illness) points to “losing [one’s] mind,” which is echoed even in ordinary speech. The fact that we have narrowed the deﬁnition considerably and have a generally more “enlightened” attitude towards the problem should not disguise the fact that the patient ordinarily experiences the progress of dementia as rather literally a loss of mind. Moreover (again, setting aside for the moment our scientiﬁc predispositions), it is hard to imagine that one could lose one’s mind (whatever we understand that to mean) without that fact ﬁnding some reﬂection in speech and language – and vice versa. The wall of separation that we have erected between thinking (the contents of our minds) and speaking (the production of a speech act) is built into our language, and for that reason alone seems to us perfectly natural and obvious. Those post-modernist theories (such as deconstructionism) that question whether discourse can ever actually get to the truth, though ordinarily taken

318

Pa˛chalska

as an attack on logocentrism, in fact reﬂect a cry of despair, which would make no sense at all if there were not still an implicit assumption, indeed an act of faith, that there could be a truth that would exist independent of the words we use to describe it. Yet in that same ancient Greek language that gave us the “logo-” of logocentrism there is no verb that denotes “thinking” independent of speech. Indeed, the basic noun logos, from which are derived such apparently disparate concepts as logic, analogy, catalogue, and the names of most of our sciences, does not mean “thought,” but rather “word,” or better, “discourse.” Thus the gospel of St. John begins, “In the beginning was the logos,” meaning the Word – and not, as our psychological theories would incline us to assume, “In the beginning was the Thought.” The thought and the speech act that embodies it evolve together, emerging from depth (drive and aﬀect) through various phases of verbalization to the surface, the level of consciousness and behavior. Separating them simpliﬁes analysis, to be sure, but at the cost of obscuring the nature of our mental life. In microgenetic theory (Brown, 1988, 2005) the process of forming a speech act is understood as a continuous stream, leading from drive through motivation to behavior, where speciﬁc mental functions are not “processors” in a data-processing system, but rather moments when the diversion or interruption of the ﬂow produces particular consequences. The process of formulating a thought ﬂows into the process of formulating a speech act in inner speech (Brown, 2004), which in turn ﬂows into a realized speech act. The mental process that leads to comprehension is a parallel ﬂow, with inner speech mediating between rules and speciﬁc mental states. Just as a mutation and a change in the environment may cause the tree of evolution to branch at a given moment, so changes in circumstances or context, both inner (within the brain) and outer (in the world “outside”), cause the microevolution of a mental state to branch in a particular way. In such a system, nothing is entirely predetermined, but then again, nothing is entirely random. Brain damage, then, including neuron loss resulting from a degenerative process, aﬀects the ensuing mental state(s) much as the damage to a branch aﬀects the growth of the tree. Further growth (i.e., the appearance of further stages in the aﬀected process) may be stopped, but more often growth continues downstream from the point of damage, though its direction and force are likely to be changed. The nature of the symptom is not merely an absence, a failure to perform, defective output from a damaged function, but a vital clue to the nature of the process itself (Brown & Pa˛chalska, 2003). Involution reveals the process by which evolution works. In microgenetic theory, then, the diﬀerence between disturbances of thinking and disturbances of speech and language is as much or more a matter of “when” as “where.” The closer the damage to the surface, the more its eﬀects are felt in the ﬁne articulation of the aﬀected behavior, the last stages of microgenesis, and conversely: the deeper the damage, the greater the number of functions that are disturbed at the outset. It is essential to emphasize that

Progressive language and speech disorders in dementia

319

in this approach the concepts of “depth” and “surface” are not used in a purely metaphorical sense, but pertain rather to the basic structure of the central nervous system, with the brainstem and midbrain at the core and the cortex at the surface. Mental states emerge along the paths laid down by evolution, from deeper, older, simpler structures, upward and outward to the youngest and most specialized regions of the cortex. In a cortical dementia, then, involution begins at the point where evolution concluded, while a subcortical dementia begins deeper, undermining the surface structures, which “cave in” as a result. If the organism survives an insult, it tries to adapt; if it does not adapt, it does not survive (Goldstein, 1995). Adaptation rarely succeeds, however, in removing the obstacle, erasing the damage; indeed, that is not what adaptation is all about. The damaged brain goes about its work diﬀerently, but neither that which is the same, nor that which is diﬀerent, simply appeared out of nowhere. Nihil de nihilo gignitur, said the Roman poet Lucretius, following his master, the Greek philosopher Epicurus: “Nothing ever happens from nothing.” The reasons for the behavior we see in the clinic must be sought not only in the disease, but also in the premorbid brain (Brown & Pa˛chalska, 2003). In dementia, then, what we are seeing is an involution of mental processes. Dementia is ontogenesis in reverse, unraveling the fabric that evolution and growth have woven. Symptoms appear as entropy expands to take in ever larger segments of mental processing. Whether this emerges as a cortical or subcortical dementia, with or without motor disturbances, with or without aphasia, depends on the point at which the entropy begins and the direction in which it spreads, whether from depth to surface or surface to depth, posterior to anterior or anterior to posterior, and so forth. The struggle to adapt, to compensate for what has been lost, is ultimately lost, and as the entropy spreads, the diﬀerences between the various diseases are gradually eﬀaced. This is why all the roads traveled by the various dementive syndromes begin very diﬀerently and end very much the same. The speech act may become ﬁrst inarticulate in its execution, then disordered in its contents, or the reverse; this may happen early or late, and it may take place quickly or slowly. In the end, however, the patient falls into global aphasia and then mutism. Logical contact is then irretrievably lost.

Conclusion There is, of course, no cure for dementia, as there is no cure for the various diseases that cause it. It is possible, however, to slow its progress and mitigate its eﬀects. In many cases, too, it may well be possible to prevent the involutionary processes from beginning. There is some evidence, though controversial, that regular mental and physical stimulation throughout life may prevent neural degeneration from beginning, even when there is a genetic predisposition (Stern, 2002). In my opinion, one of the great challenges facing neuropsychology in the century to come, as the world population ages

320

Pa˛chalska

(especially in Europe and the United States), is to develop therapeutic and preventive interventions that can keep a larger percentage of the world’s population from “losing their minds” before their natural lifespan is over. This may require some discussion and debate about where and how research resources are allocated, especially since at present the involvement of neuropsychology with dementia has been almost exclusively in the area of diagnosis. What Dylan Thomas said about death in his poem Do not go gentle into that good night (1951) could well serve as a motto for the neuropsychology of dementia in the twenty-ﬁrst century: Do not go gentle into that good night! Rage, rage! against the passing of the light!

References Ball, M. J., Code, C., Tree, J., Dawe, K., & Kay, J. (2004). Phonetic and phonological analysis of progressive speech degeneration: A case study. Clinical Linguistics and Phonetics, 18 (6–8), 447–462. Benke, T., Hohenstein, C., Poewe, W., & Butterworth, B. (2000). Repetitive speech phenomena in Parkinson’s disease. Journal of Neurology, Neurosurgery and Psychiatry, 69 (3)., 319–324. Boccardi, M., Laakso, M. P., Bresciani, L., Galluzzi, S., Geroldi, C., Beltramello, A., et al. (2003). The MRI pattern of frontal and temporal brain atrophy in frontotemporal dementia. Neurobiology of Aging, 24, 95–103. Boccardi, M., Pennanen, C. M., Laakso, M. P., Testa, C., Geroldi, C., Soininen, H., et al. (2002). Amygdaloid atrophy in frontotemporal dementia and Alzheimer’s disease. Neuroscience Letters, 335, 139–143. Brazis, P. W., Lee, A. G., Graﬀ-Radford, N., Desai, N. P., & Eggenberger, E. R. (2000). Homonymous visual ﬁeld defects in patients without corresponding structural lesions on neuroimaging. Journal of Neuroophthalmology, 20 (2)., 92–96. Borkowska, A., & Sobow, T. (2005). [Neuropsychological assessment in the diagnosis and diﬀerential diagnosis of fronto-temporal dementia] Neurologia i Neurochirurgia Polska, 39 (6)., 466–475 [Article in Polish with English summary]. Brown, J. W. (1988). The life of the mind. Selected papers. Hillsdale, NJ: Lawrence Erlbaum Associates, Inc. Brown, J. W. (2004). Word concept, verbal hallucination, and inner speech in neuropsychology. Acta Neuropsychologica, 2 (2)., 111–129. Brown, J. W. (2005). Process and the authentic life: Toward a psychology of value. Frankfurt & Lancaster: Ontos Verlag. Brown, J. W., & Pa˛chalska, M. (2003). The nature of the symptom and its signiﬁcance for neuropsychology. Acta Neuropsychologica, 1 (1)., 1–11. Büeler, H., Fischer, M., Lang Y., Biuethmann, H., Lipp, H. P., DeArmond, S. J., et al. (1992). Normal development and behaviour of mice lacking the neuronal cell-surface PrP protein. Nature, 356, 577–582. Cerhan, J. H., Ivnik, R. J., Smith, G. E., Tangalos, E. C., Petersen, R. C., & Boeve, B. F. (2002). Diagnostic utility of letter ﬂuency, category ﬂuency, and ﬂuency diﬀerence scores in Alzheimer’s disease. Clinical Neuropsychology, 16, 35–42. Code, C. (1997). Can the right hemisphere speak? Brain and Language, 57, 38–39.

Progressive language and speech disorders in dementia

321

Creutzfeldt, H. G. (1920). Über eine eigenartige herdförmige Erkrankung des Zentralnervensystems. Zeitschrift Gesamte der Neurologie und Psychiatrie, 57, 1–18. Darley, F. L., Aronson, A. E., & Brown, J. R. (1975). Motor speech disorders. Philadelphia: WB Saunders. Dierckx, E., Ponjaert-Kristoﬀersen, I., Verté, D., & De Raedt, R. (2004). Use of neuropsychological test procedures to distinguish dementia from depression in the elderly. Acta Neuropsychologica, 2 (2)., 130–141. Esmonde, T., Giles, E., Xuereb, J., & Hodges, J. (1996). Progressive supranuclear palsy presenting with dynamic aphasia. Journal of Neurology, Neurosurgery and Psychiatry, 60 (4)., 403–410. Garrard, P., & Hodges, J. R. (1999). Semantic dementia: Implications for the neural basis of language and meaning. Aphasiology, 13 (8)., 609–623. Gates, G. A., Beiser, A., Rees, T. S., D’Agostino, R. B., & Wolf, P. A. (2002). Central auditory dysfunction may precede the onset of clinical dementia in people with probable Alzheimer’s disease. Journal of the American Geriatric Society, 50, 482–488. Goldstein, K. (1995). The organism: A holistic approach to biology, derived from pathological data in man. New York: Zone Books. Grossman, M., Rhee, J., & Moore, P. (2005). Sentence processing in frontotemporal dementia. Cortex, 41, 764–777. Guiraud, P. (1956). Psychiatrie clinique. Paris: Le Francois. Gustafson, L., Elfgren, C., & Passant, U. (2004). Fronto-temporal dementia: Diﬀerentiation from Alzheimer’s disease. Polish Journal of Geriatric Psychiatry, 1 (4)., 279–292. Harciarek, M., & Jodzio, K. (2005). Neuropsychological diﬀerences between frontotemporal dementia and Alzheimer’s disease: A review. Neuropsychology Review, 15 (3)., 131–145. Heidenhain, A. (1929). Klinische und anatomische Untersuchungen über eine eigenartige Erkrankung des Zentralnervensystems im Praesenium. Zeitschrift Gesamte der Neurologie und Psychiatrie, 118, 49. Henry, J. D., Crawford, J. R., & Phillips, L. H. (2004). Verbal ﬂuency performance in dementia of the Alzheimer’s type: A metanalysis. Neuropsychologia, 42 (9)., 1212–1222. Hillis, A. E., & Selnes, O. (1999). Cases of aphasia or neglect due to Creutzfeldt-Jakob Disease. Aphasiology, 13 (9–11), 743–754. Hodges, J. R., Patterson, K., Oxbury, S., & Funnell, E. (1992). Semantic dementia: Progressive ﬂuent aphasia with temporal lobe atrophy. Brain, 115, 1783–1806. Ioannides, P., Karacostas, D., Hatzipantazi, M., & Ioannis, M. (2005). Primary progressive aphasia as the initial manifestation of corticobasal degeneration. A “three in one” syndrome? Functional Neurology, 20 (3)., 135–137. Jackendoﬀ, R. (2000). Fodorian modularity and representational modularity. In Y. Grodzinsky, L. P. Shapiro, & D. Swinney (Eds.), Language and the brain. Representation and processing (pp. 3–30). London: Academic Press. Jakob, A. (1921). Über eine der multiplen Sklerose klinisch nahestehende Erkrankung des Zentralnervensystems (spastische Pseudosklerose) mit bemerkenswertem anatomischem Befunde. Mitteilung eines vierten Falles. Medizinische Klinik, 17, 372–376. Kaplan, E., Goodglass, H., & Weintraub, S. (1983). The Boston Naming Test. Philadelphia: Lea & Febiger.

322

Pa˛chalska

Kempler, D. (1995). Language changes in dementia of the Alzheimer type. In R. Lubinski (Ed.), Dementia and communication (pp. 98–114). Los Angeles, CA: Singular Publishing. Kertesz, A. (1998a). Pick’s disease and Pick’s complex: Introductory nosology. In A. Kertesz & D. G. Munoz (Eds.), Pick’s disease and Pick’s complex (pp. 1–11). New York: Wiley-Liss. Kertesz, A. (1998b). Arnold Pick: A historical introduction. In A. Kertesz & D. G. Munoz (Eds.), Pick’s disease and Pick’s complex (pp. 13–21). New York: Wiley-Liss. Kertesz, A. (2003). Pick complex: An integrative approach to frontotemporal dementia: Primary progressive aphasia, corticobasal degeneration, and progressive supranuclear palsy. Neurologist, 9, 311–317. Kertesz, A. (2005). Frontotemporal dementia: One disease, or many? Probably one, possibly two. Alzheimer’s Disease and Associated Disorders, 19 (Suppl 1), S19–24. Kertesz, A., & Poole, E. (1974). The aphasia quotient: The taxonomic approach to measurement of aphasic disability. Canadian Journal of Neurological Sciences, 1, 7–16. Knibb, J. A., & Hodges, J. R. (2005). Semantic dementia and primary progressive aphasia: A problem of categorization? Alzheimer Disease and Associated Disorders, 19 (Suppl 1), S7–14. Knopman, D. S., Mastri, A. R., Frey, W. H., Sung, J. H., & Rustan, T. (1990). Dementia lacking distinctive histologic features: A common non-Alzheimer degenerative dementia. Neurology, 40 (2)., 251–256. Kropp, S., Schulz-Schaeﬀer, W. J., Finkenstaedt, M., Riedemann, C., Windl, O., Steinhoﬀ, B. J., et al. (1999). The Heidenhain variant of Creutzfeldt-Jakob disease. Archives of Neurology, 56 (1)., 55–61. Lebrun, Y. (2003). A. R. Luria and non-volitional verbal behaviour. Acta Neuropsychologica, 1 (1)., 22–33. Lebrun, Y., Devreux, F., & Rousseau, J. J. (1986). Language and speech in a patient with a clinical diagnosis of progressive supranuclear palsy. Brain and Language, 27, 247–256. Leszek, J., Malyszczak, K., Janicka, B., Kiejna, A., & Wiak, A. (2003). Total tau in cerebrospinal ﬂuid diﬀerentiates Alzheimer’s disease from vascular dementia. Medical Science Monitor, 9 (11)., CR484–488. Litvan, I., Agid, Y., Calne, D., Campbell, G., Dubois, B., Duvoisin, R. C., et al. (1996). Clinical research criteria for the diagnosis of progressive supranuclear palsy (SteeleRichardson-Olszewski syndrome): Report of the NINDS-SPSP international workshop. Neurology, 47 (1)., 1–9. Lund and Manchester Groups (1994). Clinical and neuropathological criteria for frontotemporal dementia. Journal of Neurology, Neurosurgery and Psychiatry, 57, 416–418. Luria, A. R. (1977). Neuropsychologial studies in aphasia. Neurolinguistics 6. Amsterdam: Swets & Zeitlinger B.V. Luzzatti, C., & Poeck, K. (1991). An early description of slowly progressive aphasia. Archives of Neurology, 48, 228–229. MacQueen, B. D. (2003). How a sentence unfolds. Acta Neuropsychologica, 1 (4)., 382–406. Mastrianni, A., & Roos, R. P. (2000). The prion diseases. Seminars in Neurology, 20 (3)., 337–352.

Progressive language and speech disorders in dementia

323

Mendez, M. F., & Cummings, J. L. (2003). Dementia: A clinical approach (3rd ed.). Philadelphia: Butterworth-Heinemann (Elsevier). Mesulam, M. M. (1982). Slowly progressive aphasia without generalised dementia. Annals of Neurology, 11, 592–598. Mesulam, M. M. (2001). Primary progressive aphasia. Annals of Neurology, 49, 425–432. Miller, B. L., Boone, K., Mishkin, F., Schwartz, J. R., Koras, N., & Kushii, J. (1998). Clinical and neuropsychological features of frontotemporal dementia. In A. Kertesz & D. G. Munoz (Eds.), Pick’s disease and Pick’s complex (pp. 23–32). New York: Wiley-Liss. Neary, D., Snowden, J. S., Northen, B., & Goulding, P. J. (1998). Dementia of frontal lobe type. Journal of Neurology, Neurosurgery and Psychiatry, 51 (3)., 353–361. Pa˛chalska, M., Kaczmarek, B. L. J., & Knapik, H. (1995). Cracow Neurolinguistic Battery of Aphasia Examination. Aphasiology, 9 (2)., 193–206. Pa˛chalska, M., Kurzbauer, H., & MacQueen, B. D. (2002). Acquired organic mutism in the course of Creutzfeldt-Jakob disease (Heidenhain variant): A case study. Stem-, Spraak- en Taalpathologie, Case Studies in Neurolinguistics, 11 (1), 38–46. Pa˛chalska, M., Kurzbauer, H., MacQueen, B. D., Formin´ ska-Kapus´cik, M., & Herman-Sucharska, I. (2003). Neuropsychological features of rapidly progressive dementia in a patient with an atypical presentation of Creutzfeldt-Jakob disease. Dementia and Depression, 2, 22–23. Pa˛chalska, M., & MacQueen, B. D. (1998). Krakowska Bateria Oceny Funkcji Prawej Półkuli Mózgu [Cracow right hemisphere functional battery]. Cracow: Foundation for Persons with Brain Dysfunction. Pa˛chalska, M., & MacQueen, B. D. (2001). Episodic aphasia with residual eﬀects in a patient with progressive dementia resulting from a mitochondrial cytopathy (MELAS). Aphasiology, 15 (6)., 599–615. Pa˛chalska, M., & MacQueen, B. D. (2002). The collapse of the US–THEM structure in aphasia: A neuropsychological and neurolinguistic perspective. In A. Duszak (Ed.), Us and others. Social identities across languages, discourses, and cultures (pp. 481–503). Amsterdam: John Benjamins. Pasquier, F., & Delacourte, A. (1998). Non-Alzheimer degenerative dementias. Current Opinion in Neurology, 11, 417–427. Ross, G. W., Cummings, J. L., & Benson, D. F. (1990). Speech and language alterations in dementia syndromes: Characteristics and treatment. Aphasiology, 4, 339–352. Selnes, O. A., & Harciarek, M. (2005). Primary progressive aphasia without dementia. In K. Brown (Ed.), The encyclopedia of language and linguistics (2nd ed., pp. 88–91). Amsterdam: Elsevier Science. Snowden, J. S., & Neary, D. (1993). Progressive language dysfunction and lobar atrophy. Dementia, 4 (3)., 226–231. Stern, Y. (2002). What is cognitive reserve? Theory and research application of the reserve concept. Journal of the International Neuropsychological Society, 8, 448–460. Stern, Y., Zarahn, E., Hilton, H. J., Flynn, J., DeLaPaz, R., & Rakitin, B. (2003). Exploring the neural basis of cognitive reserve. Journal of Clinical and Experimental Neuropsychology, 25 (5)., 691–701. Varma, A. R., Adams, W., Lloyd, J. J., Carson, K. J., Snowden, J. S., Testa, H. J., et al. (2002). Diagnostic pattern of regional atrophy on MRI and regional cerebral blood ﬂow change on SPECT in young onset patients with Alzheimer’s disease,

324

Pa˛chalska

frontotemporal dementia and vascular dementia. Acta Neurologica Scandinavica, 105, 261–269. Wechsler, D. (1981). WAIS-R manual: Wechsler adult intelligence scale–revised. San Antonio, TX: Psychological Corporation. Wechsler, D. (1986). WMS-R manual: Wechsler memory scale–revised. San Antonio, TX: Psychological Corporation.

Author index

Page entries in bold refer to tables/ﬁgures. Adams, J. H. 45 Adams, W. 304 Adolphs, R. 49, 52 Agid, Y. 147, 306 Agliotti, S. 236, 236 Aharon-Peretz, J. 46 Ahlskog, J. E. 145 Alajouanine, T. 3, 4, 169 Alarcon, N. B. 74 Albert, M. 141, 169, 178 Alexander, G. E. 137, 138, 140, 141, 142, 143, 146 Allen-Burge, R. 275, 276 Amparo, E. 45 Andelman, F. 198 Andresen, E. M. 83 Ansaldo, A. I. 294 Arabia, C. 161 Archer, B. 224, 238 Armstrong, E. 8, 93, 97, 100, 172, 181, 182, 188, 189, 195, 198, 199, 204, 205, 225 Aronson, A. E. 307 Aten, J. L. 184 Auer, P. 235 Aust, C. 24 Austin, J. 117, 293 Auther, L. 226 Avent, J. R. 184 Azrin, N. A. 73 Baer, D. M. 79, 80, 81 Bainton, D. 246 Bakay, R. A. E. 141 Baker, E. 157 Ball, M. J. 1, 3, 4, 5, 6, 8, 92, 168, 303, 315 Bara, B. G. 44, 48

Baresi 247 Barnes, M. A. 44, 46, 49, 51 Baron-Cohen, S. 48, 49 Barry, C. 59, 161, 164 Bartels, C. 19, 22 Bassich, C. J. 169 Basso, A. 39 Bastiaanse, R. 224, 245, 249, 250, 251, 253 Baum, S. R. 126 Bayles, K. A. 130 Bayley, K. 273 Bayley, M. 84 Beblo, Th. 22 Bechara, A. 49 Beeke, S. 182, 183, 233 Behrens, S. J. 125 Beiser, A. 301 Béland, R. 110 Benali, H. 292 Benecke, R. 169 Benke, T. 307 Benson, D. F. 168, 299, 316 Benzing, L. 157, 164 Berger, J. 170 Berger, P. L. 95, 96 Bergquist, T. 272 Berndt, R. S. 230, 249, 251 Bernstein, B. 108 Bernstein-Ellis, E. 98, 189 Besse, J.-M. 108 Bester, S. 79, 194, 218 Beukelman, D. R. 77, 171 Bibby, H. 49 Biber, D. 196 Biddle, K. R. 54 Bihrle, A. M. 285

326

Author index

Binder, G. M. 33, 59 Bishara, S. M. 59, 60 Bitensky, J. 84 Biuethmann, H. 309 Black, S. E. 185, 274, 275 Blanken, G. 4, 20, 156, 161, 162, 164 Bliss, L. S. 54 Blum, A. 288 Bobholz, J. A. 149, 150 Boccardi, M. 304 Body, R. 53, 55, 61, 168 Boeve, B. F. 301 Bogner, J. 272 Boller, F. 169, 178 Bollinger, R. L. 184 Bond, F. 60, 271 Boone, K. 304 Boongird, P. 130, 131, 132 Boonklam, R. 130, 131, 132 Booth, S. 182, 273, 274, 276 Borke, R. C. 141 Borkowska, A. 304 Bormann, T. 156, 162 Bornhofen, C. 46, 47, 49 Borod, J. C. 198 Boshart, J. 49 Bottini, G. 292 Boulton, C. 148 Bourgeois, M. 84, 275, 276 Bowler, D. M 48 Boylstein, C. 197 Bracy, C. A. 54 Braden, C. L. 84 Brain, R. 169 Branford, W. 232 Brassard, C. 93 Brazis, P. W. 309 Brinson, G. 146 Britz, A. 19, 22 Broadbent, G. 137 Broca, P. 92 Broe, G. A. 271 Brookshire, B. L. 55, 56, 57, 58, 62 Brown, J. W. 6, 307, 315, 318, 319 Brown, P. 43, 45 Brownell, H. H. 285, 287, 288 Bruce, C. 273 Brumﬁtt, S. 184, 194 Brunner, R. J. 140 Bryan, K. 178, 255, 273, 274, 289 Buckingham, H. W. 28, 29, 30, 35, 169 Büeler, H. 309 Buell, U. 146 Bugbee, J. K. 274

Bunning, S. 48 Burgio, L. 275, 276 Burt, D. M. 52 Buskell, R. 188, 189 Butterworth, B. 35, 36, 157, 160, 307 Button, G. 100 Buttsworth, D. L. 57 Byng, S. 72, 77, 198, 199, 274 Cabeza, R. 149, 290 Caine, E. D. 169 Caligiuri, M. P. 184 Calne, D. 306 Campbell, G. 306 Candlin, C. N. 186 Canetti 10 Cannito, M. P. 50 Capaso, R. 40 Cappa, S. F. 137, 139, 140, 141, 143, 147, 148 Caramazza, A. 40, 157, 158, 159, 160, 161, 164, 249 Cardebat, D. 285 Cariski, D. 79, 273, 274, 275 Carpenter, C. M. 225 Carrol, J. M. 115 Carson, K. J. 304 Carter, R. 196 Cavallotti, G. 140 Cerhan, J. H. 301 Chafe, W. L. 232 Champagne, M. 116, 119, 284, 288, 291 Chan, J. L. 127, 128, 130 Channon, S. 44, 47, 49 Chantraine, Y. 287 Chapey, R. 3, 83 Chapman, S. B. 53, 55, 56, 57, 58, 62, 168 Charolles, M. 118 Cherney, H. J. 140, 150 Chiarello, C. 286, 291 Chipere, N. 251 Chomsky, N. 29, 294 Christman, S. 28, 29, 35 Chung, K. 3, 4, 8 Cicerone, K. D. 49, 272, 273 Clark, H. H. 44, 118 Claughton, J. S. 232 Clinchot, D. 272 Code, C. 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 17, 18, 20, 21, 23, 24, 25, 28, 29, 42, 55, 60, 87, 92, 107, 111, 125, 136, 156, 168, 169, 170, 181, 195, 198, 213, 220, 237, 255, 259, 270, 272, 276, 277, 278, 280, 284,

Author index 288, 289, 290, 291, 293, 294, 303, 305, 315 Coelho, C. A. 55, 56, 57, 58, 59, 263, 272, 276 Cohen Conger, J. 272 Coltheart, M. 248 Combrink, J. G. H. 223 Conan, M. 181 Conger, A. J. 272 Cooper, I. S. 139 Cooper, L. J. 77 Cooper, W. E. 125, 126, 132 Copeland, G. 235 Copland, D. A. 140, 150 Corrigan, J. 272 Corrigan, P. W. 49 Corso, M. 55 Cortazzi, M. 196 Côté, H. 288, 289 Cowell, S. F. 7, 23 Cowin, K. 181 Cramon, D. 272 Cramon, G. M.-v. 272 Crawford, J. R. 49, 50, 303 Creutzfeldt, H. G. 309 Crisp, J. 182 Critchley, H. 52 Critchley, M. 169, 173, 177, 284 Croker, V. 50 Crosson, B. 44, 48, 138, 139, 140, 142, 143, 144, 145, 146, 148, 149, 150 Cruice, M. 75, 82 Crum, R. 218, 219 Crutcher, M. D. 138 Culhane, K. A. 53, 55 Cummings, J. L. 168, 299, 301, 304, 316 Curran, J. P. 272 Cutica, I. 48 D’Agostino, R. B. 301 Dahlberg, C. 272 Damasio, A. R. 52, 139, 140, 141 Damico, J. 1, 78, 92, 93, 97, 99, 100, 183, 188, 235 Danly, M. 125 Daoust, H. 288, 289 Dapretto, M. 292 Darby, D. 46, 52 Dardarananda, R. 128, 130 Darley, F. L. 92, 307 Dass, R. 218 David, R. 246 Davis, G. A. 56, 183, 184 Davis, H. L. 49

327

Davis, K. E. 95 Davis, L. E. 139 Dawe, K. 6, 303, 315 de Gaulmyn, M.-M. 108 De Long, M. R. 138, 141, 142, 143 De Raad, A. O. 77 De Raedt, R. 302 de Wilde, M. 161 DeArmond, S. J. 309 Dechongkit, S. 130, 131, 132 Delacourte, A. 304 DeLaPaz, R. 304 Delis, D. C. 287 Dell, G. S. 34, 132, 158, 159, 161 Deloche, G. 260, 261 Denes, G. 169, 178 Dennis, M. 44, 46, 49, 51 DeRuyter, F. 276 Desai, N. P. 309 Deser, T. 56 Desmond, J. E. 292 Devereux, R. 271, 272 Dierckx, E. 302 Dijkstra, K. 275, 276 Dittmann, J. 156, 161, 164 Docking, K. 138 Dolan, R. J. 52 Doody, P. 168 Dorian, N. C. 232, 233 Douglas, J. M. 53, 57, 61 Dow, R. S. 138 Doyle, D. 45 Doyle, P. 84, 86 Doyon, B. 285 Drew, E. 291, 286 Druks, J. 249 Drummond, S. S. 59, 60, 184 Dubois, B. 147, 306 Duchan, J. F. 3, 75, 83, 185, 190, 198, 274, 275 Duﬀy, R. J. 55, 56, 57, 59, 268 Durán, P. 251 Durand, E. 275 Duranti, A. 96 Duvoisin, R. C. 306 Dykes, J. C. 225 Eales, C. 181 Ebert, M. H. 169 Edwards, S. 224, 245, 246, 249, 250, 253 Edwards, W. 20 Egan, G. F. 7, 23 Eggenberger, E. R. 309 Eggins, S. 178, 185, 278

328

Author index

Eisenberg, H. M. 24, 45 Eisenson, J. 246, 284, 293 Elbard, H. 79, 194, 218 Elfgren, C. 301, 304 Eling, P. 92 Ellis, A. W. 36, 161, 163, 248, 249 Ellis, G. J. 189 Ellmas, J. 246 Elman, R. 3, 8, 75, 83, 93, 97, 98, 100, 185, 189, 255 Elsass, L. 271 Emig, J. 98 Enderby, P. 246 Engedal, K. 129 Engell, B. 80, Erb, M. 292 Erlich, J. S. 53, 55, 59 Esmonde, T. 307 Ewing-Cobbs, L. 53, 55 Fabbro, F. 235, 236 Faircloth, C. A. 197 Farrell, A. D. 272 Fatkenheuer, G. 170 Fazio, F. 147 Federmeier, K. D. 235 Feeney, T. J. 275, 276 Feeny, D. H. 83 Fehr, T. 17 Feinn, R. 55 Fenelon, B. 45, 46 Ferguson, A. 93, 181, 182, 188, 189, 190 Ferreira, A. 274 Ferstl, E. C. 46 Finegan, E. 196 Finger, S. 30 Finkenstaedt, M. 309 Finlayson, A. 79, 194 Fischer, M. 309 Fisher, C. M. 137 Flamm, L. 287 Flanagan, S. 44, 48, 49, 50, 57, 60, 272 Flynn, J. 304 Fok, A. Y.-Y. 128, 130 Foldi, N. S. 287 Foley, N. C. 84 Ford, I. 45 Fordyce, D. J. 53 Formin´ ska-Kapus´cik, M. 311 Fox, P. T. 145, 149 Frackowiak, R. S. 150 Frame, S. R. 232 Frank, A. 201 Frank, E. 50

Franklin, S. 250 Frattali, C. 87, 88, 274 Frazer, W. 140 Freedman-Stern, R. 225, 235 Frege, G. 118 Freud, S. 28, 32, 39, 87, 92, 245 Frey, W. H. 305 Fridriksson, J. 217 Friedland, D. 188 Friston, K. J. 150 Frith, C. D. 52 Frith, U. 48 Fritsch, T. 275 Fromkin, V. 127, 129, 158 Fuchs, S. 49, 50 Fugate, L. 272 Fujita, I. 235 Fukuda, M. 148 Fünfgeld, M. 19 Funnell, E. 163, 305 Gabrieli, J. D. E. 292 Gagnon, D. A. 34, 158, 159 Gagnon, J. 285 Gall, F. 92 Galski, T. 53, 56, 57, 58, 62 Gamble, A. 55 Gandour, J. 126, 127, 128, 129, 130, 131, 132 Gannaelli, T. A. 45 Gannaway, R. 232 Garcia, L. 3, 83 Gardner, H. 285, 287, 288 Garﬁnkel, H. 94, 96 Garmen, M. 250 Garratt, H. 178 Garrett, M. F. 158, 165 Gates, G. A. 301 Gennarelli, T. 45 Gergen, K. J. 95 Gerhand, S. 164 Geroldi, C. 304 Gersh, F. 141 Gersh, S. 140 Gerstle, J. 275, 276 Geschwind, N. 43, 92, 140, 157 Gibbs, R. W. 48 Giles, E. 307 Gilpin, S. 72, 77, 198 Ginet, D. 108 Giroux, F. 285, 287, 288 Gleber, J. 287 Glindemann, R. 184 Glosser, G. 56

Author index Glover, G. H. 292 Goda, A. J. 86 Godfrey, H. P. 59, 60, 271, 272 Goﬀman, E. 94, 95, 186 Goins, K. E. 205 Gokay, D. 149, 150 Goldstein, H. 78, 80, 84 Goldstein, K. 223, 319 Goloskie, S. 125, 132 Goodglass, H. 157, 247, 252, 302 Goodwin, C. 93, 96, 97, 99, 185, 233 Gordon, A. C. L. 49 Gordon, D. 45, 46 Gordon, J. K. 161 Gotts, S. J. 28, 39 Goulding, P. J. 162, 305 Goulet, P. 285, 286, 288, 289, 291 Graﬀ-Radford, N. R. 126, 139, 309 Grafman, J. 52 Graham, D. I. 45 Graham, K. S. 163 Graham, N. 100, 163 Grant, S. 277 Graybiel, A. M. 138 Green, C. D. 31 Green, R. E. A 50 Gregory, R. 148 Grela, B. 55 Grice, H. P. 44, 45, 47, 50, 53, 116, 117 Grodd, W. 292 Gross, R. E. 148 Grossman, M. 305 Grossman, R. G. 43, 48 Gubrium, J. 197 Guendouzi, J. A. 168 Guger, S. 46 Guidotti, M. 140 Guiraud, P. 305 Gumperz, J. J. 190 Gustafson, L. 301, 304 Guthke, T. 46 Guyatt, G. H. 83 Haak, N. J. 57 Haas, J. C. 156 Hadar, U. 149 Hagan, C. 53 Hale, S. 86 Hall, B. 138, 149 Halliday, G. M. 7 Halliday, M. A. K. 43, 56, 59, 172, 173, 178, 190, 206, 270, 278 Hallowell, B. 8, 181 Halson, D. 48

329

Hand, L. 51, 55, 60, 61, 273, 276, 277, 278 Hanson, W. R. 147 Happé, F. 48, 288 Harasty, J. 7, 23 Harciarek, M. 299, 301, 304, 305 Harding-Clark, J. 149 Harley, T. 28, 29, 34, 35, 36, 37, 38, 39 Harris, Z. 119, 120 Harrison, J. 140, 148 Hartley, D. 30 Hartley, L. L. 53, 55, 56, 58, 271 Harward, H. 53, 54, 55 Hasan, R. 56, 59, 278 Hatzipantazi, M. 306 Haverkate, H. 48 Havill, J. H. 272 Hayashi, M. 235 Haynes, W. O. 57 Head, H. 245 Hebb, D. O. 33 Hecaen, H. 169 Heeschen, C. 182 Heidenhain, A. 309, 311, 312 Heilman, K. M. 43, 139 Helasvuo, M. 182 Helﬀenstein, D. A. 272 Heling, G. 224, Helm-Estabrooks, N. 140, 141 Helmick, J. W. 20 Hemsley, G. 2, 3, 23, 181, 198 Hengst, J. A. 182, 190, 232 Henry, J. D. 303 Henschen, S. E. 137 Heritage, J. C. 96, 97, 99, 186 Herman-Sucharska, I. 311 Herrmann, M. 2, 3, 17, 18, 19, 20, 21, 22, 23, 24, 87, 181, 198 Herzig, A. 116, 119 Hickey, E. M. 84 Hickin, J. 181 Hickson, L. 75, 82, 272, 273 Hier, D. B. 168 High, W. M. Jr. 45 Hill, C. L. 182, 233 Hill, M. A. 168 Hillis, A. E. 157, 160, 161, 164, 310 Hilton, H. J. 304 Hinckley, J. J. 85 Hirsh, K. W. 161, 163 Hodges, J. R. 162, 163, 305, 306, 307 Hoﬀmann, C. 170 Hogan, A. 3, 21, 181 Hohenstein, C. 307

330

Author index

Hojgaard, K. 147 Holderbaum, C. S. 120 Holland, A. 3, 75, 80, 81, 84, 93, 98, 109, 184, 213, 217 Holland, D. 272, 276 Hollerbach, B. 140 Holmes, J. 201 Homskaya, E. D. 32, 39 Hopper, T. 84 Hough, M. S. 56, 287 Howard, D. 157, 160, 161, 164, 247 Huber, W. 80, 162, 169, 247, 287 Hughes, C. 49 Humphreys, G. W. 150, 159 Hunston, S. 196, 201 Hunter, M. 45, 46 Hurkmans, J. 250 Hutter, B. 80 Hydén, L.-C. 195, 197 Ioannides, P. 306 Ioannis, M. 306 Ireland, C. 72, 77, 198 Irwin, W. H. 266, 268 Israel, D. 115 Ivnik, R. J. 301 Jackson, H. F. 50 Jackson, J. H. 32, 39, 92, 245, 246 Jacob, S. 24 Jacobs, B. J. 84 Jacobs, J. R. 287 Jahn, H. 24 Jakob, A. 309 James, W. 33 Janicka, B. 300 Jbabdi, S. 292 Jeﬀerson, G. 184 Jenkins, J. J. 139, 263 Jensen, P. J. 53, 55, 56, 58 Jescheniak, J. D. 158, 160, Jiménez-Pabón, E. 139, 263 Jin, L. 196 Joanette, Y. 7, 8, 29, 119, 125, 284, 285, 286, 287, 288, 289, 290, 291, 292, 293, 294 Jodzio, K. 299, 301, 304 Johannsen-Horbach, H. 18, 19, 22 Johnson, A. F. 184, 189 Johnson, C. J. 46 Johnson, D. A. 60 Johnston, M. V. 53, 56, 57, 58, 62 Johnston, R. A. 161 Jonas, S. 139

Jones, R. H. 190 Jones, R. J. 73 Jonkers, R. 224, 249 Jordan, F. M. 57 Jordens, C. F. C. 197 Jutai, J. W. 83 Kaczmarek, B. L. J. 29, 314 Kagan, A. 3, 83, 185, 198, 274, 275 Kalinyak, M. 86 Kalmar, K. 272 Kalmek, L. 224, 238 Kameyama, S. 148 Kamio, A. 235 Kampe, K. K. W. 52 Kaplan, E. 247, 252 Karacostas, D. 306 Karaﬁn, M. S. 52 Kaszniak, A. W. 130 Katz, R. C 8, 84, 181, 259, 260, 261, 263, 264, 265, 268 Kaufman, S. 197 Kaufmann, P. M. 44, 47, 62 Kay, J. 6, 248, 249, 303, 315 Kazdin, A. E. 72, 73, 78 Keebler, M. W. 182, 205, 233 Keenan, T. 49 Keisler, L. 79, 273, 274, 275 Kelly, P. J. 145 Kemmerer, D. 249 Kemper, T. D. 96 Kempler, D. 299, 305 Kendall, E. 48 Kennedy, C. H. 74, 78, 81 Kennedy, M. 139, 140 Kenstowicz, M. 131 Kent, R. D. 177 Kersel, D. A. 272 Kertesz, A. 29, 35, 74, 126, 225, 247, 264, 304, 305, 306, 311 Keyser, A. 224 Khunadorn, F. 130, 131, 132 Kiejna, A. 300 Kimura, M. 138 Kinch, J. 44, 50, 60 Kinsella, G. 271 Kintsch, W. 57 Kircher, T. T. J. 292 Kirchner, D. M. 53 Kiss, K. 249 Klippi, A. 93, 182, 183, 185, 189, 235 Klouda, G. V. 125, 126, 134 Knibb, J. A. 305, 306 Knight, R. T. 49, 60

Author index Knight, R. G. 49, 59, 60, 271, 272 Knopman, D. S. 305 Knott, R. 250 Koch, U. 18 Kodras, J. E. 85 Kohn, S. E. 249 Koivisto, M. 285, 286 Kolk, H. 224 Koras, N. 304 Kornhuber, H. H. 140 Kozleski, E. B. 81 Kozlowski, A. 168 Krampe, H. 24, 161 Kril, J. J. 7 Kroes, H. 223 Kropp, S. 309, 311 Kubler-Ross, E. 217 Kubo, S. 116 Kufera, J. A. 54 Kuhl, D. E. 147 Kulke, F. 162 Kumpula, J. 79, 273, 274, 275 Kunz, T. 140 Kurzbauer, H. 311 Kushii, J. 304 Kutas, M. 236, 292 Laakso, M. 182, 183, 304 Labonde, E. 161 Labov, W. 196, 200, 203, 205, 225, 232, 235 Lahire, B. 108 Lakoﬀ, G. 45, 46 Lambon Ralph, M. A. 163 Lang Y. 309 Lang, A. E. 148 Lange, K. L. 230, 249, 251 Langenbahn, D. 272 LaPointe, L. L. 72, 75, 82, 84, 85, 86, 198, 289 Larkins, B. 272, 273 Lashley, K. S. 92 Lasker, J. P. 77, 85 Lassen, N. A. 147 Laughlin, S. A. 140 Lavizzo-Mourey, R. 141 Lawler, E. N. 161 Lawrence, A. E. 45 Le Blanc, B. 285 Le Dorze, G. 285 Lebrun, Y. 305, 307, 308 Lecours, A.-R. 7, 8, 29, 36, 111, 125 LeDorse, G. 93 Lee, A. G. 309

331

Lee, S. S. 292 Leer, E. V. 56, 58 Lehmann, C. 170 Leiner, A. L. 138 Leiner, H. C. 138 Leiwo, M. 235 Lemarié, J. 113 Lemieux, S. 287 Lenay, Ch. 113 Lenius, K. L. 72 Leonard, C. M. 149, 150 Lesser, R. 168, 248 Leszek, J. 300 Leube, D. T. 292 Levelt, W. J. M. 157, 158, 159, 160, 164 Levin, H. S. 43, 45, 48, 53, 55, 56, 57, 58, 62 Levine, H. L. 140 Levine, R. 79, 273, 274, 275 Levinson, S. C. 43, 45, 184 Levita, E. 43 Liang, J. 127, 131, 132 Lichtheim, L. 137, 246 Liles, B. Z. 55, 56, 57, 59 Lind, M. 253 Lindgren, A. G. H. 168 Lindsay, J. 182, 275 Ling, P. K. 287 Links, P. 250 Lipp, H. P. 309 Little, J. 197 Litvan, I. 306 Lloyd, J. J. 304 Lock, S. 273, 274 Lomas, J. 79, 194, 218 Lombardi, W. J. 148 Long, E. 46, 47, 49 Longacre, R. E. 203 Longin, D. 119 Lorch, M. P. 248 Lorenz, A. 161 LoVerme, S. R. 140 Loverso, F. L. 266, 267 Lozano, A. M. 148 Lu, L. 146 Lubinski, R. 75, 87, 190 Lucius-Hoene, G. 18 Luckmann, T. 95, 96 Ludlow, C. L. 169 Lulham, J. M. 271 Luria, A. 28, 29, 32, 33, 37, 38, 39, 92, 139, 247, 307, 315 Lustig, A. P. 76, 84 Luzzatti, C. 305

332

Author index

Lyon, J. G. 3, 13, 75, 79, 83, 86, 98, 273, 274, 275 Macaluso-Hayes, S. 225, 235 MacAndrew, S. B. G. 34, 35, 36, 37, 38, 39 Machetanz, J. 169 Macken, E. 115 MacQueen, B. D. 311, 312, 313, 314, 315, 317 Malapani, C. 147 Malec, J. 272 Malvern, D. D. 251 Malyszczak, K. 300 Mann, W. 120 Manning, M. L. 45, 46 Marie, P. 137, 246 Marquardt, T. P. 50, 235 Marrelec, G. 292 Marsh, N. V. 59, 60, 272 Martin, I. 46, 47, 48, 49, 60 Martin, J. R. 172, 173, 196, 204 Martin, N. 34, 158, 159 Martinez, A. 292 Masterson, J. 249 Mastri, A. R. 305 Mastrianni, A. 309 Matejka, J. 54 Matthiessen, C. M. I. M. 172, 173, 178 Maurel, F. 113 Maxim, J. 178, 182, 273 Mayley, Y. 186 McArdle, C. B. 45 McCabe, A. 54, 55, 170, 196 McCarney, C. T. 184, 189 McCormick, K. 224, 229, 232, 235 McDonald, S. 42, 44, 46, 47, 48, 49, 50, 51, 53, 55, 56, 57, 58, 60, 62, 271, 272, 277, 288 McFall, R. M. 43, 59, 60, 61 McFarling, D. 139 McKevitt, C. 197, 199 McLellan, D. R. 45 McPhee, J. 188, 189 Medd, J. 272 Mega, M. S. 140, 146 Mendelsohn, D. 53, 55 Mendez, M. F. 301, 304 Menn, L. 235 Messa, C. 147 Mesulam, M. M. 149, 305 Metter, E. J. 147 Meyer, A. S. 157, 158 Meyers, A. R. 83

Mezirow, J. 218, 219 Miceli, G. 40, 160, 249 Michelow, D. 125, 132, 287 Middleton, F. A. 138 Milders, M. 49, 50 Miller, B. L. 304 Miller, D. 36 Miller, G. A. 48 Mills, R. H. 260, 262, 263 Milne, E. 52 Milton, S. B. 44, 53, 59 Mintum, M. 149 Miozzo, M. 159 Mishkin, F. 304 Mitchum, C. C. 230 Moen, I. 125, 127, 128, 129, 130, 131, 132, 253 Moﬀat, N. J. 50 Mohr, C. M. 149, 150 Mojahid, M. 113 Monakow, C. von. 137 Monchi, O. 290 Monetta, L. 286, 288, 291 Monory, B. 59, 60 Monrad-Krohn, G. H. 125 Montgomery-West, P. 86 Moore, C. 150 Moore, P. 305 Moreau, N. 110 Moreno, E. M. 236 Morgan, J. 117 Morris, J. 250 Moses, J. A. 287 Moss, B. 199 Moulard, G. 260, 261 Moutier, F. 137 Mugford, J. 2, 3, 18 Müller, D. 1, 2, 3, 4, 6, 18, 20, 21, 92, 168, 181 Müller, N. 4, 6 Munoz, M. L. 235 Murasugi, K. G. 287 Murdoch, B. E. 56, 57, 136, 1371, 138, 139, 140, 149, 150 Murison, R. 75, 82 Musson, N. D. 184 Myers, P. S. 288, 289 Mysiw, W. 272 Nabeemeah, K. 224, 238 Nadeau, S. E. 139, 140, 142, 145, 146 Naeser, M. A. 128, 130, 140, 141, 142 Nagy, V. T. 261, 263, 264 Narabayashi, H. 146

Author index Nash, W. 196 Neary, D. 162, 305 Nespoulous, J. L. 7, 55, 59, 107, 108, 109, 110, 111, 113, 116, 119, 120 Neulinger, K. 46, 47, 49 Neuman-Stritzel, T. 232 Newhoﬀ, M. 217, 251, 274 Newman, J. R. 20 Newton, A. 60 Nickels, L. 157, 161, 164 Nicol, J. 126, 132 Nielsen, J. M. 137 Nocentini, U. 286, 291 Noe, A. 113 Norris, S. 190 Nyberg, L. 149 O’Brien, J. 48 O’Doherty, J. 52 O’Flaherty, C. A. 53 O’Regan, J. K. 113 Obler, L. K. 198 Ochberg, R. L. 197 Oelschlaeger, M. L. 93, 97, 99, 100, 183, 188 Ogilvy, D. 226, 238 Ojemann, G. A. 139, 143, 145 Okasha, S. 100 Oksengaard, A. R. 129 Olness, G. S. 182, 198, 199, 205, 225, 226, 233, 234 Olsen, D. R. 49 Olsen, T. 147 Olswang, L. B. 74, 84 Orchard-Lisle, V. 157 Osvaldsson, K. 184, 185 Ouellet-Plamondon, C. 290 Oxbury, S. 163, 305 Ozonoﬀ, S. 48 Pa˛chalska, M. 311, 312, 313, 314, 315, 318, 319 Packard, J. L. 130 Page, R. E. 201 Painter, C. 172, 173 Palmer, J. M. 20 Palumbo, C. L. 137, 141, 142 Papagno, C. 4, 138, 139, 140, 142, 144, 156 Papineau, D. 100 Paradis, C. 110, 111 Paradis, M. 225, 245, 254 Parker, M. 53, 168 Parkin, S. 148

333

Parr, S. 72, 75, 77, 198, 199, 274, 275 Pasquier, F. 304 Passant, U. 301, 304 Patrick, D. L. 83 Patterson, K. 162, 163, 305 Paul, K. 197 Pavard, P. 117 Pavlov, I. 28, 29, 30, 31, 32, 36, 37, 38, 39, 40 Payer, M. 288 Pearce, S. 44, 47, 48, 50, 51, 53, 57, 58, 62 Pearl, G. 181 Pell, M. D. 126 Pellijeﬀ, A. 44, 49 Penﬁeld, W. 137, 139 Penn, C. 93, 188, 222, 226, 232, 235, 237 Pennanen, C. M. 304 Perani, D. 147 Perkins, M. 53, 55, 61, 98, 99, 168, 182, 273, 274, 276 Perrett, D. 52 Perrier, D. 161 Perry, J. 115 Petersen, R. C. 301 Peterson, P. M. 149 Petheram, B. 199 Petty, S. H. 130 Pfaender, F. 113 Pfaﬀ, A. 271 Phelps, M. E. 147 Phillips, L. H. 303 Pick, L. H. 198 Pickard, L. 79, 194, 218 Pillon, B. 147 Pimentel, J. I. 55, 57, 58, 62 Pincus, D. 288 Plaut, D. C. 28, 39 Poeck, K. 162, 169, 247, 305 Poewe, W. 307 Polinsky, R. J. 169 Pollock, M. 117 Ponglorpisit, S. 130, 131, 132 Ponjaert-Kristoﬀersen, I. 302 Ponsford, J. 53, 56, 57, 59, 61 Porch, B. 8, 92, 262 Porter, G. 247 Posner, M. I. 149 Potter, H. H. 285 Pouk, J. A. 48 Pound, C. 8, 75, 181, 274, 275 Prescott, T. E. 266, 267 Prevignano, C. L. 190 Pribram, K. H. 50 Price, C. J. 149, 150

334

Author index

Prigatano, G. P. 44, 50, 53 Prince, S. 57 Prins, R. S. 250, 251 Proctor, A. 55, 56 Prutting, C. A. 53, 56, 59 Puel, M. 285 Purvis, K. 44, 49 Quinlan, P. T. 159 Rabinowitz, J. A. 272 Raichle, M. E. 149 Rakitin, B. 304 Ramsey, S. 149 Rapp, A. M. 292 Rapp, B. 157, 158, 160, 164 Read, S. 168 Reason, J. 117 Rees, T. S. 301 Reiche, W. 146 Reichle, T. 18 Reilly, K. F. 235 Reimers, T. M. 77 Reinvang, I. 130 Reivich, K. 214 Rewega, M. 84 Reynolds, A. F. 139 Rhee, J. 305 Richards, B. J. 251 Richburg, T. 50 Riddoch, M. J. 159 Riedemann, C. 309 Riege, W. H. 147 Riklan, M. 139 Riley, L. 266, 267 Ringelstein, E. B. 146 Rios-Brown, M. 50 Ripich, D. 275 Rispens, J. 249, 250, 253 Rittman, M. 197 Rizzo, M. 140, 141 Roberge, P. T. 223 Roberts, J. 233 Roberts, L. 137, 139 Roberts, P. M. 8, 181, 286, 291 Robey, R. R. 259 Robin, D. A. 126 Rochon, E. 251 Rodman, R. 127 Roelofs, A. 157, 158 Roger, P. 8 Rogers, M. A. 74 Rogers, M. F. 95 Rollins, J. 44, 50, 60

Romani, C. 157 Roncadin, C. 46 Rondeau, G. 85 Roos, R. P. 309 Rorie, K. D. 198 Rose, J. E. 43, 48 Rosenbek, J. 273, 274, 275 Rosenbek, J. 79, 273, 274, 275 Ross, G. W. 299, 316 Ross, K. B. 75, 86 Roth, D. 275, 276 Rothi, L. J. 139 Roueche, J. R. 53 Rousselle, M. 260, 261 Rowley, D. 29 Rule, A. 44, 49 Ruml, W. 40 Rustan, T. 305 Rutter, B. 4, 6 Ryalls, J. H. 125, 130, 132 Sabourin, L. 285 Sacks, H. 99, 184 Sacks, O. 195 Saddy, J. D. 287 Sadek, J. R. 146, 149, 150 Saﬀran, E. M. 34, 158, 159, 235, 251 Safran, A. 43 Saint-Cyr, J. A. 146 St. George, M. 292 Salembier, P. 117 Salmon, D. P. 162 Salter, K. 83 Samson, A. 205 Sands, D. J. 81 Santoro, J. M. 48, 49 Sarno, M. T. 43 Sasanuma, S. 235 Saunders, C. 46, 47, 48, 49, 60 Sayers, E. J. 197 Schachar, R. 46 Scheﬀ, T. J. 95, 99 Schegloﬀ, E. A. 99, 182, 184 Schenone, P. 292 Scherer, L. C. 292 Schiﬀrin, D. 274 Schlosser, R. W. 79 Schneider, S. L. 230, 249, 251 Schneiderman, E. I. 287 Schnitzer, M. L. 235 Schönle, P. W. 169 Schriefers, H. 158 Schuell, S. M. 87, 92, 139, 246, 263 Schultz, M. C. 259

Author index Schulz-Schaeﬀer, W. J. 309 Schum, D. 46, 48 Schumacher, M. 22, 158 Schunk, D. H. 44 Schwartz, I. F. 79, 80, 81 Schwartz, J. R. 304 Schwartz, M. F. 34, 158, 159, 251 Scott, R. B. 148 Searle, J. R. 43, 45, 116, 117, 293 Seger, C. A. 292 Seibert, L. K. 50 Seligman, M. 214 Selinger, M. 266, 267 Selnes, O. A. 305, 310, 312 Senhadji, N. 290 Sereno, M. I. 292 Seron, X. 260, 261 Shadden, B. 3, 75, 77, 83, 87, 198 Shallice, T. 157, 158, 159 Shamay-Tsoory, S. G. 46 Shannon, C. E. 119 Shapiro, B. E. 125 Shapiro, L. P. 230, 249, 251 Shatté, A. 214 Sheard, C. 8, 170 Sheeran, P. 184, 194 Shigaki, C. 272, 276 Shindler, A. G. 168 Shotter, J. 96 Shum, D. 46, 47, 49 Sidtis, J. J. 126 Silburn, P. A. 138, 149 Silver, C. H. 62 Silveri, M. C. 160, 249 Silverman, J. 287 Silverman, S. 251 Simmons, N. N. 274 Simmons, T. P. 184 Simmons-Mackie, N. 3, 8, 75, 78, 79, 81, 92, 93, 97, 98, 100, 185, 255, 274, 275 Simonson, H. G. 253 Simpson, T. L. 285, 286 Singh, S. 177 Sjogren, T. 168 Ska, B. 284, 287, 288, 289, 292 Skrap, M. 235, 236 Skriver, E. 147 Slade, D. 185, 278 Sleigh, J. W. 272 Smith, G. E. 301 Smith, L. 274 Smith, R. D. 266, 267 Snow, C. 250 Snow, P. C. 53, 54, 56, 57, 59, 61, 271

Snowden, J. S. 162, 304, 305 Soares, C. 125, 132 Sobow, T. 304 Soininen, H. 304 Song, J. 53, 55, 56, 57, 58, 62 Spell, L. A. 50 Spence, S. E. 60 Sperber, D. 50, 62 Spiers, M. 48, 49 Springer, L. 184 Square, P. 185, 274, 275 Squire, L. R. 147 Starr, P. A. 141 Stein, M. 276 Steinhoﬀ, B. J. 309 Stemmer, B. 287, 294 Stern, Y. 299, 304, 319 Sterzi, R. 141, 148 Stiassny-Eder, D. 141 Stiegler, L. 8, 255 Stone, V. E. 49 Stout, C. E. 55, 57, 58, 62 Strange, B. A. 52 Strawson, P. 117 Strettles, B. 271 Strick, P. L. 138, 141, 142, 143 Stubbs, M. 196 Su, M. S. 127 Suger, G. 140 Sullivan, K. 49 Sundet, K. 127, 128, 130, 132 Sung, J. H. 305 Surian, L. 48 Swabey, D. 274, 276 Swinburn, K. 247 Tager-Flusberg, H. 49 Tanaka, R. 146 Tanenbaum, L. N. 49 Tangalos, E. C. 301 Tate, R. L. 45, 46, 271, 272 Teasdale, G. 43, 48 Teasell, R. 83 Teh, M. 48 Testa, C. 304 Testa, H. J. 304 Theodoros, D. G. 138, 149 Thibault, P. J. 190 Thompson, C. K. 98, 230, 251 Thompson, D. 140 Thompson, G. 196, 201 Thompson, J. L. 182, 226, 246 Thompson, S. 120 Thompson, W. F. 50

335

336

Author index

Thomson, I. V. 43 Threats, T. T. 74, 83, 88 Thron, A. 146 Timberlake, W. H. 169, 178 Tirassa, M. 44, 48 Togher, L. 42, 48, 51, 55, 57, 60, 61, 188, 189, 270, 272, 273, 276, 277, 278 Tomer, R. 46 Tompkins, C. A. 53, 56, 57, 58, 62, 76, 80, 84, 288, 289 Toomey, R. 49 Tranel, D. 52, 249 Tree, J. 6, 303, 315 Trepanier, L. L. 148 Tsironas, D. 86 Tsohatzidis, S. L. 116 Tucker, K. 250 Turkstra, L. S. 44, 47, 56, 57, 58, 62 Ulatowska, H. K. 168, 182, 195, 198, 199, 205, 225, 226, 233, 234, 235 Urbanczyk, B. 275, 276 Vallar, G. 137, 139, 140, 141, 143, 147 Van Buren, J. M. 141 Van der Lely, H. 48 van Dijk, T. A. 57 van Heuven, V. J. 127, 131, 132 Van Hoesen, G. W. 141 Van Lancker, D. 126, 129 Van Rensburg, C. 224 van Sommers, P. 48 van Wageningen, B. 224, 250 van Zonneveld, R. 224, 249 Vanderveken, D. 116 Vanhalle, C. 287 Varma, A. R. 304 Varney, N. 141 Venter, A. 224, 226, 238 Vermeulen, J. 224, 250 Verney, N. 140 Verté, D. 302 Vignolo, L. A. 139, 140 Vigouroux, N. 113 Virbel, J. 7, 107, 111, 113, 116, 119, 120 Vitek, J. L. 141 von Bentheim, I. 224, 226, 238f von Cramon, D. Y. 46 Vygotsky, L. 32 Wacker, D. P. 77 Wagenaar, E. 249 Waletsky, J. 196 Wallace, C. 272

Wallander, J. L. 272 Wallesch, C. W. 4, 8, 18, 19, 20, 22, 29, 125, 137, 138, 139, 140, 142, 144, 156, 160, 161, 162, 164, 168, 173 Walsh, K. W. 46, 52 Walshaw, D. 182 Walter, N. 292 Wapner, W. 287 Warburton, E. 149 Ward, E. C. 138 Watamori, T. S. 20 Watson, D. R. 186 Watson, J. D. G. 7, 23 Watts, M. 44, 47, 49 Wayland, S. 251 Weaver, W. 119 Webster, E. 215, 217 Webster, J. 250 Wechsler, F. S. 47, 272, 311 Weiller, C. 146, 149 Weinstein, E. A. 284 Weiss Doyle, A. 225, 235 Weitzner-Lin, B. 190 Welkowitz, J. 198 Wells, A. 78 Weniger, D. 162, 169, 247 Wenz, C. 19 Wepman, J. M. 246 Wernicke, C. 92 Wertz, R. T. 44, 75, 86, 182, 226, 259, 260, 264, 265, 266, 268 Wheeler, K. M. 266, 167 Whelan, B.-M. 138, 149 Whitaker, H. A. 169 Whitworth, A. 168, 249 Wiak, A. 300 Wight, H. H. 251 Wilcox, J. 183, 184 Wilkes-Gibbs, D. 118 Wilkinson, M. 44, 49 Wilkinson, R. 93, 97, 182, 185, 233, 273, 274 Williams, C. L. 161 Williams, D. H. 45 Williams-Hubbard, L. J. 225 Willmes, K. 80, 162, 247 Wilson, B. M. 55, 56 Wilson, D. 50, 62 Wilson, J. 148 Windl, O. 309 Winner, E. 44, 49, 288 Winston, J. S. 52 Wise, R. J. S. 149 Wolf, M. M. 72, 73, 74

Author index Wolf, P. A. 301 Wolfson, N. 230, 232 Woolf, C. 275 Worrall, L. E. 3, 75, 80, 81, 82, 83, 88, 93, 184, 188, 189, 272, 273, 274, 276 Wright, H. H. 251 Wyen, C. 170 Xuereb, J. 307 Yamada, T. 139 Yeterian, E. H. 141 Yiu, E. M.-L. 128, 129, 130, 133, 273, 274, 276 Ylvisaker, M. 61, 275, 276, 277

Yorkston, K. M. 55, 57, 58, 62, 171 Yoshino, M. 146 Young, A. W. 248 Young, M. E. 197 Youse, K. M. 58 Zalagens, M. R. 56, 57 Zarahn, E. 304 Zawacki, T. 146 Zettin, M. 44 Zieper, I. 169, 178 Zingeser, L. 249 Ziol, E. 275 Zoghaib, C. 79, 194

337

Subject index

Page entries in bold refer to tables/ﬁgures. Acquired Immune Deﬁciency Syndrome (AIDS) 170 Adjectives in evaluation 204 in word repetition 173, 176 Age and dementia 300, 309 in testing 76, 77 Agrammatism 224 deﬁnition of 109–110 illustration 110 writing 303 Agraphia 312 Alzheimer’s disease see Dementia Amimia 305 Amyotrophic lateral sclerosis 83, 216 Anartria 137 Anomia 33, 110, 157, 160, 306 Aphasia amnesic 162 anomic 128, 131, 157, Broca’s 125, 128, 130, 131, 132, 133, 140, 205, 246, 251 conduction 128, 130, 137 deﬁnition of 294 expressive 246 ﬂuent 162, 187, 306, global 140, 164, 309, 314 jargon 301 mixed transcortical sensory 139 motor see transcortical motor nonﬂuent 18, 22, 130, 305, 313 progressive 162, 216, 305, 306 receptive 246 semantic 162 sensory see transcortical sensory striatocapsular 139, 140

subcortical 136–150 thalamic 139–140 transcortical motor 128, 140, 142 transcortical sensory 301 Wernicke’s 125, 128, 130, 140, 162 Aphasia quotient 182, 264, 311 Apraxia of speech 5–6 Artery carotid 146 middle cerebral 146 Articulation 141, 146 imprecise 170 in microgenetic theory 318 Asperger’s syndrome 48 Ataxia in Creutzfeldt-Jakob disease 309 Atrophy 300, 312 of the temporal lobe 162, 304, 305 Attitude in clinicians 317 in speakers 44, 48, 50, 51, 208 Auditory association cortex 143 Auditory comprehension in assessment 261 in the subcortical white matter pathways model 142–143 in treatment 261–263 vs. visual comprehension 23 Augmentative alternative communication (AAC) 77, 85 Basal Ganglia see also Subcortical region 22, 136, 137, 138, 140, 141, 145, 146, 149, 150, 170 Behaviourally Referenced Rating System of Intermediate Social Skills (BRISS) 272

340

Subject index

Bilingualism 223, 224, 225, 226, 234–237, 254 Body language 219 Boston Diagnostic Aphasia Examination (BDAE) see Standardized tests Brain damage and depression 216 knowledge of 33, 92 psychosocial adjustment to 2–3 and tone 127–132 Brain stem 170 Broca’s area 142 Caudate nucleus 137, 144, 150 lesion of 142 Cerebellum 138, 170, 313 Classical view of aphasia 246, 247, 293 Code-Müller Protocols (CMP) 2–3, 18, 20–22 Code-switching 225, 233, 234, 235, 236, 237 Communication Abilities in Daily Living (CADL) see Standardized tests Communication Readiness and Use Index (CRUI) 79, 86 Compensatory strategies 18, 223, 224, 235 Comprehension 7, 44, 46, 49–50, 62, 75, 118–120, 139–143, 146, 149, 163, 246–253, 261–266, 286, 292, 305–306, 315, 318 Comprehensive Aphasia Test (CAT) see Standardized tests Conversation analysis (CA) 94, 100, 183, 188, 274 Coprolalia 169 Corpus callosum 126 Counseling 181, 186, 213, 289 deﬁnition of 215 Deafness, and aphasia 113 Dementia 168, 215, 216, 299–320 and age 300, 309 Creutzfeldt-Jakob disease (CJD) 300, 309–312 deﬁnition of 317 dementia of the Alzheimer’s type (DAT) 129, 162–163, 168, 275, 300, 301–304 and depression 302 fronto-temporal dementia (FTD) 300, 304–309 history 317 MELAS syndrome 300, 312–315

semantic dementia (SD) 162–163 subcortical dementia 307 Depression 2, 20, 216–217, 271, 302 post-stroke 22–23 Discourse analysis 54–55, 100, 196 Dominance, in tonal perception 127 Dysarthria 5, 140, 170, 171, 177, 303, 307, 315, 316 Dysgraphia 307, 310 Echolalia 169, 309 Eﬃciency, in testing 259, 266, 267 Employment, prognosis and 85, 271 Epenthesis 111 Evaluation factors inﬂuencing 199 of patient 120, 288, 289 Executive dysfunction 46 FACS see Standardized test Family aﬀect of aphasia on 87 as conversational partners 276–277 counseling of 218, 220, 289 treatment and 78, 81, 213, 276 Feedback in treatment 260, 263, 267, 272 in models of word production 159 in the response-release semantic feedback model 143 Fluency 146, 247, 285, 301, 303, 305 Frontal lobe 51, 144, 145, 236, 315 Frontostriatal circuits 22 Functional approach to treatment 75, 98, 274 Functional Assessment of Communication Skills (FACS) for Adults see Standardized tests Functional magnetic resonance imaging (fMRI) 23, 149, 150, 292 Function words 160, 173 Generalization 79, 84, 261 Genetic factors 290, 319 Gesture 110, 171, 182 Grammar, evaluation of 250 Grice’s Maxims 52–53, 54, 55 Group therapy see Therapy Handedness 290 Handicap, deﬁnition of 107–108 Helm Elicited Language Program for Syntax Stimulation (HELPSS) 84

Subject index Hemispheric Asymmetry Reduction in Older Adults (HAROLD) 290 History, evaluation and 233, 237, of family 290, 310 Human Immunodeﬁciency Virus (HIV) 170 Hypokinetic dysarthria 170, 307 Infarction 146, 147 Inferential reasoning 46 Informational theory 120 Inﬂectional morphology 109–110 Inner speech 315, 318 Intonation see also Prosody 125, 127, 132, 219 Iteration 169, 173 Jargon, as symptom of aphasia 36, 301 Language acquisition 118, 161 contact 224 deﬁcits 18, 44, 137, 142, 143, 144, 145, 146, 248, 249 impairment 45, 140, 143, 182, 195, 198 modality 39, 59, 160 neurophysiology of 28, 32, 108, 292 processing 6, 7, 101, 136, 137, 139, 150, 158, 183, 213, 223, 248 rehabilitation 7 written 157 Left hemisphere 22, 119, 125, 126, 127, 128, 129, 133 Lexicon 110, 130, 132, 157, 163, 224, 285 Life Participation Approach 3, 74, 83 Linguistics 116, clinical linguistics 125 psycholinguistics 116 Logoclonia 301, 303, 305 Magnetencephalography (MEG) 23 Memory episodic memory 290 in assessment 149 semantic memory 130, 157, 285 short-term memory 301 verbal memory 139, 287 working memory 271, 287, 290, 300, 307 Mental calculation see number processing Metaphoric language 199, 206 Microgenetic theory 318–319 Multiple sclerosis 216

341

Multilingualism see also Bilingualism 222, 223, 225, 237 Mutism 110, 299, 301, 305, 310, 319 Near Infrared Spectroscopy Optical Imaging (NIS/OI) 292 Neologisms 35, 36 Neural networks 33, 286, 287, 290, 291, 292, 293 Nouns 244, 253, 254 in assessment 249 Number processing 23–24 Palilalia 169, 173, 178, 308 PALPA see Standardized tests Parkinsonism 216 Parkinson’s disease 148, 307 Perseveration 35, 39, 46, 139, 169, 205, 301 of topics 271 Personality in evaluation 199 change of 304, 305, 307 Phoneme, perseveration of 35 Phonemic decoding 130 Phonemic errors 110, 157 Phonetic decoding 130 Phonology 5, 163, 224, 250 expressive 232, 234, 242 gestural 5 government 5 and phonetics 5 underspeciﬁcation in 131 usage based 5 PICA see Standardized tests Porch Index of Communicative Ability see Standardized tests Positron emission tomography (PET) 149, 150, 292 Pragmatics 183, 224, 287–288, 294 Pragmatic Theory 43 Progressive speech deterioration 6 Progressive supranuclear palsy (PNP) 306 Proposition 204, 317 deﬁnition of 111 Prosody deﬁnition of 125–126 emotional 285 in speech perception 219 Psycholinguistic Assessment of Language Processing in Aphasia (PALPA) see Standardized tests Psychosocial factors 18–19, 20–22, 79, 86–87

342

Subject index

Psychosocial Well-Being Index (PWI) 86 Putamen 137, 138, 141, 142, 143, 146, 150 Quality of life 3, 9, 78–79, 80–81, 82, 85, 170, 266, 299 Health Related Quality of Life (HRQOL) 83 World Heath Organization (WHO) deﬁnition of 82 Reading comprehension 140 intervention 75, 263–265 testing 132, 246, 247, 252 Recurrent utterances 3–5, 169, 271 Repetitive utterances see Recurrent utterances Recovery predictions in 29 psychosocial factors in 87 the role of the right hemisphere in 7 spontaneous 216 Rehabilitation 6–7, 17, 19, 20–21, 72 goals in 21–22, 82, 273 maintenance of 80 social validation of 88 stages in 22 stimuli for 76 strategies for 289, 294 Rhetorical Structure Theory (RST) 120 Right hemisphere lesion 118, 128–129, 133, 216, 285 role in communication 5, 6–7, 126, 284, 291 Semiological substitution 113 Semantics 114, 157, 252, 285, 286, 317 Science and Technology of Information and Communication (STIC) 115 Speech apraxia of, see Apraxia of speech instrumental analysis of 5 speech automatisms see Speech automatisms Speech Act(s) Theory (SAT) 43, 62, 116–119 Standardized tests Boston Diagnostic Aphasia Examination (BDAE) 86, 247 Communication Abilities in Daily Living (CADL) 86 Comprehensive Aphasia Test (CAT) 247

Functional Assessment of Communication Skills (FACS) for Adults 182 Porch Index of Communicative Ability (PICA) 262 Psycholinguistic Assessment of Language Processing in Aphasia (PALPA) 245, 248–249, 252–253 Verb and Sentence Test (VAST) 245, 249, 250, 253–254 Western Aphasia Battery (WAB) 74, 247 Stereotypy 169 Stroke 4, 18, 19, 195–209 depression following 22–23 Sonority sequencing principle 4 Speech automatisms 3–5, 169 origins of 4 Speech tics 169 Spinal cord, results of lesion in 170 Stuttering 5, 73, 308 Subcortical region, neuroanatomy of 138 models of participation in language 141–147 Suprasegmental characteristics 6 Systemic Functional Linguistics (SFL) 59, 172, 270, 278 Syntax 84, 163, 224, 305, 317 TBI see Traumatic brain injury Traumatic brain injury (TBI) 42–63, 216, 270, 271 in children 44, 46, 51, 56, 58 Treatment see also Rehabilitation social validation of 2, 73 Thalamus aﬀect of lesion 139–140 anatomical function of 138 role in language 139, 150 role in lexical decision making model 145 role in response-release semantic feedback model 143–144 role in selective engagement model 145 Therapy of speech 18, 72 occupational 21 participants in 273 physiotherapy 21 neuropsychological 21 Group therapy 72, 84, 181, 183–184, 185, 186, 187, 189 goals 74, 79, 84–85

Subject index Theory of Mind (ToM) 48–49 Token test 182 Tone languages 127 VAST see Standardized tests Verb and Sentence Test (VAST) see Standardized tests Verbs 118, 198, 224, 225, 227, 229, 249, 252, 253–254, 266, 267, 318 copula 76 errors 226, 228 Visual impairment 309, 310, 312, 313 Visual stimuli 80, 261 Vocabulary in dementia 301 measures of 251 Voicing 5 Vowels 5, 111, 171 ratio to consonants 4

343

WAB see Standardized tests Wernicke’s Area 143 Western Aphasia Battery (WAB) see Standardized tests Word ﬁnding diﬃculties 54, 57, 139, 142, 143, 163, 182, 206, 271, 301 Word frequency 160–161, 163, 249, 252, 263 Word length 160, 263 Word order 225, 229, 230, 234, 235, 253 Word production models in 156, 158–159 Word tics 169 Writing 84–85, 140, 171, 246, 247 agrammatism 303 computerized 260–261 orthographical errors 310 samples 78 Written language 157, 172, 246

Clinical Aphasiology: Future Directions

32nd Annual Clinical Aphasiology Conference: A Special Issue of Aphasiology

Future Directions in Biocatalysis

Future Directions in Biocatalysis

Future Directions in Distributed Computing

Wto and Global Governance The: Future Directions

Travel Survey Methods: Quality and Future Directions

Energy Technology and Directions for the Future

Travel Survey Methods: Quality and Future Directions

Testosterone and Aging: Clinical Research Directions

Special Economic Zones: Progress, Emerging Challenges, and Future Directions (Directions in Development)

Care Work in Europe: Current Understandings and Future Directions

Reactive Distillation Status and Future Directions Kai Sundmacher Achim Kienle

Industrial Archaeology: Future Directions (Contributions To Global Historical Archaeology)

Stem Cells: Scientific Progress And Future Research Directions

Obsessive Compulsive Disorder. Current Understanding and Future Directions

Preharvest and Postharvest Food Safety: Contemporary Issues and Future Directions

Advances in Ubiquitous Computing: Future Paradigms and Directions

Mobile, Wireless and Sensor Networks: Technology, Applications and Future Directions

Sciences of Geodesy - I: Advances and Future Directions

Computing Tomorrow: Future Research Directions in Computer Science

Future Directions for the National Healthcare Quality and Disparities Reports

Mobile, Wireless, and Sensor Networks: Technology, Applications, and Future Directions

Airborne Geophysics and Precise Positioning: Scientific Issues and Future Directions

Gold Chemistry: Applications and Future Directions in the Life Sciences

Spirituality in business: theory, practice, and future directions

Industrial Archaeology: Future Directions (Contributions To Global Historical Archaeology)

Future Directions for Heterodox Economics (Advances in Heterodox Economics)

Biorefineries - Industrial Processes and Products: Status Quo and Future Directions

Cognition, Emotion and Psychopathology: Theoretical, Empirical and Clinical Directions

Clinical practice guidelines: directions for a new program

Clinical Aphasiology: Future Directions

32nd Annual Clinical Aphasiology Conference: A Special Issue of Aphasiology

Future Directions in Biocatalysis

Future Directions in Biocatalysis

Future Directions in Distributed Computing

Wto and Global Governance The: Future Directions

Travel Survey Methods: Quality and Future Directions

Energy Technology and Directions for the Future

Travel Survey Methods: Quality and Future Directions

Testosterone and Aging: Clinical Research Directions

Special Economic Zones: Progress, Emerging Challenges, and Future Directions (Directions in Development)

Care Work in Europe: Current Understandings and Future Directions

Reactive Distillation Status and Future Directions Kai Sundmacher Achim Kienle

Industrial Archaeology: Future Directions (Contributions To Global Historical Archaeology)

Stem Cells: Scientific Progress And Future Research Directions

Obsessive Compulsive Disorder. Current Understanding and Future Directions

Preharvest and Postharvest Food Safety: Contemporary Issues and Future Directions

Advances in Ubiquitous Computing: Future Paradigms and Directions

Mobile, Wireless and Sensor Networks: Technology, Applications and Future Directions

Sciences of Geodesy - I: Advances and Future Directions

Computing Tomorrow: Future Research Directions in Computer Science

Future Directions for the National Healthcare Quality and Disparities Reports

Mobile, Wireless, and Sensor Networks: Technology, Applications, and Future Directions

Airborne Geophysics and Precise Positioning: Scientific Issues and Future Directions

Gold Chemistry: Applications and Future Directions in the Life Sciences

Spirituality in business: theory, practice, and future directions

Industrial Archaeology: Future Directions (Contributions To Global Historical Archaeology)

Future Directions for Heterodox Economics (Advances in Heterodox Economics)

Biorefineries - Industrial Processes and Products: Status Quo and Future Directions

Cognition, Emotion and Psychopathology: Theoretical, Empirical and Clinical Directions

Clinical practice guidelines: directions for a new program

Recommend Documents