Schizoaffective Disorders: International Perspectives on Understanding, Intervention and Rehabilitation

SCHIZOAFFECTIVE DISORDERS: INTERNATIONAL PERSPECTIVES ON UNDERSTANDING, INTERVENTION AND REHABILITATION

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SCHIZOAFFECTIVE DISORDERS: INTERNATIONAL PERSPECTIVES ON UNDERSTANDING, INTERVENTION AND REHABILITATION KAM-SHING YIP EDITOR

Nova Science Publishers, Inc. New York

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CONTENTS Preface Chapter 1

Chapter 2

Chapter 3

vii Controversies and Difficulties in Theoretical Underpinning of Schizoaffective Disorders Kam-shing Yip Understanding the Needs, Resilience and Recovery of Persons with Schizoaffective Disorder: Related Theories and Conceptual Underpinnings Kam-shing Yip Schizoaffective Psychosis and Schizophrenia with- or without Affective Syndrome: A Comparative Clinical, Neuropsychological and Molecular-genetic Study V. E. Golimbet, M. V. Alfimova, V. G. Kaleda, L. I. Abramova, G. I. Korovaitseva, O. M. Lavrushina, and T. V. Lezheiko

Chapter 4

Diagnostic Controversies in Schizoaffective Disorder Nathaniel Hurwitz and C. Raymond Lake

Chapter 5

Neuropsychological Deficits in Schizoaffective Disorder Barton W. Palmer and Gauri N. Savla

Chapter 6

Ego Functioning, Cognition, and Illness Characteristics of Persons with Schizoaffective Disorder: Distinctive Features and Response to Vocational Rehabilitation Morris D. Bell, Randall Richardson, and Tamasine Grieg

Chapter 7

Chapter 8

Boredom, Hallucination-proneness and Hypohedonia in Schizophrenia and Schizoaffective Disorder McWelling Todman, Daniel Sheypuk, Kristin Nelson, Jason Evans, Roger Goldberg,and Evangeline Lehr Schizoaffective Disorder in China: Controversies and Reality in China Zhi-zhong Lian and Kam-shing Yip

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27

69

89 115

135

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vi Chapter 9 Index

Contents Managing the Suicidal Risk in Pregnant Schizoaffective Women Salvatore Gentile

197 229

PREFACE Ever since Krapelin’s (1899) classical volume on dementia praecox, persons with both features of schizophrenia and affective disorders are attended by scholars and practitioners in mental health services. Kasanin (1933) seemed to be first one in using the term `schizoaffective psychosis’ and `schizoaffective disorders’ in describing nine patients who had both psychosis and affective disorder symptoms. These patients had good prognosis and later fully recovered from the mental disorder. This new disorder, being closely resemble to both schizophrenia and affective disorder, needs a clear diagnostic criteria and operationalization in clinical practice. Robins and Gitze (1970) suggests five areas to validate schizoaffective disorder including clinical description, laboratory studies, delimitation from other disorders, follow up studies and family studies. In fact, up to now, there are still controversies in defining and interpreting schizoaffective disorder (Bottlender & Muller, 2003; Welner, et.al., 1977; Evans, et.al., 1999; Marneros & Akiskai, 2007). Despite related controversies and argument, schizoaffective disorder is a crucial mental illness that demands attention and study from both scholars and clinicians. However, most of these discussions are merely debates focused on diagnosis, etiology and genetics of persons with schizoaffective persons. Although there is a long awareness of the uniqueness of schizoaffective disorder, comparing the rich theoretical underpinnings in schizophrenia and mood disorders, the studies of schizoaffective disorder are thin and insufficient. After a long history of conceptual development, these two groups of mental illness are profoundly studied, explained and articulated by biochemical, psychodynamic, cognitive, existential, phenomenological, sociological, cultural and humanistic perspectives. In each perspective, there are numerous accounts, and research in describing persons with schizophrenia or mood disorder. For persons with schizophrenia, apart from the dominant explanations form cognitive deficit models as well as the biochemical model and genetic models, there are plies of explanations from various perspectives such as Laing’s divided self (1960) and Jaspers (1946/1963) meaningfulness of primary and secondary delusion as well as Schneider’s (1959) first rank symptoms. There seems to have enough evidence showing that severe cognitive impairment for persons with schizophrenia is due to self fragmentation, self splitting and confusion of self boundary (Blatt & Wild, 1976). Similarly, in the studies of mood disorders, there are numerous renounced theories interpreting the mood disorder in particular depressive disorder, ranging from Freud’s (1938) introjection of loss to Beck’s (1976) sense of helplessness, worthlessness and meaninglessness. There are numerous arguments such as Frankl’s (1963) loss of life meaning and Kohut’s (1971, 1972 & 1973) loss of idealized objects. There seems to have sufficient evidences that intensive negative mood and negative schema in depression may be due to the loss

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of objects, persons, interpersonal relation, personal prestige and status that the person with depression is firmly attached to. Nevertheless, all these rich and in-depth discussions are left out in conceptualizing schizoaffective disorders. Most discussions and debates in schizoaffective disorder are an entity of schizophrenia disorder, depressive disorder or a new form of disorder. The ignorance of rich theoretical traditions of mood disorders and schizophrenia may lead to a thin and insufficient theoretical underpinning in the diagnosis, treatment, intervention and rehabilitation of persons with schizoaffective disorder. The particular needs and hardships of persons with schizoaffective disorder are far beyond the agenda of scholastic research. Based on client’s in-depth interview and self narration, Yip (2006) affirmed that people with schizoaffective disorder suffered labelling and symptoms from both schizophrenia and affective disorders. In this book, the writers try to recapture such rich arguments and theoretical traditions in mood disorders and schizophrenia in describing the understanding, interacting, diagnosis, treatment and rehabilitation of persons with schizoaffective disorders. Chapter one is an outline and description about the international perspective on the controversies and difficulties in theoretical underpinnings of schizoaffective disorder. In this chapter, Kam-shing Yip outlined the development of the concepts, diagnosis and etiology of schizoaffective disorders. The concept of schizoaffective disorder began with Kraepelin’s discovery mental illness between schizophrenia and manic depressive entity. In 1930s, Kassanin was the first scholar in using the term `schizoaffective disorder’ in clinical studies. In DSM II diagnosis of schizoaffective disorder was affirmed. Previous and recent literatures tend to show that there are four controversies in the diagnosis and interpretation of schizoaffective disorder. Firstly, schizoaffective disorder can be considered as a variant of schizophrenia. Secondly, it can be regarded as a variant of affective disorder. Thirdly, it can be an intermediate entity between schizophrenia and affective disorder. Fourthly, it can be interpreted as a continuum of functional psychosis with schizophrenia at one end and affective psychosis at the other end of the spectrum. With all these theoretical positions, the writer has done a literature archives on related literatures in Science Citation Index. There are altogher 494 articles with the title of `schizoaffective disorder’ appeared in the SCI. However, most of them merely described schizoaffective disorder as an entry of schizophrenia. Majority of the articles focused on issues on biochemical and genetics, diagnosis and etiology. They tended to neglect or undermine clients’ experiences, psychosocial theories and studies on persons with schizoaffective disorder. All these articulations may have important implications on understanding, treatment and rehabilitation of persons with schizoaffective disorder. The empathetic stand towards persons with schizoaffective disorder is further extended and elaborated in Chapter two. Kam-shing Yip tried to outline a multi-dimensional frame in understanding the needs, resilence and recovery of persons with schizoaffective disorder. The chapter began with an initial articulation of subjective experiences, needs, resilience and recovery of persons with schizoaffective disorder. By means of a case illustration of a Chinese male adult, the writer attempted to recapture various theoretical underpinnings of schizoaffective disorder. As related concepts of schizoaffective disorder are comparatively thin and insufficient, the writer revisited various concepts in interpretation of schizophrenia, major depressive disorders and bipolar disorder. Within these groups of the conceptualisation, the experiences and needs of persons with schizoaffective disorder can be reconceptualized in four different ways. The first type of interpretation is to understand the experiences and needs of persons with schizoaffective disorders in terms of related theories of schizophrenia. The

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second type is to interpret the experiences and needs of persons with schizoaffective disorders in terms of related theories of depression. The third type is to interpret such experiences and needs in terms of related theories of bipolar disorder. The fourth type is to interpret such experiences and needs in terms various combinations of all these theories. There may three ways of combining theories of depressive disorders, schizophrenia and bipolar disorders. Firstly, the manifestation of one/two type/s of symptom is to cope with or suppress the manifestation of another one/two type of symptoms. Secondly, the full manifestation of one/two type/s of symptom can lead to the manifestation of another one/two types of symptoms. Thirdly, coexistence of any two/three types of symptoms implies a delicate balance for the individual in facing environmental stresses and personal conditions. Chapter three is written by Vera Golimbet and his colleagues from Russia. They reported the findings of a comparative clinical, neuropsychological and molecular-genetic study on 184 patients with schizoaffective psychosis (SA) and 872 patients with schizophrenia (170 SPA with affective syndrome and 702 SP without affective syndrome). These 3 groups have been compared for clinical symptoms, self-rated personality characteristics and neurocognitive traits. Molecular genetic study has been carried out to determine genotypes for the T102C polymorphism of the serotonin receptor type 2A (5-HTR2A) gene, the 5-HTTLPR polymorphism of the serotonin transporter gene and the Val66Met polymorphism of the brain-derived neurotrophic factor (BDNF) gene. The clinical study revealed significant between-group differences: positive symptoms were mostly pronounced in patients with SP, while the SPA and SA groups had similar scores, and negative symptoms tended to gradual decreasing as SP>SPA>SA. Patients both with SPA and SA had higher scores on anxiety and depressive-related items as compared to the SP group. The latter was featured by the highest scores on the items related to cognitive and volition symptoms which, analogous to negative symptoms, decreased gradually in the SPA and SA groups. All the groups significantly differed by personality characteristics. No between-group differences were found for neurocognitive traits. Molecular-genetic study revealed that, comparing to controls, the SA group was featured by the specific genotypes distribution, namely by the higher frequency of the ss 5-HTTLPR and the A2A2 (CC) 5HTR2A genotypes and a genetic variant represented by the combination of the 5-HTTLPR ss and the BDNF Met-allele. The results of the study revealed that SA is more closely related to SPA than to SP by clinical symptoms and molecular-genetic characteristics. Also, in genetic view, SA seems to be a separate entity, being characterized by the lowest ratings of negative symptoms, one of the most stable characteristics of schizophrenia, which is thought to be underpinned by genetic factors, and by a combination of genotypes of the candidate genes for major psychosis that discriminates it distinctly from SP and SPA. Chapter four is written by Nathaniel Hurwitz and Raymond Lake about the diagnostic controversies of persons with schizoaffective disorders. They criticize the current diagnosis of schizoaffective disorders is lack of laboratory test evidence. The ‘schizoaffective’ diagnosis cannot be reliably identified. Furthermore, it offers nothing but the opportunity cost of not treating mood, violating ‘do no harm.’ It is common to have affective and mood changes in psychotic transformation. Schizophrenia researchers disbelieve the Kraepelinian dichotomy. Unlike families with Huntington’s disease that all show the same, single abnormality, families with multiple functionally psychotic members show a variety of genetic abnormalities. Not only do gene-abnormality profiles vary across different families, but there

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are often multiple different psychiatric diagnoses within individual families − and even within individual family members. Many groups have found genetic overlap in bipolar and schizophrenia. Others have reported that all three diagnostic categories (schizophrenia, schizoaffective and bipolar) share genetic susceptibility loci. Regarding brainwave measures, a discussion of ERP findings in “schizoaffective” disorder is necessarily a discussion of findings in schizophrenia since most work has been done with patients carrying that diagnosis. Furthermore, “schizoaffective” fell under the schizophrenia section in the original DSM and remains there in the DSM-IV. Thus, many studies lump so-called “schizoaffectives” together with schizophrenics in a combined group that is then compared with a control group. There is a clinical findings showing that dysregulated mood leads to psychosis. Untreated or badly responding psychotic mood disorder ends up looking like classically described schizophrenia. Related literatures showed many functionally psychotic patients, prolonged stabilizing mood could decrease long term impairment. It can attain by mood stabilizers and gradual reduction of neuroleptics over many months while educating the patient and family about mood disorder, psychosis in mood disorder, evidence of recurrence, and an appropriate temporary adjustment in stressful life activities. Removal of the meaningless and malignant ‘schizoaffective’ label would help rekindle the lithium trial. Chapter Five is written by Barton W. Palmer, Gauri, N. Savla in United States. They attempt to describe neuropsychological deficits in persons with schizoaffective disorder. This chapter begins with an overview about the cognitive and neuropsychological deficits in schizophrenia. The writers tend to assert that neuropsychological deficits are quite similar among patients with schizophrenia and schizoaffective disorder. Related studies are consistent in showing that the level, pattern, and frequency of neuropsychological impairment among patients with schizoaffective disorder are indistinguishable from those seen in patients with schizophrenia. There is also evidence those persons with schizoaffective disorder and those with paranoid subtype of schizophrenia may, on average, have slightly better neuropsychological performance than those with undifferentiated or disorganized subtypes of schizophrenia. There is no pattern of neuropsychological deficits is unique to schizophrenia and/or schizoaffective disorder. For memory, there is limited data specifically examining savings (percent retention) for schizoaffective disorder patients separately. Compared with schizophrenia, schizoaffective disorder patients show substantial forgetting than among patients with schizophrenia. Some published reports have documented that patients with schizophrenia and schizoaffective disorder have equivalent impairments on the WCST performance. Interestingly, non-institutionalized individuals with schizophrenia or schizoaffective disorder tend to stay stable in their neuropsychological ability. However, chronically institutionalized patients appear to be at higher risk for progressive cognitive decline than expected for their age. All these have important implications in neuropsychological assessment, pharmacologic interventions and related treatments. Chapter Six is written by Morris D. Bell, Randall Richardson and Tamasine Grieg in the United States. They examined ego functioning, cognition and illness characteristics of persons with schizoaffective disorder in vocational rehabilitation services. In this chapter, the writers reported on 422 (200 with schizophrenia; 70 with schizoaffective disorders) patients enrolled in a series of vocational rehabilitation studies. They examined the differences between schizophrenia and schizoaffective disorder groups on background and illness characteristics, cognitive ability, ego functioning, and work outcome measures. Community functioning was measured using the Quality of Life Scale. A significant difference between

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the schizophrenia and schizoaffective disorder patients appeared on the Common Objects and Activities subscale (p<.009) with the schizoaffective group having more common objects. Regarding ego functioning as measured by the BORRTI, the schizophrenia and schizoaffective disorder groups were similar in terms of Alienation, Egocentricity, Social Incompetence, Reality Distortion, and Hallucinations and Delusions but differed significantly on Insecure Attachment (p<.04) and Uncertainty of Perception (p<.02). This indicates greater self-monitoring and observing ego. On Insecure Attachment, schizoaffective patients were also somewhat higher indicating greater interpersonal sensitivity and vulnerability in relationships. During the course of work rehabilitation, participants were rated bi-weekly using the Work Behavior Inventory. A MANCOVA revealed there were no significant differences on overall WBI improvement between samples, although the schizoaffective sample showed marginally (though non-significant) better improvement in the Work Habits subscale. The Work Habits subscale measures an employee’s conscientiousness, adherence to the rules of the workplace, attendance, and awareness of the norms of the work setting. Measures of work productivity including hours worked and money earned were also collected for participants in all three studies. There were no significant differences between samples on these measures. The writers concluded that schizoaffective disorder patients entering rehabilitation were similar in most regards to schizophrenia patients, but differed in several important ways. They were more likely to be females and had a higher rate of marriage. They also participated more in everyday activities, had fewer and less severe disorganization symptoms, more severe symptoms of emotional discomfort, better verbal and visual memory, better verbal fluency, better social cognition, greater interpersonal sensitivity and better observing ego. Although they were similar to schizophrenia patients on core positive and negative symptoms and on most neurocognitive and ego-function variables, whenever the two groups of patients differed, the difference favored the schizoaffective disorder samples. The findings the writers presented echoded with related literatures and add some original information, particularly regarding better social cognition and greater capacity for interpersonal sensitivity and observing ego in schizoaffective disorder. These results may indicate an endophenotypic distinction between schizoaffective disorder and schizophrenia. They support the view of schizoaffective disorder as a discrete syndrome, in which several cognitive and ego functions are better preserved than in schizophrenia. Such a view explains the counterintuitive observation that patients with symptoms of schizophrenia and affective illness have better functioning than those with symptoms of schizophrenia alone. Chapter Seven is written by McWelling Todman, Daniel Sheypuk, Kristin Nelson, Jason Evans, Roger Goldberg and Evangeline Lehr. They reported the findings of a study about the boredom, hallucination-proneness and hypohedonia in schizophrenia and schizoaffective disorder. Studies of boredom and boredom proneness in non-psychiatric and clinical populations have demonstrated that trait and state boredom are associated with depressive mood and a number of other untoward outcomes, many of which are potentially relevant to the care of patients with a severe and persistent mental illness (SPMI). For example, in a recent study conducted with college students, it was found that the impact of boredom on the quality of life and degree of unpleasantness attributed to boredom were positively correlated with a measure of hallucination-proneness. The findings of their study replicated and extended these findings in a small sample of SPMI patients. As predicted, anhedonia, hallucination-proneness, a history of auditory hallucinations, and feelings of depression

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within last 14 days were all found to have significant positive correlations with various aspects of the State Boredom Measure (SBM). The findings also underscore the importance of boredom as a potential marker for current substance use and suggest that the attributions made by patients with schizoaffective disorder about their experiences with boredom are different to those made by patients with schizophrenia or bipolar illness. Chapter Eight is written by Kam-shing Yip and Zhi-zhong Liang about the current situation in diagnosis, treatment and recovery of persons with schizoaffective disorder. The People Republic of China is the most populated country in the world. With a huge population of 1.3 billions, mental health services for persons with mental illness is certainly be a heavy burden for the central as well as local government. According to related formal documents, there are around 16 millions of persons with mental illness that necessitate prolonged treatment and rehabilitation. From related studies, it is estimated that should around 250,000 persons with schizoaffective disorder in China. Coupled with a huge and insurmountable number of persons with mood disorders and psychosis, affective psychosis, diagnosis, treatment and rehabilitation of persons with schizoaffective disorder should be a great challenge to related professionals. In China, schizoaffective disorders are diagnosed four basic clinical features. Firstly, there is co-existence or sequential occurrence of symptoms in schizophrenia and in mood disorder. Secondly, there are frequent relapses and manifestation of symptoms. Within relapses, residual symptoms are not apparently observed and occurred. Thirdly, onsets may be acute and have a family history of schizophrenia, depressive disorder or bipolar disorder. Fourthly, the age of onset is inclined to be at adolescence or youth, with female more than male. In China, the diagnosis of schizoaffective disorder follows closely to International classification of Disease ICD 10. The only difference is that in ICD related symptoms have to occur or manifest for at least one whole week, however, in China, the CCMD III (China Classification of Mental Disorder 3rd Edition) related symptoms have to sustain for at least two or more weeks. In China, due to the shortage of resources and manpower, most (around 95% ) persons with schizoaffective disorders in mental health services are treated by psychiatric medication. They are either patients in outpatient clinics or mental hospitals. For those in outpatient clinics, apart from medical treatment, they can rarely receive psychosocial treatment, partly because of insufficient manpower, partly because related professionals in outpatient clinics and mental hospitals are not well equipped with proper training in psychsocial treatment. By means of a case illustration, the writers try to discuss related issues and situation in the diagnosis, treatment, rehabilitation and recovery of persons with schizoaffective disorder in China. Chapter Nine is written by Salvator Gentile from Italy about the management of the suicidal risk in pregnant schizoaffective disorder. Suicide remains a significant public issue. Several concordant information exists suggesting that, among the psychiatric disorders, patients diagnosed with schizoaffective disorder show relatively higher rates of deaths by suicide compared with patients suffering from other mental illness. Unfortunately, in these patients, suicide is not uncommon during pregnancy. Thus, it is not surprisingly that, whereas deaths by violent means characterize most of suicides in postpartum psychosis, women attempted suicide during pregnancy prevalently by ingestion of a liquid or a solid, primarily by drug (either licit or illicit) overdose followed by ingestion of corrosive poison.

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Recent researches have demonstrated that, in pregnant women with history of psychiatric disorder, a percentage ranging from 13.1% to 33.0% of mothers may have suicidal ideation. Most of these mothers have been diagnosed with schizoaffective disorder. Either psychopathological or social specificities of schizoaffective disorder must force clinicians to consider any suicidal expression shown by these patients as a signal of possible high-lethality suicide attempts. Indeed, suicide attempts among individuals with schizoaffective disorder are often medically serious and associated with a high degree of intent. It should also be stressed that suicide attempts during pregnancy are associated with significantly higher rates of perinatal morbidity and mortality (increased rates of perinatal mortality have been recorded in women specifically requiring hospitalization after attempting suicide. Related literatures show that there are various protective factors such as safe pregnancy, children at home, life satisfaction and positive social support in alleviating the suicidal risks of pregnant women with schizoaffective disorders. However, risky factors include unplanned and unmarried pregnancy, undiagnosed psychiatric symptoms, high frequency of unfavorable life episodes during adolescence, early adulthood, incomplete schooling and unemployment. In the light of this background, the necessity exists to analyze and summarize published literature information on the teratogenic safety of antisuicidal drugs and various psychiatric illnesses such as Lithium, Clozapine as well as electroconvulsive therapy, in order to identify the safest option to treat suicidal risk during early pregnancy. The writer also investigates the difficulties of managing the suicidal risk in schizoaffective patients during the last stages of pregnancy. The writer also suggests measures to support those vulnerable mothers such as helping the patient to balance the risk of pregnancy exposure to drugs with the risks associated with the untreated psychiatric disorder; reducing patients’ access to highly lethal methods for attempting suicide; offering adequate economic and health support; discussing the difficulties to adhere to the life-style changes imposed by parenting with the mother, her partner, and the whole family, in order to identify supportive care-givers for the mother-infant pair; and facilitating social integration, especially for those women coming from disadvantaged community group.

REFERENCE Andreas, M. & Hagop, A., (2007) (Ed.) The Overlap of Affective and Schizophrenic Spectra. Cambridge, New York: Cambridge University Press. Beck, A.T. (1976) Cognitive Therapy and the Emotional Disorder. New York: International University Press. Bottlender, M. J. & Muller, A. S. (2003) `Fifteen year follow up of ICD 10 schizoaffective disorder s compared with schizophrenia and affective disorder’, Acta Psychiatric Scandianvia, 109:30-37. Blatt S.J. & Wild C.M. (1976) Schizophrenia: a Developmental Analysis, New York: Academic Press. Evans, J.D., Heaton, R.K., Paulsen, J.S., McAdams, LA., Heaton, S.C. & Jeste, D.V. (1999) `Schizoaffective disorders: a form of schizophrenia or affective disorder’, Journal of Clinical Psychiatry, 60: 874-882.

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Frankl, V. (1963) Man's Search for Meaning, New York: Pelican Press. Jaspers, K. (1946/1963) (7th edition) General Psychopathology, (J. Hoenig, & M.W., Hamilton trans.) Manchester University Press (Original work published 1923). Kasanin, J. (1933) `The acute schizoaffective psychoses’, American Journal of Psychiatry, 13: 97-126. Kohut, H. (1971) The Analysis of the Self, New York: International Universities Press. Kohut, H. (1972) `Thoughts on narcissism and narcissistic rage’, The Psychoanalytic Study of the Child, 27:360-400. New York: Quadrangle Books. Kohut, H. (1977) The Restoration of the Self, New York: International Universities Press. Kraepelin, E. (1899) Psychiatrie, 6th edition, Leipzig: Barth. Laing R.D. (1960) The Divided Self, London: Tavistock.. Marneros, A. & Akiskai, H.S. (2007) The Overlap of Affective and Schizophrenic Spectra, Cambridge: Cambridge University Press. Robins, E. & Guze, S. B. (1970) `Establishment of diagnostic validity in psychiatric illness in application to schizophrenia’, American Journal of Psychiatry, 126:983-987. Schneider K., (1959) Clinical Psychopathology, (M.W., Hamilton & Anderson, E.W., Trans) New York: Grune & Stratton, 1959. Welner, A., Croughan, J.L., Fisherman, R. & Robin, B. (1977) The group of schizoaffective and related psychosis- critique, record, follow up and family studies: a follow up study, Comprehensive Psychiatry, 18: 413-422. Yip, K.S. (2006) `Subjective experiences of persons with schizoaffective disorders’ W.H., Murray, (edited) Schizoaffective Disorders: New Research. New York: Nova Science publishers.

In: Schizoaffetive Disorders Editor: Kam-shing Yip

ISBN 978-1-60456-948-3 © 2009 Nova Science Publishers, Inc.

Chapter 1

CONTROVERSIES AND DIFFICULTIES IN THEORETICAL UNDERPINNING OF SCHIZOAFFECTIVE DISORDERS Kam-shing Yip* Department of Applied Social Sciences The Hong Kong Polytechnic University, Hong Kong

INTRODUCTION Ever since the appearance of the term `schizoaffective disorder’, there are long unsettled arguments in regarding the diagnosis, and etiology of schizoaffective disorders. These arguments can be roughly divided into three types. The first type of arguments regards schizoaffective disorder as an extension or variant of schizophrenia. The second type regards schizoaffective disorder as an extension or variant of affective disorder. The third may regard schizoaffective disorder as a new form of disorder that have no resemblance with schizophrenia and affective disorder. Finally schizoaffective disorder may be regarded as an intermediated entity between schizophrenia and affective disorder. All these differences in locating schizoaffective disorder create difficulties and problems in establishing a solid theoretical underpinning of schizoaffective disorder. In this chapter, the writer tries to describe all these controversies difficulties in details. The impacts of these controversies in affecting the diagnosis, treatmenet and rehabilitation of both related professionals and persons with schizoaffective disorder are also briefly mentioned. Also, by means of reviewing related article published in the Social Science Index, the writer tries to discuss whether such controversies were bewared, discussed and articulated by related scholars and practitioners from 1975 to 2007.

*

E-mail: [email protected]

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INITIAL CONCEPTUTALIZATION OF SCHIZOAFFECTIVE DISORDERS The concept of schizoaffective disorder originated from Kraepelin (1899) discovery of case in between dementia praecox (later named as schizophrenia by Bleuler (1911) and manic-depressive insanity. However, his colleague Zendig discovered that around 30% of Kraepelin’s patients that diagnosed as demential praecox did not demonstrated characteristics as described. Later, Kraepelin (1920) affirmed that there should be certain cases mental disorders can have characteristics of both groups. He asserted that: `We have to live with the fact that the criteria applied by us are not sufficient to differentiate reliably in all cases between schizophrenia and manic depressive insanity. And there are also many overlaps in this area.’ (Kraeplin, 1920: 28)

Later Bleuler (1911, 1924) admitted that there are cases that have both characteristics of symptoms of schizophrenia and mood disorders. However, he tended to group these cases into a new form of mental disorder but regarded them as some atypical cases (Marneros, 2007). Schneider (1959, 1973) also recognized that there are cases in between schizophrenia (of which with first rank symptoms) and mood disorder (of which with cyclothymia). For the first rank symptoms, he affirmed the following features: `We have emphasized these symptoms of first-rank importance above and illustrated them with examples. Following the order in which we have reviewed them, they are: audible thoughts, voices heard arguing, voices heard commenting on one’s reaction; the experience of influences playing on the body (somatic passivity experiences); thought withdrawal and other interferences with thought; diffusion of though; delusional perception and all feelings; impulses (drives) and violation acts that are experienced by the patient as the work or influence of others. When any one of these modes of experiences is undeniably present and no basic somatic illness can be found, we may make the decisive clinical diagnosis of schizophrenia.’ (Schneider, 1959: 133-134)

Regarding the affective disorder (cyclothymia), Schneider (1959) concluded that there should be absence of first rank symptoms. `In cyclothymia, there seem at present to be no known symptoms of first rank importance, nothing of which are can say, if this is present, then so is cyclothymia. The nearest we can get would be the vital quality of the adverse mood.’ (Schnieder, 133-134)

However, he also asserted that there were some atypical borderline cases where both diagnoses tended to be difficult. ‘In such atypical borderline cases, an arbitrary diagnosis often has to be made, either of schizophrenia with a typical course or of cyclothymia with a typical symptoms. Detailed investigation by Baume of one hundred twenty, almost all fully recovered, schizophrenia did not lead to establishing a full recovery in the case of those psychoses which had presented in the first place schizophrenic symptoms of first rank importance….. We would like to keep the term “borderline case” for those in which the diagnosis halts between the type of psychoses, ie., schizophrenia or cyclothymia, in which both diagnosis might be equally applicable for

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lack of characteristic symptomatology and we can only turn to the courses run by the illness. (Schneider, 1959: 142)

Facing these specific cases, he discovered that they are two types, the concurrent form and the sequential form. In concurrent form, persons with schizoaffective disorder have symptoms both from schizophrenia and mood disorder. In sequential form, persons with schizoaffective disorder may have symptoms of schizophrenia and then mood disorder or vice versa in a continuous sequence. Similarly, Kleist (1928) affirmed that a group of persons with `cycloid psychosis’ tend to have polarized symptoms in both schizophrenia and affective disorder but involved in onset and recoverable cycle with much better prognosis than those persons with schizophrenia (Kleist, 1928; Marneros, 2007). Kasanin (1933) was the first scholar using the term `schizoaffective’ in describing this group of mental symptom. In his study, he observed there were nine persons who have good pre-morbid functioning. They were young adults, with good social functioning and well integrated personality. They were suddenly attacked by a dramatic onset of acute psychosis in which symptoms of schizophrenia and affective disorder occurred together and were difficult to make a clear diagnosis of neither schizophrenia nor affective disorder. They might have a similar attack previously in their adolescence but recovered. Being provoked by intensive environmental stress, the onset came in with an emotional turmoil as well as a distortion of reality in forms of hallucinations but none of them possess negative symptoms, passivity and withdrawal. The situation prevailed for a few weeks or months and then recovered fully socially and psychologically (Kasanin, 1933; Marneros, 2007). Following the same line of thinking as Schneider’s cyclothymia, another prominent psychiatrist, Langfeldt (1939) described the symptoms of `schizophreniform psychosis’ that, in many ways are similar to symptoms of `schizoaffective disorders’. Related symptoms include: cyclothymic temperament, pyknic habitus, depressive symptoms, self reference tendencies, cloudiness, incoherence, catatonic or pathoplastic features and acute onset. Similar to Kasanin’s (1933) findings, Kant (1940) discovered that a group of persons with schizophrenia tended to be recoverable and with better prognosis than others persons with schizophrenia. They seemed to have shorter duration of manifestation of schizophrenic symptoms but more acute onset. Both of them and their relatives embraced bipolar moods and psychogenic natures of psychosis. All these descriptions may embrace two types of meanings and interpretation. Firstly, it clearly showed that scholars in 1890 to 1940 discovered the difficulties and discrepancies in putting clients with schizoaffective disorder as schizophrenia or affective disorder. Secondly, it may also mean problems in putting clients with mental illness into a clear category of mental symptoms. In fact, as clients with mental illness are holistic persons with their own experiences and background as well as their own process of recovery. There should always be cases in between two groups or several groups of disorders in diagnosis and treatment. Apart from schizoaffective disorder, the occurrence of various types of `personality disorders’ may also show the problem in putting clients with mental illness into a designated groups of mental symptoms and problems. Thirdly, findings of these early studies showed that persons with schizoaffective disorder may have better prognosis and recovery than those with sole schizophrenic symptoms. On the one hand, we may say schizoaffective disorders are different from schizophrenia or affective disorder. On the other hand, we may also interpret these

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findings as persons with schizoaffective disorder may use affective mental symptoms as ways to cope with their schizophrenic symptoms, especially in early psychosis while young persons feel confused, irritated, depressed or angry with their own mental illness. If this is the case, then it is highly possible that various symptoms in different types of mental illness may be interchangeable. Because of various reasons, persons with mental illness may shift from one type of mental illness to another or embrace two types of mental illness in the same time. The concurrent and sequential forms mentioned by Schneider may be one way to represent the dynamic view of mental illness, in particular in schizoaffective disorder.

CONCEPUTALIZATION OF SCHIZOAFFECTIVE DISORDER FROM 1950 TO 1980 Better Prognosis than Schizophrenia Angst’s (1966) suggested that schizoaffective disorder should be more related to affective disorder rather than schizophreina. This position was echoed by later studies by Clayton et.al. (1968), Fowler et.al., (1972) and Cadoret et.al (1974). In later study, Angst (e.al. 1979) reaffirmed his position by the findings of a study on the morbidity risk for schizophrenia among 100 first degree relatives of 150 persons with schizoaffective disorder. The findings showed the morbidity risk was 5.26% for schizophrenia and the risk for schizoaffective disorder was 6.7%. The full remission rate among persons with schizoaffective disorder was 43% and the rate for persons with bipolar disorder was 73% (Angst, et.al., 1979). The findings seemed to demonstrate that schizoaffective disorder may have better prognosis than schizophrenia and affective disorder. Angst’s views about prognosis of schizoaffective disorder were further proved by Astrup and Noreik’s (1966) findings of their studies from 1957 to 1966 on 12000 cases of schizophrenia. Their findings showed that those cases of schizophrenia (n = 131) with good recovery were those with affective symptoms such as elation of mood, psychomotor agitation, flight of ideas and mood swings.

Diagnosis as a Different Entity of Mental Illness The diagnosis of schizoaffective disorder starts with the DSM I from American Psychiatric Association in which it is regarded as a kind of variant from schizophrenia. It is regarded as `schizoaffective type’ and schizophrenic reaction’ (American Psychiatric Association, 1952; Marneros, 2007). In DSM II, the same orientation still continued regarding schizoaffective disorder as a `schizophrenia, schizoaffective type’ with a very vague definition as `a mixture of symptoms and pronounced elation of depression’ (American Psychiatric Association, 1968). Facing the controversies in diagnosis of schizoaffective disorder and schizophrenia, Vaillant (1962) suggested six variables including • •

psychotic depressive heredity; symptoms of depressive psychosis;

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onset within six months before the fully developed episode; presence of precipitating factors; absence of schizoid personality before onset; and confusion or disorientation during the acute episode (Vaillant, 1962)

By means of analyzing clients’ case history, Valient (1962) rates all these seven variables in terms of a 0-7 scale with `4’ is the cut off line. That means, the diagnosis of schizoaffective disorder was affirmed in a form of a continuum rather than a clear and differentiated category (Vaillant, 1962 &1964; Marneros, 2007). Robins and Guze (1970) suggested a five point scale of diagnostic criteria. They are clinical description, laboratory studies, delimitation from other disorders, follow up studies and family studies. Kendell and Gouraly (1970) suggested that both symptoms of schizophrenia and affective disorder should be present in schizoaffective disorder. In schizophrenic symptoms, either paranoid or schizophrenic symptoms should be presented. For affective disorder either symptoms of depression or mania should be presented. These groups of symptoms can be listed in the following: 1. Schizophrenic symptoms including: a. one of core symptom: • thought insertion • withdrawal of thought • thought broadcasting • echoes, • voices • delusions of control b. behavioral symptoms (two of objective signs) • mannerism • posturing • stereotypes • catatonic phenomena • behavioral suggesting hallucination c. affective symptom • feeling of suspicion • perplexity of affect • blunting of affect • incongruity of affect d. delusions or paranoia must be presented in a form of: • delusion of influence • persecution • reference • misinterpretation 2. Symptoms of Affective Disorders a. Depressive symptoms (four out of 16 symptoms) • sadness • loss of interest

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Kam-shing Yip • sense of inferiority • pathological guilt • hypochrondriacal delusion • nihilistic delusion • insomnia • muddled thought • poor concentration • morning depression • loss of appetite • libido or emotion b. Manic symptoms • euphoria • racing thoughts • tirelessness • delusions of special powers • delusions of grandiose identity • over activity • distractibility • irrelevant behavior • embarrassing behavior • hypomanic affects • pressure of speech • flight of idea

In 1978, the American Psychiatric Association began to recognize the controversies in regarding schizoaffective disorder as a variant of schizophrenia, a variant of affective disorder, or a continuum between schizophrenia and affective disorder (American Psychiatric Association, 1978). In the DSM III, the category of schizoaffective disorder was included but without clear diagnosis criterion. It also described as a case when the psychiatrist was unable to make a clear diagnosis as schizophrenia or affective disorder (American Psychiatric Association, 1980).

As a Variant of Schizophrenia with Similar Chronicity In a different way, Welner et.al. (1977) affirmed that schizoaffective disorder should be a variant of schizophrenia. He rejected the hypothesis that persons with schizoaffective disorder are better in prognosis and recovery than those with schizophrenia. In his study, among 114 patients with schizoaffective disorder, 70% of them had a chronic course. Among these chronic cases, 80% of them were deteriorating (Welner, et.al., 1977 & 1979). Welner and his colleagues tried to prove that persons with schizoaffective disorder are similarly chronic as those with schizophrenia (Marneros, 2007; Welner, et.al., 1977 & 1979). It seems that the argument in initial conceputalization of schizoaffective disorders before 1950 still continued in from 1950s to 1980s. In many cases, Kraepelin’s (1920) and

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Schnieder’s (1959) assumptions that borderline cases in schizophrenia have better prognosis and better recovery was further validated by large scale studies done by Angst and his colleagues from 1966 to 1979. However, this assumption was challenged by the finding of the studies done by Welner and his colleagues (1977 & 1979). Their studies strongly showed that 80% of persons with schizoaffective disorders could reach a stage as chronic as persons with schizophrenia. If the creditability of all these studies are similarly trustworthy, that means, schizoaffective disorder can be both be regarded as a variant of schizophrenia and a borderline case in between schizophrenia and affective disorder. If it is not properly treated, it can be as chronic as those persons with chronic schizophrenia. However, if persons with schizoaffective disorders have better prognosis and stronger will to recovery, they can recover better than those with schizophrenia. Within this controversy of argument in research findings, instead of recognizing that there are problems in dichotomization and categorization of clients of mental illness, some scholars still insisted that there should be a clear diagnosis of schizoaffective disorder by putting all related symptoms from schizophrenia and affective disorders. That means, Vaillant, (1962), Marneros, (2007), Robins and Guze (1970) and Kendell and Gouraly (1970) all assumed that schizoaffective disorder is a single entity of mental illness with coexistence of both schizophrenia and affective disorders. However, it seems that the related authorities such as World Health Organization and American Psychiatric Association still hesitated to give a clear diagnosis about schizoaffective disorder.

CONCEPTUALIZATION OF SCHIZOAFFECTIVE DISORDER AFTER 1980 Controversies and arguments concerning prognosis, etiology and diagnosis of schizoaffective disorder still moved on after 1980s. Jager (et.al, 2003) tried to sum up related arguments and controversies into four ways. They are: 1. Schizoaffective disorder is a variant of schizophrenia. 2. Schizoaffective disorder is a variant of affective disorder. 3. Schizoaffective disorder is an intermediate entity between schizophrenia and affective disorder. 4. There is a continuum of functional psychosis with schizophrenia at one end and affective psychosis at the other end of the spectrum.

As a Variant of Schizophrenia As a variant of schizophrenia, Evans’ (et.al, 1999) study showed that persons with schizoaffective disorder showed similar prognosis and features as those with schizophrenia.

As a Variant of Affective Disorder As a variant of affective disorder, Goldstein’s (et.al, 2005) studies by conducting cognitive test on 83 male mental patients with schizophrenia and schizoaffective disorder in a mental hospital in the United States concluded that patients with schizoaffective disorder

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were in fact, `neuropsychologically normal’ as other patients with nonpsychotic mood disorder. Several clinical implications were suggested from the findings. First, programs and interventions should focus on clients’ neuropsychologically normal and facilitate their independent living and set higher goals in their vocational rehabilitation. Secondly, as they have better cognitive ability, they can receive cognitive therapy in alleviating their mood fluctuation (Goldstein, et.al., 2004). Jager (et. al., 2003) conducted a study on 241 first admission inpatients who fulfilled the ICD-10 criteria for schizophrenia, schizoaffective disorders or affective disorders. Patients were examined at the time of first hospitalization and then followed-up after 15 years. The findings showed that clinical picture at the time of first admission, schizoaffective disorders were distinguished from both schizophrenia and affective disorder. However, long term outcome of schizoaffective disorders had similar prognosis as affective disorders (Jager, et.al, 2003). The findings imply schizoaffective disorder should be distinguished from schizophrenia. It should be a subcategory under affective disorders.

As an Intermediate Entity between Schizophrenia and Affective Disorder As an intermediate entity between schizophrenia and affective disorder, the nature of schizoaffective disorder can be reflected in the diagnosis of schizoaffective disorder in DSM IIIR, DSM IV as well as in ICD-9 and ICD-10. In DSM IIIR (American Psychiatric Associaton, 1987), the formal diagnostic criterion of schizoaffective disorder as a differential disorder with bipolar and depressive subtypes was included. Finally, in DSM IV (American Psychiatric Assocation, 1994), it further elaborated diagnostic criteria of schizoaffective was mentioned. The diagnostic criteria are listed as follows:

A. An uninterrupted period of illness during which, at some time, there is either a major depressive episode, a manic episode, or a mixed episode concurrent with symptoms the meet criterion A for schizophrenia. B. During the same period of illness, there have been delusions or hallucinations for at least two weeks in the absence of prominent symptoms. C. Symptoms that meet criteria for a mood episode are present for a substantial portion of the total duration of the active and residual period of illness. D. The disturbance is not owing to the direct physiological effects of a substance (eg. A drug of abuse, a medication) or a general medical condition). Specific Type: Bipolar Type: If the disturbance includes a manic episode (or a manic or a mixed episode and major depressive episode) Depressive Type: If the disturbance only include major depressive episode. (American Psychological Association, 1994) It is clear in DSM IV schizoaffective disorder is a single entity of mental illness with coexistence of symptoms of both schizophrenia and affective disorders. The symptoms of schizophrenia should be significantly present for a long period of time regardless of the occurrence of symptoms of affective disorder. Similarly, the symptoms of affective disorder

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should be significantly present for a long period of time regardless of the occurrence of symptoms of schizophrenia. In the same way, the classification and definition of schizoaffective disorder was included in ICD-8 (International Classification of Disease 8th Edition) (World Health Organization, 1968) and ICD-9 (World Health Organization, 1976). In ICD-10 (World Health Organization, 1992), the diagnostic criteria of schizoaffective are listed as follows: G1. This disorder meets the criteria for one of the affective disorder of moderate or severe degree, as specified for each category. G2. Symptoms form at least one of the group listed below must be clearly present for most of the time during a period of at least two weeks G3. Criteria G1 and G2 above must be met within the same episode of the disorder, and concurrently for at least part of the episode. Symptoms form both G1 and G2 must be prominent in the clinical picture. G4. Most commonly used exclusion clause. This disorder is not attributable to organic mental disorder or to psychoactive substance related intoxication, dependence, or withdrawal. (World Health Organization, 1992) According to ICD-10, schizoaffective disorder consisted of five sub-types. They are as follows: 1. Schizoaffective disorder, manic type; 2. Schizoaffective disorder, depressive type; 3. Schizoaffective disorder, mixed types; 4. Other schizoaffective disorder; & 5. Schizoaffective disorder, unspecified. In comparing with DSM IV, it seemed ICD-10 tends to regard schizoaffective disorder is dynamic and changing with different combinations of symptoms in schizophrenia and in affective disorder.

As a Continuum of Functional Psychosis with Schizophrenia at One End and Affective Psychosis at the Other End of the Spectrum As a continuum of functional psychosis with schizophrenia at one end and affective psychosis at the other end of the spectrum, it means that schizoaffective disorder can be regarded as a fusion of schizophrenia and affective disorder. This orientation seems to concur with what Schneider (1959) discovered that there are two types of borderline case in schizophrenia and cyclothymia (affective disorder), the concurrent form and the sequential form. In concurrent form, persons with schizoaffective disorder have symptoms both from schizophrenia and mood disorder. In sequential form, persons with schizoaffective disorder may have symptoms of schizophrenia and then mood disorder or vice versa in a continuous sequence. The concurrent form seems to be similar to the diagnosis of schizoaffective disorder in DSM IV and ICD-10 in which symptoms of schizophrenia and affective disorder co-exist together. The sequential form may imply a view of continuum between schizophrenia and affective disorder. Instead of a static point within the continuum, schizoaffective disorder

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may manifest as a dynamic and fluctuating state within these two extremes of the continuum. That means, on one time, the clients with schizoaffective disorder may manifest full schizophrenia symptom. On the other time, they may manifest full affective disorder symptoms. On another time, they may manifest various degrees of affective disorders and schizophrenia symptoms. Marneros’ (2007) uses the term `polymorphism’ (changes between different kinds of episodes during the long term course) to describe the dynamic and fluctuating mental state of persons with schizoaffective disorder. Marneros (2007) further elaborated that instead of a cross sectional view, a longitudinal view regarding the dynamic change and fluctuation of mental state and symptoms should be employed in the diagnosis and interpretation of schizoaffective disorder.

IMPLICATIONS TO UNDERSTANDING, TREATMENT AND REHABILITATION TO PERSONS WITH SCHIZOAFFECTIVE DISORDER Controversies in defining, diagnosing and interpreting schizoaffective disorder create challenges, difficulties and hardships for both professionals and clients in the treatment, rehabilitation and intervention with schizoaffective disorder.

Challenges and Difficulties for Professionals Under the influence of empirical based medical science, related professionals, especially medical professionals, are accustomed to follow a simple formula in diagnosis, treatment and intervention of mental illness. This formula can be roughly described as follow: This formula merely consists of several step by step procedures. Firstly, the specific deficits and symptoms of a specific type of mental disorder must be explored and identified. Secondly, these specific deficits and symptoms should be correlated with the criteria of a specific mental disorder so that a clear and specific diagnosis can be given accordingly. Thirdly, according this specific diagnosis, specific psychiatric medication is given to clients with this mental disorder as the sole treatment. Fourthly, other types of psychosocial treatments are given accordingly. If the mental disorder is in acute and severe situations, hospitalization is given so to ensure the client with this mental disorder would not impose potential harm to himself/herself and others. If the client’s mental state is comparatively stable, other psychosocial treatments such as cognitive and behavioral therapy are imposed on clients with mental illness. These types of therapy modality also required professionals to have a clear and specific assessment of related problems and deficits of clients with mental illness. Underlying this simple formula was a disease orientation with several assumptions. First, it presumes that mental disorders can be clearly and neatly diagnosed. Second, it assumes persons with mental illness are soley represented by their related symptoms in one/more than specific mental disorders. Thirdly, professional figures as pscychiatrists and clinical psychologists are the only liable ones to impose treatments and medications for the persons

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with mental orders. Finally, it tends to assume persons with mental illness are objects for various types of treatment, their potentials and strengths for their own recovery are undermined by professional authority in the process of treatment and rehabilitation. Find out the specific deficits and problems in mental illness

According to specific symptoms, make a clear and specific diagnosis of specific mental disorder

According to this specific mental disorder, specific psychiatric medication is given as sole treatment

Other psychosocial treatment such hospitalization, cognitive behavioral treatment are imposed. Some need to address specific natures of the mental disorder

Figure 1. The Simple Formula for Diagnosis, Treatment and Rehabilitation of Mental Disorder.

For persons with schizoaffective disorder, the controversies in defining and interpretation tend to challenge these assumptions. Instead of being a mental disorder that is static and can be defined and diagnosed by a clear and specific diagnosis, schizoaffective disorder tends to be a highly dynamic mental state fluctuating between schizophrenia and affective disorder. The fluctuation of these symptoms, seems to be related to clients’ psychosocial factors, such as stress in psychosocial environment, subjective experiences and coping with related symptoms (Yip, 2006: Marneros, 2007). That means, facing all these dynamic, changing and polymorphistic natures, professional figures may not be the liable ones to render proper treatment. All these imply difficulties for professionals in diagnosis, treatment, intervention and rehabilitation of persons with schizoaffective disorders. Perhaps, the follow narration from a clinician may reflect the sense of uncertainities faced by professionals. For the sake of confidentiality, personal information and identity is proper disguised. ‘Frankly speaking, I have been a medical professional for more than a decade. I have encountered more than a thousand mental patients. For every patient came to my clinic, I needed to make up a clear diagnosis. According to this diagnosis, I could render proper medication accordingly. This worked smoothly for most patients, especially for paranoid schizophrenia of which the symptoms of paranoid delusion and hallucination were clear and explicit. It worked also well for patients with depressive disorder, bipolar disorder as well as anxiety disorders. However, it did not work smoothly for patients with schizoaffective disorder. The ambiguity in diagnosis deeply challenged our professional competence and authority. I had a patient who was initially diagnosed as schizophrenia and she was previously on antipsychotic medication. One year later, she manifested severe depressive mood together with highly fluctuation of mood and occasionally with grandiose idea that he was a very rich banker in the U.S.A. Facing this situation, I had several choices in my judgement and diagnosis. The first assumption was I had made an incorrect or unpecise dignosi previouslys. That means I had to change my previous diagnosis from schizophrenia to biopolar disorders or considered it as schizoaffective disorder. The second assumption that I was right in my past diagnosis, but my patient’s mental condition changed from schizophrenia to affective disorder or schizoaffective disorder. Of course, my knowledge and training in psychiatry required me to look for coexistence of both symptoms in schizophrenia and affective disorders. However, to protect my professional identity and authority, I would rather assume that my previous dignosis was right and the client changed from schizophrenia to affective disorders. I carefully interviewed whether or not his symptoms of schizophrenia such as delusions and hallucinations were still

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Kam-shing Yip prevailed. It was a bit hard for me to distinguish clients’ delusion from grandiosity not because of my professional competence in making the distinction but because of the fact I could not afford to spend too much time in exploring clients’ subjective experiences and related symptoms. As I had lines of patients outside my office waiting for me, I could afford to spend no more than ten minutes for each patient in medical consultation. To play safe, it is better for me to include more symptoms rather than excluding symptoms. Thus, I decided to put the diagnosis of schizoaffective disorder on the patient. Nevertheless, this diagnosis did not help much in my decision in rendering proper medication. There had long been arugments that what sorts of medications I should impose on my patient. I had three options. I could render medication such as lithium on his manic episode, or antipsychotics on his grandiose like delusions, or both. From my previous treatment on this patient, it seemed that antipsychotics worked well and made him mentally stable for almost a year. But, it seemed tha the situation changed. Finally, I rendered lithium and carbamazepine, hoping that it could clam down the clients. Nevertheless, one week later, the patient family member complained to me by phone that the side effects of both drugs made the patient dull and stagnant in daily activities. Deep in my heart I understood that it was a real challenge for me to make a clear diagnosis or rendering appropriate medication for patient with schizoaffective disorder. To secure my professional image, I spoke with full competence to patient’s family member that my diagnosis and medication were absolutely right and appropriate. I added one more statement to protect both myself and my client. I told them that two weeks later when the patient’s grandiose ideas/ delusion decreased, they should consult me right away. Frankly speaking, this was the only thing I could do despite the confusion and ambivalence in schizoaffective disorder. After that, I began to question whether a high dynamic person with a highly ambivalent mental illness could be clearly diagnosed and medicated. …’

In this case illustration, it is clear the psychiatrist faced a great challenge in giving a clear dignosis for his client with schizoaffective disorder. He was puzzled among diagnoses of schizophrenia, bipolar disorders, depressive disorder and schizoaffective disorders. The changes and shifting of one type of symptoms to another types of symptoms made the diagnosis difficult. The difficulties in diagnosis further complicated the psychiatrist’s judgment in rendering proper medication. This seemed to be consistent with Marneros’ (2007) ideas of ploymorphism (changes between different kinds of episodes during the long term course) to describe the dynamic and fluctuating mental state of persons with schizoaffective disorder. The longitudinal view about the changes of symptoms also validates the diagnosis of schizoaffective disorder. However, what Marnero (2007) failed to address that a longitudinal view for clinicians implies there are should be sufficient manpower and resources so tha the clinican can follow the client with schizoaffective disorder for a long period of time. For example, a person, A, suffer from schizoaffective disorder, first he has symptoms of major depression for six months, and then he has manic episode for six months. After that, he manifests psychotic delusion for another year. Finally, he suffers both from schizophrenic symptoms in forms of delusions and hallucination as well as intensive fluctuating mood for one more year. A’s psychiarist may need to be A’s clinician continuously for at least one and half year before he can really arrives at a diagnosis of schizoaffective disorder. If the psychiatrist only looks after A for six months or one year, certainly, he only arrives at a diagnosis of `affective disorder’ or `schizophrenia’. Even if the psychiatrist looks after A for more than one and half year, facing the change of symptoms he may also feel puzzled about three types of mental illness, schizophrenia, affective disorder or

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schizoaffective disorder. The confusion in diagnoses would be intensified, if A is looked after by four different psychiatrists within two years’ time. Each of them takes care of A for around six months. The first psychiatist may give A a diagnosis of depressive disorder. The second psychiatrist may give A a diagnosis of bipolar disorder. The third one may diagnose A’s mental state as schizophrenia. Only the fourth one may come to a diagnosis of schizoaffective disorder. All these show that the controversies and arguments on the natures, etiology and symptoms of schizoaffective disorders certainly create difficulties for psychiatrists in diagnosis and treatment. The simple formula of clear and specific diagnosis and specific medication does not work well in persons with schizoaffective disorders.

Sufferings and Hardships for Persons with Schizoaffective Disorders Despite the long arguments and controversies in diagnoses and etiology of schizoaffective disorders, its impacts on the treatment and rehabilitation of clients with schizoaffective disorder are not comprehensively studies and discussed. In fact, these controversies and complexity also create a lot of burdens and difficulties for both professionals and clients with schizoaffective disorder. For example, while a psychiatrist induces anti-depressants for the client because of his diagnosis in terms of affective disorder. Another psychiatrist may induce ant-psychotic medications to the same client because of his diagnosis in terms of schizophrenia. As a variant of schizophrenia, clients with schizoaffective disorder may suffer similar symptoms, labeling and problems as a client with schizophrenia. As a variant of affective disorder, clients with schizoaffective disorder suffer similar symptoms, labeling and treatments as a client with affective disorder. As an entity of differential mental illness with coexistence of schizophrenia and affective disorders, that means, clients suffer doubly from symptoms, labeling and treatments of schizophrenia and affective disorders (Yip, 2006). What belows is a personal narration from a client with schizoaffective disorder that may illustrate this `double’ sufferings. For the sake of confidentiality, his personal information and identity was properly disguised. P said: I have been suffered from mental illness for five years. Initially I just felt highly stressful because of my highly demanding work in my office. My boss was a very tough and highly oppressive master. He demanded every one in our office to work as salve so that he could get the greatest benefit for his company. Whenever I could not fulfil his requirement, I would be cursed by him saying that I was useless, rubbish and worthless. I wanted to quit from this job. I needed this job to support my family and pay the mortgage of my flat. After several years highly stressful, demanding and oppressive work, I felt deeply depressed and fatigue. My family doctor said I was suffered from depressive disorders and suggested me to take anti-depressants. At first, it seemed to work well, apart from some side effecs, the medication did uplift my mood and I could sleep well. The situation turned worse when my supervisor and two of my colleagues in my working team tried to isolate, marginalize and oppress me. They gossiped around me, teased at me, saying that I was an outdated fat pig in the office. I worked as a senior office clerk in a finance company. In a finance and investment company, everything happened in a drastic speed according to the dynamic changes in the financial market. I worked doubly hard to support those investor and fund managers. But they did not satisfy with my job simply because of my fatness and my low academic qualification. The gossips from my colleagues deeply puzzled

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Kam-shing Yip me a lot. One year later, even though I was away from my office, I still heard they gossiped around me. The ‘voices’ troubled me a lot and I was deeply depressed. Even when I walked in the street, I heard people around me teasing at me. That was dreadfully. My family doctor advised me to consult the psychiatrist. The psychiatrist said I was suffered from schizophrenia, this term and diagnosis really threatened me. I was finally driven crazy by my boss and my colleagues. That means, I was mad, crazy and insane. I was so angry with them, but still I had to work to support my family. Once they teased as me saying that I was nothing more than rubbish and I should dump myself into the rubbish bin. I could tolerate no more. I smashed them on their faces. No sooner, a guard came forward and took me to the police station. I was sent to a hospital diagnosing them I was a patient with paranoid schizophrenia with diposition of violence. However, inside my mind, I was deeply depressed. I hated myself that I could not control my temper. I lost my job and my whole family suffered. In the period of hospitalization, my wife visited me saying that as I could not pay the mortage of our flat, it was taken away by the bank. They became homeless. They had to live with my mother in law and later depended on public security. I was so sad and depressed. I refused to eat, and spoke for a whole week in the hospital. The psychiatric nurses said I wanted to commit suicide and I was diagnosed as schizoaffective disorder: depressive sub-type with suicidal gestures. I was frustrated by this diagnosis. Frankly speaking, I did not know what was the meaning underlying this diagnosis. Did it imply that I am a combination of schizophrenia and depression? From limited knowledge of mental illness, I knew that depression meant very sad to a degree that with a will to death. Schizophrenia meant insanity and crazy. If I had schizoaffective disorder, did it mean I was so sad that I turn crazy? Did it mean I was so crazy that I want to die? Did it mean I was sad and crazy? In fact, I was so sad that I lost my job that I could not support my friend. It was true that I was crazy not because of my own faults but because of spontaneous oppression and marginalization by my colleagues. My mental state was so confused that I simply wanted to die. The nurse said that I had to keep in close ward. She said I needed to be on heavy dosage of both anti-depressants and anti-psychotics. The heavy dosage of medication made me feel dizzy, stomach ache and stagnant. I was not only frustrated by my misfortunes in job and in family, as well as my sufferings on being a mental patient, but also by the confusion in diagnosis. Two years’ of hospitalization tended to stablize my mental state but also made me become dull, institutionalized and inert. I was finally discharged and returned home. However, I could no longer work any more. I was advised by my medical social worker to work in a sheltered workshop. In there, similar to the condition in the mental hospital, workers suffered from different mental disorders. Most of them were workers with schizophrenic records. Few of them had mood disorders. Nevertheless, only I suffered from schizoaffective disorder. Even the professionals and workers there did not understand what was the exact meaning of ‘schizoaffective disorder’. They simply regarded me as suffering both schizophrenia and depression. When the professional counselor in the workshop asked me about the etiology of my mental disorders, I could simply answer that I did not know. I only followed the advice of the psychiatrist to take related medications. He asked me to narrate my experiences. I frankly told him about my story. I told him that I first started with depressive mood when I was overloaded and overwhelmed by responsibilities imposed by my demanding boss. Then, my schizophrenic delusion was nurtured by severe oppression and marginalization done by my colleagues. Finally, my suicidal gestures were provoked by sufferings of my wife and my family. However, he did not believe in my story. He affirmed that my mental disorder ought to start with co-existence of both depressive mood and schizophrenia delusion and hallucinations. He even asserted my mental disorder was not so much concern about my

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oppressive experiences in my work but merely because of my biochemical imbalance that might to deficits in genes due to heredity. His attitudes made feel really uneasy and uncomfortable. He seemed to convince me that my genetic problems and biochemical conditions in my body were all causes of my misfortunes. I felt helpless and hopeless. What could I do to recover from schizoaffective disorder provided that even among professionals themselves did not know this mental illness well. In fact, I had suffered a lot from being a patient with schizoaffective disorder.

P’s experiences clearly showed that persons with schizoaffective disorders suffered far more that persons with depression and persons with schizophrenia. Their suffering and harships can be briefly listed as follows: 1. Hardships and sufferings in facing symptoms of schizophrenia; 2. Hardships and sufferings in facing symptoms of affective disorders; 3. Hardships and sufferings in facing fluctuation of symptoms from schizophrenia and affective disorders; 4. Harships and sufferings in facing the confusion of diagnosis and treatment among affective disorders and schizophrenia; and 5. Hardships and sufferings in being labeled by others both as patients with schizophrenia and affective disorders. All these hardships and sufferings may be neglected and undermined by related professionals in the process of understanding, diagnosis, and treatment of persons with schizophrenia. It is crucial that related professionals should know the controversies and difficulties in understanding and diagnosis of persons with schizoaffective disorder. They should recognize how these difficulties create double sufferings for persons with schizoaffective disorder.

A REVIEW OF LITERATURE IN SCI LITERATURES All these controversies existed in research, clinical diagnosis, treatment, rehabilitation and community integration for persons with schizoaffective disorder. However, these controversies are arguments may not be fully addressed in recent researches and studies. To comprehend this, the writer has carrrid out a comprehensive literature on studies in schizoaffective disorder in the Science Citatin Index from 1975 to 2007.

The Literature Archieve on Schizoaffective Disorders As the Science Citation Index (SCI) has long been regarded as the most inclusive and prestigious index in scholastic publication, the writer trieds to search all related journal articles included in this index. The writer started the search by typing the term “ schizoaffective disorder’ and “ schizoaffecitive disorders” in the general search engine of the index. Also, only those articles with this term in their titles were included in the archive. There were altogether 494 journal articles with the title of `schizoaffective disorder’ appeared

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in the Science Citation Index (SCI). Around these 494 articles, their titles, abstracts and contents of articles were carefully studied and categorized. Their contents were classified according to the following groups: 1. Types of Articles: a. research article b. review and discussion article c. editorial discussion d. conference abstracts and paper 2. Topics of concern: a. medical treatment and biochemical explanation b. etiology and diagnosis c. genetics studies d. cognitive functioning e. suicide and sucidal management f. related services and policies g. psychosocial therapy and counseling h. consumers’ needs and rights i. subjective experiences 3. Positions in Etiology of Schizoaffective disorder a. as a variant of schizophrenia b. as a variant of affective disorder c. as intermediate entity between schizophrenia and affective disorder d. as a continuum between functional psychosis and affective disorder e. as a dynamic change from symptoms of affective disorders and schizophrenia from time to time. 4. Countries of authors and articles a. United States of America b. Canada c. United Kingdom d. German e. Australia and New Zealnad f. Other European Countries g. Asian Countries h. African Countries i. Central Amercian and South American Countries 5. Year of publication a. 2007 b. 2006 c. 2005 d. 2004-2002 e. 2001-2000 f. 1999-1995 g. 1994-1990 h. 1989-1980 i. 1980-1975

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17

By means of above categories, the writer did a content analysis on related literatures appear on Science Citation Index. The results of the content analysis gave the writer a view about the trends of academic discussion and research on schizoaffective disorders. Table 1. Year of Publication in Article about Schizoaffective Disorder Year 2007 2006 2005 2004 2003 2002 2001 2000 1999 1998 1997 1996 1995 1994 1993 1992 1991 1990 1989 1988 1987 1986 1985 1984 1983 1981 1980 1981

Number of Article in SCI 51 51 42 29 25 42 59 19 31 18 17 0 11 7 9 6 6 5 2 8 6 5 5 4 3 7 3 1

Percentage 10.32% 10.32% 9.1% 5.3% 5.1% 8.5% 12% 3.8% 6.3% 3.64% 3.44% 0% 2.2% 1.4% 1.8% 1.2% 1.2% 1.01% 0.4% 0.16% 0.12% 0.101% 0.101% 0.08% 0.06% 1.4% 0.06% 0.02%

Findings: Trends and Concerns in the Studies of Schizoaffective Disorders The content analysis was done on related articles appeared in Science Citation Index with titles containing the terms `schizoaffective disorder’ or `schizoaffective disorders’. The findings of the content analysis were shown in the following tables.

Year of Publication In the year of publication, it seems that around one third (29.7%) of related publication were published from year 2005 to 2007. From 2000 to 2004, there were one third (34.7% ) articles published with a title of `schizoaffective disorder; in SCI journals. The other one third

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(35.6%) of articles published in SCI journals from 1975 to 1999. Around one fifth (22.1%) of articles were published from 1990 to 1998. The disturbtion showed there was a drastic increase of concern and studies of schizoaffective disorders from 2000 to 2007.

Types of Articles The type of article with a title containing the term `schizoaffective disroder’ can be shown in the Table 2. From Table 2, it shows that most articles in discussion of schizoaffective disorder are either research articles (41.5%) or conference abstracts (49.3%). There are only a few number of them are review articles (3.3%). That means, the international academic discussion on schizoaffective disorder seems to be quite controversial and diversified. Many of them (244 articles) are only conference papers presented by various authors coming from different countries on highly diversified topics and areas of concern. These abstracts may not be matured enough in developing a well-written and reviewed article in related journals. Most research articles focused on reports of findings of related studies on a very specific area of concern. The few number of review and discussion articles (17) may demonstrate that related academics tended not to regard schizoaffective disorder as a stable and well defined mental illness that deserved attention to review related definitions, treatments, etiology and intervention methods. Table 2. Type of Article Article with `Schizoaffective Disorder’ Term in Title in SCI Types of Article

Number of Article

Percentages

Research article

205

41.5%

Review and Discussion Editorial

17 28

3.4% 5.7%

Conference Abstract and paper Others

244

49.3%

0

0%

Table 3. Topic of Concern on Article with `Schizoaffective disorder’ in title in SCI Topic of Concern Medical treatment and biochemical explanation Etiology and diagnosis Genetics studies Cognitive functioning Related services and policies, Epidemiology Psychosocial therapy and counseling Consumers’ needs and rights Subjective experiences Recovery

Number of Articles 219 130 38 28 17 20 8 3 3

Percentages 44.3% 26.3% 8% 5.7% 3.5% 4% 1.6% 0.6% 0.6%

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Topic of Concern The topic of concern appeared in article with `schizoaffective disorder’ or schizoaffective disorders’ is shown in Table 3. From the above table, it clearly shows that most articles appeared in the SCI titled schizoaffective disorder merely concern about medical treatment and biochemical explanation. (44.3%) and etiology and diagnosis (26.3%). In articles related to medical treatment, they focused on findings about how different types of psychiatric drugs such as anti-psychotic drugs or anti-depressants or mood stablizers are delivered to persons with schizoaffective disorders. There are also quite a number of article describing various biochemical hormones or neurotransmittors for persons with schizoaffective disorders with obesity, anxiety or other types of health problems. Regarding articles on etiology and diagnosis, there are articles describing examination of biochemical substance of persons with schizophrenic disorder. There are only very few number of articles discussing the controversies of etiology in discussing whether schizoaffective disorder should be regarded as a variant of schizophrenic disorder, a variant of affective disorder, a separate entity or a continium of psychotic disorder and affective disorder. Most authors, in conducting their studies and discussing their findings, simply refered to a group of patients who had been diagnosed by related psychiatrists as schizoaffective patients. They presumed that diagnoses by related psychiatrists were valid and those criteria described by DSM IV or ICD 10 were unchallenged. Position of Schizoaffective Disorder The postion of schizoaffective disorder appears in article in SCI concerning schizoaffective disorder can be shown in Table 4. From Table 4, althought there have been some heated discussion about the postion of schizoaffective disorder, however, most scholars (80%) in the SCI simply regard schizoaffective disorder as a variant of schizophrenia. Their studies were not merely focused on subjects with schizoaffective disorder, instead, they studied both subjects with schizophrenia and subjects with schizoaffective disorder. There are only 80 articles (16.2%) articles regarding schizoaffective disorder as an intermediate entity between schizophrenia and affective disorder. There are 20 articles (4%) regarding schizoaffective disorder as a variant of affective disorder. Also, only a few scholars (2%; 10 articles) regarding schizoaffective disorder as a continuum between functional psychosis and affective disorder. Table 4. Position of Schizoaffective Disroders in Article with `Schizoaffective Disorder’ Terms in Title in SCI Position of Schizoaffective Disorder As a variant of Schizoprehnia As a variant of Affective Disorder

Number of Articles

Percentages

374

80%

20

4%

20

Kam-shing Yip Table 4. (Continued) As an Intermediate Entity between Schizophrenia and Affective Disorder As a Continuum between Functional Psychosis and Affective Disorder As a Dynamic Change from Symptoms of Affective Disorder and Schizophrenia

80

16.2%

10

2%

10

2%

Country of Studies Regarding the country of the articles in the SCI, most articles (64%; 317 ) were written by scholars and practitioners from the United States. Then, 137 articles (27.6%) were written by scholars from the European countries. Among these 137 articles, 31 articles were written by scholars from the United Kingdom (6.2%); 19 article (3.8%) from German; and 87 article from other European countries such as Denmark, Norway, France and Italy. It is only a few number of articles written by scholars from Asian countries (15 artilces, 3.04%); African countries (3 articles, 0.6%); Canada (5 article, 1%) as well as Australia and New Zealand (15 articles, 3.04%). Table 5. Country of Studies Schizoaffective Disroders in Article with `Schizoaffective Disorder’ Terms in Title in SCI Countries of Studies

Number of Article

Percentages

United States

317

64%

United Kingdom

31

6.2%

German

19

3.8%

Other European countries

87

17.6%

Canada

5

1%

Australia and New Zealand

15

3.04%

Asian countries

15

3.04%

African countries

3

0.6%

Countries in South America

2

0.40%

Discussion: Challenges and Controversies The findings of the study clearly showed that the current international trend of the literatures and research in concerning schizoaffective disorder face the following challenges and controversies.

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Increasing Concern vs Decreasing Discussion All these literatures showed that there seemed to be an increasing concern on studies in schizoaffective disorder, especially in recents years from 2005, 2006 and 2007. However, the increase of concern of schizoaffective disorder in SCI seemed not to add anything new to the above mentioned controversies in diagnosis, etiology and treatment of schizoaffective disorder. Instead, most (80%) articles and discussion simply assumed that schizoaffective disorder was a variant of schizophrenia. Most authors in SCI conducted their studies towards patients with schizophrenia and patients with schizoaffective disorder. Their studies tended to reflect that in most situations, patients with schizoaffective disorders received similar types of medical treatment and hospitalization as those with schizophrenia. The above mentioned arguments on the natures of schizoaffective disorders tend to occur within a comparatively small academic circle. Their ideas and discovery on the etiology and natures of schizoaffective disorders were not echoed or considered by academics and practitioners in conducting and interpreting related studies for persons with schizoaffective disorders. Amercian Stand vs International Position Although in classical studies of schizophrenia and schizoaffective disorders, many crucial findings in etiology and natures were originated from renounced scholars in German such as Kraplien (1899 & 1920) and Bleuler (1911 & 1024). The recent discussions suggesting a dynamic change of symptoms among schizophrenia and affective disorders were merely suggested by a renounced psychiatrist Andreas Marneros and his colleagues in German (Marnerous, 2007). However, in related discussions and articles in SCI, most of them (64%) were American scholars and medical practitioners. Only a few of them (3.8%) were written by German scholars and practitioners. Similarly, only 6.2% of them were written by scholars and practitioners from the United Kingdom. Including those written by scholars and practitioners from other European countries (17.6%), there were altogether 28% of articles in SCI came from European scholars and practitioners. That means, studies of schizoaffective disorder were dominated by studies coming from Eurocentric cultural contexts. Although Asian countries housed the highest population in the world, scholars and practitioners in Asian countries tended not to take an active place or being recognized in their studies about schizoaffective disorder. The current international position in the study of schizoaffective disorder, strictly speaking, can only represents a dominating Amercian view and concern within Eurocentric cultural contexts. The entire Asicentric, Afrocentric or South American views are poorly articulated in SCI academic discussion. Medical Orienation vs Humanistic Concern As mentioned above, the controversies in etiology, diagnosis and treatment of persons with schizoaffective disorder not only create disturbance to related professionals, in fact, it also creates confusion and sufferings to clients with schizoaffective disorder. However, in the reviewing of article in SCI, it is discovered most articles and discussions focused on medical treatment, biochemical explanation (44.3%) and etiology and diagnosis (26.3%) of schizoaffective disorder. Some of them concerned about genetic studies and cognitive functioning (5.7%) of persons with schizoaffective disorder. However, only a few of them discussed related services, policy and epidemiology (3.5%) as well as psychosocial therapy and counseling (4%) for persons with schizoaffective disorder. Nevertheless, the consumers’

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need and rights (1.6%), subjective experiences (0.6%), and recovery (0.6%) were rarely discussed by related scholars and practitioners in the SCI. The inclinations to medical treatment, biochemical explanation reflect a movement that the clients’ voices, experiences, feelings and rights in the process of treatment, rehabilitaton and recovery were spontaneously neglected by scholars and practitioners.

Static Mental Symptoms vs Dynamic Manifestation Within the discussions and controversies of etiology, diagnosis and treatment of schizoaffective disorder, the early stage of discussion seems to assume that related symptoms in schizoaffective disorders are static and fixated in persons with schizoaffective disorder. They assumed that schizoaffective disorder as a variant of schizophrenia and a variant of affective disorder (Jager, et.al., 2003). These discussions only affirmed symptoms of schizoaffective disorder are regular and patterned either as schizophrenia or affective disorder. However, the later stage of development tended to regard schizoaffective disorder as dynamic manifestation of an intermediate entity between schizophrenia and affective disorder or as a continuum of functional psychosis with schizophrenia at one end and affective psychosis at the other end of the spectrum. Marneros (2007) concluded that symptoms of schizoaffectie disorder may not manifest in static form, it may change from time to time. It means, at one time, it manifests symptoms of affective disorder. At another time, it manifests symptoms of schizophrenia. At some time, there may be co-existence of both symptoms of schizophrenia and affective disorder. Marneros (2007) used the term `polymorphism’ (changes between different kinds of episodes during the long term course) to describe the dynamic and fluctuating mental state of persons with schizoaffective disorder. That means schizoaffective disoder should be regarded as a highly dynamic mental illness. However, in related articles in SCI, nearly all articles regarded related symptoms in schizaffective disorders as static and fixated and distinguishable as schizophrenia or affective disorder Most scholars (80%) in the SCI simply regard schizoaffective disorder as a variant of schizophrenia. Their studies were not merely focused on schizoaffective disorder. Instead, they studied both subjects with schizophrenia and subjects with schizoaffective disorder. There are 20 articles (4%) regarding schizoaffective disorder as a variant of affective disorder. That means, most (84%) of scholars regarded schizoaffective scholars as static and fixated symptoms without any changes in etiology and manifestation of symptoms. There are only 80 articles (16.2%) regarding schizoaffective disorder as an intermediate entity between schizophrenia and affective disorder. Also, only a few scholars (2%; 10 articles ) regarding schizoaffective disorder as a continuum between functional psychosis and affective disorder. That means only 18.4% scholars recognized the dynamic natures of schizoaffective disorder. However, very few scholars recognized and extended the stand of `polymorphism’ of schizoaffective disorders as advocated by Marneros (2007). The dynamic and longitudinal natures discovered by Marneros (2007) may create difficulties in quantitative and medical oriented research. They need to be researched by extensive longitudinal and multidimensional studies. In fact, most studies as recorded in SCI were only one time assessment that required the symptoms of schizoaffective disorder were easily distinguishable, regularized and measureable.

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23

CONCLUSION As a conclusion, this paper is an attempt to summarize and discuss the controversies and debates in interpretation, articulation and diagnosis of schizoaffective disorder. Starting with Kraepelin’s assertion that there are cases in between dementia praecox and and manicdepressive insanity. Kasanin (1933) was the first scholar using the term `schizoaffective’ in describing this group of mental symptom. The etiology of schizoaffective disorder was highly controversial and arugmentative. Some scholars and practitioners found out that persons with schizoaffective disorder had better prognosis and recovery, especially those young persons in the first episode of schizophrenia and with coxistence of mood fluctuation (Kant, 1940; Angst, 1979). However, other scholars and practitioners affirmed that persons with schizoaffective disorder manifested similar chronicty and problems in recovery, especially those with a long history of mental illness (Welner, et.al., 1977 & 1979). Controversies of research findings conclude in four different ways (Jager, et.al., 2003). The first one assumes that schizoaffective disorder is a variant of schizophrenia. The scond one assumes that it is a variant of affective disorder. The third one assumes that schizoaffective disorder is an intermediate entity between schizophrenia and affective disorder. The final one is a continuum of functional psychosis with schizophrenia at one end and affective psychosis at the other end of the spectrum. Controversies also occurred in the development of diagnosis of schizoaffective disorders in ICD and DSM criterion. Finally, based on years of research findings, Marneros (2007) concluded that symptoms of schizoaffectie disorder may not manifest in static form, it may change from time to time. It means, at one time, it manifests symptoms of affective disorder. At another time, it manifests symptoms of schizophrenia. At some time, there may be co-existence of both symptoms of schizophrenia and affective disorder. Marneros (2007) used the term `polymorphism’ (changes between different kinds of episodes during the long term course) to describe the dynamic and fluctuating mental state of persons with schizoaffective disorder. Marneros (2007) further elaborated that instead of a cross sectional view, a longitudinal view regarding the dynamic change and fluctuation of mental state and symptoms should be employed in the diagnosis and interpretation of schizoaffective disorder. All these controversies actually create difficulties and burdens in making a clear diagnosis for persons with schizoaffective disorder. It also challenges the straigth forward assumption that all persons with mental illness can be clearly diagnosed with a static and specific mental illness so that specific medication and treatment can be rendered. Furthermore, controversies in natures of schizoaffective disorder also means persons with schizoaffective disorder are spontaneously suffered doubly from symptoms, dignosis and labelling effects of both schizophrenia and affective disorders as well as confusions and puzzles in locating right kinds of diagnoses, treatments, and rehabilitation. Finally, literature review from Science Citation Index show that most articles written by scholars from 1975 to 2007 showed that most scholars tended to neglect the controversies in defining and interpretation of schizoaffective disorder. Instead of regarding schizoaffective disorder as a dynamic disorder shifting among symptoms of schizophrenia and affective disorder, they tended to regard schizoaffective disorder as a variant of schizophrenia. Also, the international position in describing schizoaffective disorder was dominated by the Amercian literature and those from European countries like, the U.K., German and Italy. Although Asian country had most of the world population, Asian scholars’ findings and stands in interpretation of

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schizaffective disorder were under represented and even neglected in the discussion of schizoaffective disorder.

REFERENCES American Psychiatric Association (1952) Diagnostic and Statistical Manual of Mental Disorders, (1st Edition) Washington: American Psychiatric Association, Mental Hospital Service. American Psychiatric Association (1968) Diagnostic and Statistical Manual of Mental Disorders,(2nd Edition) Washington: American Psychiatric Association. American Psychiatric Association (1978) Diagnostic and Statistical Manual of Mental Disorders, (Draft of 3rd Edition) Washington: American Psychiatric Association. American Psychiatric Association (1980) Diagnostic and Statistical Manual of Mental Disorders, (3rd Edition) Washington: American Psychiatric Association. American Psychiatric Association (1987) Diagnostic and Statistical Manual of Mental Disorders, (3rd R Edition) Washington: American Psychiatric Association. American Psychiatric Association (1994) Diagnostic and Statistical Manual of Mental Disorders, (4th Edition) Washington: American Psychiatric Association. Angst, J. (1966) `Zu Atiologie and nosologie endgenger depressive psychosen, Eine genetiische, Soziologische und Klinische Studie, Berlin, Heidelbergt, New York: Springer Angst, J., Felder, W. & Lohmeyer, B. (1979) Schizoaffective disorder I: Results of a genetic investigation, Journal of Affective Disorder, 1: 139-153. Bleuler, E. (1911) Dementia Praecox Order Grouppe der Schizophrenia, Aschaffenburg, Leipiz: Deuticke. Bleuler, E. (1924) Textbook of Psychiatry, translated of German edition by A.A. Vrill, New York: Macmillian. Cadoret, R.J., Fowler, R.C., McCabe, M.S., & Winokur, G. (1974) `Evidence for heterogeneity in a group of good-prognosis schizophrenia, Comprehensive Psychiatry, 15: 443-50. Clayton, P.J., Rodin, I. & Winoskur, G. (1968) `Family history studies III- Schizoaffective disorder, clinical and genetic studies- including a one to two year follow up’, Comprehensive Psychiatry, 9: 31-49. Evans, J.D., R.K., Heaton, Paulsen, J.S., McAdams, LA., Heaton, S.C. & Jeste, D.V. (1999) `Schizoaffective disorders: a form of schizophrenia or affective disorder’, Journal of Clinical Psychiatry, 60: 874-882. Flower, R. C., McCabe, M.S., Cadoret, R.J. & Winkur, G. (1972) `The validity of good prognosis schizophrenia’, Archives of General Psychiatry, 26: 182-185. Goldstein, G., Shermaksky, W. J. & Allen, D.N. (2004) `Cognitive functioning in schizoaffective disorder and clinical subtypes of schizophrenia’, Archives of Clinical Neuropsychology, 20:155-159. Jager, M., Bottlender, M. J., Strauss, A. & Muller, A. S. (2003) `Fifteen year follow up of ICD 10 schizoaffective disorder s compared with schizophrenia and affective disorder’, Acta Psychiatric Scandianvia, 109:30-37. Kant, O. (1940) `Types and analysis of the clinical pictures of recovered schizophrenia’, The Psychiatric Quarterly, 14: 676-700.

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Kasanin, J., (1933) `The acute schizoaffective psychoses’, American Journal of Psychiatry, 13: 97-126. Kleist, (1928) `Uber zykloide, paranoide und, epileptiode psychosen und uber die Frage der Degenerationspychchosen’, Schweizer Arachiv fur Neurologie and Psychiatrie, 23: 3-27. Kendell, R. E. & Gourlay, I. (1970) `The clinical distinction between affective psychosis and schizophrenia’, British Journal of Psychiatry, 117: 261-6. Kraepelin, E. (1899) Psychiatrie, 6th edition, Leipzig: Barth. Kraepelin, E. (1920) 'Die Erscheinungsformen des Irreseins, Zeitchrift fur diegesamte’, Neurologie and Psychiatrie, 63:1-39. Langfeldt, G. (1939) The Schizophrenia State, Copenhagen: Munksgaard. Marneros, A. (2007) `Paradigm of overlapping spectra’ in A. Marneros, H.S Akiskai, (Edited) The Overlap of Affective and Schizophrenic Spectra, pp, 1-22. Cambridge: Cambridge University Press. Robins, E. & Guze, S. B. (1970) `Establishment of diagnostic validity in psychiatric illness in application to schizophrenia’, American Journal of Psychiatry, 126:983-987. Schneider, K. (1959) Clinical Psychopathology, (M.W., Hamilton & Anderson, E.W., Trans) New York: Grune & Stratton, 1959. Schneider, K. (1973) Klinische Psychoapthologie, 10th edition, Stuttgart,: Thieme. Valliant, G.E. (1962) `The prediction of recovery in schizophrenia’, The Journal of Nervous and Mental Disease, 135: 534-543. Welner, A., Croughan, J.L., Fisherman, R. & Robin, B., (1977) `The group of schizoaffective and related psychosis- critique, record, follow up and family studies: a follow up study’, Comprehensive Psychiatry, 18: 413-422. Welner, A., Welner, Z. & Fisherman, R. (1979) 'The group of schizoaffective and related psychosis IV: A family study’, Comprehensive Psychiatry, 20: 21-5 World Health Organization (1968) ICD-8 International Statistical Classification of Diseases and Related Health Problems (8th edition) Geneva: World Health Organization. World Health Organization (1976) ICD-9 International Statistical Classification of Diseases and Related Health Problems (9th edition) Geneva: World Health Organization. World Health Organization (1992) ICD-10 International Statistical Classification of Diseases and Related Health Problems (10th edition) Geneva: World Health Organization. Yip, K.S. (2006) `Subjective experiences of persons with schizoaffective disorders’, in W.H., Murray, (edited) Schizoaffective Disorders: New Research, New York: Nova Science publishers.

In: Schizoaffetive Disorders Editor: Kam-shing Yip

ISBN 978-1-60456-948-3 © 2009 Nova Science Publishers, Inc.

Chapter 2

UNDERSTANDING THE NEEDS, RESILIENCE AND RECOVERY OF PERSONS WITH SCHIZOAFFECTIVE DISORDER:RELATED THEORIES AND CONCEPTUAL UNDERPINNINGS Kam-shing Yip* Department of Applied Social Sciences The Hong Kong Polytechnic University, Hong Kong

INTRODUCTION: FROM MEDICAL CONTROVERSIES TO PERSONAL EXPERIENCES There have long been controversies in etiology of schizoaffective disorder ranging from a variant of schizophrenia or a variant of affective disorder to a dynamic changes of symptoms of schizophrenia and/or affective disorder (Kant, 1940; Angst, 1966 &1979; Welner, et.al., 1977 & 1979; Jager, et.al., 2003; Marneros, 2007) However, all these discussions merely focused the perspective of medical professionals in making dignosis, rendering medical reatment as well as regading decision of hospitalization. Only a few medical professionals and scholars may consider the plights and situations of persons with schizoaffective disorder in resiliencing and recovering from schizoaffective disorders (Yip, 2006). In fact, for persons with schizoaffective disorders, they need extra courage and will power in going through various hurdles in the process of recovery. They need to motivate themselves to face challenges, hardships and difficulties in life. They need to embrace a strong will to change and to put themselves on the road of recovery. Crowdford’s narration on his own recovery from schizoaffective disorder may demonstrate this will power clearly. ‘Achieving real change is a lengthy process and it is often painful. Seeing a therapist just until you feel better for awhile is not likely to effect meaningful change.. …… There came a point….. that I noticed that I always kept falling into the same hole and that I was not having *

E-mail: [email protected]

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Kam-shing Yip any success in making my situation any better. I was on medication for much of the time since I was diagnosed and although it provided some relief. The symptoms weren't so bad with the medication but I still experienced them and life just plain sucked in general…..I made a really important decision then. … I decided I was going to see a psychotherapist and stick with it and no matter what happened that I was going to keep going even if I felt better. I was going to keep going until I was able to effect meaningful, positive, lasting change in my life. Simply deciding to see a therapist for a long time is not enough. You have to decide that you're really going to change and face up to the work it will require and face the fear that it will arouse.’ (Crawford, 2003)

Crowdford’s narration clearly showed for persons with schizoaffective disorder, they need extra courage to face their fluctuating mood and pervasive delusion and hallucination. They also need a strong will and determination that no matter what sorts of things happen, they must stick to the good advice of their related therapists that encourage them to live a normal life. Thus, in helping persons with schizoaffective disorders, related professionals need to shift their attention to medical controversies in regarding the etiology, diagnosis and treatment of schizoaffective disorder to a humanistic concern of individual experience of persons with schizoaffective disorder. This humanistic concern should consist of the following important elements.

ETIOLOGY VS PERSONAL EXPERIENCE Under the influence of the biochemical model and genetic model of explanations, related professionals tend to arise at a simple, clear and distinctive etiology of schizoaffective disorder so that they can impose related treatments in an objective but detached way. They are looking for a well defined and static etiology so that they can claim that that their professional training, authority and methods can really master the treatment process of schizoaffective disorders. The more static and distinctive the etiology is, the more virgor they can calimed their objectivity and accountability. However, as Marneros (2007) described that schizoaffective disorder is highly dynamic and changeable from a range of schizophrenic symptoms and affective disorder symptoms within a long period of time. It really creates big burdens for related professionals to arise at a well defined and static etiology to facilitate their professional performance in a highly objective but detached treatment process. Facing that sort of challenge, it is a good turning point for related professional to shift their sole attention of etiology to the personal experiences of persons with schizoaffective disorder. From time to time, a person with schizoaffective disorder may have to face several types of personal experience in facing their manifestation of related symptoms including: a.

a manifestation of symptoms of schizoprhenia such as positive symptoms and negative symptoms; b. a manifestation of symptoms of affective disorder such as major depressive episode and mania episode; c. a manifestation of both symptoms in schizoprehena and affective disorder; & d. a manifestation of chanigng symptoms from schizophrenia to affective disorder or vice versa.

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Apart from facing the experiences of manifestaton and fluctuation of psychiatric symptoms, persons with schizoaffective disorder may also need to face their personal experience in the following aspects: a.

subjective experiences in facing other labeling and perception of being persons with mental illness; b. subjective experiences in facing the diagnosis, treatment and rehabiliation by various professionals and in various service settings and units; c. subjective experiences in relying on others’ caring and help in the process of treatment and in the process of manifestation of related symptoms; & d. possible unfair treatments or exclusions in job, family, community and social life. In comparing with the focus of controversies of schizoaffective disorder, all these experiences are much more relevant and important for persons with schizoaffective disorer in their daily living. The shifting on controversies of etiology to clients’ subjective experience may make related professionals become more empathetic and understanding in the process of treatment and rehabilitation. In fact, the focus of client’s personal experience may also make related professionals more accurate in the explanation of the dynamic natures of schizoaffective disorder. Instead of regarding the schizoaffective disorder as a static nature, related professionals gradually recognize the dynamic and changing natures of etiology in fluctuating between schizophrenic symptoms and affective disorde symptoms. The focus on client’s personal experiences helps related professional to adapt a longitudinal view in understanding the etiology of persons with schizoaffective disorder. Instead of focusing on an episodic view on schizoaffective disorder, they become more alert on the change of the symptoms in the client over a long period of time.

Diagnosis vs Needs and Feeling Most medical professionals may focus their attentions in ensuring an accurate diagnosis for persons with mental illness so that appropriate medications and treatments can be rendered accordingly. The more accurate the diagnosis is, the more specific medical treatment can be imposed. Strictly speaking, the diagnosis is based on the client’s description and manifestation of symptoms in the past and in the present to predict similar symptoms s/he will experience in the future. Using the past to predict the future may have several inadequacies. Firstly, it tends to neglect the possible change of related factors that may make the client mental problems change. Secondly, it neglects the coexistence of symptoms with several types of mental illness. A person with schizophrenia can also have severe anxiety. A person with substance abuse may also suffer from depressive mood before and after the withdrawal of psychotropic susbances. Thirdly, it fails to describe the core problems behind symptoms of various types of mental illness. In schizoaffective disorder, the situation is more complicated as the diagnosis is always, in many ways, fluctuating among symptoms both in schizophrenia and in affective disorder. In many cases, the manifestation of schizophrenic symptoms may lead the practitioner to arrive at a diagnosis of schizophrenia. Later, the occurrence of the affective disorders may make the practitioner arrive at a diagnosis of schizophrenia with depressive natures. Finally,

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the coexistence of both symptoms in schizophrenia and affective disorder may make the practitioner arrives at a diagnosis of `schizoaffective disorder’. That means, different practitioners may come up with different diagnosis. Even facing the same person with schizoaffective disorder, while one psychiatrist gives a diagnosis of schizophrenia, another may arrive at a diagnosis of affective disorder and the third one may come up with a diagnosis of affective psychosis. The over concentration of arriving a clear and distinguishable diagnosis tends to exhaust all the efforts of related professionals and neglect the importance of needs and feelings behind symptoms. These may be genuine and common needs like love and being loved by other; trust and being trust; hope and being hoped as well as normal and healthy respect and interaction with others. For persons with schizoaffective disorder, if they really have choice, they prefer all these genuine and common needs can be met in facing their significant others and related professionals rather than making a clear diagnosis of variant of schizophrenia, a variant of affective disorder, a continuum between schizophrenia and affective disorder or a dynamic and changeable among symptoms of affective disorder and schizophrenia. While a client with schizoaffective disorder is expecting special concern and care from well trained and prestigious professionals so that they can regain their sense of dignity, being cared, loved and respected, s/he may be highly frustrated by the apathetic attitude of related professional, especially his psychiatrist that expresses no interest on listening to the client’s feelings and genuine needs but keeps on making a clear diagnosis so that he can render medication accordingly.

Treatment vs Resilence and Recovery The discussion about the controversies in the etiology and diagnosis of schizoaffective disorder actually aims at a clear diagnosis about a distinctive nature of schizoaffective disorder so that a specific type of psychiatric medication can be given accordingly in the medical treatment. Various interpretations of the etiology of schizoaffective disorder may imply different types of psychiatric medications given to the person with schizoaffective disorer. Regarding schizoaffective disorder as a variant of schizophrenia may mean the delivery of antipsychotic medication. Regarding schizoaffective disorder as a variant of depressive disorder may mean the delivery of anti-depressants to persons with schizoaffective disorder. Simlarly, regarding it as a variant of bipolar disorder may mean the dispensary of mood stabilizer. However, regarding schizoaffective disorder as a continuum and a dynamic change of etiology between schizophrenia and affective disorder may imply a mixture of decisions of giving various types of psychiatric medication. That means a person with schizoaffective disorder may receive mood stabilizer, anti-depressant, and/or anti-psychotic medication according different types of symptoms they manifest or different types of interpretation of etiology by their psychiatrists. Within a medical poient of view, psychiatric medication seems to be curcial in the treatment of persons with schizoaffective disorder. Depsite the adverse effects of psychiatric medication (Briggen, 1994) related professionals tend to assume that the recovery of he persons of schizoaffective disorder is mostly relied on the power of professionals and related medications, the will, coping, strengths, potentials and abilities of persons with schizoaffective disorder to recovery is not put into consideration. In fact, in the process of recovery, the persons with mental illness should have a full

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manifestation of their potentials, abilities and capabilities. In the United States, mental health recovery is defined as follows. ‘Mental health recovery is a journey of healing and transformation enabling a person with a mental health problem to live a meaningful life in a community of his or her choice while striving to achieve his or her full potential. ‘(U.S. Department of Health and Human Services, 2004)’

That means, within this concept of recovery, persons with schizoaffective disorder should have their own journey of recovery. They should have full access and right to live a meaningful life in his or her family, work, education, social and recreational activities. In this meaningful life and activities, their full potentials should thus be maximized. That means if a person with schizoaffective disorder is previously an architect, the process of recovery should be formulated that so that s/he can gradually regain his or her status as well as ability to be an architect. Even if s/he was unable to do so, s/he should be helped to do job with similar natures. S/he should not be kept in the sheltered workshop doing simple manual work simply because his or her record or experiences of schizoaffective disorder. In addition, persons with schizoaffective disorder should not be kept in close ward or occupational ward because of their records of diposition of violence or suicidal attempts. Instead, they should be helped to develop their own interests, capabilities and potentials, so that they can be healthily involved in these meaningful activities and decrease their needs to use violent acts or suicidal attempt to express their frustating emotions or profound sense of emptiness in life. Within the ideologies of recovery, the symptoms of schizoaffective disorder including both schizophrenic, depressive or/and manic symptoms can be perceived as coping mechanisms to life frustration, loss of beloved persons and objects, intense oppression from others as well ontological sense of emptiness in life. In this chapter, by means of a case vignette, the writer tries to illustrate the experiences a person in his struggle and recovery with schizoaffective disorder.

THE CASE: A RIGHTEOUS MAN WHO WANTS TO LIBERATE THE OPPRESSED James (the name preferred by the client) was a client with schizoaffective disorder. He suffered from both biopolar and schizophrenic symptoms in his medical history. He was diagnosed as having schizoaffective disorder. In his manic episode, he said that he was a righteous man who comes to the world to liberate the oppressed and disadvantaged. He approached the writer for psychosocial treatment and counseling. His consensus to use his story for academic purpose was sought. For the sake of confidentiality, his personal identity and information was properly disguised. ‘James came from a low class family in which his father was a manual labor working in a harbor in Hong Kong. His mother was a cleaner in a Chinese restaurant. Every day, his father was responsible to carry tons of goods from large cargo ships to the trucks waiting in the harbor. To face his highly labour intensive work, James’ father was accustomed to drink a large amount of alcohol to cheer him up.

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Kam-shing Yip Occassionally, James’ father was drunk and abused James and his young sister. He was also a compulsive gambler who spent all his money in gambling, drinking as well as finding prostitutes. James’ mother had to work day and night to earn enough money to support the lives of the whole family. When James was only eight years old, he was responsible to cook two meals and took care of his younger sister. James was busy with his household chores and sometimes, he needed to help his mum in earning some extra money by taking some minor processing work from nearby factories. Although James and his mother tried their every best to earn a hand to mouth living for the whole family, his father still battered them when he was drunk and snatched their money for gambling. Whenever his father battered her mother, James was very brave enough to protect his mother by fighting with his father. As a consequence, he was frequently hurt by his father abuse. In facing his father cruel abuse, James was accustomed to tolerate the abuse silently. In tolerating the painful abuse, he tried to dream that he was a superboy who came to save his mother and younger sister.. Occassionally, James was unable to pay the school fee and was too busy to attend school. Fortunately, James’ family difficulties were sympathized by his school mistress who was a kind heart nun in a catholic church. She weaved off James’s school fees and arranged some teachers to have close tutorials with James. Under the care of his school mistress and his teachers, James was able to promote to a good secondary school. James managed to finish his secondary schooling and worked as a clerk in a school. He was enthusiastic and hard working. He enrolled in a part time degree course in school counseling. At that time, James mother was died of liver cancer. James was deeply depressed by the death of his mother. He refused to eat and locked himself in his room for a few days. Fortunately, his old friend visited him and encouraged him to come out from his depressive prison. He was then become highly agitated, apart from evening study in his part time degree course. He also enrolled in a distance learning course in financial investment. He served as a committee member in a human organization that serve the poor in rural China by helping them to build their schools, rear cattle and facilitate their productive farming. James seemed to use all these activities to heighten himself from depressive mood. His colleagues and his close friend advised him to stop torturing himself by over activities. However, James said that he heard his deceased mother always talking to him saying that he ought to struggle hard to be a famous person in the world. James’ mania seemed to increase gradually. He was highly agitated in his work. He claimed that he was a righteous man coming to this world to save the oppressed and the poor. He affirmed that he represented the human organization to attend global conference in discussing measures to liberate the oppressed and the poor in China and in other underdeveloped countries. He invested most of his savings to buy numerous books about positive psychology and self development. He even convinced others to invest in his global banking network for under-developed countries. He overtly proclaimed that the more fantastic jobs he had accomplished, the happier his deceased mother would be. James manic episode finally broke out. One day, he stood in the middle of the playground of his school and uses a loudspeaker to proclaim that he was the saviour to liberate all oppressed persons in the world. James was then taken to a mental hosptial. He was diagnosed as having schizoaffective disorder bipolar type. James was then hospitalized in the mental hospitals for one year. After that James was discharged to a psychiatric half way house for psychiatric rehabilitation. At first, James seemed to be on the road of recovery, he was able to find a job as a senior clerk in a secondary school and he gradually re-continued his study in his degree in counseling. He also encountered a girlfriend in his degree study. They got along well and prepared to marry. Suddenly, his girlfriend continued his study in the U.K. and six months

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later she wrote a letter to James telling him that she had already married another man in London. James was totally shocked by the leaving of her girlfriend. He had depressed for two weeks’ time and his mania episode returned gradually. He harbored a grandiose thought that he was the representative of the People’s Republic of China to detect and save those Chinese women that committed faulty marriage in the U.K. One day, he brought an air ticket in British Airline and he personally armed with a `toy gun’ and some sharp knives and prepared to go to the airport. Fortunately, his social worker knew his critical condition, with the help of his close friends, they were able to stop James in doing that and then he was re-hospitalized for another year in the mental hospital. After that, James’ mental state seemed to be unstable and on and off in the mental hospital for around three years.

THE EXPERIENCES OF SYMPTOMS IN PERSONS WITH SCHIZOAFFECTIVE DISORDER: A MULTI-DIMENSIONAL THEORETICAL ARTICULATION Persons with schizoaffective disorder, similar to other persons with mental illness, they embrace their own experiences and needs undermining their mental symptoms. Different clinical theories tend explain these subjective experiences and needs differently. Also, there are various types of theoretical underpinnings about schizophrenia, depression and manic episode. Facing the controversies of defining, interpreting and treatment of persons with schizoaffective disorders, the discussion about integrating theories from schizophrenia and affective disorder in explaining schizoaffective disorders are rarely discussed. In fact, there are several types of explanations in interpreting and understanding the experiences and needs of persons with schizoaffective disorder. Type 1: Interpret the experiences and needs in terms of related theories of schizophrenia Type 2: Interpret the experiences and needs in terms of related theories of depression Type3: Interpret the experiences and needs in terms of related theories of bipolar disorder Type 4: Interpret the experiences and needs in terms of combinations of theories of schizophrenia, depression and bipolar disorders

Type 1: In Terms of Related Theories of Schizophrenia Related studies of subjective experiences of schizophrenia can be grouped under several schools of thought (Yip, 1998; Yip, 2002a; Yip, 2003 & Yip 2007). Firstly, phenomenological approaches asserted that psychotic experiences are inner experiences with meaningful connections (Jaspers, 1959/1963). Jaspers’ phenomenological orientation was echoed by Schneider, Gruhle, Binswanger, Erwin, and Henriey (Spiegelberg, 1972). Schneider’s (1959) first rank symptoms affirmed that there is a diffusion of ego boundary in psychotic experiences (Schneider, 1959). Similarly, Laing (1960) assumed that psychotic experience is a subjective process of self-splitting (Laing, 1960). Psychodynamic approaches in interpreting subjective psychotic experiences in terms of self fragmentation, loss of self awareness and building up one’s ominopotent self. Freud stressed that in an acute psychotic

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state, the ego is unable to perceive the external reality. Instead, the ego creates autocratically a new internal world according to the wish of the id. The distortion of the realistic world is initiated by frustration in the reality (Freud, 1924/1983). Sullivan (1956) suggested that psychotic experiences are a loss of control of awareness of the self-system. Federn (1952), Mahler (1968) and Blatt and Wild (1978) described schizophrenia as an impairment of individuals’ ability in ego boundary differentiation. Pollack (1989) thought that persons with schizophrenia are caught by the dilemma of the need to protect the self from others and the dependency upon others for emotional survival. Klein, Winnicott and Fairbairn asserted the formation of schizophrenia is closely related to problematic mother-child relationship (Stone, 1990). There are humanistic orientations in understanding subjective psychotic experiences (Strauss, 1996; Estroff, 1989). Estroff (1989) thought that underlying subjective psychotic experiences is a struggle of self-identity and self-definition (Estroff, 1989). Strauss (1989, 1991, 1994 & 1996) affirmed that persons with schizophrenia are actually functioning, interacting and coping with their illness. They have their own copings in facing their psychotic experiences. Clients’ personal accounts are also crucial in understanding subjective psychotic experiences. Leete (1989) controlled his paranoia by reality checking. He manages his delusions by obtaining feedback from others in social interaction. He reduced his sense of loneliness by initiating support from his peers. He inhibited his sense of ambivalence by participating in constructive and meaningful activities (Leete, 1989: 198). Romme & Escher’s (1989) study showed that people with schizophrenia use various means to cope with hearing voices (hallucination). Finally, Yip (2003) affirmed the content of experiences of delusions and hallucinations are closely related to superstition and religious beliefs within individual’s own cultures. In terms of related theories in schizophrenia, schizoaffective disorder is a stage of manifestation of schizophrenic symptom. While symptoms of manic and depressive moods are different experiences in regard to schizophrenic symptoms, there will be two possible proposition in regarding the combination of both symptoms in both schizophrenia and affective disorder. Proposition 1: affective episodes (manic or depressive moods) are pre or post experiences before and after manifestation of schizophrenia Proposition 2: affective episodes (manic or depressive moods) are ways to prevent further deterioration of related schizophrenic symptoms. Proposition 3: both proposition 1 and 2 occur or coexist together. Related theories in schizophrenia tend to assume that persons with schizophrenia suffer from various degrees of self fragmentation. The self fragmentation may exist in several ways: a.

diffusion of self boundary in which the individual becomes hard to distinguish him/her and other related figures in his/her delusive world (Schneider, 1959; Federn, 1952; Mahler, 1968; Blatt and Wild, 1978) b. fragmentation of self system into several sub-selves such as unembodied self, true self and false self (Laing, 1960) c. an omnipotent self that is delusive and out touch of reality (Pollack, 1989; Estroff, 1989)

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d. a loss of control self awareness in which the individuals’ delusion is a manifestation of the suppressed dreams in one’s sleeping self. In many ways, this sleeping self may also exist in forms of intensive self regression or stagnant self withdrawal. Facing these sorts of self fragmentation, in the proposition 1, affective episode occur before or after the self fragmentation in psychotic experiences. In the proposition 2, affective episodes are used to prevent the further deterioration of the self fragmentation process. In proposition 3, depressive and manic episodes both occur before, during and after the process of self fragmentation process so as to prevent persons with schizoaffective disorder further self fragmentation. In other words, for persons with schizoaffective disorders, the sense of self fragmentation in terms of diffused self boundary, fragmented self system, loss of control in self awareness and ominopotent self that is out of reality is painful and intolerable to an extent that the person with schizoaffective disorder consciously or unconsciously preserve the integrity of his or her self system by being manic and depressive in mood. The narration of James may be briefly shown the relationship between the subjective experiences of self fragmentation and bipolar mood. James said: My experiences in my childhood were painful and dreadful. I hated my father deeply. He was the one who ruin my family including my mother, myself, my young sister and himself. He was always drunk when he returned home. He snatched my mother’s money so to involve in his dreadful gambling. This was the only sum of money earned by my mother for our miminal survival. My mother fought with him so to ensure this sum of money can be secured. Then he would hit my mother fiercely. I was the only one to protect my mother and my young sister. In fact, I was fearful and deadly afraid of my father’s abuse. When he was drunk, he was a monster, using a stick to hit my body. I was hurt everywhere. It was painful, but I had to tolerate and endured it so that my mother and my sister would not be hurt. I still remembered the feelings of turning myself into a dead wood, ignored the pain and told myself that I was a hero. In fact, at that moment, my mind and my body were separated. My mind linked up with my mother and my young sister. My body tortured the endless pain from my father’s abuse.’

James’ narration clearly showed that he was accustomed to a strong sense of self dissociation in facing his father’s abuse. The sense of self dissociation was closely to the nurturing of the unembodied self as mentioned by Laing’s concept of divided self in schizophrenia. To make his sense of self dissociation meaningful and worthwhile, James tended to embrace a heightened mood of beng a suffering hero to protect his mother and his young sister from being hurt by his father. From James’ narration of his experience in onset of schizoaffective disorder, it might demonstrate that his coexistence of self dissociation and heightened mood may speed up the further onset of his manic episode. James said: `Frankly speaking, I loved my mother very much. She tolerated my father’s endless abuse and tried every means to protect us and nurture us to be well eduated youth. She worked very hard and only earned a hand to mouth living but she still insisted that I and my sister had to go to school. I struggled to do some casual work when I was only eight in nearby factory but she did not allow me to do. Instead, she tried to do one full time job and several part time jobs to support our family. I was his only son, so I had to ensure she was free from my father’s torture. Emotionally, we were together, we were linked together to support the family and to make sure my young sister could be well eduated. We attained our goals, my

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Kam-shing Yip young sister finally entered the university and became a well educated medical practitioner. My mother also encouraged me to struggle for life and to work hard. So when my mother died of cancer, I really felt that I was dead too with the collapse of my spiritual support and my mental will to survive. It was my mother who nurtured me, encouraged me and developed me physically, mentally, emotionally and spiritually strong. So I could not accept her passing away. I fully believed that her spirit still surrounded around me, protected me, encouraged and cheered me up. This was similar to the situation in my childhood, when I was abused by my father, my mother always embraced me telling that I was a brave and very courageous boy who tortured my father’s abuse so as to protect her and my sister. I fully trusted the spirit of my mother always accompanied me whenever I went.’

James’ narration might show that he had a highly enmeshed relationship with his mother to any extent that his self boundary and self system were blurred and diffused with his mother. His strong sense of self dissocation occurred during his father’s abuse also accompanied with the urge and emotional linkage to protect his mother and his sister from the abuse. Thus, when his mother died, his integrity and completeness of his self system and self boundary was thus threatened. To make the self fragmentation and diffused self boundary become integrated and functional, he embraced a strong need to be virtually linked with his deceased mother by hearing his mother’s voice. The trace of his mother’s voice in normal daily living might be sensibly controlled without affecting his normal functioning or just serve an internal encouragement for him to face manageable hardship and sufferings. However, in times of severe hardships, sufferings and difficulties, his deceased mother’s voice might be maximized in forms of auditory hallucinations so as to pull up his morale in working through and coping with all these hardships and sufferings. Also, his will power to rescue his mother and his sister from his father abuse might turn to a manic episode to save and liberate related oppressed groups. In that sense, James’ self fragmentation in terms of hallucinations with his deceased mother’s voice were closely related to his manic episode in saving and liberating oppressed group in the world. That means, for James, his manic episode may be explained by prospsition 3. That means, his manic episode was a result of his self fragmentation because of diffused self boundary of his mother in hearng his mother’s voice. However, the occurrence of the manic episode is also a mechanism to cope with his loss of his mother in his depressive episode. In the manic episode with a grandiosity to liberate to save the whole world, he revisited and revitalized the feeling of saving his mother during time being abused by his father. This feeling made him to have a sense of being together with his deceased mother in times of hardships and sufferings.

Type 2: In Terms of Related Theories of Depressive Disorder Different explanations are offered to experiences of depression. In biochemical perspective, depression is a result of low levels of norepinephrine and serotonin (neurotransmitters) as well as over-action in hypothalamic-pituitary-adrenal cortical axis in the brain (Norden, 1996; Downling-Orr, 1998). In interpersonal perspective, clinical depression is perpetuated by difficulties in interpersonal relationship in family, work and community in ones’ childhood, adolescence and adulthood (Klerman, et.al, 1984). In cognitive perspective, depression is a result of negative and self-blaming schema in forms of arbitrary inference, selective inference, overgeneralization, maximizing and minimizing

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perception and cognition towards oneself and others (Beck, 1967; Beck 1976; Wilkes, et.al., 1994). In psychodynamic perspective, depression is regarded as an introjection of loss of object. The lost object is taken inside place and there subjected to hate, till hate is expanded; and recovery from mourning or depression takes place. It may exist in form ambivalence and aggression towards the loss object and the ego (Winnicott, 1965; Jacobson, 1971). Zaslow (1994) tried to distinguish analectic depression from superego depression, in which the former one presents with object hunger, clinging dependency and feeling of weakness and incompetence and the later one is dominated by feelings of guilt and self-recrimination. For persons with depression, depression is far more than manifestation of symptoms, it is a loss of totality and meaningfulness of self in life in which they tried their best to search and relocate (Doneahue, 2000; Frankl 1963; Frank, 2000, Karp, 1996). Very often, clients’ subjective experience in depression always represents an inner cry in subjectivity of depression (Yip, 2002b; Karp, 1996; Rowe, 1996) It displays an urge for ontological being by showing her sense of ontological emptiness (Laing, 1960). Subjective experience of depression revealed a human drive for perfectionism by pointing out one’s own failure. The eagerness to be understood is suffocated by others’ labeling of her symptoms. The client searches for ultimate meaningfulness by focusing on the meaninglessness of present existence. The inner cry in subjectivity, the urge for perfection, the drive for meaningfulness and the urge to be understood may manifest in various ways of verbal construct, metaphor, myth and even silence or inertia (Rowe, 1978). Within the orientations and theories in explaining depressive disorder, schizoaffective disorder is merely a sort of depressive disorder. The occurrence of both symptoms of both schizophrenia and major depressive disorder may be explained by the following propositions: Proposition 4: schizophrenic symptom occurs after the onset of severe depression may be interpreted as results of prolonged and severe depressive mood. Proposition 5: the occurrence of schizophrenic symptoms is a way for the individual to cope with painful inner experiences from severe depression. Proposition 6: both proposition 4 and 5 occur or coexist together Related theories in depressive disorder may show that depressive mood starts with individuals’ strong sense and need of perfectionism and current loss of beloved object and end up with ontological emptiness and a severe sense of worthlessness to an extent that they may tend to end up their life. The process of depressive mood, from related theories may be summarized in several stages: Stage1. Stage 2:

Stage 3: Stage 4:

A strong sense and need of perfectionism that make the persons becoming less tolerable to loss and inperfectionism Prolonged demanding situation makes the persons accustom to involve in a self thinking that s/he should demand herself and himself more so as to live up with other expectations Recurrent unpleasant experiences and issues that results in loss of beloved objects or severe imperfection that is intolerable to the persons Development of anger feeling towards the loss objects and result in have a severe sense of imperfection

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Stage 7:

The anger feeling is internalized attributing to a self blaming schema and anger direct towards oneself. The endless struggle of anger towards oneself and others; self blaming and blaming others; and hate towards oneself and others drift off all the individuals’ psychic engery. The individual appears as empty, fatigue and loss interest in everything The self blaming schema and anger towards oneself and another may finally turn to a self destruction schema and an urge to punish, to extinct and to end up one’s life.

Within these stages of development of depressive moods, persons with schizoaffective disorder can view as a result of extremely intensive mood to an extent that the self blaming scheme and anger towards oneself and another finally result in self fragmentaiton (proposition 4). In James’ case, his subjective experiences did manifest an intensive sense of sadness and loss because of the death of his mother. Within this intensive sadness and loss, he did harbour a strong anger towards himself as well as his deceased mother and his father. What below was his self narration. James said: `The death of my mother was certainly an intensive loss to me. I was so angry with her leaving, She had suffered a lot in her adulthood. She tried her very best to nurture us and made us grew up with dignity and respect. Without her, both I and my sister would be tortured to death or we might leave our families and become delinquent adolescents. However, she left us so suddenly. It was the time for me to return her care and concern to us. I was so regreted for her leaving. If I was not so busy in my work or too committed in my study, I could have more time in accompanying with her. But now, I had no more chance. The leaving of my mother made me feel so sad and regretted to an extent that I felt extremely depressive. For more than a week’s time, I did not want to eat, to drink or to do anything. Within this week, I locked myself in my room and looked at my mother’s photo. I ventilated my sadness and emptiness. I recalled the memories with mother during my infancy, my childhood, and my adolescence.Within all these years, my mother was my sole emotional supporter as well my meaingfulness of life. Her death seemed to be the end of all these. I did want to commit suicide so that I could reunion with my mother on heaven. But one night, in my dream, I saw my mother who was so kind and caring. She stood by the side of my bed, touching my hair and encouraged to live on meaningfully. She wanted me to be a diligent and righteous man to use the rest of my life to save those oppressed and deprived. From that time on ward, I heard my mother voice always talking to me. She encouraged me wherever I went and whenever I did anything meaningful.

From James’ narration and experiences, it was clear that James’ loss of his mother provoked his onset of severe depressive mood. His anger towards the death of his mother and his own inadequacies to make his mother comfortable and enjoyable in his aging deeply frustrated him. He was absorbed in a deep depressive mood with no way out. It seemed both prospsition 4 and 5 could be applicable in explaining James situation. On the one hand, severe and prolonged depressive mood coupled with several days’ self isolation seemed to have fragmentation effects on James’ ego system. His self boundary tended to be diffused with a development of continuous hallucination that her deceased mother was speaking to him. On the other hand, it seemed that all these hallucinated voices from his mother made James have

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a pseudo-reunion with his deceased mother. It helped James to overcome his deterioration and stagnancy from his severe depression. Similar pattern happened when James faced the leaving of his girlfriend. James said: It is painful and unbearable in the leaving of my girl friend. We were so close before she went to the U.K. for further studies. She was a pretty and kind lady. We were classmates in the degree of counseling course. She was diligent and brilliant in rendering counseling. She was a full time counselor in a social welfare organization. She was empathic in listening the feeling and need of her clients. She also loved me deeply. She fully appreciated my struggle and strong endeavor in life. She also said my mother was a highly respectable woman who dedicatd her whole life to protect and bring up us. She admired my courage to protect my family by torturing my father’s abuse without complaints. She said I was the bravest and courageous man she had evere met. She loved me deeply and we planned to marry after her studies in the United Kingdom. Indeed, we had a very refined planning on our future marriage. I had brought a flat, and saved enough money for the wedding ceremony. However, things did not happen in the way you planned. After my girlfriend had arrived the United Kingdom, she was seriously sick, I could not take a long leave to take care of her. She met a male classmate there who was a male nurse and took care of her until she recovered. Their courtship developed quickly and married afterword. My girlfriend wrote a letter to me and regretted her failure to keep our promise. I was totally shocked by the news. I lost my only girlfriend, the one I loved deeply and emotionally engaged with. I was so sad and experienced similar chronic sorrow as I lost my beloved mother. Fortunately, the voice of mother kept on telling me that my girlfriend still loved me. She told me there were a lot of Chinese women in the U.K. planned to have marriage with British citizens so that they could gain their permanent residency in the U.K. They were being oppressed and raped by those indecent males in the U.K. To save all these oppressed women, properly including my girlfriend, I had to recover from my depressive mood. In fact, occasionally, I did hear the voice of my girlfriend who was crying for help in the United Kingdom.’

From James’ narration, it seemed that similar pattern occurred when James was deserted by her girlfriend. The feeling in losing of girlfriend is similar to the feeling in losing her mother. James felt dreadfully angry, sad and lost of his affective bond with his beloved one. The traumatic loss of affective bond sparkled James’ severe depressive mood to an extent that leading to possible self fragmentation with diffused ego boundary. Double loss of his mother and his girlfriend had a tremendous adverse effect on James’ mental conditions. His auditory hallucination, hearing her mother’ voices increased to an extent not only comforting him but also encouraged him to save her girlfriend from being raped by untrustworthy male in the U.K. It seemed that proposition 4 and 5 (proposition 6) could be applied to explain James’s manifestation of both depressive and schizophrenic symptoms. On the one hand, James’ depressive mood because of double loss tended to be so severe that led to a severe self fragmentation with occurrence of hallucinations (her mother’s voice as well as her girlfriend’s voice) and delusion (her mother spirit accompanied him and her girlfriend was oppressed by his husband) as well as grandiose ideas (to save all oppressed Chinese girls from the U.K.). On the other hand, all these schizophrenic symptoms tended to alleviate the painful depressive experiences in facing the double loss and related traumas. James’ hallucinations, delusions and grandiose ideas tended to creat a positive effect by revitalizing his meaning of life and recoverage from his depressive mood.

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Type 3: In Terms of Related Theories in Bipolar Disorder There are quite a number of theories in intepret experiences and symptoms of bipolar disorder. In cognitive behavioral perspective, persons with bipolar disorder have neurocognitive deficits in 1. 2. 3. 4. 5. 6. 7.

selective attention, ability to sustained attention inhibitory control (rumination, distraction, and engagement in dangerous activities) working memory verbal memory backward masking controlled visual information processing executive functioning (planning, concept formation, shifting of sets) (Jones, Sellwood & McGoven, 2005)

Within the same line of thinking, a multilevel-cognitive model is constructed to interpret the occurrence and manifestation of the manic episode (Jones, 2001；Jones, Sellwood & McGovern, 2005). This model is based on Healy and Williams (1989) multi-level works and Schematic Propositional Analogical and Associative Representative System (SPARS) suggested by Power and Dalgleish (1997). Related elements in the multi-cognitive models are as follows: 1. Events that triggers Circadian System Disruption – Increased Energy/ Mental Activity 2. Such activity provokes schemas and levels of attribution a. Schematic model level: `I am superior and Nothing can go wrong’ (Mania) b. Associate level: Internal attribution bias for energy change c. Propositional level: `I feel energetic and creative, thanks to any natural intuition and intelligence. 3. Schematic model level of mania further triggers maladaptive behaviors that further provoke stressful events in a vicious cycle. Apart from cognitive behavioral theories, there are also theories that family atmosphere and family events that trigger the onset of manic episode. These social and family factors are: 1. 2. 3. 4.

life and family events Stressful events symptoms increased in bipolar disorder following a significant goal attainment event social rhythm disruption life events preceded manic episode (Johnson, et.al, ) (Jones et.al., & Johnson, etal., 2000)

Butzalaff and Hooley (1998) found out that there is an association between high emotion expression (critical comment and emotional over-involvement of carers) and relapse in bipolar disorder. Wendel’s (et.al., 2000) study confirmed that high emotion expression of relatives of bipolar disorder viewed symptomatic behaviors as being more under the patient’s control than did those with low emotion expression.

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Confusion of social rhythm also plays a crucial role in manifestation of manic episode and mood fluctuation. Malkoff-Schwartz, (et.al, 2000) reported that social rhythm disrupting life events precede manic but not depressive, episode in bipolar disorder. Persons with schizaffective disorder actually beware that their life and life pattern are messy and out of control (Jones, et.al., 2005). They know that europhic mood is out of their control to a degree that they can not sleep, concentrate on their work and even speak a short sentence clearly. Facing the confusion in mood and daily activities, psychodynamic theories tend to offer another types of explanation of bipolar disorder, especially the manic episode. Gabbard (1992 & 1994) affirmed that manic episode is a manifestation of unconscious sexual urges and fantasies. It seems that unconsciousness sexual urges and fantasies seemed to overpower ego defense mechanism. These unconscious sexual urges seem to overpower ego defense mechanism leading to a clinical picture of hypersexuality and other symptoms of mania. Abraham (1953) affirmed that manic episode reflects an inability to tolerate childhood depression in reaction to a developmental tragedy, such as the loss of parents. Manic state is understood as a way of removing the shackles of a tyrannical superego through the merger of the ego and superego. For persons with bipolar disorder, self criticism is replaced by euphoric self satisfaction. Similarly, Lewin’s (1950) asserted that in persons with manic state, his or her ego is a purified pleasure ego. The individual uses denial to disregard unpleasant perceptions and affects. Denial is also used to distress psychic realities the results in self punishment and self criticism. Kelin (1975) described the manic depressive episode into the following stages: a.

Depressive position with intensive anxiety that one’s own aggression has result in the destruction of the important love objects. b. Defense against the persecution of bad objects by pinning the love object and generation of the depression position. Manic defenses are necessary both to control and master the dangerous bad objects and to restore and save the love good objects. c. Three Manic Defenses are used. They are omnipotence, idealization and denial. 1. Omnipotence serves: i. to deny the need for the good objects, ii. to delude oneself into feelings of self containment and grandiosity, iii. to help one feel insultated protected from assault by internal persecution. 2. Idealization and denial work together. They serve i. to deny any destructiveness or aggression in relationships. ii. to reflects the tendency to gloss over any unpleasant reality iii. to treat everything with a sense of humor and iv. to disregard for the tragic dimensions of reality, even if the situation is tragic. 3. Idealization gives way to contempt, and linked to denial: i. to disregard the importance of the loved object ii. to deny the damage has been done to them and reparation is needed iii. to minimize any distressing feelings of sorrow or regret that may arise in connection with concerns about having destroyed loved objects d. A wish to triumph over parents is often an integral part of the manic defensive posture. e. A frequent childhood fantasy is to reverse the child-parent relationship.

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The fantasy produces feelings of guilt and anxieties of a depressive nature related to the wish to destroy and replace the parents. g. Feelings of depression may develop after a job promotion or other professional success because of person’s unconscious wish to triumph over and to surpass ones’ parents has been fulfilled. In the same way, Bribring (1953) suggested that manic elation is a compensatory reaction to severe depression. For persons with bipolar disorder there exists an unconscious fulfillment of a person’s narcissistic aspiration to be loved worthy, superior and virtually flawless. Finally, Jacobson (1971) in his study of depression and related mood disorder suggested that mania is mania as transformation of the sadistic superego from a punitive tormentor to a loving and forgiving object that is idealized. He affirmed that dramatically altered superego is projected into persons in the outside world with whom the patient establishes idealized relationship that are free from any negative characteristics such as hatred and anger. The functioins of the expansive superego is to compensate the low self esteem and depression. The manfestation of superego, can be in forms of mega superego, expansive ego as well as sexually over-competence. Facing others comments, persons with bipolar disorder may regards others as lack of intelligence to understand one’s sophisticated plan. In other words, various scholars in the psychodynamic school tend to suggest that there are three crucial layers in their ego system. There are the depressive ego, the sadistic superego and the rebounding of ego (the manic episode) by the following mechanisms: i. ii. iii. iv. v. vi.

the merging of superego with ego; the use of unconscious drive for re-bounding the ego; the formation of pleasure ego; the avoidance of depression position; the denying of unpleasant reality; & the labeling of the pseudo-loving object

Facing the commenting and opposite forces from the reality, there are three ways of self defences. The first one is omnipotence. That is a deluding that one is self containment and independent of needs of need object. The second one is idealization. Individuals with biopolar disorder try to idealize that the self as well as the object. The third way is denial. Individual with bipolar disorder denies one’s depression position, inadequacy in self system and in the cruel reality. Based on above mentioned theoretical underpinning, persons with schizoaffective disorder is actually an intensive manifestation of bipolar disorder. That means, the occurrence of manic and severe depressive episode or the fluctuation of the both manic and depressive mood is the major problem leading to manifestation of schizophrenic symptoms. Under this orientaiton, it may have several propositions that are listed as follows: Proposition 7:

schizophrenic symptoms occur after the onset of severe depression may be interpreted as results of prolonged occurrence of bipolar episode In this proposition, there are three sub-propositions:

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Proposition 7a: schizophrenic symptoms occur after the onset of manic episode may be interpreted as results of prolonged occurrence of manic episode Proposition 7b: schizophrenic symptoms occur after the onset of depressive mood may be interpreted as results of prolonged occurrence of depressive episode. This seems to be similar to proposition 4 but differs in a way that the depressive mood only exists in a short period of time and is replaced by manic episode Proposition 7c: it is the shifting of mood, from manic episode to depressive episode or from depressive mood to mania that leads to the schizophrenic symptoms. That means, it is not the mood itself that relate to onset schizophrenic symptoms. Instead, it is the fluctuation of mood that works. Propositon 7c: a combination of 7a, 7b & 7c. Proposition 8: the occurrence of schizophrenic symptoms is a way for the individual to cope with painful inner experiences of bipolar episodes In this proposition, there may be three sub-propositions: Proposition 8a: Proposition 8b:

Propositin 8c:

Proposition 8d: Propsition 9:

the occurrence of schizophrenic symptoms is a way for the individual to cope with painful inner experiences of mania episode. the occurrence of schizophrenic symptoms is a way for the individual to cope with painful inner experience of depressive mood. This proposition tends to be similar to proposition 5, but differs in a way tha the occurrence of depressive mood may not be long standing. the occurrence of schizophrenic symptoms is ways to cope with or to deter the fluctuation of mood from depressive episode to manic episode or vice versa. That means, schizophrenic symptoms are ways to cope with the fluctuation of mood rather than the manifestation of mood itself. a combination of 8a, 8b & 8c. a combination of proposition 7 and propositon 8.

According to all these theoretical underpinnings, the process of having manic episode may be started by a high emotional social environment or the individual is accustomed to heighten his or her mood by committing excitement events and issues to a degree that may lead to unstable daily routine or with little awareness of limits and constraints. Within this pattern in life in encounter difficulties, once the individual is kept with traumatic loss and depressive mood, s/he may indulge in intensively exciting mood so as to pull himself or herself up and consequentally leading to the onset of manic episode. All these stages are listed as follows: Stage 1: Stage 2:

Accustom to exciting mood, unstable daily pattern as well as high emotional expression from significant others. Individuals develop a habit that s/he, in an exciting mood, can fulfill any unreasonable demands or use highly exciting mood to deal with others’ high emotional expression

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Drepssive mood being provoked by loss of beloved objects, former expectation in life, significant others or severe difficulties in fulfilling other demands. Stage 4: Development of anger feeling towards the loss objects and result of imperfection Stage 5: The anger feeling is internalized attributing to a self blaming schema and anger direct towards oneself. The senses of frustration and guilt, sadness and loss are untolerable to the individual. Stage 6: The individual tries every mean to escape from his/her depressive position by heightening his mood, s/he pushes himself and herself by building up his or her omnipotent self. Stage 7: The omnipotent self is manifested by engaging in pleasurable activities (sexual desires), grandiose ideas (mega superego), non-stopping activities (sadistic superego), irrational investment. Stage 8: The omnipotent self and grandiosity is fully intensified to a degree that the individual denies realistic limits, constraints and possible risks. Stage 9: The full manifestation of manic episode may lead to some confusion, personal loss and irreversible adverse consequences. Stage 10: The loss and adverse consequences may then sparkle another onset of depressive mood. Within all these related theories, James’ schizophrenia symptoms seem to be a way to cope with her mania episode and depressive episode. This can be shown by James narration. James said: `my psychiatrist affirmed that I was suffered from schizoaffective disorder. He insisted that I should take mood stablizer as my manic episode was the core symptoms that affect my mental stability. I admitted in times of mania episode, I was out of control. The first mania episode occurred after my mother’s death. However, my psychiatrist did not understand that I needed to be active, to be hard working, to be indulged into various types of advocating activities to fulfill my mother’s unfulfilled wishes that I had to help those in need and in adverse condition. The psychiatrist labelled this as `manic episode’. I described this as a struggle for life and ontological existence. The manic episode is crucial for me in pulling me up from the loss of my mother. The feeling of losing my mother was dreadful and untolerable. Fortunately, my mother’s voice was still there, reminding me to be strong, tough, and diligent with no fear of loneliness, and facing my depressive. With her encouragement, I was able to participate in al forms of meaningful activities like studying part time course, involving in financial investment, and being committee members in human organizations to serve the poor in rurual China. The more I engaged in these meaningful activites, the more my mother’s voice was clear and encouraging, and the more I felt my mother was so closed to me. I was so happy with them, with a sense of reconfirming my values and meaning of existence. The psychiatrist called this as mania episode. Others said I was out of my mind, but they did not understand it was a stage of heightened mood with extreme excitements and happiness. It covered up my severe depressive mood entirely, gave me extra strengths to conquer and to overcome difficulties and hardship when I indulged in a thought that I was a hero to save those oppressed and deprived. My previous tough feelings in saving my mother and my sister from the abuse of my father returned. Instead of losing the linkage of my mother, I felt united, integrated, substantial and highly competent. The feelings were so good that outraged my

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ratioality and realistic limits. That was the time people around me said I was out of my mind that might be dangerous to myself and others and should be immediatedly hospitalized.’

From James narration, it is clear that the onset of the manic episode embrace important meaning for him. The onset of manic episode went together with his relatedness with his deceased mother by reactivating his auditory halluncination of her mother’s voice. In James’ case, his first onset of manic episode can be described in the following stages: Stage 1: Loss of his mother, outbreak of his depressive mood Stage 2: The depressive position is painful and untolerable Stage 3: Development of auditory hallucination by hearing her mother’s voice of encouragement Stage 4: The growing of her mother’s voice pushed him to work hard, be ambitious and be aggressive in striving for attainment Stage 5: The development of elated mood led to the outbreak of manic episode. That means in James’ case, his schizophrenic symptoms, auditory hallucinations of her mother’s voice was closely related to James’ bipolar symptoms dialectically. On the one hand, the schizophrenic symptoms pull up his depressive mood. On the other hand, his auditory hallucination intensified with his increase of elated mood. They are closely related to one another with a result of pulling James up from his prevailing depressive mood. The manic episode tended to represent James’ inner psychic energy and power with a strong determination to reunion with her mother and to sacrifice himself to save his mother, his sister and any one in the world from oppression, tortures and unfair treatment. This can be shown by James’ self narration: James said: `People around me, including my psychiatrist, social workers and my friends all claimed that they understood me and advised me to be clam, to enjoy of being an ordinary man. Related professionals even commented me that I was out of my mind when I was in my mania episode. They only assessed my manic episode manifestation by means of related criteria of manic episode. They tended to be objective and diagnostic. But they did not understand my feelings in my manic episode, nor they understood the importance of my mother to me. They tended to judge me in terms of their own perceptions and related assessment tools. They failed to relate all these to my previous experiences in my childhood and adolescence. Frankly, in times of mania episode, it was the time where my will power to struggle with hardships and sufferings reached the maximum. It was also the time that I had a strong feeling with united feelings with my mother. Nevertheless, when I was awakened from my manic episode, I felt dreadfully empty with the death of my mother and the loss of my psychic energy to struggle with life. The loss of my mother was permanent. Although she spoke to me and I felt being united in my manic episode, she still left me with an everlasting uncompensated inner vaccum.

From James’ narration, it is clear that James suffered deeply from the loss of his mother. This loss seemed to be ontological and formulated James permanent depressive position. He could only temporarily compensate this depressive position by hearing his mother’s voice (the schizophrenic symptom of hallucintation) and involving in being diligent, saving the depowered and liberating the oppressed (the manic episode). Once, all these vanished with

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the normal stable mental health, the ontological loss might still slowly and gradually accumulate in his mind to an extent that might lead to another manic episode. Facing this sort of ontological emptiness, James’ successful courtship with her girl friend seemed to be a permanent substitute. He tended to replace the union with her deceased mother by the new union of his girl friend by preparing to marriage. However, the sudden separation of her girlfriend not only vanished his new form of ontological substitute but also deepened his sense of ontological emptiness leading to a more powerful manifestation of schizophrenic symptoms (her mother’s voice) and manic episode (to liberate all oppressed women in the U.K. ) James said: the leaving of my girlfriend was very painful and unbearable not only because I loved her so much and we were well prepared to marry, but also because it sparkled my unpleasant memory of losing my beloved mother. In my whole life, I faced many losses. I lost my childhood, I lost my chance to study full time university course. I lost the previlage to have a good and supportive father. All these were common for normal children, but for me, all these were only myths but not reality. The only worthwhile gain in my life was a caring teacher and my extremely supportive and kind mother who emotionally and physically supported me in my whole life. She worked very hard so as to support our family. She never blamed me or cursed me even when she was fatigue and worn out. Her death was an ontological vaccum deep in my mind. That could not be filled permantly. However, the occurrence of my girlfriend who was also caring, understanding and supportive seemed to fill up this vaccum. She was the one who supported me when I first relasped and stayed in a mental hosptial. At that time, she was not my girlfriend. She was my classmate. We were in the same seminar group in the degree course. She was the only classmate who visited and encouarged me to recover and get well. With her support, I was able to recover from my manic episode and found a stable job as a senior clerk in a secondary school. The leaving of her meant that my filled inner vaccum suddenly unfilled again. Her leaving not only reactivated my deep sense of loss and emptiness due to the leaving of my mother. It cut my inner wound deeper and deeper. In fact, she was still there. Frankly speaking, I did not really believe that she voluntarily left me. Instead, she ought to be forced by his boyfriend. That was why I needed to save and liberate her from being oppressed by those males in the U.K. The National Geography magazine told us that there were too many such cases in the U.K. where Chinese females were forced by British White males to marry them. For Chinese females, they had to do so. It was the only way for them to gain permanent residency in the U.K. I had to save and liberate all Chinese females in the U.K. including my girl friend.

Type 4: In Terms of Combinations of Theories from Schizophrenia, Depression and Bipolar Disorders From James narration, it was clear that his subjective experience in the manifestation and interpretation of symptoms of schizophrenia, depression and bipolar disease is highly complicated interrelated. That means, the following propositions can be applied to explain James’ subjective experience in facing schizoaffective disorder. Proposition 3: both Proposition 1& 2 Proposition 6: both Proposition 4 & 5 Proposition 9: both Proposition 7 & 8

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To embrace this sort of propositions, that means, subjective experiences and needs of people with schizoaffective disorder should not be soley explained and interpreted by theories in schizophrenia, depressive disorder, nor bipolar disorder, it should a new frame of perspective by combining all these three types of theories dynamically and flexibly. That can roughly be represented by the following diagram: From the above diagram, it shows that the manifestations of related symptoms of schizophrenia, depressive disorder ad bipolar disorder are closely related to one another. Their relationship in clients’s subjective experiences in facing schizoaffective disorder may be expressed in the following ways: Type 4A: The manifestation of one/two type/s of symptoms to cope with or suppress the manifestation of another one/two type of symptoms; Related Theories in Experiences Schizophrenia: (Self fragmentation) - Diffusion and dissociation of self boundary - self regression - omnipotent self

Related Theories in Experiences of Depressive Mood and Symptoms - Introjection of Loss - Anger towards oneself and others - Self blaming and Self distruction - Intensive sense of worthlessness, emptioness

Related Theories in Experiences of Bipolar Symptoms - Depressive Positioning - Manic Defense by sadistic superego, moral and ominopotent ego and intensification of desires

Figure 2. A combination of Related Theories in Experience of Schizophrenia, Depressive Disorders and Bipolar Symptoms.

Type 4B: The full manifestation of one/two type/s of symptoms can lead to the manifestation of another one/two types of symptoms; and Type 4C: Coexistence of any two/three types of symptoms implies a delicate balance for the individual in facing environmental stress and personal condition. In terms of related theories of these three types of symptoms, the above ways can be reinterpreted as following:

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The manifestation of one/two type/s of symptoms to cope with or suppress the Manifestation of another one/two type of symptoms

Under Type A, there may be several combinations: Type 4A1: The manifestation of schizophrenic symptoms to cope with or suppress the manifestation of depressive symptoms Type 4A2: The manifestation of schizophrenic symptoms to cope with or suppress the manifestation of manic episode Type 4A3: The manifestation of schizophrenic symptoms to cope with or suppress the manifestation of bipolar symptoms Type 4A4: The manifestation of depressive symptoms to cope with schizophrenic symptoms Type 4A5: The manifestation of depressive symptoms to cope with schizophrenia and manic episode. Type 4A6: The manifestation of manic symptoms to cope with schizophrenic and depressive symptoms Type 4A7: The manifestation of bipolar symptom to cope with schizophrenic symptoms Type 4A8: The manifestation of schizophrenic and manic symptoms to cope with the depressive symptoms Type 4A9: The manifestation of schizophrenic and depressive symptoms to cope with the manic symptoms In the case of James, it seems his situation can be described as type A8: the manifestation of schizophrenic and manic symptoms to cope with his depressive symptom. The loss of his mother provoked his depressive mood in forms of blaming his own incapability to keep his mother to live a longer life. As the depressive mood prevailed and reached an unbearable degree, the manifestation of the delusion that her mother was still alive helped James to cope with and suppress her severe depressive mood. Similarly, his manic episode in a form of liberation of others may be interpreted as way to cope with his or her prevailing depression. That means, for James, the manifestation of both schizophrenic symptoms and manic episode tend to cope with and suppress the manifestation of depressive symptoms due to the loss of her mother. However, the occurrence of delusions and hallucinations (her mother’s voice and encouragment) tended to intensify James’ manic episode to a degree that leads to another mental breakdown and relapse. James was highly confused thinking that he was a superhero, together with his mother to save those oppressed in Hong Kong and in other countries. Thus, James was mentally confused to a degree that was out the toleration limits of his significant others and people around him. As a result, he was hospitalized. In the process of hospitalized, he seemed to return to a depressive mood reminding himself about his loss of his mother as well as her girlfriend. All this may be demonstrated in the following self-narration: James said: `according to the description of the psychiatrist, I was suffered from a full boom of manic episode with mental confusion of hallucination and delusion. In my first relapse, my colleagues in my school called an ambulance and I was thus hospitalized. In the admission ward, I was injected with a strong dosage of antipsychotics and mood stabilizer. To prevent me from potential harm with oneself and others, I was tied by my bed by a restraint

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jacket. The experience was dreadful. I fell down from an elated mood (the call it as grandiose delusion and hallucination) to a deep bottom of depression where all things seemed to be meaningless and untrustworthy. The voice of my mother was still there, but the antipsychotic medicine made it so distant and weak. It strongly reminded me that my mother was dead and I was alone in the world. I was so dull and became stagnant. After several days in the admission ward, my dullness, and dead silence seemed to be a good sign showing that my mental state was stable and my manic episode was under control. I was then transferred to an open ward where I could move around. The situation was better as I could chat with other patients in the hospital ward. Some of them were young guys who were substance abusers. I talked to them and persuaded them to quit from substance abuse. When I had some meaningful things to engage, I felt much better. I got a strong feeling that I fulfilled my mother’s unfulfilled wishes to help those in need. The feelings were particular strong when one young patient complained that he was abused by a male nurse whom hit him on his stomach. No one believed in him as he was just a schizophrenic patient with prevailing delusion and paranoia. However I believed in his story as the male nurse was also quite rude to me. When I stood up and charge the male nurses together with this pateint, I got the same feeling as I protected my mother and sister from being abused by my cruel father. Time passed away and things changed, My mother was dead and my sister was married, but the feeling of being together with them still clung to my mind.’ From James’ self narration, it was interesting to see that he used both the hallucination in hearing her mother’s voice as well as liberating the oppressed in elated mood of manic episode to counteract his depressive mood in losing her mother. However, once the symptoms of hallucination and manic episode were under control of anti-psychotic drugs and mood stabilizers, he returned to his former depressive position. The situation was even worse as he was restrained and kept within the admission ward. Although, mentally, he was more stable, but feelingwise, he was painful. Without further clarification or enlightening by his hallucination and elated mood, he could further cope with sadness by meaningful encounter with other patients in the ward. He tended to engage in similar activities by being an advocater for his inmate in his hospital ward. For James, it seemed that the only way to cope with his depressive position, apart from being schizoprehenic and manic is to do some thing that may be similar in natures but be mild in degree. That is to fulfill her mother wishes by helping people around. In James’ second episode, similar natures and pattern occur again. The depressive position occurred in the leaving of his girlfriend. It sparkled James’ previous loss of his mother that had been successfully suppressed by commiting normal meaningful activities as well as by the substitution of the love and care of her girlfriend.

Type 4B: The full Manifestation of one/two type/s of symptom can lead to the manifestation of another one/two types of symptoms; and In this type of proposition, similar to type 4A, there are still several further propositions Type 4B1: The full manifestation of schzophrenic symptoms leads to the manifestation of depressive symptoms Type 4B2: The full manifestation of schizophrenic symptoms leads to the manifestation of manic episode Type 4B3: The full manifestation of schizophrenic symptoms leads to the manifestation of bipolar symptoms Type 4B4: The full manifestation of depressive symptoms leads to the manifestation of schizophrenic symptoms

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Kam-shing Yip Type 4B5: The full manifestation of depressive symptoms leads to the manifestation of schizophrenia and manic episode. Type 4B6: The full manifestation of manic symptoms leads to the manifestation of schizophrenic and depressive symptoms Type 4B7: The full manifestation of bipolar symptoms leads to the manifestation of schizophrenic symptoms Type 4B8: The full manifestation of schizophrenic and manic symptoms leads to the manifestation of depressive symptoms Type 4A9: The full manifestation of schizophrenic and depressive symptoms leads to the manifestation of manic symptoms

In more precise terms, apart from type 4A8, James’s situation could also be described by type 4B9: the full manifestation of depressive and schizophrenic symptoms leads to the manifestation of manic symptoms. That can be illustrated by James self narration of his experience in his second episode. James said: `Regarding my second relapse, it was even more painful than the first one. I lost my girlfriend. I lost my mother and my girlfriend. It was unbearable. My life was full of unbearable loss. I did not know how many lossess I had to face in my future life. Life was so unfair to me. I was so angry with myself that could not keep my mother and my girlfriend. The feeling was so unbearable and miserable. When I was small, whenever I felt unbearable and miserable, my mother comforted me saying that I was a good boy. She embraced me and telling me I was tough and could work through anything. She always said that I was so strong in protecting her and my younger sister. At that moment, my mother’s voice prevailed. The situation in my second relapse was more confusing than those in the first relapse. My mother’ voice tended to mix up with my girlfriend’s voice. My mother told me that my girlfriend was not a good girl. She deserved me. However, the voice of my girlfriend told me in another way saying she still loved me. She was threaned by his new boyfriend. Sometimes, the voice of my mother tended to argue with the voice of my girlfriend. Both of them concerned about me. But they argued with one another. Their arguments made me feel really confusing and painful. To ease up their arguments, I had to find out the truth. I had to work hard showing them I was diligent. I had read a lot of related information and news concerning Chinese immigrants in the United Kingdom. Finally, the analysis from National Geography was excellent. It told me that nurmerous Asian immigrants in the United Kingdom were painful and abused by the White males. When the voice of my mother cursed my girlfriend who was unfaithful to me, I could tell my mother that my girlfriend was in fact, faithful and loyal to me. All she did was entirely involuntary. At that moment, the voice of my mother seemed to be weakened. The voice of my girlfriend together with her cry for help was intensified. I believed that, as we deeply loved one another, we were spiritually united together. This was why I could hear her voice. I fully equipped myself with related knowledge as well as required weapons to save my girlfriend as well as other Chinese female who were oppressed by British White males. Even my mother’s voice did not agree me to do so.’

From James’s narration, it was clear that James’ manic episode, preparing himself to save his girlfriend and other Chinese females who were oppressed by White males in the United Kingdom seemed to be the result of the full manifestation of schizophrenic symptoms in terms of hearing the argument of voices between her mother and her girlfriend. Facing the loss of her girlfriend, James was kept within a deep hollow of sorrow and emptiness to an

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extent he generated hallucinations of her mother and her girlfriend as ways to cope with her emptiness and loss. That means, his manifestation of his schizophrenic symptoms was a result of the full manifestation of his depressive symptoms. However, the full manifestation of first rank symptom (Schneider, 1959) with two tracks of voices, one from his mother and one from his girlfriend arguing together, was painful and untolerable. As a way of coping, it seemed that James gradually developed his manic episode in forms of diligently searching for related information about the situation of Chinese females in the United Kingdom as well as preparing him to liberate his girlfriend in the United Kingdom. In doing so, his hallucinations on his girlfriend and his mother gradually diminished to an acceptable degree. That means, James’ manifestation of manic symptoms was a result of his full manifestation of schizophrenic symptoms. The process of James’ situations and manifestation of symptoms might be summed in the following diagram. Type 4C: Coexistence of any two/three types of symptoms implies a delicate balance for the individual in facing environmental stress and personal condition. In this proposition, an individual with schizoaffective disorder is supposed to suffer from both schizophrenic symptoms, depressive and manic symptoms. The coexistence of any two/three types of symptoms implies a delicate balance for the individual in facing environmental stress and personal condition. Under type 4C, there may be several possible combinations: Type 4C1: Coexistence of manic and schizophrenic symptoms implies a delicate balance for the individual in facing environmental stress and personal conditions Type 4C2: Coexistence of depressive and schizophrenic symptoms implies a delicate balance for the individual in facing environmental stress and personal conditions Type 4C3: Coexistence of depressive and manic symptoms implies a delicate balance for the individual in facing environmental stress and and personal conditions Type 4C4: Coexistence of manic, depressive and schizophrenic symptoms implies a delicate balance for the individual in facing environmental stress and personal conditions In James’ narration, there seems that be possibilities of some of these conditions. It seemed that James had certain periods when he embraced both depressive symptoms; and schizoprhenic symptoms and both manic and schizophrenic symptoms. The coexistence of these symptoms seemed to be a bridge between a full manifestation from one type of symptoms to another one. The coexistence of two types or three types of symptoms may imply the following meaning. First, it may mean that the persons with schizoaffective disorder, as mentioned above, use one type of symptom to suppress or the cope with another type of symptom. That mean if the client first have a full manifestation of depressive mood, the occurrence of manic episode may gradually suppress the occurrence of depressive mood. There is a period of coexistence of both depressive and manic symptoms. The gradual suppression of depressive symptoms thus leads to a full manifestation of a full manic episode.

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Full manifestation of depressive symptoms due to the loss of her mother or girlfriend

Full manifestation of schizophrenic symptoms in forms of hallucinated voices of her mother and her girlfriend

Full manifestation of manic symptoms in forms of liberation of oppressed women including her girlfriend

Figure 3. Full manifestation of depressive and schizophrenic symptoms leading to full manifestation of manic symptoms.

Secondly, in the same way, a full manifestation of manic symptoms may lead to the occurrence of a schizophrenic symptom. The occurrence of the schizophrenic symptom gradually suppresses the occurrence of the manic symptoms. Gradually, there will be a full manifestation of schizophrenic symptom. Within this transition and change of symptom, there is a period of time of co-existence of both schizophrenic and manic symptoms. Thirdly, the full manifestation of schizophrenic symptoms may lead to the occurrence of depressive symptoms. The gradual occurrence of depressive symptoms may suppress the manifestationof schizophrenic symptoms leading to a full manifestation of depressive symptoms. With this transition, there may be a period of coexistence of both schizophrenic and depressive symptoms. Fourthly, there may be time when all three types of symptoms, depressive, manic and schizophrenic symptoms existing together implying that these three symptoms try to suppress the full manifestation of one another. The co-existence of all these three types of symptoms also implies there seems to a highly unstable mental stage of the individuals searching the settlement of a full manifestation of one type of mental symptoms. In James’ case, it seems that the loss of her mother and her girl friend nurtured a full manifestation of depressive episode. Then, it turned to a full manifestation of schizophrenic episode in forms of active auditory hallucinations of her mother’s voices. Finally, it was a full manifestation of manic episode with an elated mood and strong urge to liberate all oppressed people in the world. Within these three full manifestations of different types of mental illness, there were periods of time with coexistence of two types of mental symptoms. Between the full manifestation of his depressive symptoms to a full manifestation of schizophrenic symptoms, there was a period of time with the coexistence of both depressive and schizophrenic symptoms. Between the full manifestation of his schizophrenic symptoms to a full manifestation to manic episode, there was a period of time with the coexistence of both schizophrenic and manic symptoms. The coexistence of two types of mental illness can be demonstrated in the folloing figure. The period of co-existence of two types of symptoms could be illustrated by James’ self narration. James said: ‘when my mother died, I kept myself in a severe depressive mood. Then, the hearing of my mother’s voice woke me up. At first, my depressive mood still prevailed and her voice was small and hard to hear. Later, her voice became louder and louder and my depressive mood decreased gradually as my mother’s voice gave me lot of encouragements and reinforcements. Then her voice kept on reminding me to work hard and save the oppressed in the world.

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My previous memories of protecting my mother from my father’s achieve anything in the world including saving all kinds of oppressed groups. I prepared to fight a hard battle and proclaimed to the whole world that I was a saviour of the oppressed group.’

Full manifestation of depressive symptoms due to the loss of her mother or girlfriend

Co-existence of both depressive and schizophrenic symptoms

Full manifestation of schizophrenic symptoms in forms of hallucinated voices of her mother and her

Co-existence of both schizophrenic and manic symptoms

Full manifestation of manic symptoms in forms of liberation of oppressed

Figure 4. Full manifestation of certain symptoms to Coexistence of two types of symptoms in James’ case.

In James’ narration, it was clear that at times, he suffered the coexistence of both depressive (the loss of his mother) and schizophrenic symptoms (the hearing of his mother’s voice. He also suffered the coexistence of both schizophrenic symptoms (his mother’s voice) and manic symptoms (the elated mood and grandiose thought and action in saving the oppressed groups in the world). The coexistence of both types of symptoms simply implies transferring from the full manifestation of one type of symptom to the full manifestation of another type of symptoms.

RECOVERY AND RESILIENCE OF PERSONS WITH SCHIZOAFFECTIVE DISORDERS Within the above mentioned orientation of theoretical underpinnings, persons with schizoaffective disorder are suffered from schizophrenia in forms of diffused self boundary, regression and omnipotent self; depression in forms of severe depressive mood because of intense senses of loss, anger, worthlessness, helplessness and meaninglessness; as well as manic episode in forms of elated mood and grandiosity because of the urge coming out from their depressive position by sadistic and moralistic superego and prevailing secular desires. All these symptoms are inter-related to one another, with the possibilities of the manifestation of one type of symptoms suppressing other types of symptoms; a full manifestation of one type of symptoms leading to another types of symptoms, as well as coexistence of two or three types of symptoms of schizophrenia, depressive disorder or bipolar disorder. In the process of recovery and resilience of persons with schizoaffective disorders, apart from facing their diversity and changeability of their symptoms, they still have to face several types of subjective experiences such as: • • • •

subjective experience in facing their mental symptoms; subjective experience in facing diagnosis; subjective experience in facing treatment and rehabilitation; and subjective experience in facing others’ perceptions and labeling (Yip, 2006).

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Within these four types of subjective experiences, there are unfulfilled basic human needs such as: • • • •

basic needs for physical survival such as food, employment and accommodation; gratification of human desires such as hunger, sex and aggression; psychological needs to love and to be loved, to respct and to be respected, and to care and cared by others; and social needs to interact and live with others, and to actualize one’s potentials and ability.

It is interesting to note that despite various theorectical frameworks in explaining and articulating different types of mental illness, persons with different types of mental illness may have similar types of basic needs and subjective experiences for. For James, apart from suffering from his symptoms of schizophrenia and affective disorders, he did have to face these different types of subjective experiences.

Subjective Experience in Facing Diagnosis and Symptoms As mentioned in chapter one, clients with schizoaffective disorders have hardships in facing confusion in diagnosis. The hardship involves a confusion in facing different types of symptoms of schizophrenia, depressive episode and manic episode. Similar things happen in James’s case. James said: `for me, the medical diagnosis only meant confusion and ambiguous labellings. At the time my mother died, I felt extremely sad, guilty and meaningless. I did not want to eat, drink or even said anything. My sister and my close friend escorted me to visit a private psychiatrist. He diagnosed me as suffering from major depressive disorder. My sister and close friend advised me to take the antidepressants. I took them but my sadness and depressive mood still prevailed. Not until my mother’s voice came back, my depressive mood still prevailed. When my mother’s voice gradually grew louder, my depressive feelings gradually diminished. Replacing that was a feeling of being togetherness with my beloved mother. However, my private psychiatrist said I suffered from psychotic symptoms. It seemed that the psychiatrist had every way to label your symptoms and gave you some sort of medicine accordingly. My psychiatrist said I needed anti-psychotic drug to get rid of my hallucinations and delusions. Under his advice, I did take that. The effects of the drug was a little strange, it caused me some sort of distant feeling towards my mother’s voice. I hated the label of the diagnosis of schizophrenia or psychotics making my beloved mother’s voice seemed unrealistic and delusive. In fact, every one of us does have some sort of imaginations and unfulfilled wishes. Every one enjoys the voice and togetherness of some ones we love and dream of. Even though these beloved one are away of us, it is common that we still hear their voices and feel their togetherness. Why should we label this as schizophrenia. My mother voice kept on telling me to be strong, to be tough and to be helpful to others. In our reality, we do need to be strong and tough so that we can face every challenge in our life. We do need to be helpful and supportive to one another. That is the basic mission, values and our commitment in life. I tried my best to exercise and actualize these values to a degree that my mind was full of unfulfilled missions and endeavors. I embraced a strong urge to tell

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others how important these unfulfilled missions and endeavors. At that time, the elated mood and uncontrollable urge to actualize these missions made me highly courageous to do anything. As a result, people around me said that I was out of my mind. I was thus sent to a mental hospital with a diagnosis of schizoaffective disorder with bipolar disorder. For the dignosis was nothing more than insanity or madness. The psychiatrist in the mental hospital did try to explain the diagnosis to me. He seemed to know that I was a bit confused by various types of diagnosis in my life, depressive disorder, schizophrenia and schizoaffective disorder. He explained that there was some biochemical secretions in my brain that caused my mental disorder that might be genetically determined. The different diagnoses or the final diagnosis did not mean too much to me. Although, later I tried to read related textbook about schizoaffective disorder, but it seemed that the description of various types of symptoms as well as the controversies of diagnosis in schizoaffective disorders were only games for medical professionals. They wanted to clarify and demonstrate that they knew the disorder well and had clear and precise solution accordingly. In fact, they did not, what they did was only their self fulfilling prophecy. Some of them thought that schizoaffective disorder was similar to schizophrenia and gave me antipsychotic medication. Some of them thought that schizoaffective disorder was similar to biopolar disorder and gave me mood stabilzer or anti-depressant medication. Some of them simply gave me three types of medication altogether. I thought they were highly confused and unsettled in facing my mental illness. They cared only on a clear diagnosis and medication but not my subjective experiences in my symptoms and their own feelings on the confusion of diagnosis.

Subjective Experiences in Treatment and Rehabilitation As mentioned in the first chapter, most literatures in the Social Science Citation Index on schizoaffectival treatment and biochemical explanation (44.3%) and etiology and diagnosis (26.3%). Some of them concerned about genetics studies (8%); genetics studies (8%); cognitive functioning (5.7%); related services, policies and epidemiology (3.5%); psychosocial theapy and counseling (4%). However, a very few of them discussed consumers’ needs and rights (1.6%); subjective experiences (0.6%) and recovery (0.65). Clients’ subjective experiences, especially on treatment and rehabilitation are rarely mentioned and described. In fact, client’s subjective experiences on treatment and rehabilitation are crucial in clients’ recovery process, in particular for clients with schizoaffective disorder. They need extra recognition, acceptance and support from professionals and their significant others in facing their shifting of symptoms, confusion of diagnoses and highly unstable mental conditions in the process of rehabilitation and recovery. All these can be demonstrated in James’ case. James said: ‘Indeed, I felt confused in the process of treatment, rehabilitation and recovery. In the first admission to mental hospital, I was restrained in my hospital bed to prevent me from hurting myself and other patients in my elated mood. In fact, even in my elated mood, my subjective experience was only to save those oppressed and migrated in the world but not to hurt and harm others. The days in the admission wards were dreadful, related medical professional tended to recognized my reunion with my mother by hearing my mother’s voice and my urge to help others as purely confusing psychotic and manic episode. They did not try to listen, understand and articulate my feelings, needs and meaning underlying these symptoms and diagnoses.

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It is clear that James’ subjective feelings and needs underlying his symptoms were merely regarded as signs of mental confusion that need to be controlled by heavy medication and hospitalization. He learnt to cope with this by pretending to be dull, inert and withdrawn. He also learnt to hide his symptoms in encountering with his psychiatrist so to avoid unnecessary treatment, medication and hospitalization. Similar situation occurs in his second relapse. He was retained in the mental hospital in his manic episode. James said: ‘I was kept in the admission ward when I was in elated mood to save my girlfriend and other Chinese woman in the United Kingdom. Similarly, I was restrained in my bed and was injected with heavy medication. This time, I knew the rule of game. You should never struggle and argue with medical professionals. You should behave as an innocent child and received their medication and treatment quietly and happily. You should appreciate their treatments or even maltreatment as crucial help for your mental illness. I follow all these rules of games closely and no sooner I was moved to an open ward. In the open ward, I turned a blind eye to all unfair treatments in the ward to other mental patients. I cared about myself and pretended to be happy to participate in related activities and training. One month later, I was

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discharged and returned to work. The rule of game in dealing with medical professionals was very simple. You only need to demonstrate signs of mental stability and treatment compliance. It made no difference whether you are a patient with depressive disorders, schizophrenia, bipolar disorders, schizoaffective disorders, or anxiety disorder.’

From James’ narration, it was interesting that despite the controversies and complexities in defining and diagnosing persons with schizoaffective disorder, similar to persons with other types of mental illness, what the medical professionals in mental hospitals and outpatient clinics looked for might merely be drug compliance, submissiveness to various forms of restraints, controls and manipulation. They regarded them as signs of mental stability. However, subjective feelings, meaningfulness and needs underlying symptoms were spontaneously ignored and undermined.

Subjective Experiences in Facing Others’ Perception Persons with schizoaffective disorder, similar to people with other forms of mental illness or mental problems, they are easily labeled and stigmatized by people around them or members in the community. The subjective experiences of being labeled, ignored and even oppressed in every aspect of life are painful and unbearable. They also create endless burdens for the recovery from mental illness/ problem. In James’ situation, he did suffer a lot from related labeling and stigmatization. James said: ‘After I had been hospitalized, people around me such as my friends, neighbors and members in the nearby community also labeled me as insane and mentally ill. Although many of my friends, and my colleagues were quite supportive and be empathic with my situation, they still label as insane and in many ways irrational Instead assuming and recognizing my abilities to work as a senior clerk in secondary school, they always advised me to take a longer leave or shift my full time job to a part time basis. For those nonsupportive colleagues, friends and neighbors, many of them simply looked at me in a strange way. Once they knew my record of hospitalization in mental hospital, they would regarded my actions and my thinking as insane and bizarre. Even if I spoke in a larger voice but no intention to disturb or no action to harm anyone, they might become fearful and suspicious. I was fortunate that I could find a stable job as senior clerk in a secondary school. The principal there was the best friend of the secondary school I worked previously. He was very supportive and understandable. He faced a lot of pressure from his colleagues in employing me knowing that I was a person with mental illness. He believed in my effectiveness and efficiency in work. He appreciated me to continue my part time course in counseling hoping that my training could help the counseling work in my school. I owed a lot to him.’

From James’ case, it is clear that subjective experience in perception of others seems to be crucial in the process of recovery and rehabilitation. Without the continuous support from his two bosses, James was thus labeled by his colleagues as someone that was insane and unsuitable for work or even dangerous in working with students and teachers in the secondary schools.

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CONCLUSION: RECOVERY AND RESILIENCE WITH CLIENTS’ OWN EXPERIENCE As a conclusion, this is a comprehensive chapter describing various theoretical underpinnings about the symptoms, feelings, experiences and needs about persons with schizoaffective disorders. The writer has reviewed the controversies in defining, describing and interpreting of schizoaffective disorders in details. Based on a case illustration of a Chinese male adult, James, who suffered many years from schizoaffective disorders, the writer has suggested several perspectives in articulating related theoretical underpinnings in related interpretation. Firstly, related theories about depressive disorders, bipolar disorders or schizophrenic disorders can be used in this interpretation. Secondly, all these related theories can be grouped and combined various ways in the interpretation. There may be several combinations. For instance, theories about depressive disorder can be combined with bipolar disorder. Similarly, theories about bipolar disorder can also be combined with schizoaffective disorder. Thirdly, theories from affective disorders and schizophrenic disorder can also be combined together in explaining subjective experiences, feelings and needs for persons with schizoaffective disorders. In fact, in real practice, one type of symptoms may arouse in order to cope with or suppress another type of symptoms. Also, a full manifestation of one type of symptoms may also lead the occurrence of another type of symptoms. However, all these articulations of related theoretical underpinnings may only base on professionals’ interpretation of theories from various scholastic perspectives, the subjective experiences of persons with schizoaffective disorders are always neglected, ignored and undermined in treatment, rehabilitation and community integration for persons with schizoaffective disorder. They are the actual sufferers in the controversies in diagnosis and treatment of schizoaffective disorder. In James’ case, he had been diagnosed as schizophrenia, depressive disorder, as well bipolar disorder and finally as schizoaffective disorder by concerned psychiatrists. Interestingly, within clients’ own perceptions and narration, they may not concern too much about such controversies and complexities. Instead, they may concern more about the involuntary restraints, institutionalized treatments and abuse of professional authority in the process of treatment and rehabilitation. Regardless what sort of diagnosis being imposed, they sincerely urge for genuine, empathic and caring treatment and rehabilitation environment so that they can recover from their mental illness within a supportive social environment. In fact, according to related concepts of recovery, persons with schizoaffective disorders should have their own journey of healing to live a meaningful life and actualize his potentials. ‘Mental health recovery is a journey of healing and transformation enabling a person with a mental health problem to live a meaningful life in a community of his or her choice while striving to achieve his or her full potential. ‘(U.S. Department of Health and Human Services, 2004)

Within this concept of recovery, persons with schizoaffective disorder should have their own journey of recovery. They should have their rights to live a meaningful family and work life. Also they should also have good and enjoyable education, social and recreational activities. Within their process of recovery, their full potentials should thus be maximized. In James’ case, his potential to be a senior clerk as well as to be a student in counseling course should be fully actualized. For persons with schizoaffective disorder, even if they are unable

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to restore their previous job, they should be helped to do job with similar natures. They should not be kept in the sheltered workshops doing simple manual work simply because his or her record or experiences of severe depression. Within this concept of recovery, there are 10 fundamental components of recovery. The first components is self direction. That means persons with schizoaffective disorder should exercise their own choice to determine their own path of recovery. The path of recovery should be closely related to one’s own goals and meaning of life. Self-Direction: Consumers lead, control, exercise choice over, and determine their own path of recovery by optimizing autonomy, independence, and control of resources to achieve a selfdetermined life. By definition, the recovery process must be self-directed by the individual, who defines his or her own life goals and designs a unique path towards those goals. (U.S. Department of Health and Human Services, 2004)

For persons with schizoaffective disorder, self direction means that they should be able exercise their control of their recovery. They have their own rights and autonomy to choose their own medical practitioners, treatments and control related resources such as community support, finance, related services and a meaningful and independent life. In James’ case, he should have the right to choose his psychiatrists, knowing about various effects of his psychiatric drugs. They should not be treated as institutionalized and dependent patients within mental health services and mental institutions. Nor they should be regarded as unmotivated clients that are lack of self determination and self decision making to design their own treatment and rehabilitation path. Instead, related professionals should help persons with schizoaffective disorder to formulate and actualize their own meaningfulness of life. In James’ case, it is a pity that James did not have their own rights and autonomy to choose his own treatment and recovery process. In his manic episode, he was admitted into the mental hospital involuntarily and he was even restrained and detained in the closed admission ward. The second component is individualized and person centred recovery process Individualized and Person-Centered: There are multiple pathways to recovery based on an individual’s unique strengths and resiliencies as well as his or her needs, preferences, experiences (including past trauma), and cultural background in all of its diverse representations. Individuals also identify recovery as being an ongoing journey and an end result as well as an overall paradigm for achieving wellness and optimal mental health. (U.S. Department of Health and Human Services, 2004)

For persons with schizoaffective disorder, they should construct multiple pathways to their recovery. They should not be restricted by professional designed pathway or institutionalized services in medical or social welfare services. They should be provided with different channels to restore their capabilities and potentials. They should be facilitated by their significant others and members of the community to integrate back to the society. They should also be able to participate in normalized activities such as sports, exercises and recreational programs so that they can be free from their manifestation of symptoms of schizophrenia, manic and depressive episode. They should be able to restore a positive life pattern. All these different channels in recovery are dynamic and continuous. Related parties including professionals, community members should continuously cooperate and engage together in letting persons with schizoaffective disorder to enjoy a multi-channelled recovery

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process. Similar to other persons with schizoaffective disorders, James’ process treatment was not individualized and personalized centred. Instead, it was institutionalized and collective based. In his life in the mental hospital, every day he had to follow a highly scheduled pattern of life in the hospital ward. In certain circumstances, he tried to voice out his own views in regarding his and other patients with mental illness. However, he quickly learnt that the more he adhered and complied to collective and institutionalized life within the mental hospital, the more he would be free from the labelling of the medical professionals and the more likely he would be regarded as recovered and could thus be discharged from the mental hospital. The third component in concept of recovery is empowerment. Empowerment means that persons with mental illness have the power and authority to choose suitable services and interventions. They can advocate for their rights, dignity and power in having suitable and sufficient service, treatment and quality of life. Empowerment: Consumers have the authority to choose from a range of options and to participate in all decisions—including the allocation of resources—that will affect their lives, and are educated and supported in so doing. They have the ability to join with other consumers to collectively and effectively speak for themselves about their needs, wants, desires, and aspirations. Through empowerment, an individual gains control of his or her own destiny and influences the organizational and societal structures in his or her life. (U.S. Department of Health and Human Services, 2004)

That means, persons with schizoaffective disorder should have full rights in participating in choice of medication, treatment, service programs, accommodation, job, and recreations as other persons in the society. Furthermore, persons with schizoaffective disorder, including their family caregivers or significant others can unite together. They should be able to establish their own self help groups, advocacy organization and alliance to advocate their full rights in treatment, rehabilitation, community integration and recovery. Sufficient resources should be allocated by policy makers and professionals for them to gratify their needs, wants and desires in every aspects of life. It should be an ongoing empowering process so that related parties can develop a constructive language, position and discourse with persons with schizoaffective disorder to develop their rights, dignity and assertion as other members in the society. In James’ situation, he was alone in the process of treatment, rehabilitation and recovery, there was absence of related alliance, self help groups, and advocate group for persons with schizoaffective disorders in his society. The fourth component in recovery is holistic orientation in the process of recovery for persons with mental illness. That means, recovery is not merely biochemically medicalized control of one’s body in terms of psychiatric medication. It is also a holistic recovery of one’s mind, spirit and community life. Recovery of mind is regaining one’s sense of consciousness, rationality and emotional sensitivity. Recovery of community life implies re-establishing all related aspects of life, such as housing, employment, education, social network, community participations and family support. Holistic: Recovery encompasses an individual’s whole life, including mind, body, spirit, and community. Recovery embraces all aspects of life, including housing, employment, education, mental health and healthcare treatment and services, complementary and naturalistic services, addictions treatment, spirituality, creativity, social networks, community participation, and family supports as determined by the person. Families, providers, organizations, systems,

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communities, and society play crucial roles in creating and maintaining meaningful opportunities for consumer access to these supports. (U.S. Department of Health and Human Services, 2004)

That means, persons with schizoaffective disorder should enjoy a holistic recovery process. They should not be solely dependent on biochemical anti-depressants, mood stabilizers, anti-psychotics and even minor tranquillizers that may hinder their sense of reality or high level functioning making them to be more distant to their depressive mood and elated mood, or be less responsive to their delusion and hallucinations. They should embrace a holistic sense of recovery, a sense of self mastery in life. They should have a good own supportive network. They should have their own jobs, enjoy normal community activities, participate in community activities, return to their own job and receive normal education as well as training. In the process of recovery, related services such as treatment, rehabilitation, family support and advocacy programs should be fully and adequately delivered to the persons with schizoaffective disorders. In the case of James, he did have experiences in taking various types of psychiatric medications because of various types of diagnoses imposed by different psychiatrists. These psychiatrists failed to address the James’ need of a holistic and normalized recovery process. James’ psychosocial needs of being recognized, respected and encouraged are not articulated in the treatment and rehabilitation process. Related professionals in James’ case tended to assume that medications and hospitalization as well as detention and restraints were the only ways to treat and to rehabilitate James schizoaffective disorder. The fifth component is `non liner’ in the process of recovery. That means, persons with schizoaffective disorder are not recovered in a linear way. Instead, their recovery can be fluctuating. In some period of time, their situations can be stagnant in the process of recovery. In other period of time, their conditions can be backward and deteriorating. In certain period of time, they can take stock of their own situation and make satisfactory progression in the process of recovery. In the whole process of recovery, related professionals should facilitate persons with schizoaffective disorder to face the ups and downs in treatment, rehabilitation and integration. They also have ups and downs in their searching suitable accommodation, job and social life. ‘Non-Linear: Recovery is not a step-by-step process but one based on continual growth, occasional setbacks, and learning from experience. Recovery begins with an initial stage of awareness in which a person recognizes that positive change is possible. This awareness enables the consumers to move on to fully engage in the work of recovery. (U.S. Department of Health and Human Services, 2004)’

For persons with schizoaffective disorder, their process of recovery is also non-linear. Many of them suffer from their ups and downs in their depressive, elated mood as well as outbreak of delusions and hallucinations. Very often, they may be better in some periods of time due to the support of their significant others. However, they may turn worse when their lives are full of challenges and difficulties. For James, he suffered from continuous hallucinations that her deceased mother was speaking to him in times of hardships and difficulties. He had two relapses when facing the loss of her mother as well the leaving of her girlfriend. The ups and downs of his depressive and elated mood as well as his schizophrenic

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symptoms were closely related with negative psychosocial events in his life. Nevertheless, all these ups and downs and experiences were not concerned by related professionals in his process of treatment, rehabilitation and recovery. The sixth component is strengths-based orientation. The recovery process should be an actualisation of the capabilities, strengths, resiliencies, talents, coping abilities and inherent worth of persons with schizoaffective disorders. They should be provided with good opportunities in exercising their new normal life roles as friends, caregivers, students, employees within their normal communities. Strengths-Based: Recovery focuses on valuing and building on the multiple capacities, resiliencies, talents, coping abilities, and inherent worth of individuals. By building on these strengths, consumers leave stymied life roles behind and engage in new life roles (e.g., partner, caregiver, friend, student, employee). The process of recovery moves forward through interaction with others in supportive, trust-based relationships. (U.S. Department of Health and Human Services, 2004)

Within the strengths based perspective: The recovery of persons with schizoaffective disorder should be a process in exploring, developing and manifesting their strengths, talents, and capabilities. Related professionals should fully believe that persons with schizoaffective disorder embrace their coping mechanisms and responses towards frustration, sufferings and hardship, including mental illness in their life. The process of treatment and intervention should be a collaboration with clients and their family caregivers (Saleebey, 2002; Yip, 2005). In James’ case, his potentials as a devoted teacher in the secondary school, his aspiration to help the oppressed should be suitably channeled by related professionals in his recovery. Related professionals in his recovery process seemed to concern merely on medication and hospitalization, his potentials, strengths, capabilities and talents are totally ignored and suppressed. Fortunately, his employer, the empathetic school principal did appreciate his commitment to the students and allowed him to continue his employment as a senior clerk in the school. The seventh component is peer support. Persons with schizoaffective disorder should support each other mutually, especially in sharing their experiences and wisdoms in the process of recovery. Their mutual support may create a strong sense of belonging, supportive relationship and community integration in the process of recovery in forms of self help groups, locality based supportive network, clients’ club, family mutual supportive network and day to day friendship. Peer Support: Mutual support—including the sharing of experiential knowledge and skills and social learning—plays an invaluable role in recovery. Consumers encourage and engage other consumers in recovery and provide each other with a sense of belonging, supportive relationships, valued roles, and community. (U.S. Department of Health and Human Services, 2004)

For persons with schizoaffective disorder, related professionals should facilitate them to organize their own mutual aid organizations and encourage them to establish locality based support network among their own community. They can support one another in daily life such as searching and maintaining stable employment, adjusting life difficulties. Related professionals should advocate for them to have normal friendship, job, accommodation and

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recreation. Peer support and genuine concern is also crucial for persons with schizoaffective disorders. Many of them actually have their own ways and methods to cope with and to adjust their depressive mood. For James, as mentioned above, the occurrence of one sort of symptoms may be perceived as coping mechanism for another type of symptoms. If he had good peer support from colleagues, significant others as well as other persons who successfully recovered from depressive mood, manic episode as well as delusion and hallucination, he might not need to indulge in the hallucination of his deceased mother’s voice in coping with the death of his beloved mother. The eighth element in recovery is respect. That means persons with schizoaffective disorder should be respected by others, including their colleagues, family members, peers, and members in the community and related professionals in their treatment and recovery. In interventions and services, they should be respected as consumer with consumer rights. In the society, they should be provided with equal opportunities to enjoy a normal life in work, education, recreation and other community activities. Respect: Community, systems, and societal acceptance and appreciation of consumers — including protecting their rights and eliminating discrimination and stigma—are crucial in achieving recovery. Self-acceptance and regaining belief in one’s self are particularly vital. Respect ensures the inclusion and full participation of consumers in all aspects of their lives. (U.S. Department of Health and Human Services, 2004)

For persons with schizoaffective disorder who embrace an intense fluctuation of mood, and persistently delusions and hallucination, they may suffer from an unresolved superior and inferior complex in their emotion. They may use the elated mood to pull up their intensive sense of inferiority in depressive episode. They may use their prevailing grandiose or bizarre delusions or hallucination to cover up their uncomfortable and anxious senses of inferiority, being oppressed by others or traumas in life. Fang all these unhealthy coping mechanism, normal respects from their significant others as well as from members in the community and related parties may gradually help them to come out from their involvements in their symptoms and rebuild their normal self competence, identity and image to live a normal life. As they are particularly sensitive to others’ labelling and comment, related persons in the community such as neighbours, employers, colleagues, family members, friends should play due respect to them and encourage them in regaining equal opportunities in every aspects of life in the process of recovery. In James’ case, it seems that related professionals tend not to play respect to his experiences, needs, and past experiences. They only regarded him as a patient with deficits, impairment and insane that cannot make his own decision and even determine his own recovery. His advocacy for his and other patients’ rights was only regarded as signs and symbols for mental confusion that needs to be totally controlled by medications. The ninth element in recovery is responsibility. That means persons with schizoaffective disorder should have a personal responsibility for their own recovery, including proper self care, social activities and determination to live a normal life. Related professionals should take positive steps to facilitate persons with mental illness to understand and give meaning to their own experiences and healing process. Responsibility: Consumers have a personal responsibility for their own self-care and journeys of recovery. Taking steps towards their goals may require great courage. Consumers must

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For persons with schizoaffective disorder, especially those with severe depressive mood, they may be over-anxious about their responsibility or demands imposed by other before their onset. They may even internalize others’ demands and be fully fixated and occupied by their overloading duties and responsibility making them unable to face cope with their life stress and finally breakdown mentally. However, in the stage of mental confusion, especially in severe depressive or schizophrenic symptoms, they may drastically become irresponsible to themselves to a degree that they even ignore their own personal hygiene and normal pattern of daily life. In manic episode, their highly elated mood may make them have an overwhelmed sense that they can take up all sort of grandiose responsibilities such as saving the whole world or being an outstanding banker. In James’ conditions, his unpleasant experiences in childhood made him a highly responsible son as well as a brother in protecting his mother and sister from his father’s battering. This sense of self sacrificed obligation, on the one hand becomes his aspirations in life. On the other hand, it turns to the sources of his grandiose in his elated mood. Thus, facing the dynamics and dilemmas of clients’ sense of responsibility, it is vital that related professionals can help them to develop an optimal sense of responsibility and obligation to take care of himself and others. The tenth component of recovery is `hope’. That means, in the process of recovery, persons with schizoaffective disorder should be able to nurture hope in their life so that they can have a bright future in their work, education and their community life. Their hope and recovery not only benefit their own but also their families, communities, societies and countries. Hope: Recovery provides the essential and motivating message of a better future— that people can and do overcome the barriers and obstacles that confront them. Hope is internalized; but can be fostered by peers, families, friends, providers, and others. Hope is the catalyst of the recovery process. Mental health recovery not only benefits individuals with mental health disabilities by focusing on their abilities to live, work, learn, and fully participate in our society, but also enriches the texture of American community life. America reaps the benefits of the contributions individuals with mental disabilities can make, ultimately becoming a stronger and healthier Nation. (U.S. Department of Health and Human Services, 2004)

For persons with schizoaffective disorders, related professional should help them to evolve hope and nurture a firm determination and will to live a better and more meaningful life. They do not only overcome their severe depressive mood, manic episode and schizophrenic symptoms. They may also help others to cope with their related symptoms. They may devote their lives in advocating the rights, dignity and integrity of persons with schizoaffective disorder. They do not merely retain their former standard in their living but also can advance further to live a more fruitful and meaningful life than before. They can transcend their life from secular attainment or egocentric advancement to the betterment of others and commitment to contribution to the society and country. Within these ten components of recovery, persons with schizoaffective disorder should be facilitated to rebuild their normal life within their own communities. Their potentials and

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talents should be fully manifested and actualised. Their coping mechanism in dealing with their symptoms should be fully recognized and re-channelled properly in the process of recovery.

REFERENCES Abraham, K. (1953) `Notes on the psycho-analytical investigation and treatment of manicdepressive insanity and allied conditions’ in Selected Papers of Karl Abram, p.137. Basic Books, New York. Angst, J. (1966) `Zu Atiologie and nosologie endgenger depressive psychosen, Eine genetiische, Soziologische und Klinische Studie, Berlin, Heidelbergt, New York: Springer Angst, J., Felder, W. & Lohmeyer, B. (1979) `Schizoaffective disorder I: Results of a genetic investigation’, Journal of Affective Disorder, 1: 139-153. Beck, A.T. (1967) Depression: Causes and Treatment, Philadelphia: University of Pennsylvania University Press. Beck, A.T. (9176) Cognitive Therapy and the Emotional Disorder. New York: International University Press. Blatt S.J. & Wild C.M. (1976) Schizophrenia: a Developmental Analysis, New York: Academic Press. Bribring, E. (1953) `The mechanism of depression’, P.Greenacre (ed.) Affective Disorders: Psychoanalytic Contribution to Their study, P.13. London: International Universities Press. Briggin P. (1994) Toxic Psychiatry, New York: St. Martin press. Burtzlaff, R.L. & Hooley, J.M., (1998) `Expressed emotion and psychiatric relapse: a meta analysis, Archives of General Psychiatry, 55: 50-60. Crowdford, M.D. (2003) Living with Schizaffectie Disorder, [email protected] Donahue A, B. (2000) `Riding the mental health pendulum: mixed messages in the era of neurobiology and self-help movement’, Social Work, 45(5):427-437. Downing –Orr K. (1998) Rethinking Depression: Why Current Treatment Fail, New York: Plenum Press. Estroff S.E. (1989) `Self identity, and subjective experience of schizophrenia: in search of the subject’ Schizophrenia Bulletin, 15:189 –196. Frankl, V. (1963) Man's Search for Meaning, New York: Pelican Press. Frankl, V. (2000) Man’s Search for Ultimate Meaning, Cambridge: Persus Publishing. Freud. S. (1924/1983) `Neurosis and Psychosis’ in Sigmund Freud: on Psychopathology, New York: Penguin Books Federn, P. (1952) Ego Psychology and the Psychoses, New York: Basic Books, Inc, Healy, D. & Williams J.M. (1989) `Misattributions and mania: an interaction of biological and psychological factors in the pathogenesis of mania’, Psychiatric Development, 7: 4970. Gabbard, G.O. (1992) Psychodynamic psychiatry in the decade of the brain,’ American Journal of Psychiatry, 149: 991-992. Gabbard, G.O. (1994) Psychodynamic Psychiatry in Clinical Practice: The DSM IV Edition, Washington: American Psychiatric Press.

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Jager, M., Bottlender, M. J., Strauss, A. & Muller, A. S., (2003) `Fifteen year follow up of ICD 10 schizoaffective disorder s compared with schizophrenia and affective disorder’, Acta Psychiatric Scandianvia, 109:30-37. Jaspers, K. (1959/1963) (7th edition) General Psychopathology, (J. Hoenig, & M.W., Hamilton trans.) Manchester University Press (Original work published 1923) Jacobson, E. (1977) Depression: Comparative Studies of Normal, Neurotic, and Psychotic Condition, USA: International University Press. Johnson, S.L., Sandrow, D. & Meyer, B (2000) `Increases in manic symptoms after life events involving goal attainment’ Journal of Abnormal Psychology, 109: 721-727. Jones S H. (2001) `Circadian rhythms, multilevel models of emotion and bipolar disorder – an initial step towards integration’, Clinical Psychological Review, 21: 1193-1209. Jones S.H., Sellwood, W. & McGovern, J., (2005) `Psychological therapies for bipolar disorder: the role of model-driven approaches to therapy integration’ Bipolar Disorders, 7: 22-52. Kant, O. (1940) `Types and analysis of the clinical pictures of recovered schizophrenia, The Psychiatric Quarterly, 14: 676-700 Karp, D.A. (1996) Speaking of Sadness: Depression, Disconnection and the Meaning of Illness, Oxford: Oxford University Press. Klein, M. (1975) `Mourning and its relation to manic-depressive states’, in Love, Guilt, and Reparation and Other Works 1921- 1945. p.344, New York: Free Press. Klerman, G.L., Weissman M.M., Rounsaville R.J. & Chevron, E.S. (1984) Interpersonal Psychotherapy of Depression, New York: Basic Books Laing, R.D. (1960) The Divided Self, London: Tavistock. Leete, E. (1989) `How I perceive and manage my illness’ Schizophrenia Bulletin, 22: 197200. Lewin, B.D. (1950) The Psychoanalysis of Elation, Norton, New York. Mahler, M.S. (1968) On Human Symobiosis and the Viscissitudes of Individuation, New York: International Universities Press Malkoff-Schwartz, S., Frank, E. & Anderson, et.al., (2000) `Social rhythm disruption and stressful life in the onset of bipolar and unipolar episode’, Psychological Medicine, 301005-1016. Marneros, A. (2007) `Paradigm of overlapping spectra’ in A. Marneros, H.S Akiskai, (Edited) The Overlap of Affective and Schizophrenic Spectra, pp, 1-22, Cambridge: Cambridge University Press. Norden, M.J. (1996) Beyond Prozac: Brain-toxic Lifestyles, Natural Antidotes and New Generation Antidepressants (2nd edition) New York: Regan Books. Pollack, W.S. (1989) `Schizophrenia ad the self: contributions of psychoanalytical selfpsychology’, Schizophrenia Bulletin, 15: 311-320 Power, M.J. & Dalgleish, T. (1997) Cognition and Emotion: From Order to Disorder, Hove: Psychology Press. Romme, M.A.J. & Escher, A.D. (1989) `Hearing voices’ Schizophrenia Bulletin, 22: 209210. Rowe, D. (1978) The Experience of Depression, New York: John Wiley & Sons Rowe, D. (1996) Depression: The Way out of Your Prison (2nd edition), New York: Routledge

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Saleebey, D. (2002) `Introduction: power in the people’ in D. Saleebey., (edited), The Strengths Perspective in Social Work Practice, (3rd.edition). pp.1-20. New York: Allyn and Bacon. Schneider, K. (1959) Clinical Psychopathology, (M.W., Hamilton & Anderson, E.W., Trans) New York: Grune & Stratton, 1959 Spiegelberg, H. (1972) Phenomenology in Psychology and Psychiatry, Evanston: Northwestern University Press. Strauss, J.S. (1989) `Subjective experience of schizophrenia: toward a new dynamic psychiatry II’ Schizophrenia Bulletin, 15, 179-187. Strauss, J.S. (1991) `The person with delusions’ British Journal of Psychiatry 159: 57-61. Strauss, J.S. (1992) `The person- key to understand mental illness: towards a new dynamic psychiatry III’ British Journal of Psychiatry, 162: 19-26. Strauss, J.S. (1994) `The person with schizophrenia as a person II: approaches to the subjective and complex’ British Journal of Psychiatry, 164: 103-107. Strauss, J.S. (1996) `Subjectivity’ Journal of Nervous and Mental Diseases.184: 205-212. Stone, K. (1990) `Psychodynamics of schizophrenia II: other contributors and discussion’ in Howells J.C. (Edited), The Concept of Schizophrenia: Historical Perspectives, Washington: American Psychiatric Association Press Sullivan, H.S. (1956) Clinical Studies in Psychiatry, New York: W.W. Norton & Company Welner, A., Croughan, J.L., Fisherman, R. & Robin, B., (1977) `The group of schizoaffective and related psychosis- critique, record, follow up and family studies: a follow up study’, Comprehensive Psychiatry, 18: 413-422. Welner, A., Welner, Z. & Fisherman, R. (1979) `The group of schizoaffective and related psychosis IV: A family study’, Comprehensive Psychiatry, 20: 21-5 Wendel, J. S., Miklowtz, D.J., Richards, JA. & George, E.L. (2000) `Expressed emotion and attributions in the relatives of bipolar patients: an analysis of problem solving interaction. Journal of Abnormal Psychology, 109: 792-796. Wilkes T.C.R., Belsher G., Rush A.J. & Frank E (1994) Cognitive Therapy for Depressed Adolescents, New York: The Guilford Press. Winnicott, D.W. (1965) The Maturational Process and the Facilitating Environment: Studies in the Theory of Emotional Development, London: the Hogarth Press. Yip, K.S. (1998) `Humanistic understanding of psychotic experience: its implications on social work practice with clients with schizophrenia’, Breakthrough, 2: 7-16. Yip, K.S. (2002a) ` Sullivan's approach to inner psychotic experiences: A case illustration’ Clinical Social Work Journal 30 (3): 245-263. Yip, K.S. (2002b) `Subjective experience of depression’, Social Work, 47 (4): 471-472. Yip, K.S. (2003) `Traditional Chinese religious beliefs and superstitions in delusions and hallucinations of Chinese schizophrenic patients’, International Journal of Social Psychiatry, 49 (2): 97-111. Yip, K.S. (2005) `A strengths perspective in working with an adolescent with depression’ Psychiatric Rehabilitation Journal, 28(4): 363-369. Yip, K.S. (2006) `Subjective experiences of persons with schizoaffective disorders’ W.H., Murray, (edited) Schizoaffective Disorders: New Research, New York: Nova Science publishers。

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Yip, K.S. (2007) Clinical Practice with Persons with Schizophrenia: A Humanistic and Empathetic Encounter. New York: Nova Science. Zaslow S. (1993) `Depressed Adolescents’ in J.D., O’Brien, D.J., Pilowsky, O.W. Lewis.(Edited) Psychotherapies with Children and Adolescents: Adapting the Psychodynamic Process, pp.209-230. Washington: American Psychiatric Press.

In: Schizoaffetive Disorders Editor: Kam-shing Yip

ISBN 978-1-60456-948-3 © 2009 Nova Science Publishers, Inc.

Chapter 3

SCHIZOAFFECTIVE PSYCHOSIS AND SCHIZOPHRENIA WITH- OR WITHOUT AFFECTIVE SYNDROME: A COMPARATIVE CLINICAL, NEUROPSYCHOLOGICAL AND MOLECULAR-GENETIC STUDY V. E. Golimbet*, M. V. Alfimova, V. G. Kaleda, L. I. Abramova, G. I. Korovaitseva, O. M. Lavrushina, and T. V. Lezheiko Mental Health Research Center, Russian Academy of Medical Sciences, Russia

INTRODUCTION Schizoaffective disorder (SA) is a nosological category included in many classifications of diseases, i.e. ICD-10 and DSM-IV. Main diagnostic features of the disorder are combination of schizophrenic and affective symptoms and favorable outcome. However an overlap of these criteria with both affective disorders and schizophrenia challenges the diagnostic validity of SA (Welner 1977; Tsuang & Simpson 1984). Multiple studies have been devoted to elucidation whether SA was a separate clinical entity or it should be considered as schizoaffective syndrome in clinical presentation of the above mentioned illnesses. Several hypotheses on the nature of schizoaffective psychosis have been delineated (Brockington & Meltzer 1983; Marneros 2003), according to which the disorder was supposed (1) to be a variant or an expression of either schizophrenia or affective psychosis; (2) to occur as a result of comorbidity of schizophrenia with mood disorders and (3) to be a piece of the spectrum of clinical states from “pure” schizophrenia to “pure affective psychosis”. To test these hypotheses, different designs were explored. Most often, researchers compared schizoaffective psychosis with schizophrenia and bipolar disorder with or without psychotic symptoms (Evans 1999; Benabarre 2001; Marneros 2004; Averill 2004). More detailed models analyzed a broader range of states, in particular those comprising various *

E-mail: [email protected]

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subtypes of schizoaffective psychosis, e.g. (1) mainly affective (affective dominant) and mainly schizophrenic (schizodominant) ones (Meltzer 1984); (2) “concurrent” or “sequential” subtypes (Marneros 2003-a); (3) a subtype with non-progressive phase dynamics and a schizoaffective subtype of attack-like progressive schizophrenia (Panteleeva & Bologov 2002). At the same time, the differences between SA and schizophrenia with affective syndrome (SPA) are understudied though the latter is recognized as a common and rather frequent feature of schizophrenia, ranging from 6% to 50% (Sands & Harrow 1999). Its existence and relevance were confirmed by a number of factor analytic studies of clinical symptoms (Kay, Sevy 1990; Lindenmayer 1994; Wolthaus et al 2000; Lykouras et al 2000; Lancon et al 2000; El Yazaji et al 2002) and it was suggested as a possible endophenotype of schizophrenia (McGrath et al 2004). In the present study, we compared clinical, personality, cognitive, and molecular-genetic characteristics of patients with SA, SPA and schizophrenia without affective syndrome (SP) and attempted to mark out the main features that may be specific for SA. To date, a number of studies have been conducted to differentiate SA and schizophrenia on the base of clinical variables and personality or neurocognitive characteristics. In contrast, in psychiatric genetics SA did not gain much attention as a categorical definition. A vast body of research in the field operates with so called “broad definition” of schizophrenia, which comprises SA and spectrum disorders. Due to epidemiological data, a proportion of SA cases in such investigations may vary from 10 to 30% (Meltzer et al 1984; Levinson et al 1999). To our knowledge, no studies, except that of Kaiser et al (2001), have been carried out so far to compare allele and genotype distribution of any candidate gene between schizophrenia and SA. To investigate molecular genetic characteristics of SA, SP and SPA, we selected a set of genes, which have been previously reported to play a role in etiology and pathogenesis of major psychoses. These were genes for serotonin transporter (5-HTT), serotonin receptor type 2A (5-HTR2A) and brain-derived neurotrophic factor (BDNF). 5-HTT is implicated in the regulation of serotonin neurotransmission by removing serotonin from the synaptic cleft thus modulating serotonergic signaling. The 5-HTT gene bears a polymorphism in the 5-HTT gene-linked polymorphic region (5-HTTLPR) located approximately 1 kb upstream of the transcription initiation site in chromosome 17. The polymorphism is represented by two alleles distinguished by different number of repeats and assigned the long (l) and the short (s) alleles. The alleles have been reported to determine differences in 5-HTT expression, with a higher rate of expression in case of the ll genotype comparing to the ls and ss variants (Lesch et al 1996). A number of studies demonstrated a role of the s allele in etiology of mood disorders, preferably major depressive disorder (Steffens et al 2002; Nellissery et al 2003; Nobile et al 2004; Hoefgen et al 2005) but not schizophrenia (Tsai et al 2000; Serretti et al 2002; Pae et al 2005; Dubertret et al 2005). BDNF, a neurotrophin found primarily in the neocortex, hippocampus, and amygdale, is thought to affect the mechanisms involved in cell formation, cell death, and/or neuroplasticity. In animal studies, BDNF was shown to promote the function and growth of serotonin (5-HT) neurons in the brain (Mamounas et al 1995). The gene is localized on the short arm of chromosome 11. The Val66Met single nucleotide polymorphism (SNP) that determines a valine-to-methionine substitution at position 66 has been described in the coding region and tested for association with various mental disorders. It was shown that this

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polymorphism was associated with bipolar affective disorder (Sklar et al 2002; Neves-Pereira et al 2002), with the Val allele contributing to susceptibility to the disease. The Met allele was found to be protective against depression (Strauss et al 2005) and obsessive-compulsive disorder (Hall et al 2003). However in some populations, the association between Val66Met polymorphism and affective disorders was not observed (Tsai et al 2003; Oswald et al 2004; Kunugi et al 2004). The results on relation of the Val66Met polymorphism to schizophrenia are even less persuasive. In some studies, the association between this gene and the disorder was found (Neves-Pereira et al 2005) but was not confirmed in the others (Virgos et al 2001; Skibinska et al 2004). 5-HTR2A is thought to be involved in the pathology of schizophrenia and the effects of some antipsychotic drugs as well (Dean 2003). A decrease in the number of these receptors and alterations of mRNA expression were found in the prefrontal cortex of postmortem brains of schizophrenic patients (Harrison et al 1997; Hernandez & Sokolov 2000; Matsumoto et al 2005) and in patients with depression (Mintun et al 2004). At the same time, the results of other studies revealed an increase of the 5-HTR2A in affective and schizoaffective patients (Hrdina et al 1997; Pandey et al 2003). The T102C polymorphism in exon 1 of the 5-HTR2A gene yielded the most promising results in associative studies of schizophrenia, with higher frequency of the CC genotype being observed in schizophrenic populations as compared to controls (see meta-analysis Williams et al 1997; Abdolmaleky et al 2004). Some studies, including our own, reported that the CC genotype frequency was higher in schizophrenic patients with severer negative symptoms and chronic course of the disease (Joober et al 1999; Golimbet et al 2002).

SUBJECTS AND METHODS Patients A sample included 877 patients (507 females, 370 males; age 39±14 years, age at onset 26±10.6 years) with schizophrenia and 185 patients with SA (demographic and clinical characteristics are presented in Table 1) who were admitted to clinical departments of Mental Health Research Center. Patients with organic brain disorders or severe somatic diseases were withdrawn from the study. A diagnosis was made according to diagnostic criteria of DSM-IVR and was based on the semi-structured interviews and medical records. Once established by a psychiatrist, the diagnosis was confirmed by the senior researchers (Kaleda VG & Abramova LI). When criteria for SA were met, a classification was made into manic (51 (27.6%) patients), depressed (90 (48.6%)), or bipolar (34 (18,4%)) subtypes. For 10 patients (5.4%) the subtype was not specified. The group of schizophrenic patients was stratified according to the presence or absence of affective syndrome. Out of the total sample, 170 patients had affective syndrome and 702 had not. Five patients were excluded from the study because of ambiguous data on the presence of affective syndrome. Clinical and demographic characteristics of patients are presented in Table 1. Most of schizophrenic patients (601 or 85.6%) in the SP group were diagnosed with paranoid schizophrenia; the other had a diagnosis of catatonic, hebephrenic, residual, simple and not otherwise specified subtypes. Fifty four patients (7.7%) met the diagnosis of schizotypal personality disorder and 8 (1.1%)

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– of acute psychotic disorder. In the SPA group, there were 129 (75.9%) patients with paranoid subtype of schizophrenia, 16 (9.4%) patients with other subtypes and 25 (14.7%) with schizotypal personality disorder. Thirty-two patients (18.8%) had a syndrome of mania and 138 (81.2) a depressive syndrome.

Controls A control group was recruited randomly from community and psychometrically screened before genotyping. The exclusion criteria were the presence of familial history of major psychosis and scores above 40 on Schizotypal Personality inventory (SPQ-74) and above 90 on the F scale of the Minnesota Multiphasic Personality Inventory (MMPI), which the participants have been suggested to complete. In total, 338 subjects (138 men, 250 women, mean age 32.7 (13.8) years) have been included in the analysis.

Clinical Variables Age at the initial stage of the disease was established as the time of first signs of illness that could be noticed by the relatives and significant others before patient’s referring to a psychiatrist. Age at the disease onset was registered by the time of establishing a diagnosis. Clinical symptoms were assessed by the Positive and Negative Syndrome Scale (PANSS). The PANSS (Kay et al 1987) is a widespread instrument proven to be valid and suitable for quantitative clinical studies. It includes three subscales measuring positive, negative and general psychopathological symptoms on 30 items: 7 for positive symptoms, 7 –for negative and 14 - for general psychopathological ones. Each symptom has 7 ratings (1- symptom is absent, 2- questionable, 3 – mild, 4 – moderate, 5 – severe, 6 – markedly severe, 7 –extremely severe). The PANSS interviews completed by a trained researcher were conducted one week before the patient’s discharge from the hospital. Table 1. Clinical and demographic characteristics of patients with schizophrenia with (SPA) and without (SP) affective syndrome and schizoaffective psychosis (SA) Clinical and demographic characteristics Males Females Age, years1 Age at initial stage of the disease, years Age at the disease onset, years Illness duration, years Cases with illness duration less than one year4 1

SP (n=702) 295 407 39.3 (14.0) 21.5 (9.8) 25.8 (10.5) 13.5 (3.7) 46 (6.7%)

SPA (n=170) 74 96 37.7 (14.4) 23.0 (11.5) 26.7 (11.4) 11.0 (3.1) 11 (8.5%)

SA (n=185) 81 104 30.7 (11.6)2 20.4 (8.3) 24.9 (8.5) 5.8 (3.4)3 59 (31.9%)

mean, standard deviation (SD); SP vs SA (t=7.6; df=885; p<0.0001); 3 SP vs SA (t=25.6; df=885; p<0.0001); SPA vs SA (t=15.0; df=353; p<0.0001); SP vs SPA (t=8.1; df=870; p<0.0001); 4 number of patients (%). 2

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Personality Questionnaires Translated and adapted versions of the Eysenck Personality Inventory (EPI); MMPI, and the State Trait Anxiety Inventory (STAI) were administered to measure personality traits. EPI (57 items) encompasses personality traits on two scales: Extraversion and Neuroticism. MMPI (377 item version) consists of three validity scales (L, F, K) and ten clinical diagnostic scales: Hypochondriasis (1), Depression (2), Hysteria (3), Psychopathic deviate (4), Masculinity-Femininity (5), Paranoia (6), Psychasthenia (7), Schizophrenia (8), Hypomania (9) and Social introversion (0). STAI includes 20 items measuring trait anxiety. To reduce an influence of affected status on evaluation of personality traits, the patients were administered to psychometric assessment after an improvement of their clinical state being assessed as 1 or 2 or 3 with Global Clinical Impression scale. The patients completed the questionnaires themselves or with the assistance of a psychologist. Criteria for MMPI validity were: L < 70 T-scores, F < 90 T-scores and K < 80 T-scores. Only valid profiles were used in the subsequent analysis.

Cognitive Assessment An extensive battery of neuropsychological tests was performed as described in detail elsewhere (Alfimova, Uvarova 2003). For the present analysis, 4 tasks, measuring verbal memory and executive functions, have been selected from the battery. Verbal memory tasks: •

•

An immediate 10-noun free recall test to measure short-term memory. The subject listens to a set of 10 semantically unrelated nouns and is asked to recall immediately after presentation as many as possible, in any order. This procedure is performed twice. The short-term memory score is the total number of words correctly recalled over two trials. The “Pictograms” Test to measure long-term memory. The essence of the task is that 16 words are presented to the subject who is instructed to remember them. To facilitate recalling of words, the subject is asked to draw a picture or a sign (a pictogram) for every word that may help him/her later (40-60 min after the presentation) to recall the word. If a word was recalled correctly, it was evaluated as 1 score; in a case of using synonym, the score was 0.5. The method assesses a delayed recall of deeply encoded verbal stimuli.

Executive function tasks: •

•

A variant of the Controlled Oral Word Association Test to measure verbal fluency. The subject was asked to generate as many words belonging to a designated semantic category, as he/she could in one minute. Animals and fruits were used. The total number of correct instances was included in the analysis. A serial subtraction test to measure working memory, i.e. the capacity to hold and manipulate information in mind while performing a cognitive task. Mental serial

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V. E. Golimbet, M. V. Alfimova, V. G. Kaleda et.al subtraction by seven has been utilized by psychiatrists for many years to assess the patient’s attention. Herzog and Wallace (1997) have argued that this is a measure of working memory. We used a difficult, hard-load version of the task, in which subjects were instructed to subtract successively 5 and 2, by turns, from a previous result, beginning with 200. The number of correct operations, produced within one minute, was used as a measure of sustained attention and working memory.

Ethical Requirements After being informed about the goals of the investigation, each subject gave a written informed consent to participate in the study and donated venous blood for DNA extraction. The study was approved by the Ethics Committee of Mental Health Research Center.

Genotyping To avoid ethnical stratification biases, only Russians were included in the study. DNA was extracted using phenol-chloroform method. Primers for 5-HTTLPR, 5-HTR2A and BDNF genotyping and PCR performance were as described in Lesch et al 1996, Warren et al 1993, Neves-Pereira et al 2002, respectively. To detect the 5-HTTLPR polymorphism, amplification products were resolved by electrophoresis on 5% polyacrilamide gel (PAAG). Alleles of interest were designated the “s” for 484 base pairs (bp) and the “l” for 528 bp. For the 5-HTR2A T102C polymorphism, Msp1 digestion was used with subsequent electrophoretic separation on the 2% agarose gel. The intact DNA fragment (342 bp) was assigned the A1 (T) allele and the fragment with the Msp1 restriction site presented by 2 bands (216 and 126 bp) - the A2 (C) allele. BDNF polymorphism was determined using PspC I digestion and 5% PAAG electrophoresis. The A or Met allele was represented by a 113 bp DNA fragment and the G or Val allele comprised the bands of 78 and 35 bp.

Statistical Procedures Personality and cognitive measures were compared using Student t-test. Because of rank characteristics of the PANSS ratings, Mann-Whitney (U) test was applied for between-group comparisons by the PANSS scores. Allele and genotype frequencies were compared using χ2 criterion. Odds ratio (OR) was estimated in case of significant differences between categorical variables. All statistical analyses were performed using the Graph Pad Prism 4.0 statistical package.

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RESULTS As presented in Table 1, patients’ ages at initial stage and at onset of the disease were similar in the groups studied. All the groups differed significantly (p<0.0001) in illness duration, which was the longest in SP patients and the shortest in SA ones. Also the SP group was featured by the older mean age comparing to the SA group. The number of patients with the illness duration less than one year was the highest in the SA group (31.9%) and of similar values for the SP (6.7%) and SPA (8.5%) groups. Clinical symptoms in patients measured by the PANSS are presented in Table 2. All groups differed by clinical presentations. Positive symptoms were mostly pronounced in patients with SP, while the SPA and SA groups had similar scores. Negative symptoms tended to gradual decreasing as SP>SPA>SA, with statistically significant differences between all the groups. As concerns general psychopathological symptoms, patients both with SPA and SA had higher scores on anxiety and depressive-related items as compared to the SP group. The latter was featured by the highest scores on the items related to cognitive and volition symptoms which, analogous to negative symptoms, decreased gradually in the SPA and SA groups. When compared by scores on the PANSS subscales, the SA group had the lowest ratings as on each of subscales as well in total (Table 3). All the groups differed in personality traits from the controls demonstrating higher levels of neuroticism and anxiety, lower levels of extraversion and variants of MMPI schizophrenictype profiles (Table 4, Fig.1). However there were a number of differences between the clinical groups. SA patients had better personality functioning than SP and SPA patients. Extraversion and Neuroticism scores in patients with SA did not differ significantly from controls’ values. On the STAI and MMPI scales, SA patients scored higher comparing to the controls; however none of their MMPI mean scores would be considered elevated outside of normal limits. SA had an 89 (Schizophrenia-Hypomania) profile code (Fig.1), which reflected a combination of moderately pronounced schizoid and hypomanic traits, i.e. alienation, inappropriate behavior, hyperactivity and positive affect, and indicated a relatively good psychological adjustment. Subjects with SPA showed the most deviated scores on all the personality scales that suggested they were much more compromised on the personality dimensions than subjects with SA and SP. They had a high ranging MMPI profile with marked elevations on scales 8 (Schizophrenia), 7 (Psychasthenia) and 6 (Paranoia) and secondary elevations on scales 2 (Depression) and 1 (Hypochondriasis ) that reflected significant psychological maladjustment and psychiatric symptoms, in particular confused and disorganized thinking, alienation, worring and a great deal of paranoid traits coupled with anxiety and depression. However, the profiles of the clinical groups differed mainly in level of mean scores, while the patterns were not remarkably different from each other with the exception of the Depression/Hypomania ratio. Assessment of cognitive functions (Table 5) did not reveal any significant between-group differences although there was a weak trend to better performance on the executive and shortterm memory tasks in patients with SA as compared to SP and SPA patients. It should be mentioned that all clinical groups scored significantly lower (p<0.001) on the tests than did the control group.

76

V. E. Golimbet, M. V. Alfimova, V. G. Kaleda et.al Table 2. Means and standard deviations for PANSS items in patients with schizoaffective psychosis (SA) and schizophrenia with- (SPA) or without (SP) affective syndrome SPA vs SA U

SP vs SA U

3.8 (1.8) 3.3 (1.5)

SP vs SPA U (MannWhitney) 27770* 25670*

ns ns

27690* 21380*

2.4 (1.6)

2.2 (1.6)

24770*

ns

20260*

3.1 (1.5)

2.3 (1.5)

3.0 (1.9)

28890*

7132**

ns

Grandiosity

2.4 (1.6)

1.8 (1.3)

2.1 (1.7)

31340*

ns

30460**

Suspiciousness/ persecution Hostility

3.9 (1.5)

3.2 (1.6)

3.0 (1.9)

31080*

ns

25970*

3.0 (1.6)

2.3 (1.4)

2.3 (1.6)

30450*

ns

26640*

Blunted affect

4.0 (1.3)

3.5 (1.2)

2.5 (1.2)

31240*

5205*

14600*

Emotional withdrawal Poor rapport

3.8 (1.3)

3.4 (1.3)

2.1 (1.2)

33750**

4418*

12980*

3.9 (1.3)

3.3 (1.3)

2.3 (1.3)

29170*

5365*

14050*

Passive/apathetic social withdrawal Difficulty in abstract thinking Lack of spontaneity Stereotyped thinking Somatic concern

3.9 (1.5)

3.3 (1.3)

2.0 (1.1)

32010*

4215*

11980*

3.7 (1.6)

2.6 (1.3)

2.0 (1.0)

25370*

6300*

13790*

3.5 (1.5)

2.8 (1.4)

2.1 (1.1)

31380*

6155*

16980*

3.9 (1.4)

3.1 (1.3)

1.9 (1.1)

27500*

4609*

10560*

2.2 (1.4)

2.9 (1.6)

1.9 (1.3)

29890*

5801*

31120***

Anxiety

2.7 (1.4)

3.4 (1.4)

3.1 (1.4)

29850*

ns

30530***

Guilt feelings

1.5 (1.1)

2.5 (1.6)

2.1 (1.5)

26750*

7479***

30160**

Tension Mannerism and posturing Depression

3.6 (1.4) 3.4 (1.4)

3.1 (1.3) 2.8 (1.4)

3.1 (1.3) 2.4 (1.2)

32730** 30830*

ns 7523***

28340** 21600*

2.0 (1.3)

3.9 (1.8)

3.4 (1.8)

17880*

ns

19990*

PANSS items Mean (SD)

SP (n=567)

SPA (n=143)

SA (n=126)

Delusions Conceptual disorganization Hallucinatory behavior Excitement

4.5 (1.6) 4.3 (1.3)

3.6 (1.7) .4 (1.4)

3.6 (1.8)

Schizoaffective Psychosis and Schizophrenia with- or without Affective Syndrome

*

77

Motor retardation

2.7 (1.4)

3.1 (1.5)

2.4 (1.4)

34920***

6914**

31600***

Uncooperativeness Unusual thought content Disorientation

3.3 (1.6) 3.9 (1.7)

2.5 (1.4) 2.9 (1.6)

2.1 (1.4) 2.6 (1.8)

29860* 28180*

7311** ns

20960* 22870*

1.8 (1.2)

1.4 (0.9)

1.3 (0.9)

33560**

ns

26540*

Poor attention

3.8 (1.3)

3.3 (1.2)

3.3 (1.1)

33010**

ns

26790*

Lack of judgment and insight Disturbance of volition Poor impulse control Preoccupation

5.1 (1.3)

4.2 (1.4)

4.2 (1.7)

26540*

ns

24480*

3.8 (1.3)

3.3 (1.2)

3.0 (1.1)

30770*

7583***

21920*

2.6 (1.6)

2.0 (1.3)

2.0 (1.3)

30490*

ns

26760*

4.2 (1.4)

3.8 (1.2)

3.4 (1.4)

33000**

7376***

24160*

Active social avoidance

4.0 (1.4)

3.5 (1.3)

3.0 (1.4)

30460*

7429***

1300*

p<0.0001; ** p< 0.001; *** p=<0.01; ns – non-significant. 90

80

T scores

70

60

50

40

SP SPA SA

30 L

F

K

Hs

D

Hy

Pd

Mf

Pa

Pt

Sc

Ma

Si

MMPI scales

MMPI scales: L, F, K (validity scales), Hypochondriasis (HS), Depression (D), Hysteria (Hy), Psychopathic deviate (Pd), Masculinity-Femininity (Mf), Paranoia (Pa), Psychasthenia (Pt), Schizophrenia (Sc), Hypomania (Ma) and Social introversion (Si). Subjects with SPA showed the most deviated scores on all the scales that suggested that they were much more compromised on the personality dimensions than subjects with SA and SP. Figure 1. MMPI profiles of the SP, SPA and SA groups.

78

V. E. Golimbet, M. V. Alfimova, V. G. Kaleda et.al Table 3. Means and standard deviations for PANSS subscales in patients with schizoaffective psychosis (SA) and schizophrenia with (SPA) - or without (SP) affective syndrome

PANSS subscales

SP (n=567)

SPA (n=143)

SA (n=126)

SP vs SPA U (MannWhitney)

*

Positive

24.7 (7.8)

Negative

26.3 (7.8)

General psychopathological Total

50.2 (12.0) 101.2 (27.5)

19.0 (7.6) 22.2 (6.7) 48.5 (11.5) 89.7. (25.8)

SPA vs SA U

SP vs SA U

19.3 (9.1)

27090*

ns

28760*

14.5 (6.1)

30250*

4667*

10510*

42.0 (13.0) 75.8 (28.1)

ns

7839*

27080*

28890*

7132*

28060*

p<0.0001; ns – non-significant.

Table 4. Means and standard deviations for the personality traits in patients with schizoaffective psychosis (SA) and schizophrenia with- (SPA) or without (SP) affective syndrome Personality traits Mean (SD) EPI Extraversion

SP

SPA

SA

controls

(n=282) 10.3 (3.7)

(n=93) 9.1 (3.2)

(n=118) 11.1 (3.9)

(n=292) 11.6 (3.8)1

Neuroticism

12.9 (5.3)

15.0 (4.9)

13.4 (4.9)

12.7 (4.8)2

MMPI Hypochondriasis

(n=169) 60.8 (13.8)

(n=71) 66.7 (12.7)

(n=110) 57.0 (13.2)

(n=296) 53.3 (11.3)3

Depression

60.6 (13.9)

70.2 (14.2)

56.2 (13.4)

50.4(11.9)4

Hysteria

58.6 (11.9)

62.8 (11.7)

56.4 (11.0)

53.5 (10.7)5

Psychopatic deviate

59.6 (11.3)

65.3 (9.7)

56.4 (11.7)

53.8 (10.7)6

MasculunityFemininity Paranoia

54.8 (11.6) 64.3 (11.5)

52.8 (10.9) 69.1 (19.2)

52.8 (12.6) 60.4 (15.9)

51.5(11.6)7 53.7(12.6)8

SP vs SPA

SP vs SA

SPA vs SA

t=2.8; df=373; p=0.005; t=3.4; df=373; p=0.001

ns

t=4;df=209 ; p<0.0001 t=2.4; df=209; p=0.02

t=3.1;df=238 ; p= 0.002 t=4.852 df=238; p<0.0001 t=2.5; df=238 p= 0.01

t=2.9; df=277; p=0.02 t=5.8; df=277; p<0.0001 ns

t=3.7; df=238; p=0.0003 ns

t=2.3; df=277; p=0.02 ns

t=4.9; df=179; p<0.0001 t=6.704 df=179; p<0.0001 t=3.7; df=179; p=0.0003 t=5.3; df=179; p<0.0001 ns

t=2.4; df=238; p=0.02

t=2.4; df=277; p=0.02

t=3.3; df=179; p=0.001

t=3.166 df=398; p=0.002;

Schizoaffective Psychosis and Schizophrenia with- or without Affective Syndrome Psychasthenia

64.3 (14.0)

73.4 (13.9)

62.4 (14.4)

56.3 (11.9)9

Schizophrenia

71.7 (18.9)

80.2 (19.2)

66.1 (17.6)

55.7 (14.3)10

Hypomania

63.0 (12.4) 56.2 (12.2)

63.1 (11.8) 61.5 (11.4)

65.0 (13.2) 53.0 (10.4)

60.2 (11.3)11 50.6 (11.7)12

(n=285) 48.4 (9.3)

(n=88) 53.5 (11.9)

(n=115) 47.6 (9.9)

n=290 44.5 (8.7)13

Social introversion STAI Trait anxiety

ns

79

t=4.6; df=238; p<0.0001 t=3.2; df=238; p=0.02 ns

t=2.484 df=277; p=0.01 ns

t=5.1;df=1 79; p<0.0001 t=5.1; df=179; p<0.0001 ns

t=3.1; df=238; p=0.02

t=2.3; df=277; p=0.02

t=5.2; df=179; p<0.0001

t=4.2; df=371; p<0.0001

ns

t=3.8; df=201; p=0.0002

SA vs controls: 1 – ns; 2 -ns; 3 - t=2.8; df=404; p=0.005; 4- t=4.2; p<0.0001; 5 - t=2.4; p=0.02) ; 6 – ns; 7 – ns; 8 – t=4.4; p<0.0001; 9 - t=4.3; p<0.0001; 10 - t=6.1; p<0.0001; 11- t=3.6; p=0.003; 12 – ns; 13 t=3.1; p=0.002.

All clinical groups differed significantly (p<0.001) from the controls in the cognitive traits measured. The distribution of 5-HTTLPR, 5-HTR2A and BDNF genotypes was in accordance to Hardy-Weinberg equilibrium, that is, it did not differ from the one expected. Alleles and genotypes frequency of the polymorphisms studied was similar to those of European populations. The results on allele and genotype distribution are presented in Tables 6 and 7. There were no significant differences in the distribution of 5-HTTLPR alleles and genotypes between the SP, SPA and control groups though the ss genotype frequency tended to be higher in the SPA group (p=0.14). However, in patients with SA, frequency of the s allele and the ss genotype was significantly higher (p=0.02) comparing to SP patients and controls (p=0.01) but did not differ from that in SPA patients. When the SA and SPA groups have been combined, the ss genotype prevalence still remained significantly higher (p=0.02) as compared to either the SP or control groups. Table 5. Means and standard deviations for the cognitive variables in patients with schizoaffective psychosis (SA) and schizophrenia with- (SPA) or without (SP) affective syndrome Cognitive variables Mean (SD) Short-term memory Long-term memory Verbal fluency Sustained attention and working memory

SP

SPA

SA

Controls

(n=205) 8.5 (2.7) (n=94) 8.3 (3.6) (n=223) 27.0 (9.5) (n=65)

(n=48) 9.3 (2.3) (n=11) 8.7 (2.3) (n=48) 29.4 (10.2) (n=11)

(n=43) 9.7 (1.8) (n=23) 7.9 (2.9) (n=43) 29.6 (9.1) (n=20)

(n=223) 11.0 (2.3) (n=214) 12.5 (2.8) (n=230) 41.3 (8.6) (n=162)

9.9 (6.5)

7.9 (6.5)

11.2 (5.4)

17.2 (6.9)

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Table 6. The 5-HTTLPR, 5-HTR2A and BDNF genotypes distribution (frequency and number of cases) in the clinical groups and controls Genotype Group LL SP 36.6 (98) SPA 29.3 (27) SA 31.6 (24) Controls 36.6 (142)

5-HTTLPR LS SS 47.0 16.4 (126) (44) 48.9 21.7 (45) (20) 36.8 31.6 (28) (24) 46.6 16.8 (181) (65)

n 268 92 76 388

A1A1 16.2 (66) 18.7 (26) 12.9 (19) 22.7 (76)

5-HTR2A A1A2 A2A2 41.5 42.3 (169) (172) 48.9 32.4 (68) (45) 41.5 45.6 (61) (67) 42.1 35.2 (141) (118)

n 407 139 147 335

Met/Met 2.3 (4) 1.9 (2) 3.4 (5) 2.7 (9)

BDNF Met/Val Val/Val 39.0 58.7 (67) (101) 31.4 66.7 (33) (70) 29.5 67.1 (44) (100) 36.9 60.4 (124) (203)

n 172 105 149 336

Between-group differences in the ll and the ss genotypes frequency: SA vs controls - χ2 =5.9; df= 1; p=0.01. OR 2,2 (CI 95% 1.2-4.1); SA vs SP - χ2 =5.6; df= 1; p=0.02. OR 2.2 (CI 95% 1.4-4.3); SA +SPA vs controls - χ2 =5.7; df= 1; p=0.02. OR 1.8 (CI 95% 1.1-3.0) SA +SPA vs SP - χ2 =5.3; df= 1; p=0.02. OR 1.95 (CI 95% 1.1-3.2). Between-group differences in the A1A1 and the A2A2 genotypes frequency: SP vs controls - χ2 =6.3; df= 1; p=0.01. OR 1.7 (CI 95% 1.1-2.5); SA vs controls - χ2 =8.5; df= 1; p=0.003. OR 2.4 (CI 95% 1.3-4.3); SA vs SPA - χ2 =5.1; df= 1; p=0.02. OR 2.3 (CI 95% 1.1-4.6).

For the 5-HTR2A polymorphism, the genotype distribution was similar for SP and SA patients. Comparing to the control group, higher frequency of the A2 allele and the A2A2 genotype (p=0.01) was observed in the SP and SA groups but not in the SPA group. Also, there was significant difference in the frequency of the A1A1 and A2A2 genotypes between the SA and SPA groups. Table 7. The 5-HTTLPR, 5-HTR2A and BDNF allele distribution (frequency and number of cases) in the clinical groups and controls Genotype Group SP SPA SA Controls

L 60.1 (322) 53.8 (99) 50 (76) 59.9 (465)

5-HTTLPR S 39.9 (214) 46.2 (85) 50 (76) 40.1 (311)

n 536 184 152 776

A1 37 (301) 43.2 (120) 33.7 (99) 43.7 (293)

5-HTR2A A2 63 (513) 56.8 (158) 66.3 (195) 56.3 (377)

n 814 278 294 670

Between-group differences in the l and the s alleles frequency: SA vs controls - χ2 =5.2; df= 1; p=0.02. OR 1.5 (CI 95% 1.1-2.1); SA vs SP - χ2 =4.9; df= 1; p=0.03. OR 1.5 (CI 95% 1.1-2.2). Between-group differences in the A1 and the A2 genotypes frequency: SP vs controls - χ2 =7.0; df= 1; p=0.008. OR 1.3 (CI 95% 1.1-1.6); SA vs controls - χ2 =8.6; df= 1; p=0.003. OR 1.5 (CI 95% 1.1-2.0).

Met 21.8 (75) 17.6 (37) 18.1 (54) 21.1 (142)

BDNF Val 78.2 (269) 82.4 (173) 81.9 (244) 78.9 (530)

n 344 210 298 672

Schizoaffective Psychosis and Schizophrenia with- or without Affective Syndrome

81

The distribution of the BDNF alleles and genotypes did not differ in all the groups studied. A trend to higher frequency of the Met allele-contained genotypes (Met/Met +Val/Met) that failed to reach a level of significance was found in the combined group of SA and SPA patients as compared to SP patients (p=0.08) and control group (p=0.12). The distribution of combined genotypes for 5-HTTLPR and BDNF genes has been also studied. We assumed that these genes might have an additive or interactive effect on the phenotype, especially in case of SA, because BDNF was reported to modulate serotonin transporter function in cells depending on a 5-HTTLPR genotype (Mossner et al 2000). The combinations of interest were as follows: (1) the BDNF Met allele and the 5-HTTLPR ll genotype due to their plausible protection effect against affective disorders and (2) the BDNF GG and 5-HTTLPR ss genotypes, which may predispose to affective disorders. As expected, we found a higher frequency of combined genotypes (Met/Met + Met/Val + ll) versus a genetic variant, comprising Val/Val + ss genotypes, in the control group (49 versus 37 cases respectively). In contrast, an opposite ratio was observed for the above mentioned combinations in the SA group (5 versus 15 cases). This between-group difference in genotype ratio was significant (Chi2=6.0; df=1; p=0.01; OR 4.2; CI 95% 1.3-13.6).

CONCLUSION Therefore, we demonstrated that patients with SP, SPA and SA had significant differences in clinical, personality, and molecular genetic, but not cognitive, characteristics. Patients with SA were featured by the lowest ratings of negative symptoms, milder psychotic and affective symptoms and less pronounced personality changes. Notably, the dramatic gap was detected between SP and SA whereas the difference between SPA and SA was less striking, especially with regard to positive, affective and disorganization (e.g. conceptual disorganization, unusual thought content) symptoms. Clinical symptoms tended to descend from SP to SA, with SPA taking an interim position, thus suggesting an existence of a certain kind of continuum between these groups. Indirect evidence for the lack of the transparent differentiation is provided by the finding of the younger age at the time of examination, shorter illness duration and a higher percent of the cases with the disease duration less than one year in patients with SA. This fact can be explained by the possibility of changing the diagnosis of SA for SP during the disease progression. A possibility of such changes has been argued earlier (Avrill et al 2004). Interestingly, a study of Fenton & McGlashan (1989) on diagnostic efficiency of schizophrenia revealed that the most valid definition of the disease is based on characteristic symptoms plus absence of affective symptoms plus 6-months duration. It should be mentioned that our study is in line with some previous investigations into clinical symptoms of schizophrenia and SA. The absence of the differences in age at onset between SP and SA was reported by a number of researches (Evans et al 1999; Benabarre et al 2001). There are controversial findings as well, for example, Ricca et al (1997) reported the same levels of perception and thought disturbances in SP as well as in SA patients. However, the results have been obtained in a relatively small sample, which in total included 58 patients with schizophrenia and SA. With regard to personality, each group showed a pattern of traits reflecting schizophrenia-type personality changes as measured by MMPI. Besides, higher levels of neuroticism and anxiety and lower level of extraversion were found in all clinical groups that

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V. E. Golimbet, M. V. Alfimova, V. G. Kaleda et.al

was in accordance with the results reported by other authors, who studied combined samples of schizophrenic and schizoaffective patients (Lysaker & Davis 2004; Camisa et al 2005). It should be noted that self–ratings of SPA patients were severest though they were rated by clinicians mainly as intermediate between SP and SA patients. This may be due to their high levels of depression and anxiety and reflects significant amount of subjective distress. The SA group demonstrated the mildest personality changes, the finding being mainly consistent with the PANSS results. Notably, in this group, there was a discrepancy between clinically and subjectively rated levels of depression. In particular, given established links between personality and general outcome, including sense of well being in schizophrenia spectrum disorders (e.g. Lysaker & Davis 2004), one might suggest different prognoses for SPA and SA patients despite their resemblance on symptom ratings. In contrast to symptoms and personality traits, cognitive functioning was similar in all clinical groups that was consistent with other studies (Miller et al 1996; Manschreck et al 1997; Beatty et al 1993; Evans et al 1999; Gooding & Tallent 2002; Goldstein et al 2005), which have reported the same level of cognitive deficits both in schizophrenia and SA. Interestingly, the fact that schizoaffective patients did not differ from schizophrenics in cognitive functioning even prompted some researchers to challenge a validation of SA as a diagnostic category (Gooding & Tallent 2002). The results of molecular genetic study revealed that all clinical groups had both the differences and similarities by genotype distribution. The SA group was closer to the SP group by the prevalence of the A2A2 5-HTR2A genotype and to the SPA group by higher frequency of the ss 5-HTTLPR genotype and the BDNF Met allele. However, only the SA group had a specific genotype combination, namely higher frequencies of the 5-HTTLPR s allele and ss genotype, the A2 5-HTR2A allele and A2A2 genotype and the genetic variant the ss and the Met allele, which differentiated it distinctly from the control group. Notably, in accordance to OR estimation, possession of these variants raised liability to SA by 2 to 4 times. A contribution of the 5-HTTLPR, 5-HTR2A and BDNF polymorphisms to SP and SPA was less obvious. There were no genetic variants associated with SPA, 5-HTR2A polymorphism only being found to contribute to schizophrenia with OR 1.7. The results of our molecular genetic study, to a certain extent, replicated the earlier reports on the relation of 5-HTTLPR and 5-HTR2A polymorphisms to schizophrenia and SA. For example Kaiser and associates (2001) have found higher frequency of the ss genotype in patients with SA as compared to patients with schizoparanoid or residual subtypes of schizophrenia. The samples used in positive association studies of the 5-HTR2A polymorphism in schizophrenic populations (Williams et al 1997) comprised a portion of SA cases with higher frequency of the A2A2 genotype comparing to the A1A1 genotype. As it has been mentioned earlier, genetics of SA is poorly understood. Family studies (for review see Abrams 1984) seem to reveal both a schizophrenic and affective genetic contribution to schizoaffective disorder, which differentiates it from either schizophrenia or affective disorder. Our molecular genetic findings support this observation. In compliance with literature, the 5-HTTLPR polymorphism is related to depression and anxiety (Mossner et al 2001; Mueller & Kranzler 2003; Golimbet et al 2004) while the 5-HTR2A polymorphism is associated with schizophrenia symptoms (Joober et al 1999; Golimbet et al 2002). In our study, both the “depression prone” ss 5-HTTLPR genotype and the schizophrenia-related 5HTR2A A2A2 genotype were associated with schizoaffective psychosis.

Schizoaffective Psychosis and Schizophrenia with- or without Affective Syndrome

83

Based on the results of the study, the following conclusions may be drawn out: (1) the presence of affective syndrome in the course of psychotic episode in schizophrenia is correlated with particular clinical presentations and personality changes of schizophrenic patients; (2) SA is more similar to SPA than to SP with regard to clinical symptoms and molecular-genetic characteristics; (3) SA is characterized by some specific features, namely, by the lowest ratings for negative symptoms, one of the most stable characteristic of schizophrenia, which is thought to be underpinned by genetic factors, and by a combination of genotypes of the candidate genes for major psychosis. Taken together, these factors discriminate SA distinctly from SP and SPA in genetic view.

ACKNOWLEDGMENTS We wish to thank clinical psychiatrists Mrs. T.S. Kaidan, T.K. Ganisheva, A.A. Muratova, K.V. Chubabria, M.A. Streltsova, T.K. Shemyakina, L.F. Frolova for their assistance in providing patients for the study.

REFERENCES Abdolmaleky, HM; Faraone, SV; Glatt, SJ; Tsuang, MT. Meta-analysis of association between the T102C polymorphism of the 5HT2a receptor gene and schizophrenia. Schizophr Res 2004, 67(1), 53-62. Abrams, R. Genetic studies of the schizoaffective syndrome: a selective review. Schizophr Bull 1984, 10(1), 26-29. Alfimova, M; Uvarova, L. Cognitive peculiarities in relatives of schizophrenics: heritability and EEG-correlates. Int J Psychophysiol 2003, 49, 201-216. Averill, PM; Reas, DL; Shack, A; Shah, NN; Cowan, K; Krajewski, K; Kopecky, C; Guynn, RW. Is schizoaffective disorder a stable diagnostic category: a retrospective examination. Psychiatr Q. 2004, 75(3), 215-227. Beatty, WW; Jocic, Z; Monson, N; Staton, RD. Memory and frontal lobe dysfunction in schizophrenia and schizoaffective disorder. J Nerv Ment Dis 1993, 181(7), 448-453. Benabarre, A; Vieta, E; Colom, F; Martinez-Aran, A; Reinares, M; Gasto, C. Bipolar disorder, schizoaffective disorder and schizophrenia: Epidemiologic, clinical and prognostic differences. European Psychiatry 2001,16(3), 167–172. Brockington, IF; Meltzer, HY. The nosology of the schizoaffective psychosis. Psychiatric Developments 1983, 1, 317-338. Camisa, KM; Bockbrader, MA; Lysaker, P; Rae, LL; Brenner, CA; O'Donnell, BF. Personality traits in schizophrenia and related personality disorders. Psychiatry Res 2005; 133, 23-33. Dean, BB.The cortical serotonin2A receptor and the pathology of schizophrenia: a likely accomplice. J Neurochem. 2003, 85(1), 1-13. Dubertret, C; Hanoun, N; Ades, J; Hamon, M; Gorwood, P. Family-based association study of the 5-HT transporter gene and schizophrenia. Int J Neuropsychopharmaco. 2005, 8(1), 87-92.

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In: Schizoaffetive Disorders Editor: Kam-shing Yip

ISBN 978-1-60456-948-3 © 2009 Nova Science Publishers, Inc.

Chapter 4

DIAGNOSTIC CONTROVERSIES IN SCHIZOAFFECTIVE DISORDER Nathaniel Hurwitz1,* and C. Raymond Lake2 1

New Mexico VA Heath Care System, 1501 San Pedro SE (116), Albuquerque, NM 87108, USA 2 Psychiatry and Behavioral Sciences, University of Kansas School of Medicine 3901 Rainbow Boulevard, Kansas City, KS 66160-7341, USA

INTRODUCTION Diagnosis in psychiatry is unlike that in internal medicine due to the absence of ‘gold standard’ measures. A gold standard unequivocally establishes diagnosis. In internal medicine, for example, venogram for deep vein thrombosis (DVT) is the gold standard against which the diagnostic values of venous doppler, D-dimers, and Homan’s sign (pain on dorsiflexion of the foot) have been assessed. Though once standard, Homan’s sign is now discouraged since poor sensitivity/specificity for DVT make it useless, and worse yet, checking for it may even contribute to increased morbidity when a clot is present [1, 2]. This Chapter asks the questions: 1. How, given the absence of a single diagnostically useful lab test (save toxicology screening), let alone ‘gold standards’ for such problems as suicidality and psychosis, should we move towards maximizing patient benefit until labs become available?, 2. What is the pitfall of inventing more and more diagnoses, like ‘schizoaffective disorder’ without lab test evidence for their existence? and 3. What diagnostic strategy would best lead towards the development of meaningful lab tests?

DIAGNOSTIC HISTORY IN RELATION TO PHARMACOLOGY It is instructive to review the ‘schizophrenia’ versus ‘psychotic mood disorder’ diagnostic history first since those are the two diagnoses that were merged to create ‘schizoaffective *

Email: [email protected]

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disorder’. Kraepelin described two separate psychiatric disorders based on his belief that thedegree of symptom severity and chronicity differentiated the two: 1. dementia praecox (renamed ‘schizophrenia’ by Bleuler), and 2. manic-depressive insanity (now called bipolar disorder) [3, 4]. According to Bleuler, the presence of any single psychotic symptom was pathognomonic for the diagnosis of schizophrenia, which, he argued was the third most common psychiatric condition following ‘oligophrenia’ (mental retardation) and alcoholism [5, 6]. In 1959, Kurt Schneider, echoed Bleuler codifying eleven psychotic symptoms (Schneiderian First Rank Symptoms or FRSs), the presence of any one of which was supposedly pathognomonic for schizophrenia [7]. Despite numerous studies showing a lack of diagnostic, prognostic, or treatment response specificity, FRSs remain among diagnostic criteria for schizophrenia in the DSM-IV [8]. The concepts that formed the schizophrenic view of psychosis predate psychopharmacology. Both chlorpromazine and lithium became available around 1950, but lithium was pulled off the American market shortly thereafter due to its use as a salt substitute and consequent deaths from heart failure. Lithium didn’t reappear in the USA for treatment of manic depressive illness until 1970. Consequently, schizophrenia was diagnosed five to ten times as often as manic depression in the United States versus Europe between 1950 and 1970, with reversed ratios in Europe [9-11]. As a strategy to correct this cross-ocean diagnostic disparity, the DSM III-R (1987) introduced into the schizophrenia categories: 1. a six month chronicity requirement, and 2. the requirement that a patient’s illness is not better accounted for by mood disorder. A series of studies in the mid to late 1970s revealed no difference in symptoms, family histories, or prognoses between ‘good prognosis schizophrenia’ (characterized by positive symptoms, and now frequently called ‘positive syndrome schizophrenia’ and/or ‘paranoid schizophrenia’) versus manic depression (now called bipolar illness) [Reviewed in Pope and Lipinski, 1978] [12]. By some counts, relative diagnostic rates have changed- more affective psychosis and less schizophrenia [13]. Akin to epilepsy, mood episodes exhibit kindling, or the tendency for discrete affective (depressed, manic, or mixed) episodes to occur more frequently and to become more severe over time, without treatment [14-18]. Parallel mood stabilizing and anti-epileptic effects of certain anti-seizure medications further support the kindling model [14, 16]. In susceptible patients, severe episodes manifest psychosis (reality distortion in the form of hallucinations, delusions, or disorganization). Multiple lines of research suggest that psychotic states are neurotoxic [19-25]. As well, unpredictable and dangerous behavior can manifest in acute psychotic states. The risk/benefit ratio for neuroleptics in acutely psychotic states favors their use, despite their malignant side effects with long term use. Some diagnostic labels, including diabetes, hypertension, schizophrenia, and psychotic mood disorder suggest a need for chronic prophylactic medication. All functional psychiatric labels are based solely on observed behavior and reported symptoms. The schizophrenia and schizoaffective diagnostic labels carry the implication that chronic neurolepticization is indicated. There is a key difference in the case of risk/benefit ratio assessment in internal medicine versus psychiatry. Since diagnosis in internal medicine (like hypertension) is generally based on specific measurements (like blood pressure), and pharmacologic interventions (like hydrochlorothiazide) are titrated to achieve specific endpoints (BP < 135/85) to prevent known consequences of non-treatment (increased probability of stroke, renal disease, etc.), it is clear when a drug is working or not. The diagnosis is essential hypertension, but in a

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refractory case, alternate diagnoses (like pheochromocytoma, renal artery stenosis, etc.) must be considered. In psychiatry, however, diagnostic labeling occurs in the absence of lab testing. Thus, unlike in internal medicine, there is in psychiatry a risk/benefit ratio to the diagnosis itself. The exceptions to the ‘unlike’ status in internal medicine are areas where the diagnosis is very uncertain, or where it is not based on any reliable criteria as is the case for ‘fibromyalgia’. Fibromyalgia is solely based on patient’s complaints since the ‘finding’ that was originally argued to define this ‘disease’, namely ‘trigger points’ (knots on your back), can not be reliably identified [26-30]. One must consider the risks of unemployment or iatrogenic opiate dependance when diagnosing someone with fibromyalgia. The risks of chronic neurolepticization have to be included in the risk/benefit ratio assessment of diagnosing schizophrenia, or any ‘schizo’ prefaced label, including ‘schizoaffective’. We are dealing more in the realm of opinion than fact when it comes to diagnostic labels in psychiatry (ie: in your opinion, did you ever have a two week period when you felt really blue?) except when it comes to documented observed behavior (ie: police brought patient in for going door to door preaching frantically). Psychosis is impressive, thus it is not missed when it is obvious. Its psychological effect on clinicians invokes the words, “schizophrenia” and “schizoaffective”, which has become the way that the expert psychiatrist relates that he/she detected psychosis. Patient care considerations dictate risk/benefit assessment of competing diagnostic options. Whether or not a given case is better prognosis (ie: affective), the opportunity cost of diagnosing schizophrenia early is chronic neurolepticization at the expense of anti-kindling strategies. In other words, the early diagnosis of schizophrenia (bad prognosis illness) becomes a self fulfilling prophecy in missed psychotic mood disorder. Schizoaffective disorder, which falls under the schizophrenia section in the DSM-IV, also leans clinicians towards prolonged neurolepticization and away from the strategy of acute stabilization with neuroleptics while initiating prophylactic mood stabilizing medications, and subsequent tapering off neuroleptics. For the most acutely ill patients, risk benefit ratios dictate immediate stabilization due to the danger component. Patients who are blatantly seeking means to do immediate harm are given haloperidol and ativan or similar medications. There are predictable dose dependant responses in acute decompensation due to the sedation endpoint. EPS are minimized and D2 effects of the typical are potentiated by the benzodiazepine. There is no tardive dyskinesia risk with acute stabilization. A similar approach is used in stabilizing soon-to-be dangerous psychosis, like refusal to eat or drink due to fear of being poisoned. But the risks/benefits of chronic neurolepticization are entirely different. Aside from the obvious, tardive dyskinesia and metabolic syndrome, there is a more subtle ill effect of dopamine blockade. Dopamine mediates drive. Typicals exhibit more D2 binding activity than atypicals by pet studies, but the atypicals still show significant ventral striatal D2 blockade. All motivated pleasure/fulfillment seeking behavior has been linked to dopamine activity at the nucleus accumbens in the ventral striatum [31-37]. All antipsychotic medications tested to date block D2 receptors and stabilize acute mania (including Chlorpromazine, as was shown over 50 yr ago) [38-40]. Acute mania is characterized by euphoric or irritable mood in the context of marked increase in the rates and quantity of thoughts, but with a decreased need for sleep. Patients present as if they are on cocaine [dopamine reuptake inhibiter], but they are not. A series of studies showed that the antipsychotic potencies of traditional neuroleptics is dose dependent on their D2 dopamine receptor binding affinities [41-43]. This led to the dopamine theory of schizophrenia

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(psychosis). Atypicals work in acute mania, but their role in maintenance is unclear. Clozapine may have a maintenance role in refractory bipolar illness [44-46]. Several newer atypical antipsychotics have received FDA indications for the treatment of bipolar illness though studies have been too short to document anti-kindling effects. Their actions may, like chlorpromazine and haloperidol, only stabilize mania, but not prevent recurrence. Next to Lithium, Divalproex and Carbamazepine, both antiepileptic mood stabilizing agents, show greatest anti-kindling efficacy. Lithium has beaten all other medications for the treatment of bipolar illness in all meta-analyses to date. Psychotic mood episode frequency and severity during critical vulnerability stages may dictate long term outcome. Studied for over 50 years, lithium has been shown to both reduce the frequency and severity of mood episodes over time, as well as reduce suicide rates [47-51]. Several studies suggest anti-kindling lithium effects in recurrent depression as well [52-54]. Classic descriptions of schizophrenia involve a prodromal 2-4 year period of relatively depressed mood followed by a subacute withdrawn, severely dysphoric and anxious episode culminating in frank psychosis, or ‘psychotic break’. That is, ‘classic’ schizophrenia describes textbook psychotic depression. In fact, some have called such a depressive trajectory, “double depression” which means major depression (the subacute phase with marked withdrawal) superimposed on dysthymia (a dysphoric overall adjustment for years) [55-57]. Hafner et al (2005) performed a retrospective assessment of psychotic, depressive and negative symptoms from onset of symptoms to time of admission in N = 232 first admission schizophrenia cases [58]. A representative subset (N = 130) were also studied retrospectively from time of admission to 6 mo later. “The lifetime prevalence of depressive mood (>or=2 weeks) at first admission for schizophrenia was 83%.” In the first psychotic episode, 71% had clinically significant depressive symptoms. The N=130 subset were compared with N=130 controls and N=130 new onset unipolar depressed patients. Both ill groups showed parallel prodromal depressive symptoms. It was not until emergence of psychosis, years after onset of symptoms, that the schizophrenia versus the depression groups could be distinguished from eachother. In a follow up paper, the authors report data they gathered from 107 first episode cases of schizophrenia, whom they followed for an average of 11.2 years showing [1] depression is the most frequent symptom throughout the course of schizophrenia, and [2] “psychosis risk increases when depressive and anxiety symptoms increase and decreases when these symptoms decrease” [59]. A diagnosis of psychotic depression, but not schizoaffective, would have begged lithium trial which would likely have improved many patients’ outcomes. Occam’s Razor (if one thing explains multiple findings it is probably their cause, rather than the coincidental occurrence of multiple independent events), is a basic diagnostic tenet. Psychotic mood disorder explains psychosis and mood disturbance. By the current DSM (DSM-IV) the rates of “non-affective psychosis” depend on how broadly one defines mood. Broad ways to define mood episodes would be around a couple of weeks of not functioning normally because one is too depressed, or [2] a few days of being noticably exceedingly abnormally hyper or talking way too much while not needing sleep and feeling unlike oneself. But, “patients don’t read textbooks” (presentations don’t correspond to classic descriptions), and the clinician really wants to know if anything like any of that ever happened. The next step is contacting the witnesses of the abnormal state (often family) to ensure that multiple streams of information dovetail. The reason this is so important is that the real question one is asking oneself is, “is there evidence that this patient has a recurrent mood episode component

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to his/her illness dictating prevention of kindling as a primary intervention to prevent secondary psychotic exacerbation?” Even in well defined illness, like clot-rupture and subsequent myocardial infarction, patients don’t present with consistent symptomatic reports. Given the complexity of the protein cascades involved with mood and psychosis regulation, the subjective retrospective endorsement of episodes of psychosis without mood symptoms doesn’t specify anything of known meaning. Thus, while as for psychotic mood disorder, the checklists for schizoaffective disorder also explain multiple findings, there is no clinical or scientific justification for the inclusion of the items that purport to define schizoaffective as a specific illness. The approach of those clinicians who aggressively stabilize their patients’ moods is to work under a presumption of psychotic mood disorder in new onset functional psychosis until proved otherwise. The only clinical pharmacologic question is what medication trials are most appropriate to maximize the probability of optimizing the patient’s function. The goal is to optimize mood stabilization, then gradually taper off antipsychotic medications, as tolerated, several months down the road, due to their malignant side effects (more later) and not adding anything. There will be some patients who will not do well and will require permanent clozapine or other antipsychotic medications to even function at a markedly subpremorbid level, but others can be stabilized and rejoin peers. Concerns have been raised that young mood disordered patients are diagnosed with ‘schizo’ prefaced illness and consequently denied a lithium trial [60, 61]. Mood disorder kindles resulting in adverse outcomes [62, 63].

THE INTERVENTION AND ULTIMATE RISE OF SCHIZOAFFECTIVE In 1933, in an American Journal of Psychiatry article entitled, “The acute schizoaffective psychoses”, Dr Kasanin, who was working under a grant to study schizophrenia, described a set of 9 cases initially diagnosed with dementia praecox or schizophrenia. Though these patients had hallucinations and/or delusions, they differed from the classic Bleulerian description of schizophrenia due to: 1. active premorbid social adjustment and acute onsets, 2. prominent mood symptoms, and 3. return to normal function following brief psychosis (weeks to months) [64]. Based on literature search for articles citing schizoaffective disorder, the diagnosis received little attention through the mid 1960s [65, 66]. Still, it was included in the DSM in 1952. Subsequent to its inclusion, there was a precipitous rise in publications about schizoaffective [66]. There has been robust debate as to the validity of Kraepelinian dichotomy versus a continuum of functional psychotic illness from worst to best prognosis. In other words, are bipolar illness and schizophrenia two separate illnesses, or is there one problem that can manifest different levels of severity? Schizoaffective offers a simple route to say both and neither, somewhere in between, and depression too. But while in concept, schizoaffective is largely thought of as a merging of schizophrenia and affective disorder, with an intermediate prognosis between the two, in practice, the term is often applied to impoverished chronically cocaine or phencyclidine exposed patients. This is partially driven by an insurance-reimbursement for hospitalization requirement to label patients with diagnoses other than psychosis or mood disorder from neurotoxic drug exposure. In fact the population of crack addicted patients labeled schizoaffective by the

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psychiatrists at one major east coast university is so high, that some residents and faculty have at times renamed the category ‘schizocrackfective’. There is ample evidence that chronic cocaine exposure is neurotoxic; where is Occam?. Part of the rationale in claiming that recurrent affective illness is diagnostically legitimate is its response to specific disease modifying drug properties. Lithium reduces the frequency and severity of recurrent mood episodes in psychotic mood disorder. There is no ‘antischizophrenia’ drug. There are only antipsychotics, which reduce psychosis; And psychosis is not disease specific. One pillar of the dopamine theory of schizophrenia (psychosis) is that the typicals’ antipsychotic potencies vary in a dose dependant manner on D2 occupancy. Specific PET demonstrates similar levels of D2 blockade (70-80% D2 occupancy) for both typical and atypical antipsychotics. But the distribution of D2 blockade is different [67-70]. The atypical antipsychotic medications show a relatively lower striatal (roughly 55% D2 occupancy) but higher temporal lobe D2 occupancy by raclopride PET studies, compared to typical antipsychotics. This might account for their different pharmacodynamic properties. Clearly, dopamine may represent a common final pathway in functional psychosis. By analogy, opiate analgesics reduce acute pain across numerous diagnoses, but other question lists, physical examination, and lab test data are required to diagnose the source of pain. Notably, while undoubtedly effective in acute pain, multiple studies have demonstrated detrimental effects of chronic opiate administration on pain control [71-73]. Some patients complain of severe pain but seem to ambulate and interact with no difficulty at all. Video cameras have caught patients receiving disability for severe joint conditions engaging in extremely strenuous activities. Similarly, some seemingly fully functional patients happily tell us that they are hearing voices and see knives flying about. We have no lab tests for pain and no lab tests for auditory hallucinations. Yet, in severely ill patients, these symptoms clearly exist. Neuroimaging studies demonstrate neural underpinnings. For instance, all studies of chronic pain show anterior cingulate activation regardless of primary source (arm, leg, gut, etc.) [65, 74-80]. And fMRI studies of humans diagnosed with schizophrenia indicating with button presses the onsets and offsets of perceived auditory hallucinations show temporal lobe speech area activation [81]. Though still in the experimental stages, transcranial magnetic stimulation timed to decrease activity in Wernike’s area decreases auditory hallucination complaints in patients diagnosed with schizophrenia [82]. The connection between auditory hallucinations and L temporal lobe speech mediating regions is strong. L temporal lobe dysfunction has been identified in patients described as bipolar, schizoaffective, schizophrenic and depressed [55, 83]. Discussion in the literature raises several possible links between “schizoaffective disorder” (SAD), schizophrenia, and mood disorders. We assessed a fairly large sample of articles (N=257) which weighed in on the differential diagnosis of functional psychosis. Based on our interpretation of the author’s conclusions, we assigned each article to one of the following five categories: [1] SAD = schizophrenia, [2] SAD = continuum/heterogeneous, [3] SAD = mood disorder, [4] SAD = separate disease, or [5] inconclusive/ambivalent. We submit that the author’s diagnostic and not their scientific impressions likely mediated their differences of opinion since groups generally agree about findings. But two groups could report a set of genetic testing results that show the greatest number of abnormalities in schizophrenia followed by schizoaffective, then bipolar I, and the first group could say this

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suggests that schizoaffective is schizophrenia, while the other group could say that those findings are consistent with schizoaffective’s being a distinct disease. It might best serve patients to consider functional psychosis as [1] a severity marker for hereditary affective illness, or [2] an extremely rare debilitating syndrome characterized by early childhood aloofness, gradual peri-adolescent mood decline, subacute withdrawal, then disorganization, and subsequently a persistently much lower level of functioning. Some might agree to this, but insist on calling syndrome 2 schizophrenia. The problem with the term ‘schizophrenia’ is that treatment courses and outcomes, and family and patient expectations are very different for ‘schizophrenia’ versus the indistinguishably presenting psychotic depression. The two diagnoses compete for the same presentation. The opportunity cost of not treating the possible mood component far exceeds problems with not diagnosing nonaffective psychosis.

UNRELIABILITY The relative merits of various semantic options depend, to some degree, on their reliability. The DSM was largely developed as a research tool so separate groups who study the same disease category would be studying similar patients. This says nothing about validity (truth), only whether different diagnosticians will agree. Clinicians cannot agree about who has schizoaffective disorder [84-86]. Volmer-Larsen et al (2006) used a checklist based diagnostic algorithm and two psychiatrist reviewers to reevaluate all cases (N=59) discharged with a diagnosis of schizoaffective in 2002 from two university hospitals in Copenhagen. Reevaluation diagnoses were allocated by algorithm results and crossvalidated by reviewer consensus. None met DSM-IV life-time criteria for schizoaffective disorder [87]. Maj et al (2000) reported that while Cohen’s kappa inter-rater reliability for DSM-IV items defining a manic episode were .71, and for a major depressive episode .82, it was .22 for schizoaffective disorder [88]. Reduction in severity and frequency of affective episodes with appropriate pharmacotherapy can be demonstrated. Thus, in identifying affective psychotic episodes, reliability translates in a very real way to outcomes for patients, regardless of the validity of attached semantics. But the ‘schizoaffective’ diagnosis cannot be reliably identified. Furthermore, it offers nothing but the opportunity cost of not treating mood, violating ‘do no harm.’

PSYCHOSIS AS SEVERITY For now, it makes sense to use psychosis as a severity modifier. By analogy, respiratory failure occurs across a variety of different pneumonias, which are labeled ‘pneumonia’ until an organism is grown from a sample, at which time the disease receives a more specific label like ‘Klebsiella pneumonia’. But the respiratory failure aspect relates to severity, and requires non-specific care across the etiologically different pneumonias. Specific antibiotics attack infection based on antibiotic susceptibility testing. Patients are weaned from ventilator as soon as possible due to the malignant effects of being ventilated. Similarly, psychosis is nonspecific and requires treatment with antipsychotic medications across the variety of causes

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(cocaine induced, dementia associated, affective, etc.); And the parallel goal is limiting exposure to toxic but necessary, acutely-stabilizing antipsychotic medications. The long term SE profiles for neuroleptics are considerably worse than for mood stabilizers, though lithium is much less safe in noncompliant patients due to its narrow therapeutic window. The underlying cause of psychosis dictates the long term plan. Cocaine dependence requires substance use therapy. Cocaine immunization to prevent it’s crossing the blood brain barrier may someday be available [89-91]. Alzheimer’s medications may temporarily delay further cognitive decline [92, 93]. Mood stabilizing/antidepressant/anti-anxiety medications are titrated to optimally regulate mood and prevent reemergence of psychosis [94]. Since the vast majority of schizophrenia diagnosed patients enrolled in studies have been chronically ill, it is possible that highly kindled mood disorder accounts for their chronic psychosis. There is no way to know. Multiple studies using a variety of outcome measures show a spectrum of disease severity by diagnostic group: affective psychosis is best, schizoaffective intermediate, and schizophrenia worst prognosis. For affective disorders, the DSM-IV uses psychosis as a severity modifier only, but psychosis serves as diagnostic criteria for schizoaffective and schizophrenic illness. Some might argue that the question of diagnostic labels is purely semantic. But it is not since semantics dictate treatment. It is hard to imagine psychotic transformation without mood disturbance. Both depression [95-98] and sleeplessness heralding onsets and exacerbation of psychosis are described in schizophrenia [99, 100]. This alone indicates that schizophrenia researchers disbelieve the Kraepelinian dichotomy. Some might legitimately object to the notion of eliminating the use of ‘schizo’ prefixed terms based on so-called “negative syndrome” schizophrenia: patients with lower intellectual capacity who are aloof and odd as children, then become progressively more constricted in late adolescence, then exhibit stable constricted disorganization as adults. Schizophrenia might seem an appropriate term for these very rare negative syndrome patients. And negative syndrome schizophrenia has shown higher concordance than positive syndrome in monozygotic twins [101, 102]. For such cases, the diagnosis ‘Psychosis NOS’ seems most appropriate. Ongoing review of the history and search for organic factors is indicated. Past depressive episodes may be hard to identify when superimposed on adolescence, a time of rapid brain change and expected mood fluctuation [56]. A difficult process of sequential pharmacologic trials seeking optimal stabilization should be undertaken. The bottom line is that, in reality, broad application of the term schizophrenia to both positive and negative syndrome patients often undermines assiduous pursuit of target mood symptoms. This harms patients.

GENETICS Concordance for psychotic illness (schizophrenia diagnosis) in monozygotic twins is high (50-80%), but not 100% [103-106]. Most diagnosis heritability studies show that mood disorders in first degree relatives of schizophrenics are more common than schizophrenia is in relatives of patients with mood disorders. Studies show a mixture of both in the relatives of so-called “schizoaffective” probands [107, 108]. Genetic studies could help sort this out. The human genome has been sequenced and a search for the genetic causes of functional psychosis is under way. However psychiatric genetics faces unique difficulties. Unlike

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families with Huntington’s disease that all show the same, single abnormality, families with multiple functionally psychotic members show a variety of genetic abnormalities. Not only do gene-abnormality profiles vary across different families, but there are often multiple different psychiatric diagnoses within individual families − and even within individual family members. Many groups have found genetic overlap in bipolar and schizophrenia [109-118]. Others have reported that all three diagnostic categories (schizophrenia, schizoaffective, bipolar) share genetic susceptibility loci [119, 120]. The presence in one person of more than one susceptibility locus may cause a multiplicative susceptibility effect [121]. Valles (2000) reported that an increased number of bipolar-diagnosed relatives was associated with increased diagnostic rates for schizophrenia in a family [122]. Valles and others suggest that psychosis is “a non-specific indicator of illness severity” and that “it may be useful to consider the combined findings [about heritability] in a framework of a ‘continuum of severity’.” Ketter (2004) conclude there is “a broad genetic vulnerability to psychosis in general” rather than specifically to schizophrenia or bipolar disorder [123]. Torrey et al 2005 examined 100 candidate RNA, protein and other neurochemical markers in 60 brains post mortem (15 controls, 15 schizophrenic, 15 bipolar, 15 non-psychotic depression). Abnormalities in bipolar and schizophrenia overlapped 65% [124]. DISC1 (disrupted in schizophrenia 1) is one example of a genetic abnormality associated with psychosis [125-127]. DISC1 was first identified in a large Scottish family with a chromosomal abnormality that segregated with mental illness. Mental illness was defined broadly and included schizophrenia, schizoaffective disorder, recurrent major depression, adolescent conduct disorder, and emotional disorders [128]. None of the normal karyotype family members carried a psychiatric diagnosis. In mice, DISC1 is involved with two critical brain development periods: [1] E13.5, consistent with neurogenesis and neuronal migration, and [2] postnatal at P35 consistent with onset of puberty [129]. DISC1 abnormalities have been linked to abnormalities in verbal working memory and P300 amplitude reductions. A number of key central nervous system proteins have been linked to DISC1 leading to “the concept of the DISC1 pathway in normal and disturbed brain development and function” [125]. One wonders if DISC1 pathway derangements play a role in the prodromal mood episodes of DISC1 mutant patients who subsequently become psychotic. Since they point to more reliable diagnoses, and thus pave the way for more appropriate treatments, strides in genetic research are encouraging. One obvious question is, if there are valid markers, why are we employing an extraneous diagnostic terminology at all? That is, if genetic cluster A responds to drug AA, who needs irrelevant labels like schizophrenia, schizoaffective, depression, or bipolar? The answer is that not only is the genetic marker level currently in early investigational stages, but since concordance for psychotic illness is less than 100% in monozygotic twins, the genes are not the disease. Someday genetic profiles will likely demonstrate who is vulnerable to severe functional psychotic disease, and which specific (hopefully benign) supplements or other therapies will prevent it. Until then, the semantics matter, and the use of affective labels for almost all functional psychosis would optimally serve patients. Though some patients would get and fail a lithium trial, many patients who now suffer disabling disease kindling would be helped−possibly even saved from ever experiencing psychosis.

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BRAIN MAPPING Rather than trying to cover fMRI, PET and other imaging modalities, our discussion will focus mainly on evoked response potential (ERP), the oldest and best-established brain mapping technique. ERPs are brainwave measures generated by averaging many brain responses to the same stimulus type. The term "endophenotype", meaning a subtle vulnerability-associated brain processing abnormality, has been applied to brainwave findings that differentiate psychiatrically diagnosed versus control groups. A discussion of ERP findings in “schizoaffective” disorder is necessarily a discussion of findings in schizophrenia since most work has been done with patients carrying that diagnosis. Furthermore, “schizoaffective” fell under the schizophrenia section in the original DSM and remains there in the DSM-IV. Thus many studies lump so-called “schizoaffectives” together with schizophrenics in a combined group which is then compared with a control group [130-136]. The most common ERP paradigm is the auditory oddball, so named because it involves a sequence of 2 tones: an infrequent ‘oddball’ tone (about 20% of stimuli), and a frequent ‘standard’ tone (80%). Subjects press a button upon detecting the oddball (target) but not the standard (non-target) tones. The oddball target P300 (“P” for positive, and “300” for 300 milliseconds or about 1/3 of a second after the target tone) is linked to the referencing of the incoming tone with temporarily stored ‘target’ and ‘non-target’ tone information (working memory). The most reported finding in psychiatric ERP research is oddball-generated target P300 amplitude reduction. Initially reported and highly replicated in schizophrenia research [137143], P300 reductions have also been reported in groups diagnosed with bipolar [137, 144], acute mania [143], depression [145-147], PTSD [148-150], alcoholism [151, 152], antisocial personality [152-154], borderline personality [155, 156], and OCD, as well as in relatives of manic depressive probands [157]. The New York High-Risk Project gathered auditory oddball ERP data at mean age 15 and diagnostic measures at mean age 25 from offspring of the following three groups: schizophrenic disorder N=24, affective disorder N=26, and normal N=70. Reduced P300 amplitude at mean age 15 associated with worse Global Personality Function at mean age 25 for subjects from both the schizophrenic and affective parental groups versus the control parental group. Unlike the P300 which depends on factors involved with consciously manipulating information, the earlier P50 brain response is considered ‘automatic’. Gating refers to the relative reduction in ERP component amplitude, in response to the second versus the first of two proximate stimuli. The standard method to elicit P50 gating is to administer sets of paired clicks (1/2 second apart) with about 8 seconds between serial pairs. Normal 'gating' is considered around a 70% reduction in amplitude of the second click's P50 versus the first. Gating is thought to mirror circuitry normally responsible for ignoring irrelevant sensory input, like background noise. Reduced P50 gating was first described as an endophenotype for schizophrenia and has since been reported in bipolar, and PTSD diagnosed patients [158] [ [159-161]. Due to poor signal to noise ratio (the P50 is often not much larger in amplitude than many people’s ‘background’ alpha rhythm), reliability for P50 gaiting is good only within a few labs. Still, although many labs cannot demonstrate P50 gating, it does exist; Just like the auditory

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oddball, P50 gating has been demonstrated with intracranial electrodes in surgical epilepsy patients. MEG, the magnetic cousin of EEG might someday solve the poor signal to noise ratio problem from which P50 gating suffers. Lu et al (2007) demonstrated reduced M50 (magnetic P50) noise with MEG versus EEG [162]. A specific allelic variation in a region coding a promotor for the alpha-7 acetylcholine nicotinic receptor on chromosome 15 (CHRNA7) has been associated with P50 gating suppression. As well, that smoking normalizes P50 gating-reduction in schizophrenia diagnosed subjects has been linked to abnormalities in the alpha-7 nicotinic receptor. Martin et al (2007) studied the association of CHRNA7 allelic promotor variants with abnormal P50 gating in patients diagnosed with bipolar-type schizoaffective disorder. Data previously obtained from schizophrenia-diagnosed and control subjects were used for group comparisons. Subjects with diagnosed schizophrenia, regardless of allele status, demonstrated abnormal gating. But in both schizoaffective and control subjects gating was variant dependant. The authors concluded that “in persons with bipolar type schizoaffective disorder, CHRNA7 promoter region allelic variants are linked to the capacity to inhibit the P50 auditory evoked potential and thus are associated with a type of illness genetically and biologically more similar to schizophrenia,” though their results show parallels between gating-variance dependance in the schizoaffective and control groups, distinct from the schizophrenia diagnosed group. Mismatch Negativity (MMN) is an ERP measure reflecting automatic environmental change detection [163]. Hall et al (2007) gathered P300, P50, and mismatch negativity (MMN) from 10 monozygotic twins discordant for bipolar illness, six monozygotic twins concordant for bipolar illness, and 78 control twin pairs [144]. Results showed reduced P300 and P50 gating, but no MMN difference in bipolar patients. That this study shows P50 reduction in bipolar diagnosed but not their very close relatives, while another study, cited above, showed P50 reduction in relatives of bipolar probands, speaks to the difficulty with this technique. Unlike the P50, a different ERP measure - N100 - shows its changes clearly to the naked eye. Furthermore, the N100 is barely detectable in 5-6 year olds and steadily and markedly deepens with increasing age through around 18 years old. In schizophrenia diagnosed patients, decreases in N100 are as robust as the changes in P300. Were high-risk children routinely tracked, it is possible that N100 amplitude trajectories would be found to fall off normal growth curves. One could hypothesize that the N100 changes would be coincident with the dysthymic/depressed/withdrawn episodes and/or the anxiety/sleep-disturbance episodes that usually precede obvious frank psychosis. We should note that a teenager acting ‘moody’ for a couple weeks does not constitute an affective episode. However, a significant interruption in normal development might be suspected in a teen who is uncharacteristically ‘moody’ or withdrawn, and has a newly abnormal ERP marker (e.g. age-specific N100 amplitude drops by one standard deviation). When normative data become available, and atrisk children are routinely tracked, the goal of early intervention may become a reality. P50 gating (and P300 reduction) may someday prove to be non-specific markers for susceptibility to develop whatever more specifically runs in the family. As with genetic studies, the most-replicated ERP findings in schizophrenia research were subsequently sought and found in groups carrying other diagnoses including bipolar, depressed and “schizoaffective”. Also, similarly to genetic markers, some ERP measures may differentiate schizophrenia versus bipolar diagnosed groups. That would be an expected result from

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comparing highly kindled versus stabilized affective psychosis groups. Since longitudinal studies that could differentiate malignant versus expected changes over time have not been performed, it is not yet known whether candidate 'endophenotypes' have predictive value. Several high-risk (to develop schizophrenia) studies have followed families with schizophrenia-diagnosed parents [164-167]. Were normative data available and P300, N100, MMN and P50 measures gathered, relationships between endophenotypes and developing psychosis might have been delineated. Over 20 years ago, Roth et al asserted that "it remains to be determined to what extent [P3 amplitude reduction] reflects a global impairment, regardless of specific clinical state or diagnosis, and to what extent it reflects specific symptomatology or disorder subtype." This is still the case.

RESEARCH STRENGTHS AND PITALLS It has been argued that since the diagnosis of schizophrenia is itself questionable, the research conclusions in schizophrenia are invalid. That is not the case. The more basic research is, the more broadly it can be applied. Substituting the word “psychosis” for the word “schizophrenia”, it becomes clear that the groundwork to optimally treat, and someday prevent, functional psychosis has been laid. Meaningful measures like the oddball target P300, N100, P50 gating, and MMN, have been well enough characterized that it is evident that they should be gathered on a large scale to define population norms. The pitfall is that translating basic findings from benchside to bedside cannot be accomplished without logical diagnostic terminology. It is instructive to note that the nature of chest pain is completely non-diagnostic for myocardial infarction, but troponin is. Patients with auditory hallucination complaints (AH) are an unequivocal group. They are undoubtedly complaining of hearing voices. Then, those with abnormal baseline Wernike’s activation by fMRI could be identified as Wernike’s Activation + AH patients (WAH), and that actually means something as opposed to ‘schizoaffective’ or ‘schizophrenia’. Patients with explosive aggression undoubtedly have that. Holes in walls prove the point. But considering that aggressive children are labeled ‘ADHD’ and increasingly labeled ‘bipolar’, those words in children tell a person nothing about those labeled. Freud initially had a neurobiological bent, but became frustrated. Like Bleauler and Kaepelin, Freud’s crossectional descriptions of behavior were on the money, but etiologic arguments were off base. His thought that major psychotic illness was a consequence of oral stage fixation illustrates the need to stay with neurobiological pathways. Still, around the age of one, maximal synaptic density is achieved, followed by successive waves of synaptogenesis and larger scale synaptic reduction, thus, Freud was correct in noting critical developmental stages for future vulnerability to mental illness. Notably, there is a vast change in brain architecture around the time of malignant psychiatric transformation in functional psychosis, and under influence of the same hormones that effect puberty. The term ‘pruning’ has been applied to the 40-60% reduction in synaptic connections that progresses from back (visual cortex) to front (auditory/verbal cortex) from about the ages of 10 through 25 [168]. Prodromal affective symptoms are described during this time frame, and late-pruning auditory cortical dysfunction and functional psychosis associate [169].

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Woods et al (2003) recently assessed a large number of local teenagers who responded to adds targeting teens experiencing perceptual disturbance symptoms [170]. Subjects were randomized to olanzapine versus placebo arms. Results did not show strong efficacy, but weight gain was very problematic. Still, the feasibility of studying earlier brain changes and attempting primary prevention was demonstrated. The key weakness might have been that subjects were not preselected for positive family histories of psychosis. Computer modeling has been used to explore the effects of pruning [171]. Reducing connections between two input/output structures improved the efficiency of a neural network tasked with using a limited set of words to form sentences. However, over pruning inserted words and neologisms where the rule set dictated pauses [171, 172]. Progress in schizophrenia research has laid the foundation to pursue a logical roadmap towards optimal neuroprotection. NMDA receptors, calcium channel-associated glutamate receptors subserving biochemical memory formation, play a key role in psychosis associated neurotoxicity. Adults but not children manifest psychotic reactions to NMDA blockers. That is why ketamine is routinely used in pediatric but seldom in adult medicine. Parallel time courses for NMDA-blocker induction of psychosis and endogenous functional psychosis has led to the glutamate hypothesis [173-176]. Excitotocicity, or free radical formation resulting from the leakage of high energy electrons along the electron transport chain associated with glutamatergic dysfunction, is the primary neurotoxic process implicated in functional psychosis. There is, by most counts, hippocampal cell loss, but no gliosis (scarring) in postmortem brains from functional psychosis patients [177-183]. What is suggested is an early migrational abnormality which subserves mood disorder followed by malignant psychotic transformation in a percentage of those affected. Excitotoxicity and associated apoptosis (programmed cell death) are the only known mechanisms yielding agliotic neuronal cell loss. NMDA blockade induced excitotoxicity in animal models is reduced by preapplication of D2 blocking drugs, and those atypicals tested demonstrated an approximately 2:1 increased experimental neuroprotective effect [184-187]. Lithium frustrates excitotoxicity in animal models as well [188-197]. Decreased superoxide dismutase blood levels (free radical scavenging capacity) has been demonstrated in new onset functional psychosis [24]. Cytochrome C in the electron transport chain shares a key role in both generation of free radicals in excitotoxicity and as an obligate docking site for apoptosis mediating proteins [198-207]. Thus, excitotoxicity and apoptosis are directly linked. In fact, it is because cell loss in excitotoxicity is apoptosis mediated that scarring does not occur. Tracking at risk groups through the pruning period is clearly indicated. Our question is, in light of the mood disorder that precedes psychotic break by years, and the demonstration of lithium’s neuroprotective effects against excitotoxin damage, shouldn’t we be asking if treating the prodrome could prevent the subsequent need for antipsychotic medications? Children’s head circumferences, weight, and height are routinely measured and plotted on standardized growth curves. Rapidly changing percentiles in these parameters clue clinicians to developing problems, allowing further investigation and early intervention. There are cheap, valid, and readily available methods to measure attention and auditory cortical development [208-213]. In the audiology literature, small but adequately powered studies have shown a vast change in a standard auditory-evoked-potential (AEP) measure which can be seen very clearly with the naked eye [211-219]. Yet normative data have not

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been gathered to allow the same ‘growth curve’ type of measurements that are done for pediatrics to be done for psychiatry. Rather, the vast majority of psychiatric research continues to focus on chronically ill adult patients who have been medicated for years and are diagnosed with schizophrenia. Resources must be allocated towards following large samples who have yet to develop disease and away from studying functional abnormalities in already diagnosed patients. That would gather normative data and track changes heralding malignant transformation. In other words, clinically useful lab tests should be developed. The genetic testing of multiply effected families yields critically important information. But, again, the yet undiagnosed children in these families must be tracked with functional measures. In high risk studies, approximately 20 percent of male and 10% of female offspring develop disease. That is a high percentage, and if population norms were delineated, prospectively following a large number of high risk children with a battery of brain measurements should allow the assessment of prodromal stabilization and primary prevention of psychosis. But before progressing from benchside to bedside, the pitfall of employing diagnostic terminology whose seminal concepts predate biological pathway considerations must be overcome. When we study problems like aggression, depression, psychosis, and kindling, we will develop the means to determine initial treatment and monitor treatment response in psychiatry as is the case for the rest of medicine, with meaningful lab tests.

CONCLUSION There is a clinical concept that in susceptible patients, dysregulated mood leads to psychosis. And instability begets worse future instability. One consequence of the existence of ‘schizo’ prefaced diagnoses is diminished efforts to regulate mood. Resultant kindling of psychotic mood disorder and associated neurotoxicity may thereby yield the clinical picture of persistently low functioning. That is, untreated or badly responding psychotic mood disorder ends up looking like classically described schizophrenia. Peri-adolescence appears to be a critical period of vulnerability, though there are features including genotypes that could be identified very early. Definitive tests unequivocally identifying patients’ illnesses will someday eliminate the ‘risk/benefit’ ratio assessment of applying a label. Early stabilization of psychosis is essential, as psychosis is a toxic state. Prevention of recurrence is essential as well. Many already chronically ill patients will likely require permanent stabilizing neurolepticization. It is not known in how many of them mood stabilization would have been neuroprotective. And the linearity of the process is unknown- it may be that preventative strategies through the pruning stage would completely eliminate the need for later treatment. Labels that emphasize basic description, like acute, subacute, chronic, and psychosis, mania, and depression leave open the door for further exploration: ie: 1. “why is he depressed?”, or 2. “why is she psychotic?”. 3. “why is he manic?” [does he need an inpatient drug rehabilitation?]. But the labels schizophrenic and schizoaffective do not lead to the question, “why is he schizophrenic?”, and “why is she schizoaffective?”. In a high paced world, “schizo” prefaced labels translate directly into chronic neurolepticization. The literature suggests that in a large number of functionally psychotic patients, diligently stabilizing mood could decrease long term impairment. One clinical strategy is to

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aggressively pursue mood stabilization and then gradual reduction of neuroleptics over many months while educating the patient and family about mood disorder, psychosis in mood disorder, evidence of recurrence, and an appropriate temporary adjustment in stressful life activities. Many patients who’ve had functionally psychotic episodes function normally for years on lithium. Removal of the meaningless and malignant ‘schizoaffective’ label would help rekindle the lithium trial.

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[157] Pierson, A., , Information processing deficits in relatives of manic depressive patients. Psychol Med, 2000. 30(3): p. 545-55. [158] Freedman, R., , The genetics of sensory gating deficits in schizophrenia. Curr Psychiatry Rep, 2003. 5(2): p. 155-61. [159] Hong, C.J., , Association study of the human partially duplicated alpha7 nicotinic acetylcholine receptor genetic variant with bipolar disorder. Neurosci Lett, 2004. 355(1-2): p. 69-72. [160] Schulze, K.K., , P50 Auditory Evoked Potential Suppression in Bipolar Disorder Patients With Psychotic Features and Their Unaffected Relatives. Biol Psychiatry, 2006. [161] Olincy, A. and L. Martin, Diminished suppression of the P50 auditory evoked potential in bipolar disorder subjects with a history of psychosis. Am J Psychiatry, 2005. 162(1): p. 43-9. [162] Lu, B.Y., , Improved test-retest reliability of 50-ms paired-click auditory gating using magnetoencephalography source modeling. Psychophysiology, 2007. 44(1): p. 86-90. [163] Ford, J.M., W.T. Roth, and B.S. Kopell, Attention effects on auditory evoked potentials to infrequent events. Biol Psychol, 1976. 4(1): p. 65-77. [164] Mednick, S.A., A longitudinal study of children with a high risk for schizophrenia. Ment Hyg, 1966. 50(4): p. 522-35. [165] Mednick, S.A. and T.F. McNeil, Current methodology in research on the etiology of schizophrenia: serious difficulties which suggest the use of the high-risk-group method. Psychol Bull, 1968. 70(6): p. 681-93. [166] Mirsky, A.F. and C.C. Duncan, Pathophysiology of mental illness: a view from the fourth ventricle. Int J Psychophysiol, 2005. 58(2-3): p. 162-78. [167] Mirsky, A.F., , Adult outcomes of high-risk children: differential effects of town and kibbutz rearing. Schizophr Bull, 1985. 11(1): p. 150-4. [168] Huttenlocher, P.R. and A.S. Dabholkar, Regional differences in synaptogenesis in human cerebral cortex. J Comp Neurol, 1997. 387(2): p. 167-78. [169] Feinberg, I., Schizophrenia: caused by a fault in programmed synaptic elimination during adolescence? J Psychiatr Res, 1982. 17(4): p. 319-34. [170] Woods, S.W., , Randomized trial of olanzapine versus placebo in the symptomatic acute treatment of the schizophrenic prodrome. Biol Psychiatry, 2003. 54(4): p. 45364. [171] Hoffman, R.E. and T.H. McGlashan, Synaptic elimination, neurodevelopment, and the mechanism of hallucinated "voices" in schizophrenia. Am J Psychiatry, 1997. 154(12): p. 1683-9. [172] Hoffman, R.E. and S.K. Dobscha, Cortical pruning and the development of schizophrenia: a computer model. Schizophr Bull, 1989. 15(3): p. 477-90. [173] Krystal, J.H., , NMDA receptor antagonist effects, cortical glutamatergic function, and schizophrenia: toward a paradigm shift in medication development. Psychopharmacology (Berl), 2003. 169(3-4): p. 215-33. [174] Abi-Saab, W.M., , The NMDA antagonist model for schizophrenia: promise and pitfalls. Pharmacopsychiatry, 1998. 31 Suppl 2: p. 104-9. [175] Olney, J.W. and N.B. Farber, Glutamate receptor dysfunction and schizophrenia. Arch Gen Psychiatry, 1995. 52(12): p. 998-1007.

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In: Schizoaffetive Disorders Editor: Kam-shing Yip

ISBN 978-1-60456-948-3 © 2009 Nova Science Publishers, Inc.

Chapter 5

NEUROPSYCHOLOGICAL DEFICITS IN SCHIZOAFFECTIVE DISORDER Barton W. Palmer* and Gauri N. Savla University of California, San Diego, Department of Psychiatry 3350 La Jolla Village Drive, 116A-1, San Diego, CA 92009, USA

INTRODUCTION As reflected in the World Health Organization’s (WHO) International Classification of Diseases (ICD-10) [1] and the American Psychiatric Association’s (APA) Diagnostic and Statistical Manual (DSM-IV-TR) [2] the focus in diagnosis of schizoaffective disorder, as well as its treatment, is on the presence of affective and psychotic symptoms. By contrast, neuropsychological deficits are not generally among the first characteristic which comes to mind when thinking about schizoaffective disorder. Nonetheless, as with schizophrenia, a majority of persons with schizoaffective disorder exhibit mild-to-moderate neuropsychological deficits [3-8]. These neuropsychological deficits may have a deleterious effect on everyday functioning beyond the effects of primary psychopathology, and thus represent potentially important, albeit traditionally ignored, targets of primary intervention [9, 10]. In the following pages we provide an overview of neuropsychological functioning in schizoaffective disorder in terms of conceptual history, contemporary findings regarding neuropsychological deficits in schizoaffective disorder, and the relationship of neuropsychological deficits to level of everyday functioning. We also consider the effects of treatment on neuropsychological deficits in schizoaffective disorder, including recent efforts to develop pharmacologic and psychosocial (cognitive rehabilitative) interventions that directly target the neuropsychological deficits associated with psychotic disorders.

*

Email: [email protected]

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HISTORICAL CONSIDERATION Origin and Controversies of the Construct of Schizoaffective Disorder The distinction between schizophrenia and mood disorders is generally traced to Kraepelin’s division of dementia praecox from what he labeled ‘manic-depressive insanity’ [11, 12]. Descriptions of persons whose symptoms involved a combination of the two syndromes were published virtually simultaneously with Kraepelin’s efforts to distinguish the two conditions (e.g. see Dunton [13]). Kraepelin [14] acknowledged the existence of patients with a mixture of such symptoms, but generally held that a distinction could be drawn based on course and outcome of the condition. In particular he posited that dementia praecox was characterized by a pattern of progressive deterioration versus a more benign course and outcome characterizing affective disorders [15, 16]. (As discussed below, subsequent evidence suggests that the typical long-term course of schizophrenia is more stable than Kraepelin initially believed.) Although its conceptual roots are even older [16-18], the term “schizoaffective” was introduced in 1932 by Kasanin [19] when he described a series of cases of persons evidencing what he labeled “acute schizoaffective psychoses.” Kasanin did not provide a detailed description of cognitive functioning among these patients, but he did note that each had average or superior intelligence, and that intellectual functions were “intact” during the clinical mental status examinations. The patients were also noted to have good premorbid psychosocial functioning, with acute onset. This relative sparing of intellectual functions, as well as the acute (rather than insidious) onset stood in contrast to what Kasanin and Bowman [20] contemporaneously described as “constitutional schizophrenia,” the latter resembling more recent descriptions of “ “type II” or deficit syndrome: schizophrenia [21, 22]. Contemporary diagnostic criteria for schizoaffective disorder emphasize the prominence and pattern of schizophrenic and affective symptoms [1, 2], rather than the acute onset or longterm course, so the degree to which the syndrome described by Kasanin actually overlaps with the contemporary concept of schizoaffective disorder is unclear. The concept of schizoaffective disorder has been controversial from its inception [16, 23]. For instance, in 1936, Hunt and Appel [24] stated, “As to the actual existence of this mixed group of schizo-affective or thymo-phrenic psychoses there can be no doubt” (p. 314), whereas one of the discussants for the same paper (whose comments were included at the end of the published manuscript) asserted “though the symptoms of manic-depression and of schizophrenia may blend, the roots are different” (p. 337). Today, there remains little disagreement that some patients present with a mixture of symptoms of schizophrenia and mood disorders, but there remains considerable debate and uncertainty regarding whether schizoaffective disorder is a distinct condition, a variant of schizophrenia, or a variant of psychotic mood disorders [7, 23, 25]. The appropriate grouping of schizoaffective disorder may also depend on subtype (bipolar or depressed) [26]. There are also suggestions that a categorical nosology is fundamentally flawed, and that a multidimensional model might have better construct validity and clinical/research heuristic value [11, 27, 28].

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Historical Considerations of Schizophrenia as a Neurocognitive Disorder The historical view of neurocognitive impairment in schizophrenia has itself had a long and circuitous history. Kraepelin [14] described dementia praecox as involving impairment in “volition” and “will,” and Zec [29] has made an cogent argument that Kraepelin’s views very much parallel contemporary descriptions of schizophrenia as a disorder of executive functions. Kraepelin [14] also suggested that dementia praecox was associated with neuropathology in the frontal, as well as the temporal brain regions, writing, “If it should be confirmed that the disease attacks by preference the frontal areas of the brain, the central convolutions and the temporal lobes, this distribution would in a certain measure agree with our present views about the site of the psychic mechanisms which are principally injured by the disease. On various grounds it is easy to believe that the frontal cortex, which is specially well developed in man, stands in closer relation to his higher intellectual abilities…On the other hand, the peculiar speech disorders resembling sensory aphasia and the auditory hallucinations, which play such a large part, probably point to the temporal lobe being involved” (p. 219).

Together with the cortical-subcortical connections, the frontal and temporal regions remain among the areas and systems of primary focus in contemporary neurophathological models of schizophrenia [30-35]. Despite the initial momentum toward a neurocognitive model of schizophrenia provided by Kraepelin’s descriptions of dementia praecox, and consistent psychometric reports documenting the frequency of intellectual/cognitive impairments among persons with schizophrenia [36-41], the first half of the 20th century included considerable debate regarding psychogenic versus biological (“organic”) models of schizophrenia [39, 42-44]. Through the late 1960s, there was a tendency among some researchers and clinicians, at least within the United States, to interpret deficient performance on neuropsychological tests by patients with schizophrenia and other “functional psychosis” as reflecting deficits engaging in the tasks (due to symptoms and motivation) rather than reflecting the genuine neurocognitive dysfunction associated with “organic” dysfunction [38, 45, 46]. The “functional” versus “organic” argument faded in the last third of the 20th century with the rise in biological psychiatry and cognitive neuroscience, as well as accumulating evidence that patients with “functional psychoses” had neurocognitive deficits that were often indistinguishable from those with documented “organic” brain injuries [38, 45].

CONTEMPORARY FINDINGS ON NEUROPSYCHOLOGICAL ASPECTS OF SCHIZOAFFECTIVE DISORDER Neuropsychological Deficits in Schizoaffective Disorder and Schizophrenia The historical and ongoing controversy regarding the concept of schizoaffective disorder has substantially influenced the neuropsychological literature on this condition. In particular, the vast majority of neuropsychological studies in which patients with schizoaffective disorder have been examined as a group distinct from schizophrenia were focused on

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evaluating the validity of that distinction from a neurocognitive perspective [3-8, 26, 47-56]. The findings from such studies are consistent in showing that the level, pattern, and frequency of neuropsychological impairment among patients with schizoaffective disorder are indistinguishable from those seen in patients with schizophrenia [4, 5, 7, 8, 48, 51-54]. A few studies have found isolated group mean differences between schizoaffective versus schizophrenia patients on specific neurocognitive test scores [3, 50, 55, 56], but such differential impairment findings generally emerged from post-hoc analyses (rather than as confirmation of specific a priori hypotheses) within the context of many non-significant neurocognitive differences between the two groups. No clear pattern of consistent differences on any particular cognitive ability emerged across studies. Moreover, schizophrenia and schizoaffective patients show similar impairment in mean neuropsychological performance relative to healthy controls [3, 7, 47, 51, 57, 58], and with isolated exceptions [56] relative to those with bipolar disorder [51, 58] and/or unipolar depression [5, 51, 54]. In part due to relatively small subgroup sample sizes, most of the studies comparing neuropsychological performance of patients with schizoaffective disorder to those with schizophrenia have emphasized whole groups, rather than subtype analyses (such as depressed versus bipolar subtypes of schizoaffective disorder, and/or standard schizophrenia subtypes). However, there is some evidence those persons with schizoaffective disorder and those with paranoid subtype of schizophrenia may, on average, have slightly better neuropsychological performance than those with undifferentiated or disorganized subtypes of schizophrenia [6, 47]. Indeed, one of the rationale for considering schizoaffective disorder as a subtype of schizophrenia, at least from the perspective of neuropsychological data, is that there exists at least as much heterogeneity within the standard category of schizophrenia as between schizoaffective disorder and schizophrenia. Because of such considerations, many of the neuropsychological studies of schizophrenia include and combine patients with schizoaffective disorder within the schizophrenia group [59].

Severity and Prevalence of Neuropsychological Deficits As true with virtually every dimension of schizophrenia and schizoaffective disorder, even within the traditional clinical subgroups, there is substantial within-group heterogeneity in terms of the range and pattern of neuropsychological functioning [6, 60]; the neuropsychological deficits can range from minimal to severe impairment. On average, however, patients with schizophrenia evidence mild-to-moderate neuropsychological deficits across a range of more specific cognitive abilities [61-63]. Based on a comprehensive metaanalysis of 204 studies published between 1980 and 1997, Heinrichs and Zakzanis [64] concluded that 60-80% of people with schizophrenia have at least mild neuropsychological deficits. That conclusion is consistent with findings from our research group at the University of California, San Diego [60] and others [6, 65, 66] indicating that approximately a quarter of patients with schizophrenia or schizoaffective disorder retain normal range neuropsychological profiles. The degree or proportion of such persons who would have had even higher neuropsychological abilities in the absence of schizophrenia or schizoaffective disorder remains a point of controversy [65-68].

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Specific Neuropsychological Abilities and their Measurement There is no pathognomonic neuropsychological sign of schizophrenia and/or schizoaffective disorder, i.e., no pattern of neuropsychological deficits is unique to schizophrenia and/or schizoaffective disorder, nor has one been found that is common to all patients or an independently identifiable subtype [69, 70]. However, some of the most frequently impaired abilities include attention, working memory, auditory and visual episodic learning and memory, psychomotor speed, and executive functions [61, 63, 64, 71]. Comprehensive review of the multitude of neuropsychological tests used to operationalize these and other potentially relevant neuropsychological constructs, and the range of neuroantomic and neurophysiologic substrates of each, would go beyond the intended scope of the present chapter (interested readers are referred to Lezak [72] and to Sharma and Harvey [73]). Nonetheless, as the labels for neuropsychological constructs and measures are not used in a fully uniform or consistent way across all research or clinical settings, it may be helpful to consider some examples of the array of different tests used to measure a few of these more specific neuropsychological constructs.

Attention As true of the standard labels for many neuropsychological abilities, “attention” is a broad term that covers a number of more specific behaviors, subsumed by an array of different neurophysiologic processes, and the ways in which the term is used colloquially, in clinical psychology and clinical neuropsychology, and in cognitive neuroscience are not always fully synonymous [74, 75]. One skill generally included under the rubric of attention is “vigilance.” Vigilance involves maintaining “response readiness” for a particular stimulus or event [75]. An example of a vigilance task used widely in schizophrenia research is the identical pairs version of the Continuous Performance Test (CPT-IP) [76], during which the examinee must rapidly respond when he or she detects a pair of identical successive numbers during computer presentation of a series of numbers. Because first-degree relatives of persons with schizophrenia also show impaired CPT-IP performance, the latter task has been suggested as a potential endophenotype measure for use in genetic studies of psychosis [77]. Another common meaning or form of “attention” is the ability to choose or filter relevant from irrelevant stimuli. The idea that schizophrenia may be fundamentally characterized by deficits in selective attention (or “filtering”) has a long history [14, 78, 79]. One example of such a task the Digit Span Distractibility Task [80], in which the examinee is presented with two intermingled strings of digits, one spoken with a male and the other with a female voice. The task is to ignore (filter out) the man’s voice, and attend to and immediately recall the number string spoken by the woman. (This task was used in one of the early randomized clinical trails suggesting second generation antipsychotic medications might have a beneficial, albeit quite modest, effect on neurocognitive deficits [81].) It might also be noted that outside the context of clinical neuropsychological tests, there has also been considerable interest and research on pre-conscious or sensory gating mechanism in schizophrenia and related psychoses [82]. An advantage of the latter forms of measures, in addition to the fact that they target more circumscribed neurocircuits or systems, is that the measures of sensory/pre-conscious are not dependent on the patient’s conscious effort. It is therefore easier to disintangle primary attentional (or pre-attentional) deficits from the potential interference of psychotic symptoms on sustained effort. (Interested readers are

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referred to Braff and Light [82] for an excellent review of the use of such measures in schizophrenia research.)

Working Memory “Working memory” is a concept closely related to attention as well as to executive functioning; it involves the ability to hold and manipulate information in one’s mind for brief durations of time (generally on the order of seconds) while that information is processed [83, 84]. The essential form of Baddeley’s [83, 84] widely used model of working memory consists of three primary components: (a) two resource limited systems for short term storage and manipulation of auditory versus visual information (the “phonological loop” and “visuospatial sketchpad”), and a “central executive” responsible for allocation of resources between the auditory versus visual systems. The prototypic example of auditory working memory is the Digit Span task from the various incarnations of David Wechsler’s intelligence and memory scales [85]. In this task the examinee is asked to repeat strings of numbers (or increasing length) in forward order, and later in reverse order. (This forward task is sometimes describes as a meaure of “basic attention,” but it is highly correlated with the backward span task so may be more accurately described as a transient working memory task [86].) A common form of spatial working memory task used in schizophrenia research involves presenting a stimulus somewhere on a visual array, and then requiring the examinee to recall the position after a delay (with or without an intervening distracter task) [87]. There is also a spatial analogue to the Digit Span task on the Wechsler Memory Scale – Third Edition (WMS-III) [88], although there has been some debate regarding whether the Spatial Span and Digit Span tasks are fully analogous as measures of spatial and auditory working memory, resepctively [89]. As noted in a recent meta-analysis from Lee and Park [90], working memory deficits in schizophrenia are common; deficits in at least the visual form of working memory have also been reported specifically for patients with schizoaffective disorder [7, 50]. Indeed, some investigators and theorists have suggested that deficits in working memory may underlie many of the other schizophrenia-related deficits including executive dysfunction and some aspects of thought disorder [91]. Auditory and Visual Episodic Declarative Learning and Memory Although cognitive neuroscience has delineated a wider typology of memory systems, (see Squire [92]), much of the research on memory in schizophrenia has been on declarative episodic memory for auditory or visually presented stimuli, such as learning and recall of word lists, memory of story passages, and/or memory of geometric designs [93]. For example, prototypical word list learning tasks involve reading a word list to an examinee, asking him or her to repeat back as many words as he or she can recall, and then repeating that procedure over several trials to evaluate his or her ability to learn the information [9496]. Some versions include implicit semantic categories which may aid learning and recall if the examinee thinks to organize his or her learning or recall strategy in reference to semantic relationships [94, 96]. Research is quite consistent in demonstrating patients with schizophrenia often have impaired performance on tasks of episodic declarative memory [93]. For instance, in their meta-analyses of studies published between 1980 and 1997 that compared neuropsychological

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performance among schizophrenia patients versus healthy comparison subjects, Heinrichs and Zakzanis [64] found the mean effect size (corrected for sample size differences) for verbal memory was d = 1.41 (the lowest two effect sizes were Block Design, a measure of visualconstructional ability, d = 0.46, and Vocabulary, a measure of crystallized verbal ability, d = 0.53). In Fioravanti ’s [71] meta-analysis of studies published between 1990 and 2003, they also found the highest mean effect sizes in terms of memory tests, but they also noted the considerable heterogeneity in observed effect sizes between various studies It may be important to distinguish between difficulties with acquisition of new information and/or efficiency of its retrieval, from actual loss of the memory trace. To distinguish encoding, forgetting, and retrieval deficits, clinicians as well as researchers frequently compare delayed versus immediate recall scores, and free-recall versus recognition scores [97]. For instance, a substantial decline in free recall performance from the immediate to delayed recall trials may indicate “rapid forgetting”; the latter is considered a hallmark of Alzheimer’s disease [98], but is rare among persons with schizophrenia or schizoaffective disorder [62]. In that sense of the word “memory” as “forgetting”, memory tends to be relatively unaffected in schizophrenia. Of note, the latter suggestion is also consistent with Kraepelin’s [14] observations of patients with dementia praecox, as he wrote “Memory is comparatively little disordered. The patients are able, when they like, to give a correct detailed account of their past life, and often know accurately to a day how long they have been in the institution (pp. 17-18).” [Although there is limited data specifically examining savings (percent retention) for schizoaffective disorder patients separately, it appears that if anything, even fewer schizoaffective disorder patients show substantial forgetting than among patients with schizophrenia [3)].] Alemen ’s [93] meta-analysis of different types of memory test scores suggested that free-recall measures yield the largest mean effect size (overall free recall d=1.21; verbal free recall d = 1.20 to 1.22; visual free recall d = 1.00 to 1.09). The mean recognition memory effect size (patients versus healthy comparison subjects) found in Alemen ’s [93] metaanalysis was d=0.64. Although the latter is within the range traditionally labeled as a “medium” effect size [99], it contrasts with the “large” mean effect size, d=1.21, seen for free recall. Paralleling the findings of Fioravanti et al, however, Alemen noted considerable heterogeneity in the size of effect sizes observed among the individual studies.

Psychomotor Speed The term “psychomotor speed” may be conceptualized as having two primary components: (a) mental processing speed (independent of the motor requirements), and (b) efficiency of psychomotor integration (requiring translation of thoughts or intentions into action) [63]. Two of the most widely used measures of psychomotor speed the Digit Symbol task and the Trail Making Test. As noted in Boake’s [100] and Tulsky ’s [101] fascinating overviews of the origins of cotemporary of intelligence tests, the present form of the widely used Digit Symbol-Coding task [102] has undergone only minor modifications since first introduced in the early 1900s. The test consists of a series of nine numbers printed at the top of a page, each paired with a unique symbol. Below this number-symbol key, is a matrix of numbers with blank boxes below each number. The examinee’s task is to rapidly fill in the boxes below each number with the symbol that is paired with it per the key. Very rapid performance taps into visualmemory, as quick response is facilitated by learning the pairings (rather than requiring

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repeated checking of the key). However, the test is most frequently interpreted in terms of psychomotor speed. The stimuli for the Trail Making Test also have undergone relatively little modification over the past 60 to 70 years [103]. The most widely used contemporary form consists of two parts [104]. In part A, the examinee is required to rapidly connect a series of circled numbers, without lifting his or her pencil from the page, in ascending order. Part B consists of intermixed circled letters and numbers. The examinee’s task is to rapidly alternate between the letters and numbers in ascending order, i.e., drawing a line from the number 1 to the letter A, to the number 2, to the letter B, and so forth.. As the latter task requires repeated switching between two series, it is sometimes described as a test of “mental flexibility” and is thereby categorized with “executive functions.” Psychomotor speed tasks are purported to be among the most sensitive to virtually any form of neurological injury [72]. Indeed, in a recent report of a meta-analysis of schizophrenia studies employing Digit Symbol, Dickinson [105] concluded “digit symbol coding yields the largest impairment documented in the schizophrenia clinical neuropsychology literature” (p. 539).

Executive functions Pinning down a precise definition of “executive functions” is difficult. Faced with a similar challenge in a prior review of executive dysfunction in schizophrenia (see Palmer and Heaton [106]), we previously suggested the following functional description of executive skills as “those cognitive processes which permit an adaptive balance of initiation, maintenance, and shifting of responses to environmental demands permitting goal directed behavior” (pp. 63-64). We also previously noted that “abilities underlying such activities may include: search of knowledge, abstraction and planning, evaluation/decision-making skills, initiation, self-monitoring, mental-flexibility and inhibition of immediate/reflex responses in pursuit of a longer term goal” (p. 53). There is also an overlap between the construct of executive functions and working memory, in that the “central executive” aspect of working memory is itself a type of executive function [107]. The Wisconsin Card Sorting Test (WCST) [108, 109] has perhaps been the single most widely used measure of a specific neuropsychological ability in schizophrenia research [110]. This task consists of four stimulus card which vary in terms of the shape (form) of objects, the number, and the color of the depicted objects. The examinee’s task is to sort a series of cards in a deck in reference to the four stimulus cards. No information is provided to the examinee regarding the potential dimensions against which to sort, but after each response the examinee is told whether the card placement was correct or incorrect (thus, the examinee must abstract and test out different possible sorting rules). Unbeknownst the examinee, the sorting principle changes several times during the test; thus successful performance also requires him or her to be able to abandon a previously adaptive response in favor of the new implicit rule. The test yields a number of different scores, but the one most frequently examined in reference to schizophrenia is the number of “preservative responses” (reflecting a failure to adaptively switch sorting strategies) [111]. The first published study documenting that patients with schizophrenia show impaired performance on the WCST was reported over half a century ago [37]. A number of published reports have documented that patients with schizophrenia and schizoaffective disorder have equivalent impairment on this task [3, 4, 7, 48, 49].

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Another widely used “executive function” test with a long history in schizophrenia research is the Stroop task [112, 113]. There are a number of different forms of the Stroop task, but the core common component involves presenting the examinee with a series of words that refer to color names; the words are printed in ink of different colors (usually a color discordant with the content of the word), such as the word “blue” printed in green ink. The examinee’s task is to ignore the meaning of the word, and instead vocalize the name of the color of ink it is printed in. Although there is not full consensus on the precise cause of the “Stroop effect”, this task can be quite difficult because it requires inhibition of what is usually a more automatic (or quickly processed) reading response, in favor of a less automatic or habitual (and slower) color naming task demand [112, 114]. (Note, this task is sometimes categorized, perhaps appropriately as a measure of selective attention [113]. The uncertainty regarding which cognitive function under which to categorize such a widely used measure further illustrates the need to attend to the specific manner in which neuropsychological constructs are operationalized, not simply the verbal summary labels.)

Course of Neuropsychological Deficits in Schizophrenia and Schizoaffective Disorder Premorbid and Peri-onset Cognitive Deficits A wealth of data support the prevailing model of schizophrenia as a neurodevelopmental condition [110, 115-117]. Included in that support is evidence of subtle premorbid impairment in cognitive functions among some of those who subsequently develop schizophrenia or schizoaffective disorder [118-120]. For instance, Reichenberg [53] presented an interesting retrospective analysis of premorbid cognitive and behavioral data collected by the Israeli draft board (when subsequent patients were age 16 or 17 years) on persons who were subsequently developed schizoaffecitve disorder, schizophrenia, or bipolar disorder. The the patients with schizoaffective disorder and schizophrenia showed premorbid deficits relative to non-patient matched comparison persons, whereas the persons who developed bipolar disorder manfests less premorbid cognitive or behaviorl dysfunction. Bilder et al [118] estimated that approximately 60% of the cognitive deficits in schizophrenia or schizoaffective disorder accumulates during early childhood and adolescence, but they also provide evidence that a further decline in neurocognitive functioning typically occurs around the time of initial onset (“first episode”) of the psychopathologic symptoms. Long-term Course of Cognitive Deficits As noted above, Kraepelin’s view was that dementia praecox was characterized by a progressively deteriorating course of mental functioning. This pessimistic view of the longterm prognosis for schizophrenia was influential throughout much of the 20th century [121, 122]. However, a wealth of contemporary neuropsychological data reported in the last two decades has persuasively refuted that view. Among non-institutionalized individuals (who make up the bulk of patients with schizophrenia today [123, 124]), patterns of neuropsychological ability tend to stay remarkably stable even with fluctuations in severity of symptoms; this is true regardless of which specific neurocognitive abilities are examined

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[125-128]. The one exception to this generally positive and remarkably consistent finding is that elderly patients who have been chronically institutionalized appear to be at higher risk for progressive cognitive decline than expected for their age [129]. This decline does not appear to be attributable to an increased risk of Alzheimer’s disease [129].

RELATIONSHIP IN EVERYDAY FUNCTIONING Neuropsychological abilities are among the strongest predictors of functional independence in schizophrenia, such that persons with worse neuropsychological abilities tend to have lower levels of everyday functioning, e.g., in basic and instrumental activities of daily living, as well as the broader aspects of social/occupational functioning [10, 130, 131]. Neurocognitive deficits also appear to be among the strongest predictors of functional outcome among patients with bipolar disorder [132, 133]. Severity of negative symptoms is also associated with worse functional independence. However, outside the context of acute exacerbations of psychoses, severity of positive symptoms (such as delusions and hallucinations) have little discernable influence on functioning [10, 131]. Findings in regard to the relative importance of specific neurocognitive abilities as predictors of specific or overall everyday functioning are more equivocal [134]. Based on the frequency with which specific neuropsychological abilities have been reported as significant correlates of specific components of everyday functioning, there had been some suggestions that verbal episodic and working memory, certain executive functions, and/or certain aspects of attention/vigilance might be particularly important for certain types of independent functioning and community outcome [10]. Although such differential relationships seem likely from a rational viewpoint, efforts to empirically document differential relationships are hampered by the multifactorial nature of most neuropsychological tests [135, 136], and the long-recognized but persistent problem of a lack of measures of different cognitive abilities with documented psychometric equivalence [137]. In clinical application, as well as future research, further clarity might be garnered through deconstruction of the neurocognitive and functional constructs into more specific terms, e.g., by examining the relative functional impact of different forms of “executive functions” (cf. Jefferson et al [138]). Paralleling the approach taken in clinical neuropsychological assessments, particularly emphasized in the “process approach” [139], it may also be helpful to examine the patterns of specific errors on neuropsychological tests and functional outcomes.

TREATMENT ISSUES Effects of Psychotropic Medications The classic empirical literature on the neuropsychological effects of conventional neuroleptic medications in patients with schizophrenia yielded somewhat equivocal results, but the overall conclusion was generally that any deleterious or beneficial were minimal relative to the existing inter-patient heterogeneity in cognitive functioning [140, 141]. Results

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from a more recent meta-analysis, however, suggest that there might be some beneficial neurocognitive effects which at least warrant further empirical inquiry [142]. Over the past ten years, there have been a number of studies and meta-analyses (e.g. see Woodward [143]) on the neuropsychological effects of second-generation (a.k.a. ‘atypical’) antipsychotic medications. There appears to be some evidence of modest neurocognitive improvements, but there is no full consensus on such efficacy [144]. Most researchers seem to agree that any improvement that is present is modest relative to the overall cognitive deficits. That is, the effects are at best characterizable as improvements, rather than a “normalization” of the cognitive functions. One recently published large scale head-to-head comparison of four antipsychotic medications (three second generation, and one conventional) showed modest improvements with all compounds, but no differential cognitive benefit from any one of the antipsychotic medications over the others (including the conventional neuroleptic.) [145]. Among the mood stabilizers, lithium appears to have some modest adverse effects on psychomotor/mental processing speed, and episodic verbal memory [146-148]. There are also potential subtle cognitive effects from other mood stabilizers and antidepressant medications, but the overall neuropsychological effect of such medications does not appear to be substantial relative to the overall impairments associated with schizophrenia or bipolar disorder [149].

Neuropsychological Deficits as a Target of Treatment As exemplified by the Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS) and Treatment Units for Research on Neurocognition and Schizophrenia (TURNS) projects, there has been recent interest among academic researchers, government agencies, and the pharmaceutical industry in the possibility of developing medications which directly target the cognitive deficits associated with schizophrenia [9, 150, 151]. This line of inquiry remains in its early stages, but the breadth and magnitude of these efforts provides reason for optimism about the long-term possibility of developing effective pharmacologic treatments for the neurocognitive deficits in schizophrenia and schizoaffective disorder. Beyond pharmacologic treatments, there is an also increased interest in the potential added value of non-pharmacologic interventions in reducing neurocognitive deficits in schizophrenia, or at least reducing their functional impact [152, 153]. Restorative interventions, as the name implies, are aimed at “restoring” (or at least improving) cognitive functions toward “normal” levels. Given the neurodevelopmental nature of the cognitive deficits in schizophrenia and schizoaffective disorder, the notion of “restoration” may not be fully applicable [152, 153], so these may be more appropriately conceptualized as “cognitive enhancing” interventions. Compensatory approaches, also called “cognitive prosthetics” aim at training patients to bypass their deficits and word around them. Environmental approaches generally fall under the broad realm of compensatory approaches, but involve overt manipulations in the patients’ home, school or work environment to reduce cognitive demands [152, 153]. While most studies of the current cognitive interventions demonstrate an improvement in cognitive test performance and/or a reduction in the functional impairment, additional research is still needed to document the degree of, and factors fostering real-world

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generalizability of skills and long-term maintenance of effects in terms of real-world functioning (see review by Twamley [152]).

CONCLUSION Neuropsychological impairment is a functionally and clinically important dimension of schizoaffective disorder. Although the psychotic and affective symptoms associated with this condition are often appropriately the initial focus of acute treatment, stabilization of psychopathology should be viewed as one of the tasks, not the sole task, in clinical management of this condition. Although there is considerable variability between patients in terms of the level and pattern of impairment, most individuals have some areas of relative strength. Thus, while pharmacologic interventions resulting in substantial, functionally relevant, degrees of neurocognitive improvement are still in the relatively early phases of development, neuropsychological assessment can be of considerable aid in treatment planning and management even in the absence of readily available methods to eliminate such deficits [154]. Because of the relevance of cognitive deficits to functional living skills, neuropsychological assessment should be considered as an integral part of overall patient care to aid in long-term treatment planning, and to identify neuropsychological areas of cognitive strengths that may be utilized to compensate for other deficits.

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[103] Partington JE, Leiter RG. Partington's Pathways Test. Psychological Service Center Journal. 1949l 1:11-20. [104] Reitan RM, Wolfson D. The Halstead-Reitan neuropsychological test battery: Theory and clinical interpretation. 2nd ed. Tucson, Ariz.: Neuropsychology Press 1993. [105] Dickinson D, Ramsey ME, Gold JM. Overlooking the obvious: a meta-analytic comparison of digit symbol coding tasks and other cognitive measures in schizophrenia. Arch Gen Psychiatry. 2007 May;64(5):532-42. [106] Palmer BW, Heaton R. Executive dysfunction in schizophrenia. In: Sharma T, Harvey P, eds. Cognition in Schizophrenia: Impairments, Importance and Treatment Strategies. New York: Oxford University Press 2000:52-72. [107] Baddeley A. The central executive: a concept and some misconceptions. J Int Neuropsychol Soc. 1998 Sep;4(5):523-6. [108] Berg EA. A simple objective technique for measuring flexibility in thinking. J Gen Psychol. 1948(39):15-22. [109] Heaton R, Chelune G, Talley J, Kay G, Curtiss G. Wisconsin Card Sorting Test Manual. Revised and Expanded. Odessa, FL: Psychological Assessment Resources, Inc. 1993. [110] Green M. Schizophrenia from a neurocognitive perspective: Probing the inpenetrable darkness. Boston: Allyn and Bacon 1998. [111] Li CS. Do schizophrenia patients make more perseverative than non-perseverative errors on the Wisconsin Card Sorting Test? A meta-analytic study. Psychiatry Res. 2004 Dec 15;129(2):179-90. [112] MacLeod CM. Half a century of research on the Stroop effect: an integrative review. Psychol Bull. 1991 Mar;109(2):163-203. [113] Henik A, Salo R. Schizophrenia and the stroop effect. Behav Cogn Neurosci Rev. 2004 Mar;3(1):42-59. [114] Dyer FN. The Stroop phenomenon and its use in the study of perceptual, cognitive, and response processes. Memory & Cognition. 1973 Vol. 1(2), Apr:106-20. [115] Rapoport JL, Addington AM, Frangou S, Psych MR. The neurodevelopmental model of schizophrenia: update 2005. Mol Psychiatry. 2005 May;10(5):434-49. [116] McGrath JJ, Feron FP, Burne TH, Mackay-Sim A, Eyles DW. The neurodevelopmental hypothesis of schizophrenia: a review of recent developments. Ann Med. 2003;35(2):86-93. [117] Lencz T, Cornblatt B, Bilder RM. Neurodevelopmental models of schizophrenia: pathophysiologic synthesis and directions for intervention research. Psychopharmacol Bull. 2001 Winter;35(1):95-125. [118] Bilder RM, Reiter G, Bates J, Lencz T, Szeszko P, Goldman RS, Cognitive development in schizophrenia: follow-back from the first episode. J Clin Exp Neuropsychol. 2006 Feb;28(2):270-82. [119] Cannon TD, Bearden CE, Hollister JM, Rosso IM, Sanchez LE, Hadley T. Childhood cognitive functioning in schizophrenia patients and their unaffected siblings: a prospective cohort study. Schizophr Bull. 2000;26(2):379-93. [120] Davidson M, Reichenberg A, Rabinowitz J, Weiser M, Kaplan Z, Mark M. Behavioral and intellectual markers for schizophrenia in apparently healthy male adolescents. Am J Psychiatry. 1999 Sep;156(9):1328-35.

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[121] Jeste DV, Symonds LL, Harris MJ, Paulsen JS, Palmer BW, Heaton RK. Non-dementia non-praecox?: Late-onset schizophrenia. American Journal of Geriatric Psychology. 1997;5:302-17. [122] Palmer BW, McClure FS, Jeste DV. Schizophrenia in late life: findings challenge traditional concepts. Harv Rev Psychiatry. 2001 Mar-Apr;9(2):51-8. [123] Cohen CI, Cohen GD, Blank K, Gaitz C, Katz IR, Leuchter A, Schizophrenia and older adults. An overview: directions for research and policy. Am J Geriatr Psychiatry. 2000 Winter;8(1):19-28. [124] Horan ME, Muller JJ, Winocur S, Barling N. Quality of life in boarding houses and hostels: a residents' perspective. Community Ment Health J. 2001 Aug;37(4):323-34. [125] Kurtz MM. Neurocognitive impairment across the lifespan in schizophrenia: an update. Schizophr Res. 2005 Apr 1;74(1):15-26. [126] Rund BR. A review of longitudinal studies of cognitive functions in schizophrenia patients. Schizophr Bull. 1998;24(3):425-35. [127] Heaton RK, Gladsjo JA, Palmer BW, Kuck J, Marcotte TD, Jeste DV. The stability and course of neuropsychological deficits in schizophrenia. Arch Gen Psychiatry. 2001 Jan;58(1):24-32. [128] Nayak GV, Moore DJ, Roesch SC, Jeste DV, Heaton RK, Palmer BW. Use of hierarchical linear modeling to evaluate longitudinal neuropsychological performance in middle-aged and older schizophrenia patients J Int Neuropsychol Soc. 2005;11:175. [129] Harvey PD. Cognitive impairment in elderly patients with schizophrenia: age related changes. Int J Geriatr Psychiatry. 2001 Dec;16 Suppl 1:S78-85. [130] Green MF, Kern RS, Braff DL, Mintz J. Neurocognitive deficits and functional outcome in schizophrenia: are we measuring the "right stuff"? Schizophr Bull. 2000;26(1):119-36. [131] Kurtz MM. Symptoms versus neurocognitive skills as correlates of everyday functioning in severe mental illness. Expert Rev Neurother. 2006 Jan;6(1):47-56. [132] Dickerson FB, Boronow JJ, Stallings CR, Origoni AE, Cole S, Yolken RH. Association between cognitive functioning and employment status of persons with bipolar disorder. Psychiatr Serv. 2004 Jan;55(1):54-8. [133] Martinez-Aran A, Vieta E, Colom F, Torrent C, Sanchez-Moreno J, Reinares M, Cognitive impairment in euthymic bipolar patients: implications for clinical and functional outcome. Bipolar Disord. 2004 Jun;6(3):224-32. [134] Velligan DI, Bow-Thomas CC, Mahurin RK, Miller AL, Halgunseth LC. Do specific neurocognitive deficits predict specific domains of community function in schizophrenia? J Nerv Ment Dis. 2000 Aug;188(8):518-24. [135] Gladsjo JA, McAdams LA, Palmer BW, Moore DJ, Jeste DV, Heaton RK. A six-factor model of cognition in schizophrenia and related psychotic disorders: relationships with clinical symptoms and functional capacity. Schizophr Bull. 2004;30(4):739-54. [136] The Psychological Corporation. WAIS-III/WMS-III Technical Manual. San Antonio, TX: Author 1997. [137] Chapman LJ, Chapman JP. Problems in the measurement of cognitive deficit. Psychol Bull. 1973 Jun;79(6):380-5. [138] Jefferson AL, Paul RH, Ozonoff A, Cohen RA. Evaluating elements of executive functioning as predictors of instrumental activities of daily living (IADLs). Arch Clin Neuropsychol. 2006 May;21(4):311-20.

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[139] Kaplan E. A process approach to neuropsychological assessment. In: Dennis M, Kaplan E, Posner MI, Stein DG, Thompson RF, eds. Clinical neuropsychology and brain function: Research, measurment, and practice. Washington D.C.: American Psychological Assocation 1988:129-67. [140] Cassens G, Inglis AK, Appelbaum PS, Gutheil TG. Neuroleptics: effects on neuropsychological function in chronic schizophrenic patients. Schizophr Bull. 1990;16(3):477-99. [141] Spohn HE, Strauss ME. Relation of neuroleptic and anticholinergic medication to cognitive functions in schizophrenia. J Abnorm Psychol. 1989 Nov;98(4):367-80. [142] Mishara AL, Goldberg TE. A meta-analysis and critical review of the effects of conventional neuroleptic treatment on cognition in schizophrenia: opening a closed book. Biol Psychiatry. 2004 May 15;55(10):1013-22. [143] Woodward ND, Purdon SE, Meltzer HY, Zald DH. A meta-analysis of neuropsychological change to clozapine, olanzapine, quetiapine, and risperidone in schizophrenia. Int J Neuropsychopharmacol. 2005 Sep;8(3):457-72. [144] Carpenter WT, Gold JM. Another view of therapy for cognition in schizophrenia. Biol Psychiatry. 2002 Jun 15;51(12):969-71. [145] Keefe RS, Bilder RM, Davis SM, Harvey PD, Palmer BW, Gold JM, Neurocognitive effects of antipsychotic medications in patients with chronic schizophrenia in the CATIE Trial. Arch Gen Psychiatry. 2007 Jun;64(6):633-47. [146] Pachet AK, Wisniewski AM. The effects of lithium on cognition: an updated review. Psychopharmacology (Berl). 2003 Nov;170(3):225-34. [147] Honig A, Arts BM, Ponds RW, Riedel WJ. Lithium induced cognitive side-effects in bipolar disorder: a qualitative analysis and implications for daily practice. Int Clin Psychopharmacol. 1999 May;14(3):167-71. [148] Lund Y, Nissen M, Rafaelsen OJ. Long-term lithium treatment and psychological functions. Acta Psychiatr Scand. 1982 Mar;65(3):233-44. [149] Bearden CE, Hoffman KM, Cannon TD. The neuropsychology and neuroanatomy of bipolar affective disorder: a critical review. Bipolar Disord. 2001 Jun;3(3):106-50; discussion 51-3. [150] Fenton WS, Stover EL, Insel TR. Breaking the log-jam in treatment development for cognition in schizophrenia: NIMH perspective. Psychopharmacology (Berl). 2003 Sep;169(3-4):365-6. [151] Gold JM. Cognitive deficits as treatment targets in schizophrenia. Schizophr Res. 2004 Dec 15;72(1):21-8. [152] Twamley EW, Jeste DV, Bellack AS. A review of cognitive training in schizophrenia. Schizophr Bull. 2003;29(2):359-82. [153] Velligan DI, Kern RS, Gold JM. Cognitive rehabilitation for schizophrenia and the putative role of motivation and expectancies. Schizophr Bull. 2006 Jul;32(3):474-85. [154] Palmer BW. The expanding role of neuropsychology in geriatric psychiatry. Am J Geriatr Psychiatry. 2004 Jul-Aug;12(4):338-41.

In: Schizoaffetive Disorders Editor: Kam-shing Yip

ISBN 978-1-60456-948-3 © 2009 Nova Science Publishers, Inc.

Chapter 6

EGO FUNCTIONING, COGNITION, AND ILLNESS CHARACTERISTICS OF PERSONS WITH SCHIZOAFFECTIVE DISORDER: DISTINCTIVE FEATURES AND RESPONSE TO VOCATIONAL REHABILITATION Morris D. Bell*, Randall Richardson, and Tamasine Grieg Department of Psychiatry, Yale University School of Medicine, Psychology Service 116B, VACHS, 950 Campbell Avenue, West Haven, CT 06516, USA

OVERVIEW Patients entering rehabilitation with a diagnosis of schizoaffective disorder are regarded as having deficits similar to those with schizophrenia. Yet, they often have a history of better psychosocial functioning, which suggests that they might respond better to rehabilitation than their counterparts with schizophrenia. In this chapter, we review literature on features of schizoaffective disorder that may be distinctive from schizophrenia. We then examined these features in a large sample of patients who entered a vocational rehabilitation program, comparing them with patients with schizophrenia in the same program. Finally, we looked for differences between the two groups in their rehabilitation course and outcome.

*

E-mail: [email protected]

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THE SCHIZOAFFECTIVE CONUNDRUM: TWO DISORDERS OR ONE Related Debates Since Kasanin first used the term “schizoaffective” in 1933 to identify a psychotic syndrome marked by mood disturbance, there has been persistent debate as to the validity of the diagnostic category. Like schizophrenia patients, schizoaffective patients experience hallucinations and delusions, thought disorder, negative symptoms, and poor cognitive functioning. On the other hand, they also display many symptoms associated with major depression or bipolar disorder such as depressed mood, disinterest in activities, frequent crying, heightened activity, expansiveness and irritability. This has caused some to question whether schizoaffective disorder shouldn’t be viewed as more similar to an affective illness with psychotic features. However, the persistence of psychotic symptoms in the absence of mood disturbance in schizoaffective disorder is the key factor that distinguishes it from mood disorders with psychotic features (DSM-IV-TR; APA, 2000). If patients have schizophrenia symptoms and also have mood symptoms, one might reasonably expect that they would have a worse course than patients with just schizophrenia symptoms. After all, having two sets of symptoms should be more disabling than one. And indeed, in their self-report, schizoaffective patients tend to rate themselves as the most severely ill. According to clinician ratings on the other hand, they are generally viewed as intermediate between schizophrenia and bipolar disorder in terms of illness severity (Averill , 2004). But even in clinician ratings, perspectives diverge: on cross-sectional assessments of symptoms schizoaffective patients are typically placed closer to the schizophrenia end of the spectrum. When the course of illness is taken into consideration however, the prognosis is more akin to that of bipolar patients, suggesting an intermediate outcome (Benabarre , 2001). Those that argue for a unitary syndrome point to differences in presentation, course and outcome from either schizophrenia or bipolar disorder. At the same time, the disorder combines some features of both diagnostic categories. The complexity of the diagnosis, and absence of clear nosologic boundaries between schizoaffective disorder and related syndromes has led some psychopathologists (e.g., Taylor & Amir, 1994; Yasamy, 1987) to suggest that schizoaffective disorder highlights the failure of categorical diagnosis based on signs and symptoms. This view has encouraged some researchers in the phenomenology of the psychoses to call for a dimensional perspective, in which key features such as cognitive impairment, positive symptoms and mood disturbance are viewed as independent continua; the extent of each in a single individual determining the diagnostic picture (Harrow , 2000). According to this perspective, schizoaffective disorder is diagnosed when pathology is present on each of these three dimensions. Yet others (e.g. Ketter , 2004) support a mixed dimensional/categorical perspective, in which these disorders are viewed along a continuum for the purpose of understanding their shared and discrete characteristics; yet viewed categorically for the purpose of making reliable diagnoses.

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Genetics of Schizoaffective Disorder Research into the genetic underpinnings of schizoaffective disorder has thus far failed to clarify the discussion surrounding this syndrome. Family and genetic studies have drawn into question the nosological distinctions between schizophrenia and affective disorders that have been historically assumed (Berretini, 2000a). Findings from the New York High Risk Project have shown that schizoaffective disorder is as likely to occur among the relatives of schizophrenia probands as those of probands with bipolar disorder (Erlenmeyer-Kimling , 1995). Similarly, Bramon and Sham (2001) have reported that there are no risk factors that set schizoaffective disorder apart from either schizophrenia or affective disorders. Although the genetic profiles underlying schizophrenic and manic syndromes appear to have shared, as well as discrete features (Berretini, 2000b), there is no evidence at present to suggest that the genetic liability to schizoaffective disorder is in any way distinguishable from the other two syndromes (Maier , 2005). Indeed, studies attempting to define the specific loci on the human genome that may be associated with these disorders have found that the loci that are implicated in schizoaffective disorder can be found in both schizophrenia and affective disorders (Berretini, 2000a). Perhaps for this reason researchers have been unable to clearly document genetic transmission of schizoaffective disorder as a diagnostic entity (Abrams, 1984).

Neurocognition in Psychosis Cognitive deficits are now recognized to be a central feature of schizophrenia (Bartok , 2005), appearing in the prodromal stage (Niendam, 2003), following remission of acute phases (Bilder , 2000), and in the residual stages (Harvey, 2001). Cognitive impairments also appear in the first order relatives of schizophrenic probands (Niendam, 2003). Children who later develop schizophrenia and their siblings show similar patterns of deficits involving spatial reasoning, verbal knowledge, perceptual-motor speed, and speeded processes of working memory. However, the probands exhibit more severe deficits in perceptual-motor speed and speeded processes of working memory than their unaffected siblings (Niendam, 2003). Similarly, a meta-analysis of studies examining cognitive deficits in schizophrenia patients found that 87% of their cognitive deficits can be explained by a general slowdown of processing speed (Schatz, 1998). Still, there is continuing debate about whether these impairments are generalized or converge in a profile that may be specific to schizophrenia (Dickinson , 2004).

Neuroleptics and Neurocognition Although medications have proved quite helpful in improving clinical symptoms, they have been relatively ineffective in addressing cognitive impairments. This is a crucial target area because these impairments are believed to have a significant impact of psychosocial functioning (Green, 1996). Prevailing opinion holds that conventional neuroleptics have not been helpful in improving cognitive symptoms, although a recent meta-analysis of clinical trials revealed small to moderate cognitive advantage among patients taking these

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medications (Mishara & Goldberg, 2004). The claims of cognitive improvements from treatment with second generation neuroleptics appear to have been overstated however (Harvey & Keefe, 2001), and a large study performed by investigators independent of industry found no support for such claims (Lieberman , 2005).

Cognition in Schizoaffective Disorder Despite a growing awareness literature on cognitive impairments in psychotic disorders, relatively little has been said about cognitive impairments with regard to schizoaffective disorder in particular. Investigations have yielded mixed results, suggesting alternately that schizoaffective patients were indistinguishable from non-clinical controls (Buhler , 1991); were similarly impaired as schizophrenic patients (Miller , 1996); were no different from nonpsychotic affective disorder patients (Zihl , 1998) and were intermediate between schizophrenia and affective disorder patients in memory and general intellectual ability (Maj, 1986). More recent studies have examined differential performance between schizoaffective and schizophrenia patients in key domains of processing. For example, Stip and colleagues (2005) found differences between these diagnostic groups in visual-motor speed and explicit memory. Other researchers have found that memory disorders are shared between the two groups, rendering them distinct from non-psychotic affective disorders on this dimension (McIntosh , 2005). A recent cluster analysis revealed that cognitive functioning is a heterogeneous dimension in psychosis, such that some patients are severely impaired, whereas others appear neuropsychologically normal. These researchers determined that schizoaffective and paranoid schizophrenia appear at all levels of performance, but are more likely to be in the upper end of the functional continuum, while disorganized and undifferentiated patients are more likely to be at the lower end of the continuum (Goldstein et al, 2005).

EGO FUNCTIONING IN SCHIZOPHRENIA AND SCHIZOAFFECTIVE DISORDER Given the better premorbid function and milder course of schizoaffective disorder than schizophrenia, it is worthwhile to consider whether their capacity for psychological integration will also be better. One approach to defining and measuring psychological fitness relies on the psychoanalytic concept of ego functioning. This term refers to the set of psychological qualities that permit an individual to cope with both internal and external pressures and to navigate the world in an effective way. To accomplish these aims an individual must employ several skills adaptively, including reality testing, interpersonal relatedness, and self-regulation. Several researchers have attempted to operationally define and quantify ego functioning as the psychological basis for mental health and illness. Most notably, Bellak, Hurvich and Gediman (1973) reviewed the historical literature on ego functioning and defined 12 key components. This framework was the foundation upon which Bell (1995) constructed the Bell Object Relations and Reality Testing Inventory (BORRTI).

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Object relations and reality testing were selected for scientific study because they represented central features of psychotic disorders and were amenable to a nomothetic approach to psychometrically sound instrument development. The object relations scales include Alienation, Insecure Attachment, Egocentricity and Social Incompetence. Reality testing scales include Reality Distortion, Uncertainty of Perception, and Hallucinations and Delusions. The BORRTI has been found to have excellent discriminant validity between schizophrenia, borderline, other Axis II disorders and healthy community adults (Bell, 1995). Six distinct BORRTI profiles within schizophrenia samples have been identified and found to have predictive and discriminant validity as well (Bell , 1986; Bell , 2001). The BORRTI also has cross-cultural validity, as shown in a study of schizophrenia patients in Brazil (Bell & Bruscato, 2002). In the study described here, we compare ego functioning in patients with schizophrenia and schizoaffective disorder. To our knowledge this is the first attempt to quantify and characterize these two diagnostic groups on this dimension.

VOCATIONAL REHABILITATION, SCHIZOPHRENIA AND SCHIZOAFFECIVE DISORDER Diagnosis has generally been a weak predictor of vocational outcomes in psychiatry. The first statement on the issue was by Anthony and Jansen (1984), who argued that diagnosis and symptoms were unrelated to vocational functioning within psychiatric populations. However, more recent work has found that having a schizophrenia diagnosis as compared to affective illness or other diagnosis is a negative predictor of supported employment success (Cook, 2005). Some have argued that any differences in outcomes between schizophrenia patients and others diminish with better rehabilitation programming (Mueser & McGurk, 2004). Whether patients with schizoaffective disorder have a better rehabilitation course than patients with schizophrenia remains an open question. Although the literature cited earlier concludes that patients with schizoaffective disorder demonstrate better community functioning, it is unknown whether these advantages translate into improved outcomes in vocational rehabilitation.

THE CURRENT STUDY In this chapter we report on 422 patients enrolled in a series of vocational rehabilitation studies. We examined the differences between schizophrenia and schizoaffective disorder groups on background and illness characteristics, cognitive ability, ego functioning, and work outcome measures. We hypothesized that differences would generally favor schizoaffective patients and that such differences might influence the course and outcome of vocational rehabilitation.

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n Schizophrenia Subtype Paranoid Disorganized Residual Undifferentiated Gender Male Female* Ethnicity White Black Hispanic Asian Other Ever Married* Age Education Full Scale IQ Age at 1st Hosp. Lifetime Hosp.

Medications Atypical Conventional Both None

Schizophrenia (n=302) %

N

Schizoaffective (n=121) %

203 20 23 56

67 7 8 18

— — — —

— — — —

278 24

92 8

102 19

84 16

189 95 13 4 1 97 Mean 42.19 12.77 92.88 24.59 9.54

63 31 4 1 0.33 32.55 Std Dev 8.37 2.34 14.37 6.69 10.11

85 33 3 0 0 61 Mean 43.28 13.02 95.31 26.45 9.49

71 27 2 0 0 50 Std Dev 9.29 2.27 16.02 7.71 8.95

n 86 92 10 12

Schizophrenia (n=200) % 43 46 5 6

N 39 25 6 2

Schizoaffective (n=72) % 54 35 8 3

*p<.01

Procedures and Results Four hundred and twenty-three outpatients with diagnoses of schizophrenia or schizoaffective disorder were enrolled in a series of three vocational rehabilitation studies between the years of 1995-2005. Procedures and evaluations differed slightly across studies with some measures collected for all three studies and some for one or two. The number of participants included in each analysis is noted in the tables. Diagnoses of schizophrenia or schizoaffective disorder were determined by doctoral level psychologists who conducted the Structured Clinical Interview for DSM-IIIR (SCID; Spitzer, Williams, Gibbon, & First, 1989). Participants met diagnostic criteria based on the Diagnostic

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and Statistical Manual of Mental Disorders (DSM –IIIR; American Psychiatric Association, 1987) and were eligible for the study if they were clinically stable (i.e., no housing changes, psychiatric medication alterations, or psychiatric hospitalizations in the 30 days prior to intake). Patients with a history of traumatic brain injury or known neurological diseases were excluded.

Sample Characteristics Participant demographics are presented in Table 1. While similar in most respects, there were several notable differences between the schizoaffective and schizophrenia groups. People diagnosed with schizoaffective disorder were twice as likely to be female and to have ever been married. Having been married is generally acknowledged as an indicator of better premorbid functioning; as such this finding indicates that the patients with schizoaffective disorder in our rehabilitation sample were similar to other schizoaffective disorder samples in the literature.

Clinical Features Symptoms were evaluated by trained raters using the Positive and Negative Syndrome Scale (PANSS; Kay , 1987). The PANSS measures 30 symptoms common to schizophrenia. This study utilized the 5 factor-analytically derived component scores (i.e., positive, negative, cognitive, hostility and emotional discomfort). The items on each scale, psychometrics, and a discussion of replication analyses are reported in Bell (1994). The PANSS cognitive component taps attention, conceptual disorganization and difficulty in abstract thinking. Patients with schizoaffective disorder were given significantly lower ratings on this dimension than those with schizophrenia (p<.04). In contrast, people with schizoaffective disorder had significantly higher scores on the emotional discomfort component of the PANSS which measures anxiety and depression. Schizoaffective patients had a significantly lower total score on the PANSS, although the effect size was small (Cohen’s D=0.21). These PANSS results indicate that impairments in cognition and formal thought processes are less common and less severe in schizoaffective disorder than in schizophrenia, whereas symptoms of mood disturbance, anxiety and guilt are more common and more severe. Importantly, positive symptoms and negative symptoms, core features of schizophrenia, are similar in both disorders.

Community Functioning Community functioning was measured using the Quality of Life Scale (QLS; Heinrichs , 1984). Scores are based on a structured interview and yield information on social and vocational involvement. The QLS is comprised of four subscales that examine different aspects of a patient’s intrapsychic and interpersonal functioning, role functioning, and engagement with everyday objects and activities. A significant difference between the schizophrenia and schizoaffective disorder patients appeared on the Common Objects and

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Activities subscale (p<.009) with the schizoaffective group having more common objects (e.g., keys, map of the city, library card, stamps) and engaging in more activities (e.g., reading a newspaper, paying a bill, shopping for food, attending a sporting event). Other aspects of community functioning including interpersonal relationships, productive activity, and intrapsychic experiences of purpose and meaning were similar between groups. Thus, patients with schizoaffective disorder in our sample showed selective differences in their community functioning, but in many important domains of life they functioned no better than schizophrenia patients.

Cognitive Functioning As routine procedure for all three studies, participants completed a battery of psychological and neuropsychological instruments at intake. The battery differed somewhat according to the study. Attention, executive function, working memory, visual and verbal memory, verbal fluency, processing speed, and social cognition, including theory of mind (Hinting Task; Corcoran & Frith, 1995) and affect recognition (BLERT; Bell , 1997) were domains tapped by the various neuropsychological measures listed in the tables. Ego functioning was measured using the Bell Object Relations & Reality Testing Inventory (BORRTI; Bell, 1995), which was described in the introduction. Table 2. Positive and Negative Syndrome Scale Ratings

Positive Negative Cognitive* Hostility Emot. Discomfort.* Total Score*

Mean 18.80 18.27 18.69 7.66 11.65 75.08

Schizophrenia (n=302) Std Dev 5.97 6.24 5.23 2.97 3.56 14.30

Mean 17.86 17.31 16.96 7.83 12.34 72.33

Schizoaffective (n=121) Std Dev 5.22 5.98 4.78 3.35 3.35 12.99

Mean 20.78 19.46 1.02 7.27 48.54

Schizoaffective (n=73) Std Dev 5.91 8.35 2.46 2.2 15.08

*p<.005

Table 3. Quality of Life Scale

Intrapsychic Found. Interpersonal Rel. Instrumental Role Objects & Activities* Total Score *p<.009

Mean 19.45 17.68 1.25 6.50 44.88

Schizophrenia (n=200) Std Dev 5.73 9.18 3.04 2.15 16.00

Ego Functioning, Cognition, and Illness Characteristics of Persons … Table 4. Neuropsychological Variables

Mean Wisconsin Card Sort Perseverative Errors Conceptual Level Categories Correct

Schizophrenia (n=300) Std Dev

81.05 81.16 3.39 Mean

19.94 17.86 2.28 Schizophrenia (n=200) Std Dev

WAIS-III Digit Symbol 6.43 Information 9.58 Picture Completion 7.97 Digit Span 8.12 Block Design 8.17 Similarities 8.82 Letter Number Sequence* 7.39 Wechsler Memory Scale-R Logical Memory I* 21.91 Logical Memory II** 19.98 Visual Reproduction I 39.35 Visual Reproduction II 29.95 Mental Control 4.69 Figural Memory* 5.89 Hopkins Verbal Learning Trial 1 4.41 Trial 2 6.13 Trial 3 7.06 30 min recall 5.97 Continuous Performance Test Number Correct 43.77 Misses 6.87 Wrong 13.55 Absolute % 87.21 Relative % 81.13 Bell Lysaker Emotion Recognition Test (BLERT) Total Score** 12.66 Proverb Test Gorham’s (Bizarreness) 2.51

82.14 81.77 3.62 Mean

18.23 18.37 2.15 Schizoaffective (n=73) Std Dev

6.48 10.07 7.63 8.51 8.51 9.04 7.95

1.96 3.41 2.79 2.58 3.05 2.98 2.96

22.98 20.63 34.76 32.43 1.46 1.71

29.30 27.82 48.24 34.54 4.99 6.42

24.81 23.97 37.22 35.33 1.26 1.81

1.63 1.87 2.18 2.62

4.58 6.36 7.30 6.24

1.58 1.92 2.45 2.83

9.11 11.03 22.95 17.71 22.06

42.97 7.03 11.42 85.95 82.31

9.97 9.97 19.81 19.92 22.49

3.88

14.04

3.43

3.39

1.81

2.86

Schizoaffective (n=46) Mean Std Dev

0.39 2.13 25.17 65.03 3.96

0.24 1.04 38.93 107.47 17.39

0.60 1.85 13.69 59.81 2.44

12.45

37.20

14.74

Schizophrenia (n=70) Mean Std Dev Controlled Word Association Test (COWAT) Categories*** 32.98 10.37 * p<.05 ** p<.01 *** p<.001

Schizoaffective (n=121) Std Dev

2.18 2.96 2.94 2.43 2.69 2.64 3.05

Schizophrenia (n=104) Mean Std Dev Trailmaking Trails A errors 0.16 Trails B errors 1.31 Trails A time* 47.37 Trails B time 123.87 Hinting Task*** 15.41 Controlled Word Association Test (COWAT) F-A-S 35.55

Mean

Schizoaffective (n=29) Mean Std Dev 40.72

9.94

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Schizophrenia Schizophrenia

Schizoaffective Schizoaffective

70

65

BORRTI Subscale T-Score BORRTI Subscale T-Score<

60

55

50

45

40

35

0 Alienation

Insecure *Insecure Attachment

Egocentricity

Social Reality *Uncertainty Uncertainty Hallucinations Incompetence Distortion ofofPerceptions Perceptionsand & Delusions Delusions

< Scores greater than 60 indicate clinically significant pathology. Clinical cutoffs based on nonpathological norms. * p>.05 Fig.ure 1. BORRTI Subscale Profiles of Schizophrenia and Schizoaffective Groups.

Table 5. Bell Object Relations and Reality Testing Inventory

BORRTI Subscale Alienation Insecure Attachment* Egocentricity Social Incompetence Reality Distortion Uncertainty of Perception* Hallucinations & Delusions * p<.05

Mean 0.53 -0.03 0.50 0.41 0.77 0.14 1.10

Schizophrenia (n=301) Std Dev 0.88 0.88 0.92 0.88 1.27 0.86 1.57

Schizoaffective (n=121) Mean Std Dev 0.57 0.89 0.14 0.82 0.45 0.83 0.46 0.87 0.68 1.25 0.35 0.88 1.02 1.50

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Ego Functioning Regarding ego functioning as measured by the BORRTI, the schizophrenia and schizoaffective disorder groups were similar in terms of Alienation, Egocentricity, Social Incompetence, Reality Distortion, and Hallucinations and Delusions but differed significantly on Insecure Attachment (p<.04) and Uncertainty of Perception (p<.02). On the latter two measures, the differences in effect size between the diagnostic groups were small (Cohen’s D, IA=0.19; UP=0.24). Schizoaffective patients were somewhat higher on the Uncertainty of Perception scale indicating that they were more uncertain of the veracity of their perceptions as they should have been given their very high score on Hallucinations and Delusions. This indicates greater self-monitoring and observing ego. On Insecure Attachment, schizoaffective patients were also somewhat higher indicating greater interpersonal sensitivity and vulnerability in relationships. The schizophrenia and schizoaffective disorder groups were similar on most neuropsychological measures. Whenever differences emerged, the results favored the schizoaffective disorder sample. Areas of strength for the schizoaffective group included episodic memory (Logical Memory I and II), visual memory (Figural Memory), motor speed and attention (Trails A; Reitan, 1992), and verbal fluency (COWAT Categories; Spreen & Strauss, 1991). Importantly, the schizoaffective sample scored significantly higher on measures of social cognition including the Hinting Task, which is a measure of Theory of Mind, or the ability to infer the thoughts and intentions of others; and the BLERT, a measure of affect recognition. These relatively better cognitive functions may provide a neurocognitive foundation for the better social functioning we inferred from higher rates of marriage and observed on the QLS in terms of greater participation in common activities.

Work Rehabilitation During the course of work rehabilitation, participants were rated bi-weekly using the Work Behavior Inventory (WBI; Bryson , 1997). The WBI is a work assessment instrument designed to evaluate the performance of employees with severe mental illness. It is rated by trained job specialists based on a fifteen-minute behavioral observation of the worker and brief interview with the worker’s supervisor. Each of 5 subscales—Cooperativeness, Work Habits, Work Quality, Social Skills, and Personal Presentation—is comprised of a number of items rated along a five-point Likert scale from significant work weakness (1) to significant work strength (5). The sum of all five scales yields the total score. To examine change in work performance over time, we used the average of the first two evaluations as the initial assessment and the average of the last three evaluations as the final assessment. By using more than one measure at the beginning and end we were increasing the stability and reliability of measurement. We then compared the schizoaffective disorder sample with the schizophrenia sample on WBI score improvement by analyzing their average final WBI ratings, with the average of the initial ratings as a covariate. A MANCOVA revealed there were no significant differences on overall WBI improvement between samples, although the schizoaffective sample showed marginally (though non-significant) better improvement in the Work Habits subscale. The Work Habits subscale measures an employee’s conscientiousness, adherence to the rules of the workplace, attendance, and awareness of the norms of the work

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setting. Measures of work productivity including hours worked and money earned were also collected for participants in all three studies. There were no significant differences between samples on these measures.

CONCLUSIONS We found that schizoaffective disorder patients entering rehabilitation were similar in most regards to schizophrenia patients, but differed in several important ways. They were more likely to be female and had a higher rate of marriage. They also participated more in everyday activities, had fewer and less severe disorganization symptoms, more severe symptoms of emotional discomfort, better verbal and visual memory, better verbal fluency, better social cognition, greater interpersonal sensitivity and better observing ego. Although they were similar to schizophrenia patients on core positive and negative symptoms and on most neurocognitive and ego-function variables, whenever the two groups of patients differed, the difference favored the schizoaffective disorder sample. Table 6. Work Behavior Inventory

Pre Mean WBI Subscale Cooperativeness Work Habits Presentation Work Quality Social Skills Total Score

Schizophrenia (n=150) Post SD Mean SD

23.80 23.43 23.09 22.41 20.28 113.02

4.38 5.18 4.29 5.29 4.11 20.56

26.00 24.45 24.88 24.72 22.58 122.63

4.58 6.13 4.53 5.64 5.11 23.24

Schizoaffective (n=57) Pre Post Mean SD Mean SD 23.43 22.64 23.49 21.26 21.18 112.01

4.11 4.94 4.32 4.31 3.11 18.43

26.16 24.78 25.32 25.13 23.61 125.01

4.47 6.01 4.74 5.57 4.22 23.17

These results are consistent with other reports that schizoaffective patients tend to function better, despite having symptoms of both schizophrenia and affective disorder. Yet, these advantages in functioning did not lead to differences in work performance improvement or vocational outcomes in our rehabilitation program. The most likely explanation is that the rehabilitation program provided sufficient individualized training and accommodations that small differences in capacity were compensated by the supports the patients received. It is also possible that the world of work provides niches for people who may have interpersonal and cognitive deficits; as such rehabilitation outcomes are not affected by the differences we found in our samples. We therefore conclude that diagnosis of schizoaffective disorder is associated with better cognitive and ego functioning but that it is not a useful predictor of rehabilitation outcomes. Regarding the discriminant validity of schizoaffective diagnosis from schizophrenia, our findings support the contention that schizoaffective disorder is not schizophrenia plus mood symptoms, but its own diagnostic category lying along a continuum of psychosis and severity from schizophrenia to bipolar disorder. This conclusion has been reached by others with

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regard to positive symptoms (Evans , 1999) cognitive symptoms (McIntosh , 2005), genetic vulnerability (Bramon & Sham, 2001; Berretini, 2000; Maier , 2005), and clinical outcome (Grossman , 1991; Harrow , 1984; Steinmeyer , 1989); and we may now add ego functioning to this list. The findings we present are in keeping with the literature and add some original information, particularly regarding better social cognition and greater capacity for interpersonal sensitivity and observing ego in schizoaffective disorder. These results may indicate an endophenotypic distinction between schizoaffective disorder and schizophrenia. They support the view of schizoaffective disorder as a discrete syndrome, in which several cognitive and ego functions are better preserved than in schizophrenia. Such a view explains the counterintuitive observation that patients with symptoms of schizophrenia and affective illness have better functioning than those with symptoms of schizophrenia alone.

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Maj M., (1986). `Neuropsychological functioning in schizoaffective disorder, depressed type’. Acta Psychiatrica Scandinavica 74:524-8. Marengo J., Harrow M., Rogers C., (1980). A manual for Scoring Abstract and Concrete Responses to Verbal Tests. New York, NY: Microfilm Publications. McGurk S.R., Mueser K.T., (2004). `Cognitive functioning, symptoms, and work in supported employment: a review and heuristic model’. Schizophrenia Research, 70:14773. McIntosh A.M., Harrison L.K., Forrester K., Lawrie S.M., Johnstone E.C., (2005). `Neuropsychological impairments in people with schizophrenia or bipolar disorder and their unaffected relatives’. British Journal of Psychiatry, 186:378-385. Miller L.S., Swanson-Green T., Moses J.A. Jr., Faustman W.O., (1996). `Comparison of cognitive performance in RDC-diagnosed schizoaffective and schizophrenic patients with the Luria-Nebraska Neuropsychological Battery’. Journal of Psychiatric Research, 30:277-282. Mishara A.L., Goldberg T.E., (2004). `A meta-analysis and critical review of the effects of conventional neuroleptic treatment on cognition in schizophrenia: opening a closed book’. Biological Psychiatry, 55:1013-1022. Niendam T.A., Bearden C.E., Rosso I.M., Sanchez L.E., Hadley T., Nuechterlein K.H., Cannon T.D., (2003) `A prospective study of childhood neurocognitive functioning in schizophrenic patients and their siblings’. American Journal of Psychiatry,160: 20602062. Reitan, C., (1992). The Trail Making Test: Manual for Administration and Scoring. Tucson, AZ: Reitan Neuropsychological Laboratory. Schatz J., (1998). `Cognitive processing efficiency in schizophrenia: generalized vs. domain specific deficits’. Schizophrenia Research, 30:41-49 Spitzer R.L., Williams J.B., Gibbon M., First M.B., (1989). Structured Clinical Interview for DSM-III-R-patient version (SCID-P, 9/1/89 version). New York: Biometrics Research Division, New York State Psychiatric Institute. Spreen O., Strauss E. (1991). A Compendium of Neuropsychological Tests: Administration, Norms, and Commentary. NewYork: Oxford University Press. Steinmeyer E.M., Marneros A., Deister A., Rohde A., Junemann H., (1989). `Long-term outcome of schizoaffective and schizophrenic disorders: a comparative study. II. Causalanalytical investigations’. European Archives of Psychiatry and Neurological Science, 238:126-34. Stip E., Sepehry A.A., Prouteau A., Briand C., Nicole L., Lalonde P., Lesage A., (2005). `Cognitive discernible factors between schizophrenia and schizoaffective disorder’. Brain and Cognition, 59:292-295. Taylor MA, Amir N., (1994). `Are schizophrenia and affective disorder related? The problem of schizoaffective disorder and the discrimination of the psychoses by signs and symptoms’. Comprehensive Psychiatry, 35: 420-429. Wechlsler D., (1987). The Wechsler Memory Scale-Revised. New York: NewYork Psychological Corporation. Wechsler D., (1997). WAIS-R Manual: Wechsler Adult Intelligence Scale-III. New York, NewYork Psychological Corporation. Yasamy M.T., (1987). `Schizoaffective disorder: a dimensional approach’. Acta Psychiatrica Scandinavica, 76: 609-618.

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In: Schizoaffetive Disorders Editor: Kam-shing Yip

ISBN 978-1-60456-948-3 © 2009 Nova Science Publishers, Inc.

Chapter 7

BOREDOM, HALLUCINATION-PRONENESS AND HYPOHEDONIA IN SCHIZOPHRENIA AND SCHIZOAFFECTIVE DISORDER McWelling Todman*, Daniel Sheypuk, Kristin Nelson, Jason Evans, Roger Goldberg, and Evangeline Lehr Department of Psychology, New School For Social Research, The New School, 65 Fifth Ave., Room 335, New York, NY 10003, USA

INTRODUCTION As in the case with other negative emotions, boredom is an affect that we constantly strive to limit and avoid - sometimes to the point of preoccupation. And like anxiety, boredom has an important signal function: it informs us that the behavioral strategies currently in use have ceased to be effective in extracting novelty and positive reinforcement from a given environment. For most clinicians, however, boredom has remained largely irrelevant to serious discussions about psychopathology. Hence, there are no questions about its frequency or severity on the standard psychiatric interview, nor are there instruments that are routinely used in clinical settings to assess an individual’s susceptibility to boredom. It is difficult to provide a definitive reason for this neglect, but there are probably at least four factors that have played a role obscuring the importance of the role of boredom in the manifestation of psychopathology. The first and perhaps most obvious reason is that it is an extraordinarily ubiquitous emotion. Too common, some would argue, to serve as a useful cue in the exploration of the complex, inner life of another individual. A second reason is probably due to the prominent role that the construct of anxiety has played in Freudian psychoanalysis and other early theories of psychopathology. In psychoanalytic theory, anxiety (and its variants of fear and terror) was conceived as the central and determinative emotion in psychological adjustment and maladjustment. Boredom, on the other hand, was seldom mentioned in early psychoanalytic discourse and was seen by most theorists as having very *

E-mail: Todmanm @Newschool.edu

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little to contribute to the grand theatre of the mind. A third reason, albeit one that is somewhat more difficult to validate, is the observation that complaints of persistent boredom are often attributed to something akin to a weakness of character. Like the habitual drug user or the overeater, individuals who are frequently bored are perceived to be making a conscious choice to live their lives in ways that perpetuate their feelings of boredom. After all, the solution seems simple enough: find environments and tasks that capture and hold one’s interest and then make the effort to ensure that they can be accessed on a regular basis (ironically, full-fledged substance dependence is one such solution). The fourth and final reason, and something that will figure prominently in the current thesis, is the notion that the effects of boredom are often hidden from view, exacerbating coexisting problems or giving rise to problems that would otherwise not exist. Indeed, precisely because boredom is so undervalued as a clinical symptom, clinicians seldom inquire about its frequency and intensity, and patients, for their part, almost never spontaneously volunteer information about its prevalence in their daily lives. This is made all the more interesting by the fact that clinicians routinely inquire about anhedonia (i.e., loss or reduction in interest in activities that were formerly pleasurable and/or interesting) despite its obvious phenomenological and conceptual similarities with the construct of boredom. But what are we to make those cases where the experience of boredom is unrelenting or unusually intense, or where it has become reliably associated with an unusually large proportion of the activities and environments that are valued and prescribed by the host culture? Is the information conveyed by such conditions as trivial and irrelevant as current clinical practice would seem to suggest? Research over the last 30 years would seem to strongly suggest that the answer to this question is a resounding “no”. Numerous studies, across broad range of populations, have clearly demonstrated that there are significant individual and group differences in the susceptibility to boredom (e.g., Sundberg , 1991) and that a high level of boredom proneness, assessed psychometrically, is associated with a wide range of untoward outcomes and characteristics, including alcohol dependence in men (Orcutt, 1984; Wiesbeck , 1996), reduced sociability (Leong and Schenller, 1993), and higher levels of negative affect, including hostility (e.g., Farmer and Sundberg, 1986; Gordon, Wilkerson, McGown and Jovanoska, 1997) Consistent with this growing awareness of the possible clinical importance of boredom, Todman has attempted to make the argument on the basis of evidence from case studies that there are unrecognized, clinically relevant boredom-related adaptations and responses that are often present among the severely and persistently ill (SPMI). He has also suggested that changes in reported boredom might be an important warning sign of a worsening clinical status (Todman, 2003). More recently, we have been able provide some direct and indirect empirical support for notion that boredom plays an important role in the course and symptom manifestations in psychosis and other forms of psychopathology. For example, we have been able to demonstrate in a non-clinical sample that both state and trait boredom are associated with psychometrically assessed levels of anhedonia and hallucination-proneness, with persistent state boredom also being predictive of current drug use (Todman, 2007). In yet another study, this time with methadone patients, we have also found that persistent levels of state boredom are positively associated with global measures psychiatric symptom severity and continued use of opioids based on urine toxicology results (Rajaratnam, , 2007; Todman, 2007).

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The research described in this chapter can been viewed as an extension of the line of inquiry that began with a series of case studies and continued with the aforementioned research with college students and methadone patients (Todman, 2003;2007). The latter studies provided support for the hypothesized relationships between boredom and measures of anhedonia, hallucination-proneness, symptom severity and substance use, but were limited by the fact that they did not include patients with psychotic disorders. The current research was an attempt to determine whether similar relationships can also be found in a heterogeneous sample of SPMI, consisting of individuals with schizophrenia, schizoaffective disorder and mood disorders. Importantly, the observed relationship between boredom and anhedonia in non-clinical samples is actually a negative one, suggesting that persistent feelings of boredom engender a type of abstinence or interest-craving syndrome. This counter-intuitive relationship, Todman has suggested, reflects an exaggeration of the normal response to a monotonous experience – the seeking of a more interesting environment (Todman, 2007). Consequently, of particular interest in the current study was the question of whether boredom, a negative affect with an inverse relationship to anhedonia in a non-clinical population assumed a positive relationship to anhedonia in a sample of individuals with schizophrenia and schizoaffective disorder. As explained below, we are of the opinion that anhedonia and boredom exist on functional continuum of severity, with anhedonia occurring when a persistently bored individual concludes that the source of their boredom is internal, uncontrollable, inescapable and permanent. We conjectured that this was far more likely to occur in the case of individuals with severe and persistent mental illnesses such as schizophrenia or schizoaffective disorder. Another question of interest revolved around the inter-correlations between boredom, anhedonia and depressed mood. Since the diagnosis of schizoaffective disorder requires that a mood episode be present for a substantial portion of the duration of the illness, there was the expectation that boredom would be more pervasive in schizoaffective disorder than in schizophrenia. Finally, we also wanted to determine whether boredom was associated with actual history of clinical hallucinations (rather than psychometrically determined hallucination-proneness); and whether current substance abuse status could be discerned on the basis of boredom prevalence, as was found to be the case in other populations. However, before describing the study and its rationale in greater detail, it would be helpful to review some of the key constructs and issues associated with study of boredom and monotony.

DEFINING BOREDOM Boredom is as difficult to define as it is commonplace, and attempts to do so have generally failed to satisfy almost everyone. The research that will be described in the following pages has been guided by a definition that is similar to the views of several different authors, including that of Mikulaus and Vodanovich (1993) who have proposed that boredom is a ‘state of low arousal and dissatisfaction, which is attributed to an inadequately stimulating situation’ (p.3). Although our own definition is similar to that of Mikulaus and Vodanovich, there are some important differences worth mentioning. First, Mikulaus and Vodanovich believe that the feeling of constraint is not an integral part of the boredom experience. However, we are

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very much of the opinion (as are most other researchers in the field) that attentional constraint is both central and critical to the experience of boredom. The source of the disagreement appears be in how the term ‘constraint’ is defined. Mikulaus and Vodanovich (1993) appear to restrict its meaning to external constraints, stating, for example, that “constraints take many forms including physical, social, legal and practical/financial” (p. 7). However, we would contend that the most important constraints are probably psychological in nature, as they include the covert coping strategies (e.g., daydreaming) that we all employ to deal with monotonous environments. If these strategies are inefficient or inaccessible, then, for all intents and purposes, they are constraints. Second, there is the issue of Mikulaus and Vodanovich’s ‘inadequately stimulating situation’, which we contend should be replaced with the construct of ‘uninteresting environments’. Individuals are not just stimulated by environments, they explore them physically and psychologically (Csikszentmihali, 2000). This emphasis on reciprocity makes explicit the widely assumed Interest-Boredom continuum and makes obvious the fact that individuals learn not only how to cope with boredom, but also how to anticipate it by monitoring their capacity to sustain interest in a particular endeavor. Indeed, this is a critical point when considering the capacities of cognitively compromised populations such as individuals with schizophrenia and schizoaffective disorder. Boredom can also be defined by its adaptive function, and like anxiety, it is generally assumed to have a signaling function with respect to an individual’s relationship to a given environment. Specifically, it is a cue that the current strategy for exploring a particular environment has exhausted all available stores of novelty and positive reinforcement (Todman, 2003). Despite its similarity to depression, Todman has suggested elsewhere that there are important differences between the two. The most important distinction lies in the fact that depressed/sad mood is a consequence of the conviction that negative reinforcement is inevitable and beyond one’s control (e.g., Alloy , 1984). Bored individuals, by contrast, are convinced that positive reinforcement is no longer attainable and beyond their control (Todman, 2003; 2007) Finally, there is the important trait vs. state boredom distinction; a distinction that is not always made clear in the extant literature. The subjective experience of boredom results from an interaction between individual differences in the predisposition to perceive environments as monotonous and variations in the intrinsic capacity of environments to evoke feelings of sameness. Consequently, any serious study of boredom obligates the researcher to distinguish between the concept of susceptibility to boredom (trait boredom) and the actual experience of boredom (state boredom). There are now several well-validated psychometric scales such as the Boredom Proneness Scale (BPS; Farmer & Sundberg,1986) and the Boredom Susceptibility Scale (BSS; Zukerman, 1979) that are routinely used to assess trait boredom. Indeed, the development of the BPS, in particular, has been a major catalyst in the growth of research on boredom over the last 20yrs. By contrast, state boredom has been typically assessed using ad hoc single-item measures that require the individual to indicate (usually on a Likert-type scale) the degree to which they currently feel bored or have felt bored during a recent time period. The State Boredom Measure (SBM; Todman, 2004), the state measure that is employed in the current study represents an attempt to develop a more structured and systematic method for assessing state boredom. The scale is described in greater detail below and appears in Appendix 1.

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It is important to appreciate that the trait-state distinction is more than an academic exercise. For example, if a measure of trait boredom was found to be positively associated with an important outcome such as relapse among recovering addicts, it would be important to know whether prolonged exposure to intrinsically monotonous environments in otherwise low boredom prone individuals produced the same effect. Since environments are usually easier to modify (or avoid) than personality traits, the clinical implications in this hypothetical scenario are obvious.

BOREDOM, ANHEDONIA AND HALLUCINATION-PRONES IN NON-CLINICAL SAMPLES Anhedonia Todman has suggested that it might be useful, at least heuristically, to think of boredom as a multi-dimensional construct, along the lines depicted in Figure 1 (Todman, 2007). In this model, the dimensions represent expectancies about future encounters with new environments, and anhedonia is construed as a type of boredom that is distinguished by extremely high levels of persistence (high frequency/duration) and ubiquity (high extensiveness/ubiquity). Such a state would ultimately give rise to the apathy and disinterest in the future that tends to characterize episodes full-blown anhedonia. In other words, the anhedonic individual is inclined to make attributions about the source, controllability and permanence of their uninteresting existence in a way that effectively shuts down pleasure seeking and expectations of novelty and positive reinforcement. By contrast, we hypothesized that in the case of chronically bored individuals the experience is not apathy but rather an abstinence-like, hedonic-deficit state that manifests itself in the form of exaggerated compensatory subjective craving for positively reinforcing (i.e., interesting) experiences. We therefore expected that this hedonic deficit would result in a negative association between measures of anhedonia and feelings of persistent/frequent boredom in populations where the prevalence of an anhedonic adaptation to persistent boredom was assumed to be low (e.g., among college students). In the study described in this chapter, we anticipated that the among SPMI patients, an anhedonic adaptation (i.e., attributions of uncontrollability, ubiquity, and permanence) to persistent boredom would be more far more common than in non-clinical populations and would result in a positive association between boredom and anhedonia.

Hallucination-Proneness There is of course a considerable amount of anecdotal evidence that suggests that psychotic patients are more likely to hallucinate under conditions of extreme over-stimulation and under-stimulation. However, the hypothesized boredom-hallucination-proneness association was based on two intersecting points that were originally articulated in the context of a published case study that involved hallucinatory behavior as coping strategy for boredom (Todman, 2003). First, is the widely accepted view among researchers that hallucinations are not pathognomonic of mental illness and, in fact, are quite common in the general population

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(Slade & Bentall, 1988). Second, there is the observation that the environmental conditions that have been shown to promote and exacerbate hallucinations in hallucination-prone individuals are strikingly similar to the conditions that are known to induce feelings of boredom (i.e., stimuli that are high in redundancy, of low complexity, and which provide limited opportunities for engagement or exploration) (Margo et al, 1981). Hence the expectation of a boredom-hallucination-proneness association. The predicted associations between boredom and hallucination proneness, and boredom and anhedonia were tested in a sample of 84 participants had been recruited from the student population at the New School for Social Research. Demographically, the sample consisted of 60 women and 24 men, ranging in age from 18 to 42 years of age (Mean age= 28.7, SD= 9.5) and was 78% Caucasian, 12% Asian, 5% African American, 3% Hispanic, and 2% other. The participants were administered the following measures in a large group setting: The Boredom Proneness Scale (BPS; Farmer and Sundberg, (1986), a measure of trait boredom; The Boredom Susceptibility Scale (BSS; Zukerman, 1979), another measure of trait boredom; The Launay-Slade Hallucination Scale (LSHS; Launay & Slade, 1981; Slade & Bentall, 1988), a measure of hallucination-proneness; The State Boredom Measure (SBM; Todman, 2004; see Appendix 1.), a measure of state boredom; and a modified version of The Snaith-Hamilton Pleasure Questionnaire (SHPQ-M; Snaith & Hamilton, 1995), a measure of anhedonia. With the exception of the SBM, all of the measures were administered only once. The SBM was administered a second time, approximately one month after the first administration. The scores for each of the eight items on the SBM were summed across the two administrations to yield a single composite score for each item, thus reflecting the degree to which reported levels of boredom were sustained over the one-month period. In keeping with the hypothesized existence of the exaggerated, abstinence-like state described, boredom frequency (SBM1) and boredom duration (SBM2) over the preceding two weeks were both found to be positively correlated with scores on the SHPQ-M. (note: lower scores on the modified SHPQ are associated with higher levels of hypohedonia). Two items from the SBM (i.e., degree of unpleasantness [SBM4] and impact on quality of life [SBM5] over the preceding two weeks), were also positively correlated with the LSHS, suggesting that individuals who were the most bothered by boredom (functionally and affectively) were also the individuals who were more likely to be hallucination-prone. Interestingly, controlling for state boredom (SBM) through a partial correlation analysis effectively eliminated the association between the trait boredom measure (BPS) and hallucination-proneness, but not the association between anhedonia and BPS (r=.26, P< .029), indicating that there is more to the latter relationship than sustained state boredom or its aversiveness. Finally, state boredom items were found to be the only significant predictors of current drug use. Self-identified substance users reported feeling frequently bored and that the quality of their lives was being negatively affected by boredom. However, they did not feel that they had been experiencing unusually long periods of sustained boredom (quite possibly because of their drug use). By contrast, the only significant predictor of past involvement in drug treatment was the feeling that boredom was having a negative impact on the quality of life.

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Frequency/Duration + High

Intensity /Unpleasantness + High

Low 0

Extensiveness/Ubiquity + High Figure 1. A Hypothetical Model of the Relationship between Anhedonia and Three Subjective Dimensions of Boredom. Solid Circle Represents the Clinical State of Anhedonia = Expectancies of High levels of Persistent and Frequent Boredom + Expectancies of High Levels of Extensive Boredom + Expectancies of High Levels Boredom Intensity.

BOREDOM IN METHADONE PATIENTS We have also employed the SBM (Todman, 2004) and a number of other measures to examine the role of state boredom in sample of patients in a methadone maintenance treatment (MMT) program in NYC (Rajaratnam, , 2007; Todman, 2007). The study was conducted in the context of a larger study, which focused on the effects of aging and long term treatment with methadone. The inclusion of a state boredom measure in this study was prompted by findings from studies that have suggested that there is an association between boredom and the tendency to use alcohol and other psychoactive substances (Johnston & O’Malley, 1986; Iso-Ahola & Crowley, 1991; Orcott, 1984). However, to our knowledge, there had been no studies to date that had been able to demonstrate a relationship between state boredom and a patient’s ability to remain abstinent while participating in a methadone maintenance treatment program. Moreover, since state boredom by definition varies over time and circumstance, we conjectured that if an association were to be found, it would be of considerably greater clinical utility than the trait-based associations that had been found in previous studies. Briefly, The study consisted of a sample of 156 methadone participants, with a mean age of 45 years of age. Sixty-six percent of the participants were male. The average amount of time in methadone treatment had been appoximately 10 years. All of the patients were paid for their participation. As part of a larger battery of assessments patients were administered the following scales: The SBM (Todman, 2004), the Brief Symptom Inventory (BSI; Derogatis & Melisartos, 1983) and the Barratt Impulsiveness Scale (BIS; Barratt, 1993).

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Additionally, Information regarding urine toxicology results were obtained from the patients’ clinical records. In keeping with the initial prediction that state boredom would be associated with greater symptom exacerbation and subjective distress, patients who reported more state boredom, particularly in terms of frequency, duration and impact on quality of life, were more likely to report higher elevations on almost all of the scales of the BSI, including Depression, Somatization, Interpersonal Sensitivity, Anxiety, Phobic Anxiety, Hostility, Paranoid Ideation, Psychoticism and Global Severity. Another equally interesting finding was that participants who reported finding boredom particularly unpleasant over the preceding 14 days but who did not experience long periods of sustained boredom, were more likely to be have drug-free urine toxicology results at 30days and at 60days prior to the administration of the SBM. Furthermore, and consistent with this finding, individuals who reported having protracted periods of boredom over the previous 14 days were more likely have urine samples that were positive for opiates at 30 and 60 days prior to the SBM administration. Taken together, these findings suggest that despite an equal aversion to boredom, the abstinent patients, unlike those who continue to use opiates, may have developed coping mechanisms that have allowed them to avoid extended periods of boredom. (It is also important to note that the scores for depression, anxiety (from the BSI) and impulsivity (BIS) were also entered into the regression analysis with the SBM items but did not prove to be particularly effective predictors of either drug free urine toxicology results or continued opiate use.) Finally, the SBM provided no predictive value with toxicology results that were obtained 12 months prior to the administration of the SBM. This type of temporal gradient in predictive efficiency is consistent with the status of the SBM as a state measure.

STUDY RATIONALE Although various theorists have suggested that some of the negative symptoms typically associated with schizophrenia and might not be endogenous in origin, but rather the byproduct of an under-stimulating treatment environment (e.g., Wing and Brown, 1970), there have been few attempts to empirically support this claim. In earlier writings, Todman has speculated about the various manifestations and consequences of boredom in psychotic disorders and have presented a series of case studies to illustrate the range of behavioral adaptations and responses that are likely to triggered by boredom and/or attempts to avoid it (Todman, 2003). In a recent study with a sample of college students, two of the associations that were predicted on the basis of the case studies (i.e., boredom/boredom proneness – hallucinationproneness; and boredom/boredom proneness – anhedonia) were confirmed (Todman, 2007). The present study was undertaken in an effort to extend these findings into an actual SPMI population. In addition to the general goal of replicating some of the previously obtained boredom-related associations in a sample of individuals with actual histories of psychotic illness, we hoped to address several other questions and predictions. They included the following: 1. The observed relationship between boredom and anhedonia in the non-clinical sample have been found to be a negative one, suggesting that persistent feelings of

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boredom engender a type of abstinence or interest-craving syndrome (Todman, 2007). It was hypothesized that this inverse relationship reflects an exaggeration of the normal response to a monotonous experience – the seeking of a more interesting environment. Of particular interest in the current study was the question of whether this relationship would be reversed in a sample of individuals with schizophrenia and schizoaffective disorder. We expected this to be case based on the hypothesis that anhedonia and boredom exist on functional continuum of severity, with anhedonia occurring when a persistently bored individual concludes that the source of their boredom is internal, uncontrollable, inescapable and permanent. We conjectured that these types of attributions were far more likely to occur in the case of individuals with severe and persistent mental illnesses such as schizophrenia and schizoaffective disorder; 2. Another question of interest was issue of the differential prevalence and experience of boredom among the constituent diagnostic groups of the SPMI population. Specifically, we wanted to know whether boredom, a correlate of depressed mood, restlessness and feelings of general dissatisfaction (e.g., Kavanagh, et al, 1981), tended to be more pervasive in the more mood-involved disorders in the SPMI (i.e., schizoaffective disorders, major depression and bipolar disorder). We also speculated that if anhedonia does in fact involve the attribution of permanence and ubiquity to feelings of boredom, we should also expect fewer external, situational attributions about the source of boredom in conditions in which anhedonia is expected to be particularly prevalent; 3. Since psychometrically determined hallucination-proneness is not the same as a documented history of having hallucinations, we wanted to determine whether boredom was in fact associated with an actual history of hallucinations in a SPMI population; 4. And finally, we wanted to find out whether current substance abuse status could be discerned on the basis of boredom prevalence, as was found to be the case in both college student and MMTP populations.

METHOD Participants Thirty-five participants were recruited from a community-based day treatment program for SPMI patients in New York City. The sample consisted of 13 individuals with schizophrenia, 10 individuals with schizoaffective disorder, eight individuals with Bipolar disorder, three individuals with Major Depressive Disorder, and one individual with psychotic disorder NOS. Because of the small cell sizes, the latter two diagnostic groups were excluded from most of the analyses. The mean age of the overall sample was 46, with a range of 26 to 82 years of age. A more complete description of the demographic and clinical characteristics of the sample is provided in Table 1. All of the participants were paid for their participation.

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McWelling Todman, Daniel Sheypuk, Kristin Nelson, et al. Table 1. Sample characteristics including frequencies and percentages across demographic and clinical features. N= 35

Race/ Ethnicity

Gender

history of depression

depression in last 14 days

Heard voices in last 14 days

history of hearing voices

poor compliance

substance abuse history

Current Substance User

Freq.

%

African Am. Hispanic Asian Total Male Female Total

26 8 1 35 20 15 35

74.3 22.9 2.9 100.0 57.1 42.9 100.0

no yes Total

11 24 35

31.4 68.6 100.0

no yes Total

23 12 35

65.7 34.3 100.0

no yes Total

28 7 35

80.0 20.0 100.0

no yes Total

14 21 35

40.0 60.0 100.0

no yes Total

23 12 35

65.7 34.3 100.0

no yes Total

5 30 35

14.3 85.7 100.0

no yes Total

25 10 35

71.4 28.6 100.0

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Materials and Procedure The participants were recruited by case managers who were blind to the goals of the study. Each participant was interviewed individually by a trained Masters level graduate student in clinical psychology. In addition to the administration of the scales and measures listed below, the following information was obtained from the patient’s clinical record: Current diagnosis; current medications; last inpatient stay; evidence of prior substance and/or alcohol abuse; evidence of current substance and/or alcohol abuse; and evidence of poor compliance with prescribed psychotropic medications. (All of the forgoing information was confirmed for accuracy and currency with the treating psychiatrist and the assigned case manager.). In addition, the following information was obtained directly for the patient: whether or not they had a history of hearing voices; whether or not they had heard voices during the previous 14 days; whether or not they had a history of depression; whether they had felt depressed during the previous 14 days; and a list of five activities that they enjoy and engage in on a regular basis. Finally, using a five point likert-type scale, ranging from Not at all to Constantly, two clinicians familiar with each of the participants in the study were asked to rate each of the patients on the extent to which they were: 1. Perceived to be Withdrawn and isolated; 2. Perceived to be Apathetic; 3. Perceived to be Non-communicative;4. Perceived to be Exhibiting Flat affect; and 5. Perceived to be Unable to enjoy anything. The two clinicians were also asked to give an overall rating of symptom severity using a fivepoint likert-type scale, ranging from None (1) to Profound (2). A third set of ratings for 16 of the 35 patients were provided by another clinician who was insufficiently familiar with the remaining patients to provide ratings for the entire sample. The participants were also administered the following scales and measures during a single session while attending the clinic:

Launay-Slade Hallucination Scale (LSHS; Launay and Slade, 1981; Slade and Bentall, 1988) This self-report scale consists of 12 items and was designed to evaluate an individual’s propensity to hallucinate based on the view that hallucinatory events lie along a continuum that includes both nonrmal and pathological anomalous perceptual experiences. Slade and Bentall (1988) established the reliability and validity of the LSHS on a non-psychiatric control sample (N = 150) and modified the scale by substituting the true/false dichotomy with a 5 point Likert Scale. Levitan, Ward, Catts, and Hemsley (1996) subsequently proposed a four factor structure to the LHS: Factor 1, consisting of items concerning vivid daydreams (items 2,3,5,6,9); Factor 2, consisting of items reflecting hallucinatory experiences in psychosis (items 7,9,10, 11,12); Factor 3, consisting of items tapping intrusive, vivid thoughts (loading > 0.3, items 1,3,4,12); and Factor 4 consisting of items tapping perceptual abberations (items 8,9). The present study employed the Slade and Bentall (1988) modified version of the scale. The Snaith-Hamilton Pleasure Questionnaire- Modidfied (SHPQ-M; Snaith and Hamilton, 1995) This scale is a 14-item self-report scale that asks respondents indicate the extent to which they would expect to derive pleasure from certain activities and experiences. Overall, the

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SHPQ has been found to be psychometrically sound (Snaith & Hamilton 1995). In the original scoring scheme by Snaith and Hamilton, there are four scoring categories: “Definitely agree” and “Agree”, both of which receive as score of “0”, and “Disagree” and “Definitely disagree”, both of which receive a score of “1”. Consequently, a high score is associated with anhedonia and a low score with normal hedonic tone and hedonic strivings. Based on a study of sample of individuals with Major Depression Snaith and Hamilton have suggested that scores above 2/3 are indicative of clinically significant levels of anhedonia. In the approach adopted in this study, the 4-category scoring system was replaced by a 7-point likert-type scale ranging from “strongly disagree” (1) to “strongly agree” (7). Hence, the higher score, the higher the hedonic tone and hedonic strivings. Importantly, by providing a middle response category between “agree” and “disagree” this approach makes the assumption that individuals can be ambivalent or unsure in their responses to statements such as “I would get pleasure from helping others” or “I would enjoy being with family or close friends”. Consequently, in addition increasing sensitivity and variability, hedonic tone /hedonic strivings is conceived as a truly continuous dimension with no a priori claims being made with regard to the threshold for clinical significance. Accordingly, the modified SHPQ (SHPQ-M) represents a continuum of expectancies regarding hedonic strivings that range from unusually low levels (hypohedonia) to the highly exaggerated levels (hyperhedonic pleasure cravings) that have been found to be positively associated with boredom proneness in non-clinical populations (Todman, 2007).

The State Boredom Measure (SBM; Todman, 2004) The SBM is designed to be a state measure. It consists of eight questions about different aspects of the boredom experience, each of which is associated with a seven-point Likert-type scale (see Appendix 1). The participant is asked to base his/her responses on their recollections about boredom experiences during the preceding 14 days. The eight questions were created through a rational-theoretic process. Each of the test items can be grouped into one of four clusters or dimensions: Frequency/ Duration; Degree of Unpleasantness/ Aversiveness; Tolerance; Internal/External Attribution. Reliability and Validity were established using a sample of 160 adults, ranging in age from 24 to 65. The scale has good internal consistency (Alpha = 0.81), item-total correlations range from .67 to .30, and test-retest reliability ranges from .78. to .45, across the eight items (Todman, 2004). In terms of validity, the eight items have been found to have correlations with the two best known measures of trait boredom, the Boredom Proneness Scale (BPS; Farmer and Sundberg, 1986,) and the Boredom Susceptibility Scale (BSS; Zukerman, 1979) that range from .82 to .37 and .78 to.25, respectively. The Satisfaction with Life Scale (SWL: Diener,, 1985) is a concise and 5-item measure, which targets an individual’s overall (general) satisfaction with life.. Life satisfaction is considered to be one of three factors in the more general construct of subjective well being, which is believed to consist of positive affective appraisal, negative affective appraisal, and life satisfaction. Life satisfaction is distinguished from affective appraisal in that it is assumed to be cognitively driven, rather than emotionally driven. The SWL has been widely used to assess satisfaction with life in a variety of domains and populations and has been shown to have good psychometric stability (Arrinddell, Meeuwesen & Huyse1991; Neto, 1993; Pavot & Diener,1993).

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RESULT AND DISCUSSION The inter-correlations between the eight SBM items and the other measures in the study are presented in Table 2. Although the sample is prohibitively small, many of the associations are consistent with the study predictions, as well as the results obtained in non-clinical samples (Rajaratnam, , 2007; Todman, 2004; 2007). Specifically:

Hallucination Proneness LSHS, the measure of hallucination proneness, correlated positively with six of the eight items of the SBM. Of particular notice is the large correlation coefficients associated with the LSHS scores and the degree to which patients’ experienced boredom as being unpleasant (SBM4; r= .69, p<.001) and/or particularly disruptive (SBM5; r = .66, p<.001) over the previous two weeks. Importantly, controlling for a history of auditory hallucinations and having auditory hallucinations within the last two weeks had minimal effect of the strength of the observed associations.

History of Hearing Voices and Voices during the Last 14 Days Only two items correlated with a self-reported history of hearing voices (i.e., lifetime history). They were the patient’s self-described capacity to tolerate boredom (SBM3: D; r = .36 p< .05) and LSHS (hallucination proneness) scores. In addition to validating the utility of the hallucination proneness measure, this finding also supports a central claim made about the predicted association between boredom and hallucination proneness: hallucinations, like daydreaming and other covert forms of self-stimulation, enhance the individual’s capacity to “tolerate” boredom (Todman, 2003). It is of course possible that hallucination prone individuals are simply more sensitive to anomalous subjective experiences, or are perhaps more willing to report them. However, if this is the case, then it is surprising that there were not more significant associations found between the LSHS and the other variables in the study. Of the variables assessed, only self-reported feelings of depression during the previous 14 days was found to be significantly associated with patients’ actual reports of hallucinatory experiences during the preceding 14 days. This finding leaves open the possibility that complaints of recent/current hallucinations and depressive affect may be in part expressions of current distress.

Depressive Feelings during the Last 14 Days Consistent with the predicted relationship between boredom and depressive mood, significant associations were found between the degree of unpleasantness attributed to boredom (SBM4) and reported depression during the pervious 14 days (r = .45, p < .01).

Table 2. Inter-correlation matrix consisting of the component items of the State Boredom Measure (SBM), The Satisfaction with Life Scale (SWL), the Launay-Slade Hallucination Scale (LSHS), the Snaith-Hamilton Pleasure Questionnaire- Modified (SHPQ), Poor compliance with medication, History of hearing voices, History of depression, Substance Abuse history, depression within the last 14days, heard voices within the last 14days, Current Substance Abuse, and Gender, (N= 31) A A B

G ender F re q u e n c y F r e q . B o re d o m

SBM 2

SBM 3

SBM4

SBM 5

SBM 6

SBM 7

SBM8

C

D

E

F

G

H

I

-0 .2 5

H ig h T o le r a n c e U n p le a s a n tn e s s

-0 .0 5

0 .5 0 **

B o re d o m Im p a c t B o re d o m C o m p a re d

-0 .0 2

0 .5 2 **

0 .4 4 *

B o re d o m A ttrib B o re d o m A ttrib

P

Q

R

1 .0 0

0 .0 5

0 .1 5

0 .3 2

0 .4 2 *

1 .0 0 .

-0 .3 8 *

0 .4 4 *

0 .6 1 * *

0 .4 4 *

0 .5 7 **

1 .0 0 .

-0 .0 4

-0 .1 6

0 .0 4

-0 .1 5

-0 .3 1

0 .1 1

1 .0 0 .

-0 .1 0

0 .1 1

0 .3 6 *

0 .1 1

0 .5 4 * * 0 .4 8 **

0 .0 4

to M e d ic a l P r o b . I

O

.

to T e n Y e a r s A g o H

N

1 .0 0

o n L ife Q u a lity G

M

.

o f B o re d o m F

L

1 .0 0

fo r B o re d o m E

K

.

L o n g e r T h a n 3 H o u rs D

J

1 .0 0

o f B o re d o m C

SBM 1 B

1 .0 0 .

-0 .3 0

0 .2 7

0 .2 7

0 .2 8

-0 .3 4

-0 .1 6

-0 .2 2

-0 .2 2

0 .3 4 0 .5 7 **

0 .0 4

0 .4 1 *

1 .0 0

to S o c ia l P r o . J

to ta l s a tis fa c tio n

-0 .2 9

-0 .2 1

-0 .1 4

-0 .3 2

-0 .3 1

1 .0 0

w ith life K

h a llu c in a tio n

-0 .3 6 *

0 .1 6

0 .3 8 *

0 .4 0 *

0 .6 9 **

0 .6 6 * *

-0 .2 5

-0 .3 6 *

0 .3 6 *

0 .4 0 *

-0 .1 5

1 .0 0

p ro n e n e s s L

a n h e d o n ia

M

s u b s ta n c e a b u s e h x

N

p o o r c o m p lia n c e

0 .0 5 -0 .3 9 * -0 .2 2

-0 .1 9 -0 .5 2 * *

-0 .2 0

0 .0 3

-0 .2 2

-0 .2 3

-0 .1 7

0 .2 1

-0 .2 0

1 .0 0

-0 .0 9

0 .1 1

-0 .1 5

-0 .0 7

0 .1 4

0 .0 0

0 .0 5

0 .0 5

0 .2 1

0 .3 0

-0 .1 9

1 .0 0

0 .2 9

0 .0 4

0 .0 4

0 .1 5

0 .1 6

-0 .1 9

-0 .1 0

0 .2 2

0 .0 4

0 .2 2

-0 .0 3

0 .0 1

w ith m e d s O

h is to ry o f

1 .0 0 .

0 .0 0

-0 .0 1

0 .0 8

0 .3 6 *

0 .3 1

0 .1 3

-0 .2 0

-0 .0 2

0 .0 1

-0 .0 2

0 .4 3 *

-0 .1 1

0 .1 9

0 .1 7

h e a r in g v o ic e s P

h e a r d v o ic e s

1 .0 0 .

-0 .1 5

0 .0 0

-0 .0 8

0 .0 9

0 .2 6

0 .2 3

0 .0 8

0 .0 3

0 .1 9

-0 .2 5

0 .3 4

0 .2 0

-0 .0 8

0 .0 8

0 .2 7

in la s t 1 4 d a ys Q

h is to ry o f

1 .0 0 .

0 .0 3

0 .1 5

0 .2 6

0 .1 5

-0 .0 3

0 .2 0

0 .2 5

0 .1 5

0 .2 6

0 .1 8

-0 .4 0 *

0 .1 1

0 .1 8

0 .3 2

0 .2 4

-0 .2 3

0 .2 2

0 .0 9

0 .0 1

0 .0 0

-0 .0 1

0 .0 8

0 .1 6

0 .0 4

1 .0 0

d e p re s s io n R

d e p re s s io n

0 .4 5 *

0 .2 9

-0 .0 4

-0 .4 0 *

0 .4 4 *

0 .3 5 *

0 .2 7

0 .4 5 *

0 .3 3

in la s t 1 4 d a ys S

C u rr e n t

1 .0 0 .

0 .0 3

0 .3 8 *

0 .2 7

0 .2 0

0 .1 5

0 .2 3

-0 .0 6

-0 .1 7

0 .1 3

-0 .4 0

0 .3 4

-0 .2 3

0 .2 1

0 .4 2 *

0 .0 7

0 .1 6

0 .1 4

0 .3 2

S u b s ta n c e U s e

* = Pearson Correlation is significant at the 0.05 level (2-tailed). **= Pearson Correlation is significant at the 0.01 level (2-tailed). N = 31 (Mood Disorder and Psychotic Disorder NOS excluded from analysis).

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167

Although it was not surprising to find that depressive feelings during the last 14 days were also correlated (negatively) with SWL scores (r= -.40, p < .03), as noted above, the association of recent/current depressive feelings with LSHS (hallucination proneness) scores ( r = .44, p .<.03) and reported hallucinations during the previous 14 days (r = .45, p .<.01) was unexpected. Also surprising was the association between recent/current depressive mood and non-compliance with prescribed psychotropic medications (r =.35 p <.05). These findings, together with the association with SMB4 (boredom unpleasantness), suggest that the changes in the experience of boredom are likely to accompany more general disturbances in mood and symptom severity.

History of Depression The relationship between the SBM and self-reported prior episodes of depression is somewhat more complicated. The SBM item pertaining to the feeling that boredom is currently less pervasive than it has been in the past (i.e., 10 years earlier) was the only variable significantly associated with a reported history of depression (SBM6; r= – .40, p < .03). Specifically, despite reporting similar levels of current boredom (i.e., in terms of frequency [SBM1], duration [SBM2] and unpleasantness [SBM4]), individuals who reported having a history of depression also reported that they were currently less bored in relation to the past (M = 2.33) than patients who reported no history of depression ( M = 3.40). Moreover, this difference proved to be significant, even when controlling for depressive mood during the previous 14 days, F(1, 28) = 5.54, p <.0.01. This negative association between reports of prior depression and current levels of boredom relative to the past is intriguing and suggests that for many patients with prior periods of depressive mood, boredom figures prominently in the representation of the memory of the depressive experience. This would be consistent with the aforementioned positive association between current/recent depressive mood (i.e., feelings of depression in the last 14 days) and the degree of unpleasantness associated with boredom.

Anhedonia (SHPQ-M) In a previous study with college students the SHPQ-M was found to be positively associated with both state and trait boredom, leading to the hypothesis that sustained boredom in non-psychiatric populations typically results in heightened expectations of pleasure/interest in future environments and activities. Moreover, it was suggested that such a state might reasonably be expected to lead to increased pleasure/interest seeking behaviors on the part of the individual (e.g., drug seeking and drug use) (Todman, 2003; 2007). Todman has also argued that this inverse boredom-anhedonia relationship underscores the fundamental difference between the experience of mere chronic boredom, and its most severe manifestation, anhedonia. He has proposed that anhedoia should be construed as not only a diminution of the capacity to derive positive reinforcement from current activities and environments (i.e., boredom), but also the expectation that positive reinforcement (i.e., interesting and pleasurable experiences) will continue to be unattainable (Todman, 2003). It therefore follows that we might expect a different type relationship between boredom and the

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SHPQ-M in populations that are at risk for diminished expectations of future positive reinforcement (such as the SPMI). Several aspects of the current findings are consistent with this conjecture. First, as seen in Table 3, compared to the SHPQ-M mean of the college sample from the Todman (2007) study, the mean of the SPMI sample is significantly higher, indicating truly outsized expectancies of pleasure/interest on the part of the SPMI when asked predict their affective response to potentially pleasure-inducing environments/activities such as those implied by the SHPQ statement, “I would find pleasure in small things such as bright sunny day” (Snaith & Hamilton, 1995). Second, as in the case with the college sample, SHPQ-M scores were significantly correlated with the prevalence of boredom lasting longer the three hours (SBM2; r = -.52, p < .001) - but in the opposite direction. Moreover, individuals who reported higher levels of anhedonia also reported that boredom had a significantly greater impact on the quality of their lives (SBM5; r = -.36, p < .05). This seems to indicate that among the SPMI, individuals with the most persistent and disruptive boredom were also more likely to have greater diminishment in their expectancies for positive reinforcement from future environments and activities. It is as if some of the SPMI individuals, long constrained by their disabilities, relatively monotonous treatment environments and limited options for stimulating employment and recreational activity, had begun to habituate to the sameness of their lives. Consistent with this notion is the fact that no association was found between the SHPQ-M and boredom’s perceived unpleasantness (SBM4), nor were there associations between the SHPQ-M and satisfaction with life (SWL) scores, or between LSHS scores and reports of depression in either the recent or not so recent past. Table 3. Comparison of group means on the SBM, SHPQ & LSHS across Combined SPMI vs. College Student sample. GROUP

N SHPQ

LSHS a

3.13

2.26

SBM B4 B5 B6 B7 B8 a 3.35 3.87 2.84 2.68 2.61 2.61

b

3.33

2.46

3.14

3.77

2.98

3.20

2.31

22.13

3.28

2.40

3.20

3.80

2.94

3.06

2.39

B1 a

Combined SPMI*

31 85.35

22.13

College Students

84 26.86

b

12.52

Total

115

85.35

B2

B3

b

3.41

3.19

a-b = significant difference between means at the 0.05 level; SBM = State Boredom Measure; SHPQ =Snaith Hamilton Pleasure Questionnaire; LSHS = Launay-Slade Hallucination Scale.

It is of course important to acknowledge that SPMI status is inextricably confounded with income level and educational/occupational history, with most of the SPMI falling at or below the poverty level. It is therefore possible, and indeed likely, that much of the exaggerated expectations of enjoyment from relatively mundane activities such as taking a warm bath or eating one’s favorite meal are a stark reflection of the history of privation common to many in the SPMI sample. Even so, the fact remains that individuals who reported a higher prevalence of periods of sustained boredom also reported decreased levels of expected enjoyment from typically pleasurable activities and environments, suggesting that in the SPMI, sustained boredom, not depressive mood per se, may be the best indicator for hypohedonia.

Boredom, Hallucination-proneness and Hypohedonia …

169

Current Substance Abuse State boredom, as assessed by the SBM, was found in previous studies to an effective predictor of current substance use in both college students and patients in methadone maintenance treatment (Rajaratnam, , 2007; Todman, 2007). An important question in the current study was whether a similar relationship would obtain in a sample of SPMI; a population for which the rate of dual diagnosis (i.e., a co-occurring substance related disorder and another Axis I disorder, such as schizophrenia) is notoriously high (e.g., Kessler , 1997). As shown in Table 1, the rate of prior substance use in the current sample is extremely high (85.7%) and well within the range reported in the literature (Kessler , 1997). Moreover, because of the high base rate of prior substance use in the sample, substance abuse history was not found to be significantly correlated with current substance use, underscoring the value of identifying alternative markers in the monitoring of SPMI patients for current use (see Table 2). In fact, only three variables significantly correlated with current substance use: frequency of boredom (SBM1), SWL and poor compliance with prescribed medication. Working on the assumption that non-compliance with prescribed medications is probably a consequence (rather than an antecedent) of current substance abuse, a binary logistic regression analysis using SWL and boredom frequency as the predictor variables correctly identified 60% of the current substance abusers and 92.0% of the current non-users, for an overall accuracy rate of 82.9%, [χ2 (2, N = 35) =10.9, p< .004]. Moreover, since all of the 10 current substance users also had a history of substance abuse, adding substance abuse history to the list of predictors - despite its weak correlation to current use - improved the identification of non-users to 100%. Even though these results are consonant with previous findings from the previous studies with MMTP and non-psychiatric particpants, the sample size in the current study is probably too small, and the effects too modest, to place an inordinate amount of confidence in the findings. Nonetheless, the findings are promising, and as such, remain very much in line with the notion that boredom is probably an important (and under-appreciated) factor in the motivation to use substances among the SPMI.

Schizoaffective Disorder vs. Schizophrenia A major goal of the present study was to determine whether boredom as assessed by the SBM is experienced differently by individuals with schizoaffective and bipolar disorder than individuals with schizophrenia. It was hypothesized that individuals with schizophrenia would experience boredom less frequently and for shorter periods of time than individuals with disorders in which mood disturbances, especially depressive mood, were more prominent. This prediction was not confirmed. (Because of the small sample size, individuals with major depression and the single individual with psychotic disorder NOS were not included in the analysis.) The frequency, duration and unpleasantness of boredom among individuals with schizoaffective disorder were not found to be significantly different from mean levels among individuals with bipolar disorder and schizophrenia. A follow-up analysis was conducted to ascertain whether the assumption that the rates of depressive feelings were differentially distributed across the three diagnostic groups was in

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fact correct. The results confirmed that none of the inter-group differences in reported lifetime occurrences of depression were statistically significant. Specifically, 53.8% of individuals with schizophrenia, 80% of the individuals with schizoaffective disorder, and 75% of the patients with bipolar illness reported having a history of depression. In terms of the reported incidence of recent/current depressive feelings (during the last 14 days), significantly more individuals with bipolar illness (62.5%) reported having current or recent feelings of depression than individuals with schizophrenia (15.4%) [(χ2 = 1, N= 21) = 4.94, p < .026], but there were no significant differences found between schizoaffective disorder group (30%) and the other two diagnostic groups. Overall, the findings suggest that the differences in patientreported depression across diagnostic groups may not have been sufficiently robust (at least in the small sample used in the current study) to adequately test for differences in the incidence and duration of boredom as function of diagnosis. There were, however, significant differences between the three disorders in terms of the attributions made regarding the capacity to cope with and avoid boredom. Controlling for recent/current depression in an analysis of covariance (ANCOVA) individuals with schizophrenia (M= 3.16; p<. 03), as well those with bipolar disorder (M=3.26; p <. 04), were found to be significantly more likely to attribute their inability to cope with boredom to medical reasons (SBM7) than individuals with schizoaffective disorder (M = 1.42) (F(2, 27) = 3.46, p <. 04). On the other hand, individuals with schizophrenia (M=1.69) were significantly less likely than individuals with bipolar disorder (M = 3.50) to attribute their inability to avoid boredom to their social circumstances. (SBM8; F(1, 19) = 6.06, p <. 02), but only if recent/current depression was not entered as a covariate. The difference between schizophrenia and schizoaffective disorder approached but did not reach significance (M = 1.69 v 3.10, respectively) (F(1, 21) = 3.81, p <. 06). A related question that might be asked about the SPMI and boredom is whether the prevalence of boredom as measured by the SBM is significantly different from that of individuals who do not have significant psychiatric histories or diagnoses (i.e., college students). To answer this question, boredom scores on the SBM from two administrations approximately one month apart from the college sample described above (Todman, 2007) were averaged and compared with the scores from the SPMI participants in the current sample. As seen in Table 3., the only significant difference between the two groups on the SPM is on the item that assesses the degree to which the individual attributes situational or social problems to their inability to avoid boredom (SBM8). In a subsequent set of analyses in which the college sample was compared to the each of the diagnostic groups separately, only the schizophrenia vs. college sample comparison yielded a significant difference on any of the SBM items. Specifically, the patients in the schizophrenia diagnostic group were found to be significantly less likely to attribute their difficulties in avoiding boredom to current social circumstances (SBM8).

Staff ratings of Negative Symptoms, and Overall Severity Three staff members, blind to the hypotheses and the scores obtained by the various participants on the various measures administered, were asked to provide their impressions regarding the following patient features using a likert-type rating scale that ranged from 1= Not at all, to 5 = Constantly:

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1. 2. 3. 4. 5.

171

The degree to which the patient is perceived to be Withdrawn and Isolated The degree to which the patient is perceived to be Apathetic The degree to which the patient is perceived to be Non-communicative The degree to which the patient is perceived to have Flat Affect The degree to which the patient does not seem to Enjoy Anything

Two of the three staff raters provided ratings for the entire sample, the third rater completed 16 of the 35 participants using the same criteria. The staff raters were also asked to give an impression of the overall severity of the patients’ illness on a likert-type scale, ranging from 1= None, to 5 = Profound Apart from clarifying the definitions of the various terms used to describe the behaviors associated with the negative symptoms referred to in the questions, formal training was not provided to the raters, nor was there an attempt to establish inter-rater reliability. In short, we were interested in obtaining ecologically valid judgements from the clinical staff about the clinical status of the clients, much as they typically do on a daily basis without the benefit of standardized measures or checks for inter-rater agreement. In so doing, we hoped to get a sense of the degree to which the judgments of trained clinicians about the presence of negative symptoms and signs correlated with patients’ reports of boredom as measured by the SBM. (Note: Two of the raters were experienced psychiatric social workers with advanced degrees. The third rater was a trained and experienced Ph.D candidate in clinical psychology) In terms of internal consistency, two of the raters demonstrated a considerable amount of internal consistency in their ratings across the five negative symptom items (Alpha = .93 & . 87). The third rater evidenced a somewhat lower level of internal consistency (Alpha = .68). Interestingly, for two of raters, none of their negative symptom ratings correlated with their ratings of overall severity. In the case of the third rater, only two of the five items, “Apathy” and degree of “Withdrawal and Isolation”, were significantly correlated with severity (r = .48, p < .01 and r= .41, p < .02, respectively). Furthermore, while ratings of two of the raters significantly covaried with four of the six items ( range: r = .84 to r =.54 ), there was no significant covariation found between the ratings for the remaining rater and the ratings by the other two raters. The only items that failed to show significant inter-rater covariation between any two raters was overall severity and non-communicative behavior. None of the items on the SBM correlated significantly with the ratings of severity provided by the three raters. However, it is particularly notable that for one of the raters the patients’ reported frequency of boredom significantly correlated with the rater’s impressions of the patients’ degree of Withdrawal and Isolation (r = .63, p < .01), Apathy (r = .59, p<. 02) and capacity to Enjoy Anything (r = .62, p < .02). Smaller but still significant associations were also found between the patients’ reported capacity to tolerate feelings of boredom on the SBM and the raters’ impressions of the patients’ level of Apathy (r= .360, p <. 047), capacity to Enjoy Anything (r =. 350, p<. 05) [same rater], and degree of Flat Affect (r= -.42, p<.02). Collectively, these findings suggest, but don’t confirm, that expressions of patient boredom may be capable of influencing the clinical impressions of trained clinicians, even with those clinicians have frequent and extend contact with the patient.

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CONCLUSION It perhaps goes without saying that the small sample sizes and the fact that no corrections were made for the large number of comparisons requires that the findings be interpreted with extreme caution. Indeed, if a conservative adjustment such as the Bonferroni correction for alpha levels had been employed, most of the findings would have failed to reach significance. In short, the findings are at best, provisional. Even so, most of the findings were based on predictions drawn from previous studies with non-SPMI participants, thus not the product of blind, exploratory analyses. Consequently, the current set of findings, if nothing else, should provide incentive and justification for taking a more serious look at boredom and its utility in care and rehabilitation of the SPMI. If the behavioral choices associated with an anxiety-provoking situation can be reduced to the overworked phrase, “flight or fight”, then the choices associated with boredom might well be described as “fidget or flee”. A working premise of the present study has been that fidgeting and fleeing, much like fighting or taking flight, are often maladaptive responses in a complex social world. And while most of us acquire a broader and more flexible repertoire of coping skills as a product of the normal psychosocial developmental process, there is no guarantee that these skills will be necessarily effective in all circumstances or that they will be used appropriately. Indeed, it is almost universally assumed by clinicians that the coping skills of individuals with severe and persistent mental illnesses such as schizophrenia and schizoaffective disorder are likely to be less effective, less efficient, less well developed and used less competently than those of healthy controls (e.g., Rosenfarb et al, 2000). It would therefore seem safe to assume that this would also apply to the coping strategies typically employed to avoid and manage boredom. Consistent with this view were the findings from a study with MMTP patients whose levels of reported boredom were found to be positively correlated with almost all of the clinical and summary scales of Brief Symptom Inventory (Derogatis & Melisaratos, 1983), including the Global Severity Index (Todman, 2007). Consequently, the findings from the current study (despite the presence of some marginal effects) are somewhat surprising and are contrary to the expectation that the SPMI would be particularly vulnerable to feelings of monotony, especially in the highly routinized, understimulating, community-based facilities in which they often receive care and support. Nonetheless, differences were found between individuals with schizophrenia and college students in terms of the attributions made about boredom, with the former being less likely attribute their inability to avoid boredom to social circumstances. One of interpretation of this finding that is consistent with the predictions of the study is that individuals with schizophrenia are more inclined to perceive their boredom as a product of non-social, possibly internal factors that are less controllable and/or subject to modification. The finding that individuals with schizophrenia, when compared to individuals with schizoaffective disorder are more inclined to attribute their inability to avoid boredom to medical reasons bolsters this conjecture. In other respects, study was successful in generating supporting evidence for at least some of our initial predictions. Most notable were the following results: 1. As was the case in previous studies with other populations, the SBM demonstrated robust correlations with hallucination proneness (LSHS). Moreover, tolerance for

Boredom, Hallucination-proneness and Hypohedonia …

2.

3.

4.

5.

173

boredom (SBM3) was found to be correlated with self-reported histories of actual auditory hallucinations. Also predicted and confirmed was the finding that current substance abuse is associated with the frequency of boredom (SBM1), demonstrating the potential utility of state boredom as a marker for a patient’s current risk for substance abuse in populations where the base rate of substance abuse history is likely to be extremely high (e.g., the SPMI). In a previous study with a non-clinical sample, expectancies of reinforcement from future environments and activities and boredom were found to be positively correlated. It has been argued that like daydreaming, outsized expectancies of positive reinforcement through alternate activities and/or environments reflect a covert expression of the normal motivational and cognitive concomitants of the “flee or fidget” reaction to sustained boredom. The current study replicated the finding of an association between expectancies of reinforcement from future environments and activities and boredom, but also demonstrated that among the SPMI, the relationship is inverted so that greater amounts of sustained boredom is associated with diminished expectations of future reward. We interpret this finding as being consistent with a conception of anhedonia as an extreme adaptation to sustained boredom in which there is an increasing conviction that monotony is permanent, ubiquitous, and largely uncontrollable. Consonant with the notion that such an adaptation is probably more prevalent among the individuals with schizophrenia in the current sample was the fact that they were less likely to attribute their inability to avoid boredom to external, social factors (SBM8) and more likely to report that they were more bored today than they were 10 years (SBM6). Also, the more frequently individuals with schizophrenia experienced periods of sustained boredom (SBM 2), the greater their reported satisfaction with life (r= .609 p <. 029) Although there is no good way to know for sure, one interpretation of this seemingly paradoxical finding is that the avoidance of anxiety is paramount for these individuals, and to do so requires a sort of Faustian bargain in which protracted periods of boredom (anxiety’s conceptual opposite) are accepted as a normal, if not desirable, state of being (Csikzentmihalyi, 2000). By contrast, for patients with bipolar disorder, the correlations between sustained boredom and satisfaction with life and expectancies of positive reinforcement were negative and large (r = -.908 p <. 002; r = -.743 p<.035, respectively). This suggests that while boredom plays a very prominent role in the motivational dynamics of patients with bipolar illness, it seems to play a relatively less important role (at least in relation to anxiety) in the dynamics of individuals with schizophrenia. That no associations were found between boredom and either the SWL or the SHPS among patients with schizoaffective disorder speaks to a potentially important distinction between schizoaffective disorder and the other two diagnoses. Although boredom has been accused of masquerding as a negative symptom for decades (e.g.,Wing and Brown, 1970) the present study is one of the few that has been able to demonstrate empirically that there is a correspondence between patients’ reports of boredom and the attributions of negative symptoms on the part of experienced clinicians. The position taken in this chapter, however, is that boredom

174

McWelling Todman, Daniel Sheypuk, Kristin Nelson should be regarded as a negative symptom in its own right and that it exists on a functional continuum with anhedonia. 6. Finally, the strong correlation between noncompliance and substance use is consistent with other similar findings in the literature (e.g., Kessler et al 1997). It is therefore not surprising that the diagnostic group with by far the largest percentage of active substance users, bipolar disorder, is also the diagnosis with the largest proportion of noncompliant individuals. It is also interesting that the bipolar group is the diagnostic group that is most likely to attribute their boredom coping problems to both social (external) and medical (internal) obstacles.

APPENDIX 1: THE STATE BOREDOM MEASURE (TODMAN, 2004) 1. Over the last two weeks: How often would say that you can remember feeling bored? 1

2

3

4

5

6

7

never or

most or all

very rarely

of the time

2. Over the last two weeks: How often would you say that you can you remember feeling bored for longer than three hours at a time? 1 Never or Very Rarely

2

3

4

5

6

7 Very Frequently

3. Over the last two weeks: What is the longest period of time that you could tolerate being bored before trying to do something about it? 1 Only for very brief periods

2

3

4

5

6

7 For very long periods of time of time ( eg. less than few minutes) (e.g. more than two hours)

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175

4. Over the last two weeks: How unpleasant was the experience of boredom for you? 1 Not Unpleasant

2

3 Mildly Unpleasant

4

5 Moderately Unpleasan

6

7 Extremely Unpleasant

5. Over the last two weeks: Compared to how you felt ten years ago, would you say that you were: 1 Bored Much LESS Often

2

3 Bored Somewhat LESS Often

4 No Difference

5 Bored Somewhat MORE Often

6

7 Bored Much MORE Often

6. Over the last two weeks: Have there been physical or medical problems that you believe have made it more difficult to avoid being bored? 1 Strongly Disagree

2

3 Disagree

4 Not Sure

5 Agree

6

7 Strongly Agree

7. Over the last two weeks: Have there been situational or social problems (e.g., issues at work or home) that you believe have made it more difficult to avoid being bored? 1 Strongly Disagree

2

3 Disagree

4 Not Sure

5 Agree

6

7 Strongly Agree

REFERENCES Barratt, E.S. (1993). Impulsivity: Integrating cognitive, behavioral, biological and environmental data. In W.B. McCown, J.L Johnson and M.B. Shue(Eds.), The Impulsive Client: Theory, Research and Treatment (pp.39-56) Washington, DC: American Psychological Association. Bogenschutz M.P & Siegfried S.L. (1998). Factors affecting engagement of dual diagnosis patients in outpatient treatment. Psychiatric Services 49:1350-1352. Csikszentmihalyi, M. (2000). Beyond boredom and anxiety. Jossey-Bass Inc. Davies, A. H. (1926).The physical and mental effects of monotony in modern industry. British Medical Journal 2: 472-479. Derogatis, L.R & Melisaratos, N. (1983). The Brief Symptom Inventory. An introductory report. Psychological Medicine, 13(3): 595-605

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Farmer, R., and Sundberg, N.D. (1986).Boredom Proneness- The development and correlates of a new scale. Journal of Personality Assessment 50: 4-17. Gordon, A., Wilkinson, R., Mcgown, A., and Jovanoska, S. (1987). The psychometric properties of the Boredom Proneness Scale: An examination of its validity. Psychological Studies 42: 85-97. Johnston, L. D. & O'Malley, P. M. (1986). Why do the nation's students use drugs and alcohol? Self-reported reasons from nine national surveys. Journal of Drug Issues, 16: 29-66. Kavanagh, M.J, Hurst, M.W., and Rose, R. (1981). The relationship between job satisfaction and psychiatric health symptoms for air traffic controllers. Personnel Psychology 34 (4): 691–707. Kessler, R.C., Crum, R.M., Warner, L.A., Nelson, C.B.,Schulenberg, J., & Anthony, J.C., (1997). Lifetime co-occurrence of DSM-II-R alcohol abuse and dependence with other psychiatric disorders in the National Comorbidity Survey. Archives of General Psychiatry, 54: 313-321. Launay, G and Slade, PD.(1981). The measurement of hallucinatory predisposition in male and female prisoners. Personality and Individual Differences, 2: 221–234 Leong, F.T., and Schneller, G.R. (1993).Boredom proneness: Temperamental and cognitive components. Personality and Individual Differences 14: 233-239. Levitan, C, Ward, PB, Catts, SV, Hemsley, DR. (1996). Predisposition toward auditory hallucinations: The utility of the Launay-Slade Hallucination Scale in psychiatric patients. Personality and Individual Differences, 21: 287–289. Margo, A., Hemsley, D.R., and Slade, P.D. (1981) The effects of varying auditory input on schizophrenic hallucinations. British Journal of Psychiatry 139: 122-7. Mikulas, W.L., and Vodanovich, S.J. (1993).The essence of boredom. The Psychological Record 43: 3-12. OHanlon, J.F. (1981) Boredom: A review. Human Factors 23: 329-340. Orcutt, J.D. (1984). Contrasting effects of two kinds of boredom on alcohol use. Journal of Drug Issues 14: 161-173. Rajaratnam, R., Sivesind, D., Todman, M., Roane, & Seewald, R. (2007). Characteristics of Older Adults Enrolled in Methadone Maintenance Programs American Association for Geriatric Psychiatry AAGP Annual Meeting - New Orleans, LA, March 1. Rosenfarm, I.S., Neuchterlein, K.H., Goldstein, M.J., & Subotnik, K.L., (2000). Neurocognitive vulnerability, interpersonal criticism, and the emergence of unusual thinking by schizophrenic patients during family transitions. Archives of General Psychiatry, 57: 1174-1179. Slade, P.D., and Bentall, R.P. (1988) Sensory Deception: A Scientific Analysis of Hallucination. Croom Helm Snaith, R.P, Hamilton, M. (1995). A scale for the assessment of hedonic tone: the Sanith Hamilton Pleasure Scale. British Journal of Psychiatry 167: 99-103 Sundberg, N.D., Latkin, C.A., Farmer, R.F., and Saoud, J. (1991). Boredom in young adults: Gender and cultural comparisons. Journal of Cross-cultural Psychology 22: 209-223. Todman,M. (2003). Boredom and psychotic disorders: Cognitive and Motivational Issues Psychiatry: Interpersonal and Biological Processes 66(2): 146-167.

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Todman, M (2004). The dimensions of state boredom: frequency, duration, unpleasantness, consequences and causal attributions. Unpublished Document. New School for Social Research Vodanovich, S.J., and Kass, S.J.(1990).A factor analytic study of the Boredom Proneness Scale. Journal of Personality Assessment 55: 115-123. Wangh, M. (1975). Boredom in psychoanalytic perspective. Social Research 42: 538-550. Wiesbeck, G, A., Wodarz, N., Mauerer, C., Thome, J., Jakob, F., and Boening, J. (1996). Sensation Seeking, alcoholism and dopamine activity. European Psychiatry 11: 87-92. Wing, J. K. and Brown, G. W. (1970) Institutionalism and Schizophrenia. London: Cambridge University Press. Zukerman, M. (1979). Sensation Seeking: Beyond the Optimal Level of Arousal. Hillsdale, NJ: Erlbaum, Zukerman, M., Eysenck, S., and Eysenck, H.J. (1978). Sensation seeking in England and America: Cross-cultural, age and sex comparisons. Journal of Consulting and Clinical Psychology 46: 139-149. Zurita, A., Murua, S., and Molina, V. (1996). An endogenous opiate mechanism seems to be involved in stress-induced anhedonia. European Journal of Pharmacology 299: 1-7.

In: Schizoaffetive Disorders Editor: Kam-shing Yip

ISBN 978-1-60456-948-3 © 2009 Nova Science Publishers, Inc.

Chapter 8

SCHIZOAFFECTIVE DISORDER IN CHINA: CONTROVERSIES AND REALITY IN CHINA Zhi-zhong Liang and Kam-shing Yip* Department of Applied Social Sciences The Hong Kong Polytechnic University, Hung Hom, Kowloon, Hong Kong

INTRODUCTION: MENTAL HEALTH SERVICE IN CHINA The People Republic of China is the most populated country in the world. With a huge population of 1.3 billions, mental health services for persons with mental illness is certainly be a heavy burden for the central as well as local government. According to related formal document, there are around 16 millions of persons with mental illness that necessitate prolonged treatment and rehabilitation, 30 millions of children and adolescents with behavioral and emotional problems, and 6 millions with persons with epilepsy and numerous elderly persons with mental problems (Ministries of Health, Civic Affairs, Public Security, and China Federation of Disabled People, 2002). Facing this huge demand, it is very hard for the federal and local government to supply sufficient mental health services as well as well trained mental health professionals for the dignosis, treatment and rehabilitation of persons with mental illness including those with schizoaffective disorder. The difficulty was further complicated by poor mental health literacy and services coverage. In 1987, it was estimated the 80% of persons with severe mental illness did not receive any mental health services and 95% of them did not able to be admitted by mental hospitals (Ministry of Public Health, Ministry of Civic Affairs and Ministry of Public Security, 1987). Although, there seemed to be much better in service coverage in 2000, the demand of mental health service were still difficult to reach. It was estimated that, despite many efforts input by related parties, the mental health literacy for general population was still very limited. The details can be shown in the following Table 1 (Yip, 2007):

*

E-mail: [email protected]

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Zhi-zhong Liang and Kam-shing Yip

Table 1. Estimated Mental Health Literacy in China in 2005 and in 2010 (summarized from Ministry of Public Health, Ministry of Civic Affairs, Ministry of Public Security and Disabled Persons’ Federation, (2002 ) General Awareness about Mental Illness

Estimated Target of Mental Health Literacy of General Population in 2005

General Awareness about of Mental Illness General Awareness of Mental Problems of Adolescent and Children General Awareness of Mental Illness of Women General Awareness of Elderly Mental Problems (such as elderly depression and senile dementia)

30%

Estimated Target of Mental Health Literacy of General Population in 2010 50%

40%

60%

30%

50%

30%

50%

As all these percentages are actually targets suggested by central policy makers that should be met by related parties in improving mental health services in China, that means in 2005, there were at least 70% population in China did not know mental illness. Furthermore, there were at least 60% population in China did not have any awareness of mental illness or problem of adolescents and children. Similarly, there were at least 70% population did not beware of mental problems of women. Finally, in 2005, there should be at least 70% population did not have any general knowledge of elderly mental problems in particular elderly depression and senile dementia. For persons with schizophrenia in China, it was targeted in 2005, only 50% of them could receive treatment. In 2010, it is hoped that only 60% of them will receive treatment. In other words, there were at least 50% of persons with schizophrenia did not receive any treatment or care in 2005. Also, there will be at least 40% of persons with schizophrenia did not receive any treatment and care in 2010. All these imply that there are strong unmet demand of mental health services in China that are difficult challenges for policy makers and professionals in the coming years. Within this circumstances, there may be many challenges in the diagnosis, treatment and rehabilitation of persons with schizoaffective disorder in China. In this paper, by means of a case illustration, the writers try to illustrate these in details. Table 2. Estimated Number of Persons with Schizophrenia in China in 1993 (Calculated from the study by Zhang, et. al., 1998; cited in Yip, 2007) Mental Disorder Identified by Psychosis Screening Schedule Schizophrenia Affective Psychosis

Total Prevalence 6.55 per 1000 persons 0.10 per 1000 persons

Estimated Number of Adult Persons with Mental Illness 8.45 millions 0.13 million

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Table 3. Life Prevalence of Elderly with Mental Problems in 1993 (Summarized and adapted from: Lau. et.al., 1998 cited in Yip, 2007) Mental Illness of Elderly Schizophrenia Affective Psychosis Reactive Psychosis Schizoaffective Psychosis

Life Prevalence 9.88 % 1.20 % 0.60 % 0.30 %

SCHIZOAFFECTIVE DISORDER IN CHINA Prevalence in China Up to now, there were no large epidemiological studies in study the prevalence of schizoaffective disorder in China. We can only estimate it from related studies in national epidemiological studies of mental illness in China. The second national epidemiological studies in China in 1993 showed that the prevalence of mental illness is 13.47 (per 1000 persons). It implied that there were at least 17.5 millions of persons with severe mental problems including mental retardation. In this study, the prevalence of schizoaffective disorder was not well articulated but the prevelances of schizophrenia and affective disorder were reported. The estimated number of persons with schizophrenia and affective psychosis from the findings of 1993 epidemiological study is shown in Table 2. Regarding the life prevalence for elderly with schizophrenia and affective psychosis, related results can be showed in Table 3. From the above tables, it is estimated that there should be around for every 100 persons with elderly persons with schizophrenia there may be 3 persons with schizoaffective disorder. Provided that ration of adult with schizoaffective disorder is close to elderly persons with schizoaffective disorder. That means there should around (8.45 million x 0.30% ) 253,500 persons with schizoaffective disorder in China. Coupled with a huge and insurmountable number of persons with mood disorders and psychosis, affective psychosis, diagnosis, treatment and rehabilitation of persons with schizoaffective disorder should be a great challenge to related professionals.

Diagnosis and Etiology of Schizoaffective Disorder in China Yang (et.al. 2004) from his 12 years clinical practice as a psychiatrist in China, he encountered 29 cases who first diagnosis as schizoaffective disorders. Among them 20 cases’ (69%) diagnoses remained stable and unchanged. In comparision with those with affective disorders and schizophrenic disorder, persons with schizoaffective disorder then have earlier onset, short duration of illness. It seems that females are more inclined to have schizoaffective disorder than males. In China, schizoaffective disorders are diagnosed four basic clinical features. Firstly, there is co-existence or sequential occurrence of symptoms in schizophrenia and in mood disorder. Secondly, there are frequent relapses and manifestation of symptoms. Within

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relapses, residual symptoms are not apparently observed and occurred. Thirdly, onsets may be acute and have a family history of schizophrenia, depressive disorder or bipolar disorder. Fourthly, the age of onset is inclined to be at adolescence or youth, with female more than male (Zhang & Zhiu, 2005). In psychiatric wards in Kunming hospital, there are around 3% patients suffer from schizoaffective disorder. In China, the diagnosis of schizoaffective disorder follows closely to International classification of Disease ICD 10. The only difference is that in ICD related symptoms have to occur or manifest for at least one whole week, however, in China, the CCMD III (China Classification of Mental Disorder 3rd Edition) related symptoms have to sustain for at least two or more weeks. There are some difficulties and controversies of diagnosis of persons with schizoaffective disorders. Firstly, In CCMD III, similar to ICD 10 related symptoms in manic and depressive episode have to sustain and last for at lease one week. This may be inconsistent in comparing with the diagnosis of schizoaffective disorder that requires at lease two weeks’ manifestation of both schizophrenic and manic or depressive symptoms. This is particular difficult when persons with schizoaffective disorder are normally changeable, dynamic and fluctuating in manifestation of symptoms. In addition, in China, as persons with mental illness have to pay their medical fees in related treatments in outpatient clinics or in hospitalization in mental hospitals. That means, many patients may not be affordable to stay in the mental hospital or have repitative visits to the clinics. Also, to facilitate greater utlitiy rate of hospital bed, patients’ duration in mental hospital may normally be regularized to around no more than 15 days. Thus, within a short period of time, their symptoms may be subsided making the diagnosis inclining merely to either mood disorder or schizophrenic disorder. Thirdly, as manifestation of symptoms in schizoaffective disorder is highly dynamic and controversial. Jager (et.al, 2003) tried to sum up related arguments and controversies into four ways. They are: i. Schizoaffective disorder is a variant of schizophrenia. ii. Schizoaffective disorder is a variant of affective disorder. iii. Schizoaffective disorder is an intermediate entity between schizophrenia and affective disorder. iv. There is a continuum of functional psychosis with schizophrenia at one end and affective psychosis at the other end of the spectrum Within these four types of possibilities, medical practitioners may need to be well equipped with related knowledges and experiences in distinguished schizoaffective disorder from schizophrenia, major depressive disorder and bipolar disorder. However, in China, specialized psychiatric training of mental health professionals such as psychiatrists is still inadequate (Yip, 2007). Many psychiatrists in China are only equipped with general medical training. Those in rural areas may even be originated from paramedical background. Thus, it may be commonly observed that psychiatrists in China, because of limited formal training in psychiatry, may have problems to make a clear diagnosis of schizoaffective disorders. Some of them may confuse manifestation of symptoms of schizoaffective disorder with symptoms of schizophrenia, depressive disorder and bipolar disorders. This type of confusion may demonstrate in the following case illustration. Related parties’ consensus in using their stories for academic purposes was sought, their personal identity and information were properly disguised to ensure confidentiality.

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‘Mr. C was a young man with schizoaffective disorder in Yunan in China. He came from a grassroot family. Under the single child policy, Mr. C was the only son in the family. His parents loved him very much and tried their best to nurture him and used most of their saving for him to receive university education in another city in China. Initially, his son was able to find a job in this city after university graduation to support the family. Unfortunately, his son had an active delusion that someone followed him and intended to harm him. On his way back home, Mr. C deluded that his former female classmate in his secondary school loved her and wanted to marry him. Thus, he went down to the small town near Kunming and tried to connect with this former female classmate. As his behaviours was odd and bizarre with unstable mental condition. His mother escorted him to Kunming hospital for treatment. At first, related psychiatrists were confused by the complexity of Mr. C’s mental symptoms and just gave a rough diagnosis as `depressive disorder’ and mental problems and required Mr. C for immediate hospitalization. In the first few days in his hospitalization, his responsible psychiatrist diagnosed Mr. C as schizophrenia and requiring him to take antipsychotic medication. However, a close observation of Mr. C’s behaviours in related programs in the mental hospital reviewed that Mr. C’s mood was elated and easily provoked. After a thorough discussion with related medical professionals and Mr. C’s mother, the diagnosis was finally settled as `schizoaffective disorder, bipolar type.’

Furthermore, the diagnosis of schizoaffective disorder may be closely related to a diversified cultural and social contextual interpretation, coupled with the instability of manifestation of symptoms of schizoaffective disorder. For example, traditional Chinese culture may be more acceptable to the onset and manifestation of depressive mood, those clients with depressive mood and schizophrenic symptoms may thus be soley considered as schizophrenia rather than schizoaffective disorder.

Treatment and Rehabilitaton of Schizoaffective Disorder in China In China, due to the shortage of resources and manpower, most (around 95% ) persons with schizoaffective disorders in mental health services are treated by psychiatric medication. They are either patients in outpatient clinics or mental hospitals. For those in outpatient clinics, apart from medical treatment, they can rarely receive psychosocial treatment, partly because of insufficient manpower, partly because related professionals in outpatient clinics and mental hospitals are not well equipped with proper training in psychsocial treatment. A psychiatrist in an outpatient clinic has to look after forty to fifty cases a day normally. In peak season, the caseload is even more. Thus, s/he can only afford very limited time in diagnosis and treatment of every patient. For teaching hospitals, related psychiatrists should also take up heavy teaching, training, administrative and academic duties in addition to direct clinical work with patient. They can hardly afford sufficient time to render counselling, psychotherapy as well as family work with patients with schizoaffective disorder. All they can afford may only be brief consultation of patient’s current social, mental, and medical conditions and rendering psychiatric medications accordingly.

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Zhi-zhong Liang and Kam-shing Yip Table 4. Commonly used medication for schizoaffective disorder in China

Antipsychotic medication Types of Psychiatric Medications Antipsychotic Medication Antidepressants Mood Stablizers

Included Medication The first generation: Cholorpromazine, Parphenazine The second generation: Quetiapine, Risperidone The first generation: Imipramine The second generation: Fluoxetine Lithium Carbonate, Topiramate

For those who needed to be treated in mental hospital, their duration in the mental hospital is limited by related policy. For psychiatric wards in large hospitals in important cities, there are strict requirement in having a high turn over rate. Most patients are limited to stay in their hospital bed no more than two to four weeks. For mental hosptials, their length of stay in the hospital is a bit longer, around four to tweleve weeks, or may be longer. In some hospitals, they may require the accompany of patients’ relatives. Under the current health policy in China, patients have to afford their own fees of treatment. Various fees and charges were introduced in mental hospitals in China to ensure their incomes. That includes charges on medical treatment, medical consultation, medication and daily charges on hospitalization (Yip, 2007). According to Zhek (et.al, 2003), the average charge of medical consultation in outpatient clinics in large cities in China is around 140 RMB. The average charge of hospital bed per day is 84 RMB. The average charge of every discharge patient, including mental paitent is around 6151 RM. It may charges less in hospitals in town and rural areas (Zhek, etal., 2003). The medical charges and fees are still going up in recent times. Without medical insurance, the medical fees are unaffordable for most families in China. Facing the possibility of acute onset but frequent relapase, persons with schizoaffective disorder may be unafforadable to seek for medical treatment. Even during the time on onset of relapse, they may not able to receive treatment in outpatient clinic or stay in mental hospitals. Even if they stay in mental hospital, their duration of stay may be short and insufficient to have appropriate treatment. For those who are discharged from mental hospital, they may not able to afford to seek follow up treatment in outpatient clinics. Major of patients with schizoaffective disorders in China are treated by psychiatric medication. Only a few of them are treated by psychosocial treatment such as counselling, psychotherapy and recreational groups. Various types of psychiatric medications are used such as mood stabilizers, antidepressants and antipsychotic medication. They are listed inTable 4. For those patients who can afford expensive medication, psychiatrists in China may render the second generation medication with few side effects, in comparing with the first generation medication. Usually, for those patients with bipolar symptoms, we normally treated them with mood stablizers first. When patients’ mood is stablized, then antipsychotic medication is used. For those with major depressive episode, antidepressants are used together with antipsychotic medication. In some cases, electric shock therapy is used to stablize the condition of the patients. In terms of rehabilitation, because of insufficient resources, patients with schizoaffective disorder are dependent on the acceptance and support of their significant others in family,

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work and community. In those large integrated hospitals or mental hospital in Beijing, Nanjing, Shenyang, Wuhan, Kunming, Zhanjiang, Chengdu, Chengsha, Guangzhou and Shanghai, thy have initiated some programs and counselling for mental patients and family caregivers, including those with schizoaffective disorder. Related literatures showed that these services and interventions for persons with mental illness including, such as home based beds, guardianship networks, psychoeducational programs, family counseling and therapy as well as hotline services (Yip, 2007). These services may only be available in the above regions of China. The future development of related rehabilitation services is limited by several factors. Firstly, there is insufficient manpower and training to implement psychiatric rehabilitation services. Secondly, current psychiatric services in China are heavily medicalized and treatment oriented. Psychosocial orientation and rehabilitation as well recovery focus is only recognized by few medical professionals in some large integrated hospitals and mental hospital in a few well developed cities in China.

CASE ILLUSTRATION The causes, diagnosis, treatment and rehabilitation of persons with schizoaffective disorder in China can be further elaborated and discussed in the following case illustration. The client’s consensus to use his story was sought. To ensure confidentiality, his personal information and identity were properly disguised.

Mr. W’s Onset, Manifestation, Struggle, Resilience and Recovery from Schizoaffective Disorder ‘Mr. W was a Chinese male adult aged 44 and lived in a city in China. He was diagnosed as suffered from schizoaffective disorder, depressive type. He had been hosptialized five times in Yunnam in China. He ranked the eighth within his nine siblings. When he was only three years old, his mother gave him to his aunt as her adopted son as his aunt was unable to bear child. From that time onwards, he lived with his aunt and uncle and became their only son. In the 1980s, Mr. Ws uncle (adopted father) became rich by running a shoe factory. Mr. W was also the chef in the canteen of a large factory for twenty years. At first, their lives were stable and selfcontained. Later, Mr. Wang fell in love with his girlfriend. He committed pre-marital relationship with her but later left her. He then met another girlfriend and married. However, his uncle and aunt (adopted parents) had severe conflicts with her wife’s parent. The conflict resulted in the first divorce of Mr. W. In the second marriage, his second wife committed adultery and left him. Mr. W’s misfortune started at 1992 when his adopted father’s factory was bankrupted. In 1994, he divorced with his first wife and his adopted mother was stroked. In 1995, his brother cut his palm in an accident. In 1996, his mother died. In 1998, his adopted father died leaving him a great amount of debt. From that time onwards, to pay off his adopted father’s debt, he had to work day and night as a security guard and a shoe polisher. He felt dreadfully tired, fatigue, worthless and helpless. In 2000, he was mentally broken down. From 2000 to 2005, he relapsed and was hosptialized for five times. He suffered from schizoaffective disorder. In acute psychotic state, he harboured active delusions that someone was dead in upper floor. Then the dead body was

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Zhi-zhong Liang and Kam-shing Yip dropped down. Furthermore, others also shot him by gun. Finally, his previous superivisor in the factory criticized him spontaneously. In his depressive episode, he felt dreadfully meaningless, empty and sad with an intensive suicidal ideation. He recalled his experiences of hospitalisation as inhumane detention in corrective institution. He had problems in paying his charges in hosptialization. In his last hospitalization, a supportive psychiatrist encouraged him to recover and affirm that his employer could pay related charges. He then determined to get well from his mental problems. He was currently lived on public assistance. He still worked as a shoe polisher to support his family. He tried to stop from the reliance on psychiatric medication. He insisted a normal and healthy daily pattern in his recovery. Every day he tried his very best to have regular physical exercise, social activities as well as some casual work. He had lost his wives. Both his parents and adopted parents were dead. He was currently lonely and single but he still insisted he should live a meaningful and productive life in the future.’

Mr. W’s story clearly showed that his schizoaffective disorder was closely related his misfortunes in his life. The leaving of his natural parents; the turning from a wealthy life to a hard and difficult life after the bankruptcy of his adopted father’s business; divorce and leaving of his first and second wives; the difficulties to pay off his adopted father’s medical fees, and death of his natural parents seemed to contribute his onset and relapses of his schizoaffective disorders. He tried very hard to cope with his harships, sufferings and challenges in his life. He felt depressive, confused and helpless in difficult times. He was the only one to face all these difficulties, hardships and challenges, which were all out his coping limits. As a result, his sense of depression prevailed to become major depressive episode. His sense of confusion and isolation accumulated to become an outbreak of schizophrenic symptoms. The threats from delinquents in nearby neighborhood towards his business and employment nurture the contents of his paranoid delusions and halluciations. He relapsed several times, every time, his relapse and manifestation of schizoaffective disorder seemed to be closely related to his plights and predictments in life. Medication treatments and hospitalization tended to be the only alternatives in controlling his prevailing schizoaffective disorder but related medical fees also added to his unaffordable loans and burdens. He even felt insulting by being supervised by a female nurse in his bathing in the mental hosptial. Facing all these, it seemed that he had already lost his hope, determiantin and will power to get well and recovey. The turning point occured when he encountered a genuine and caring psychiatrist in the fifth relapse. He did several things to re-develop Mr. W’s will to get well. Firstly, he showed genuine empathy to W and tried all means to understand W’s needs, feelings and frustration. Secondly, he helped Mr. W’s to weave off his medical charges by claiming medical insurance from Mr. W’s working units. Thirdly, he encouraged Mr. W to get well. Fourthly, he advised Mr. W to take the minimum medication so that he could free from further medical fees. All these seemed to reactivate Mr. W’s will to get well from his schizoaffective disorder. Mr. W finally discharged from the mental hospitals, on his way home, he determined to throw away all psychiatric medication. He retired from his work and took some part time jobs to maintain his living. He managed to have highly scheduled life pattern in terms of physical exercise, writing calligraphy, and other routine and healthy daily life pattern to put himself in good physical and mental condition. In the following sections, we tried to look into all these in details.

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Client’s Family Background and Relationship with His Parents ‘My mother and my adopted mother were two sisters. My current adopted mother was the younger sister. She could not bear child due to some physiological problems. However, my mother had nine children and I was the eighth one. As my grandfather deeply concerned about the loneliness of my adopted mother in her life, he arranged me to be her only adopted son.’ Client’s Mother My mother was stroke in 1994, the next year after my wife’s pregnancy failed. In 1996, she died. Client’s Adopted Mother My adopted mother was an implusive woman. She was very strong and stubborn in her character. Whenever she felt angry, she would try to blame others. If you tried to argue with her, she would be furious. She might even require us to drink the urine in the container or swallow her saliva in front of her. Client’s Adopted Father My adopted father was a shoe maker. Before that, he was a solider. He urged to be an outstanding person in the society. Thus, he was ambitious in establishing his own business. He was clever and had an amazing memory. After reading the bible for one year, he could fully memorize the content every page in details. In 1982 and 1983, he became rich and his business was good. However, he looked down upon me, thinking I was not diligent and was lazy. He was angry with my poor academic performance. Occassionally, he bit me because of my laziness. He was stern, serious and demanding. He always complained me that I was lazy and was unable to study hard and reached a good academic standard. In fact, my whole was being fooled by my adopted father. He did not pass his property and fortune to me. He lagged behind the modern development of the society seriously. He was well educated and had wisdom in interpreting social problems. However, he was seriously tortured by others in the Cultrual Revolution. Thus, he was afraid of continuous development in his business and property. His conservative attitude made our family decline. He simply thought that he owed the money and he could survive well. He did not recognize that things changed. Everything can be out of your estimation and care. That was why he failed. Later, he suffered from chronic illness in his lung and heart. He was hospitalized. However, his own company could only afford 40% of the medical cost. My family had to pay 4000 RMB. This was a huge sum for us. My whole monthly salary was only 200 RMB. He had been hospitalized for four times and spent around 100,000 RMB. All our family fortune and property was spent in paying off this medical cost. By the end of day, I still had to owe a huge debt for my family. He died of chronic illness at 1998, the year after my second divorce.

W’s self narration clearly showed that the client’s family background was a bit complicated. As her natural parents had many children but her aunt had none, he was adopted by his aunt and uncle as the only son. Facing that sort of changes, there might be a difficulty for Mr. W to build up a clear self identity. Deep down in his heart, he might get a feeling that he was only regarded as an object/ gift for his parents to donate to his sister. Fortunately, his adopted parents were quite caring and supportive. They managed to give him a decent and wealthy life in his childhood and adolescence. However, his adopted mother was implusive and stubborn in character. In temperament, she might abuse W. His adopted father was clever but conservative. On the one hand, he cared about W. On the other hand, he demanded W to

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be outstanding in academic performance. As W was rebellious and lazy in his study, he tended to look down upon W. However, it seemed that W’s affective bonding with his father was very strong. He still loved and regarded his adopted father as model in business and earning money. Thus, when W’s father was in final days of chronic illness in his lung and heart, W still tried his best to look after him. All these could serve as participating factors contributing to W’s onset of schizoaffective disorder. Firstly, in the developmental process, W might have identity crises because of he was adopted by his uncle and aunt. Secondly, W might have psychological and physical burdens in taking care of two pairs of parents, his natural parents and his adopted parents. Thirdly, he might also feel highly stressful under his adopted mother’s verbal abuse and his father demanding critism on her academic performance. All these may serve as long term potential contributing factors in W’s onset of schizophrenic and depressive symptoms.

Client’s Courtship and Marriage Client’s Narration of his First Courtship ‘My first courtship happened when I was only in the third year of my secondary school. I fell in love with a beautiful girl in my class. We sat in the same long chair. She was so beautiful and attractive and I was also handsome and well dressed. We loved each other well. At that time, we were so updated and advanced we went to western restaurant and night club. After four and five years, we got so intimate that we had pre-marital sex. My girlfriend was preganent. Under my advice she did abortion. The whole abortion was performed in a highly secret way. Later, we separated as my girlfriend’s father had chosen a husband for her. She could not oppose her father’s authority and decision. I did feel guilty for her. Indeed, I tried to compensate my fault. We still got along well after our own marriage. I tried every mean to help her. Up to now, we are still good friends.’

Clients’ Self Narration of his First Marriage and Divorce ‘The second courtship was introduced by others. As it is not the first time, everything seemed to be more at ease. In fact, I was not choosy in my marriage. I married with my third girlfriend. She was a worker in a water factory. She came from a middle class family and was a secondary school graduate. At that time, it was already a good education. We married after nine months courtship. Later, she was pregnant. It should be a good news for me. Unfortunately, the pregnancy was an abnormal one. I urged her to have medical check up but she and her mother insist to tolerate it. One month later, she embraced problems in the preganacy. She was sent to the hospital urgently. My adopted mother kneeled down on the corridor of the hospital pray and cried loudly so that God could save her life. Finally, she had to undergo the abortion. Blood coming out her body was dreadfully red. I was very angry with her who did not listen to my advice and had medical check up early. It was her who killed my son. After she recovered from her abortion, I told her that we should end up our marriage by divorce.’

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Client’s Self Narration of Second Marriage and Divorce ‘My second wife was a young lady, however, she was also highly materialistic. She had his first marriage with a young man who ran his small business. After her first child was born, she did not like his first husband criticizing that he was poor and dirty. She gave the husband some money and then worked as a dancing girl in the night club. At first, I was fond of her as she was open and frank in character. I married her. No sooner, I discover she was a highly demanding woman. She yielded at me saying that I could not have extra marital relationship with other women or else she would make love with another man in front of me. Her accussation was highly dreadfully. I told her that I married her I had to take dual responsibilities in taking care of her and her son that was not my real son. That child was very clever. He stole money. One year later, I started my business and ran my own restaurant. One day when I was cooking food in my restaurant, a young guy approached my wife. He held her hand and took her away. Indeed, I was so furious and cursed this young guy. Furthermor, I slapped my wife’s face. Her mother later told me that this young guy was her previous boyfriend. They lived together for three years before he married me. He was also married. As he could not divorced his wife and his son, this courtship ended up with my marriage with her. Later, I also divorced this wife as she was not faithful to me.’

From client’s self narration, clients’ courtship and marriage was full of hardships, difficulties and frustration. He could not get along and marry his beloved girlfriend. He felt highly guilty in making his girlfriend became pregnant but persuaded her to abort their unborn child. His first marriage was pre-arranged by his parents. He was very angry and hated his first wife as she did not listen to his advice to have early body check up so that he can safe her pregnancy. He divorced her first wife. Her second wife was unfaithful to him. All these unhappy experiences in courtship and marriage made W deeply frustrated. He did not have a stable and warm family life. He did not have any strong affective bond with his wives or adopted children. He might lost his trust on marriage and family cohesiveness. Emotionally and mentally, he may be deeply frustrated. Continuous loss of love and trust from her girlfriend, first wife, second wife may serve as powerful ingredients in sparkling and nurturing her depressive mood and frustration. The client frankly expressed that in his whole family, he encounter numerous unhappy issues in his family life. The loss of his natural parents and adopted parents, as well as the problems in her courtship, first and second marriage all made him felt highly stressful, empty, unhappy, frustrated as well as totally loss of meaningfulness and direction in life.

Client’s Onset and Relapse of Schizoaffective Disorder Client’s Self Narration of Experience of the First Onset ‘At that time, I felt deeply depressed. Following this was delusion, feeling of being followed by others everywhere I went. I sensed that some one hated me and wanted to take revenge on me. I was afraid of everything. I did not want to talk to anyone. I was unable to sleep for a long period of time. Everyday I could only sleep for two to three hours. Because of paying the debt, I had to sell my house. Everyday, I worked hard but could earn around 200 dollars per month. After a long day’s work, I took a nap of around two hours. Then I went up to repair shoes. My father left a huge amount of debt around 7,000 dollars for

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Zhi-zhong Liang and Kam-shing Yip me to pay off. Life was so hard. In selling my house, I also owed others an amount of 10,000 dollars. This huge amount of money imposed insurmountable pressure to me. I was terribly afraid of being chased by others, especially the governmental official. You know, in the past, I had seen gang fighting. It was so dreadful that even the intestines came out from the wound. The gang fighting concerned with my previous business, I needed to protect my own territories. However, some underground society claimed the ownership of our territories and required us to pay for our business terrorities. If we failed to do so, they would attack us with weapons. Life was so hard for us. You knew corruption, bribery and oppression were common in our society. Under these aversive conditions, life of citizens in our society was painful and full of hardships. I got a feeling I was fallen off from the peak of wealth to the bottom of poverty. Everything was loss. I had nothing but debt from my step father.’

From client’s narration of his first onset of his schizoaffective disorder, it was clear that clients harbored paranoid delusions and hallucinations as well as a strong sense of losing of his fortune as well as his meaningful of life. The clients had paranoid delusions and hallucinations that everywhere he went, there is someone who followed him closely. These guys hated him so much and wanted to take revenage on him by being violent to him. He was deeply threatened by the memories of gang fighting in his region with a lot of blood and intestine flowing out from the wound. It seemed that the first onset of his schizoaffective disorder is closely related to harships in his psychosocial and financial situations. It was also closely related to his unpleasant past experiences in life. The negative impacts of all these stressful events in W’s life may be demonstrated in the following figure. From figure one, it showed that there were two types of factors that led to the onest of Mr. W’s schizoaffective disorder. The first type is precipitating and accumulative factors that nurture Mr W’s schizoaffective disorder. The first factor might be the sense of confusion in his sense of identity and self image. His natural parents gave him to his uncle and aunt as the only son. On the one hand, Mr. W might harbor some anger towards his natural parents. On the other hand, he still cared about them. Same dilemma occurred in dealing with his adopted parents. He might both love and hate them. He loved them because they did regard him as his only son. He hated them because they took them from the affective bond of their natural parents. Furthermore, instead of having two parents to be responsible and care for, he had four. All these may add to Mr. W’s burdens when their parents became old and sick. The second factor seemed to be the manipulation and maltreatment of his adopted parents. Although they regarded them as the only son, they were still manipulative and a bit rejecting. His mother was highly implusive and cursed him whenever she was in bad mood. In extreme case, she even required him to swallow her saliva. His father always looked down upon W saying that he was lazy and not academic. His father also said he was worthless and useless. That means, W was thoroughly frustrated by his adopted parents’ comments in his childhood and adolescence. In addition to frustration from parents, W’s life in courtship and marriage was not happy too. He was deeply frustrated by the leaving of his beloved girlfriend as well as full of a sense of guilt in making her aborting their baby. The first marriage ended up with divorce as his wife failed to protect her pregnancy. The second wife betrayed him and involved in ex-marital relationship. All these were accumulative factors making W felt that his life was meaningless and worthlessness. It also made him felt that despite his life long struggle and resilience, he was still in a bad fortune.

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Precipitating and long terma acculumative factors of W’s Schizoaffective Disorder

Unhappy Childhood: The natural parents gave him to his uncle and aunt as adopted son (Loss or Confusion of Self Identity)

Adopted Parents’ were protective but highly manipulative and implusive (Adopted mother was highly impulsive and stubborn. Adopted father looked down upon him)

Unpleasant past experiences in Courtship and marriage (Guilt in the abortion of his beloved girlfriend in courtship, intensive anger and in the divorce of his first wife)

Provoking factors of W’s first onset of schizoaffective disorder

Unpleasant recent life experience (The downfalls of his adopted father’s business and he had to earn his own living. Divorce of second marriage and a strong sense of being betrayed by his second wife)

Loss of Family Members (The death of his adopted father and natural parents because of chronic illness)

Severe Hardship in Life (Inability to pay off the huge debt left by his deceased father even though he sold the house and worked very hard; Threats by others in his business and work)

Figure 1. Accumulative and Provoking Factors Leading to W’s Onset of Schizoaffective Disorder.

The second type of factors may be provoking factors that provoke the onset of W’s schizoaffective disorder. According to W’s self narration, W felt highly frustated by about her second wife. He was betrayed by his second wife as she still continued extra-marital relationship with her former husband and they even had a child. All these were out of the knowledge of W. In addition to this deep frustration, W’s adopted father died leaving a huge loan to him. Because of his father’s chronic illness, W had to shoulder his father medical fees that were far out of his affordability. At the same time, W’s work as a chef was terminated by the closing down of his factory. W had sold his house, worked doubly hard as security guard

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as well as shoe polishers. Still he was unable to play back all his loans. Coupled with struggles and threats from loan sharks and underground societies in his work, W’s physical and mental conditions reached a breakpoint. He was desperate, lonely, helpless, fearful, and fightening in facing all these hardships. Facing all these losses, he felt highly depressed. In facing all these unpaid loans and the threats from underground societies, gradually, he developed hallucinations and delusions that corrupeted governmental officials and members from underground societies followed him everywhere and tried hard to hurt and even killed him.

Client’s Self Narration of Experience of Relapse The First Relapse ‘The second onset occurred soon after the first one. I just felt terribly upset. I did not want to eat, to sleep and to speak with others. I stayed there for sometimes.’

The Second and Third Relapse ‘The third onset was full of delusion and hallucination. I got a strong feeling that some one in my upper floor of my house was dead and jump off from there. Someone used their guns and shoot at me. Some corrupted government official tried to oppress me. They wanted to take revenage on me.’ In fact in the third and fourth onset in 2000 and 2001, my whole life was highly messive. My personal hygiene was extremely poor. I did not wash my clothes. I was dirty and depressive thinking my whole life was entirely meaningless and emptiness. I simply wanted to die. My step mother was fierce. She quarrelled with me everyday making me felt heavily annoyed. I simply wanted to swallow all medications and died immediately.’

The Fourth Relapse ‘At that moment, I was mentally sick. Even though my factories wanted me to work over-time additional work but I could not. I could not eat. I could not sleep. My sister in law he worked in a carpentry factory. He knew the policy of my factory. He told me that my factory was bankrupted. He advised to stay on my job, and asking for compensation of salary. I was a man with dignity. I knew that was serious corruptions in my factory. I did not trust that the new young manager could ease the financial situation of the factory. They were too young and unable to handle dirty policits and dynamics in our corrupted societies. Some leader took the money and made the factory in debt. I thus decided to retire from my work. I harbored a strong delusion that there were persons around me who decided to kill others. My father told me to admit to the Yunnam Mental Hospital.’

From W’s self narration, it was clear W’s frequent relapse was closely related to his harships and sufferings in his work, his family and in the society. Even though W had received appropriated medication. W’s related symptoms still prevailed because of all these difficulties and harships. He still had to should the loan from his father’s medical treatment. He still had to work doubly hard to pay off his loand. Moreover, W’s mother was still grumbling and complaining. Facing all these severe stress, W’s symptoms quickly intensified and his second onset followed closely to his first onset. He still harbored intensive deluions

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and hallucinations that someones were chasing around him and wanted to harm and threaten him. Medical treatment and brief hospitalization seemed to do nothing to alleviate his stress and hardships in life. Instead, heavy charges and fees for medical treatment and brief hospitalization tended to accumulate his life stress. He relapsed again and again when his life stresses and frustrations reachable an unbearable limit. His physial and psychosocial conditions deteriorated. In the second relapse, W harbored a strong delusion and hallucination that some one in his upper floor of his house was dead and jumped over his house and someone shot him by gun. Corrupted government official took a full revenage on him. All these might reflect W’s anger and frustration towards the corruption and unfairness in his work and the society. In the third relapse, his own life was highly messy with poor hygiene and a strong urge to end up his life. The final relapse was happened in a severely depressive mood and confusing delusions someones in his factories were all corrupted and tried to kill one another. He trusted nobody. All these clearly showed that the onset and relapse of his schizoaffective disorder were closely related to his stress, frustration and hardships in life. It seemed that continuous medications made no improvement in his mental conditions nor gave him any will power to recover from his depressive mood, confusing paranoid delusions and hallucinations.

Client’s Treatment and Recovery Client’s self Narration of Experience of First Treatment ‘In my first treatment, I did not have any feelings. My only memory was that I lived in the second floor. I felt I slept and behaved like a small infant, navie and did not know anything, stipud. I was afraid of any noises nearby. My ear was very sensitive to any noice nearby. I stayed there for two week.’ ‘My psychiatrist approached me and told me to take psychiatric medication and injection. They did not let me work. It might be because there were severe fightings in our society especially when one needed to protect his territories in business. In fact, I did not want to take medication. I just felt that I did not have any mental illness or problems. I slept better with the antidepressant and my conditions seemed to be better. They said I suffered from major depressive disorder.’ ‘The experiences in the second, third and fourth treatment were not much different from the first one. I felt being controlled, as well as manipulated by nurses. When I was bathing, a female nurse stood by my side and ordered me to finish them quickly. The psychiatrists there did not speak much. They simply told me to swallow my medication and reminded me to pay my medical charges. In fact, I did not have even a cent to pay all these. I could not afford to pay the medical charges of my father. How could I pay my medical fees. The side effects of the medication made feel dizzy, inert and withdrawn.’

The first treatment, in no way, was a pleasant experience for W. He felt deeply humiliated in the process of treatment and hospitalisation. Within a highly institutionalized hospital settins, W felt being controlled and manipulated in the mental hospitals. It seemed related medication only made him felt dizzy, inert and sleepy. It did not have crucial effects in enlightening his stresses in life, nor gave him wisdoms to deal with his situations. He felt being ignored and neglected by medical professionals.

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Client’s Self Narration of his Recovery ‘My experiences in the fifth hospitalization were a crucial turning point for my recovery. This time, the psychiatrist was a very humane and empathic professional. He approached me and challenged me that how many sleeping pills I needed to take so that I could fall into sleep everyday. I said I need two and half pills. Also, if there was any noise outside such as thunderstorm, I would wake up immediately. He knew that I had many worries especially concerning the fees for hospitalization. Frankly speaking, I had no money to pay off all the charges in hospitalization. The charges for the first and second hospitalization were paid by my factory where I was the security guard. Unfortunately, the factory was brankrupted. The psychiatrist ensured me that all these charges could be weaved off by the new factory. He comforted me and sternly affirmed that I ought to stay in the hospital peacefully unitl my mental illness was cured. I felt much more secure and being understood. Whenever I stuck to my sick role and did not want to eat and do anything, he approached me and cheered up. He even ordered me to eat and to do constructive thing or else he might tied my up. Under his affirmative supervision, I embraced a strong will to recover. With his help, I gradually reduced the dosage of my medication including the antidepressant as well as the antipsychotic drugs. In 2004, when I was discharged from the mental hospital, he said this is the slightest dosage that he could give to his patient. I rode on my bicycle and return home. On the way, I strongly affirmed myself I had to recover from my mental illness. I was determined to recover from all these mental problems. At that moment, my mind was clear and my will was strong. I threw all related medication into the rubbish bin. From that time onward, I did not eat any medication. I knew that I would still be troubled by my depressive mood and my occasionally occur paranoia. But I still have time. I remembered my deceased father told me that if you did not attain something good enough in your life, the best thing you can do was to do this thing better in your retirement. I submit my retirement to my supervisor and determined to try every mean to recover from my mental illness. Every day, I get up early in morning, eat my breakfast and then spent my time on practicing calligraphy, reading newspaper and sometimes talking with others. In the afternoon, I insisted to walk around six to eight kilometers as exercises. Then I eat my dinner. I normally go to bed around 10 p.m. If I wake up at the mid night, I may smoke a cigarette and go to sleep again. Simple and regular life make me feel much better. It gives me extra strength to recover from my mental illness. Frankly speaking, starting from 2005 July onward, I had not take any medication and my mental state is still stable and satifactory.’

From W’s self narration, his recovery seemed to consist of several crucial ingredients. The first was humanistic care and empathic concern from related professionals. In his last hospitalization, he was lucky enough to encounter a humanistic and empathic psychiatrist. Instead of only ordering him to swallow psychiatric medication, this psychiatrist concerned his health and recovery. He advised him to stop abusing sleeping-pills. He encouraged W to recover by his own will. All these concerns and empathy were very important for W. He had long been deprived from love and concern from his natural parents, adopted parents, wives and relatives in his own life. The encouragement from a father like authority figure gave him courage to restore his own dignity and meaningful life by recovering from his schizoaffective disorder. The second ingredient was ways to ease his financial burdens. The psychiatrist helped him to apply and pay off his medical fees from his new factory. He also helped W how to think way to resolve the medical fees of his deceased adopted father. Resolving

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psychosocial stresses, in many ways are crucial in the recovery of persons with schizoaffective disorders. It gave clients a supportive psychosocial environment free from stress and frustration that nurture recovery and rehabilitation. The third ingredient was that encouragement and facilitation of clients to live a normal integrated life. W was encouraged by his psychiatrist to live a normal life and keep his medication to a minimum so that he would not be solely dependent on psychiatric medication. It is crucial for W to regain his determination and will to live a normal and integrated life. Whe he discharged from the hospitals, his mind was clear and affirmed to throw all medications into the rubbish bin. From that time onwards, he tried every means to live a normal and integrated life. He retired from his stressful job and insisted on a regular life pattern. Every day, he got up early and ate his breakfast. He then, spent his time in practicing calligraphy and reading newspaper. In the afternoon, he walked six to eight kilometers everyday. He went to bed at around 10:00 p.m. every night. He affirmed that he still felt depressed and occasionally disturbed by paranoia. However, he learnt how to live with them. He tried to make his life meaningful and simple. Even though he got up in the mid night, he learnt to take it easy. He smoked a cigaretter and got relaxed and slept again. In fact, the recovery of W’s schizoaffective disorder is closed to the ideologies of recovery currently promoted by the National Consensus Statement on Mental Heatlh Recovery in the United States. In this statement, self direction, individualized or person centered, empowerment, strengthes based, peer support, holistic, non-linear, respect, responsibility, and hope should be stressed and ensured in the recovery of persons with mental illness (United States Department of Health and Health Sciences, 2004) Firstly, the recovery of W is self directedness. He affirmed his will power to recover without dependency on related medications. He encouraged himself to live an independent live even though most of his significant others including his natural parents, adopted parents and his wives left him. His recovery is also person centred. Within his own living habit and Chinese culture, he insisted a normal daily life with regular schedule and practicing Chinese calligraphy, reading local newspaper and walking in nearby neighborhood. All these were specially designed for himself in the process of recovery. His recovery process is also based on his own strengths and power. He determined to have early retirement so that he could live on a simple life on public assistance rather than being involved in endless busy work life that was oppressed, depowered and controlled by others. From a hopeless and meaningless life, he strived to a self defined meaningful life with hope, respect and responsibility to himself to live a normal and healthy life. Interestingly, the starting and determination to do all these were sparkled, facilitated and initiated by the spontaneous encouragement of a genuine, accepting and warm psychiatrist, who trusted and believed W, despite all his frequent relapses and mental confusion still harbored strengths, abilities and potentials to recovery. Perhaps, in Chinese culture, as Yang (1995) suggested, the respect of authority figure plays a crucial role in building up individual’s self image, will power and determination in personal achievement and attainment.

CONCLUSION As a conclusion, this paper addresses and discusses related issues in diagnosis, treatment and rehabilitation of persons with schizoaffective disorder in the People Republic of China. As the most populated country in the world, the number of persons with schizoaffective

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disorder should be huge and insurmountable. It created great burdens and challenges to related diagnosis, treatment and rehabilitation. By means of a case illustration, the writers demonstrated all these challenges and burdens in refined details. It seemed that there exist an urgent need to input sufficient manpower, resources and training so that related professionals can perform accurate diagnosis, holistic treatment as well as integrated rehabilitation and recovery for persons with schizoaffective disorder.

REFERENCES Jager, M., Bottlender, M. J., Strauss, A. & Muller, A. S. (2003) `Fifteen year follow up of ICD 10 schizoaffective disorder s compared with schizophrenia and affective disorder’, Acta Psychiatric Scandianvia, 109:30-37. Lau, C.K., Ng, F.M., Shen, Y., (et.al) (1998) `Prevalence of mental problems of elderly in seven regions in China’, China Journal of Psychiatry, 31(2): 126. Ministry of Public Health, Ministry of Civic Affairs, Ministry of Public Security and Disabled Persons’ Federation, (2002) The Future Plan of Chinese Mental Health Work (20022010). The People’s Republic of China: www.cma-mh.org/p/lawConsult. United States Department of Health and Health Sciences (2004) National Consensus Statement on Mental Health Recovery, Washington, DC: United States Department of Health and Health Sciences. Yang, K.S., (1995) `Chinese social orientation: an integrative analysis’ in T.Y. Lin., W.S. Tseng. & E.K. Yeh (ed.) (1995) Chinese Societies and Mental Health, Hong Kong: Oxford University Press. Yang, K. K., Ko, F. & Lu, A. M. (2004) ` The stability of diagnosis of schizoaffective disorder’, Journal of Clinical Psychosomatic Illness, 10(2): 89. Yip, K.S. (2007) Mental Health Service in the People’s Republic of China: Current Situation and Future Development, New York: Nova Sciences. Zhang, C., Zhiu, C.Y. (2005) `Clinical analysis of 60 cases with schizoaffective disorder’, Harbin Medicine, 25(3): 33. Zhang, W.X., Shen, Y.C., Li, S. R., et.al (1998) `Epidemiological investigation on mental disorders in 7 areas in China’ China Journal of Psychiatry, 31(2): 69-71. Zhek, K., Zhui, C., Lu., K.C., Zhang, Y., (2003) `A research on cost effectiveness of mental health work II, Shanghai Archives of Psychiatry, 15(6): 371- 375.

In: Schizoaffetive Disorders Editor: Kam-shing Yip

ISBN 978-1-60456-948-3 © 2009 Nova Science Publishers, Inc.

Chapter 9

MANAGING THE SUICIDAL RISK IN PREGNANT SCHIZOAFFECTIVE WOMEN Salvatore Gentile* Department of Mental Health ASL Salerno 1, Head, Mental Health Center n. 4, Piazza Galdi 84013, Cava de' Tirreni, Salerno, Italy

UNNATURAL DEATHS AMONG THE SCHIZOAFFECTIVE PATIENT POPULATION Suicide remains a significant public issue. [1] In 2002, an estimated 877 000 lives were lost worldwide through suicide, representing 1.5% of the global burden of the disease or more than 20 million disability-adjusted life-years (years of healthy life through premature death or disability). [2] In virtually all countries reporting suicide statistics to World Health Organization, the suicidal risk increases with age in both sex, and rates for men in older adulthood are generally higher than those for women. [3] Overall, deaths by suicide are more frequent in men that in women, whereas nonfatal suicide attempts occur more frequently in women. Two exceptions are: 1) United States, where during the last 20 years suicide has increased up to 80% in specific populations, such as Afro-Caribbean women, and 2) China, where the suicidal rate in women is much greater than in men. [4, 5] Notably, psychiatric disorders are present in at least 90% of suicides and more than 80% are untreated at time of death. [6, 7, 8] Several concordant information exist suggesting that, among the psychiatric disorders, patients diagnosed with schizoaffective disorder show relatively higher rates of deaths by suicide compared with patients suffering from other mental illness. A generally increased mortality has been already reported in these patients. [9] In fact, a Swedish study demonstrated that the increased mortality in inpatients who had been admitted with schizophrenia was 2.8 for men and 2.4 for women, whereas a further 30% significantly increased risk was specifically associated with the diagnosis of schizoaffective disorder. [10] Specifically, however, while either bipolar and schizophrenic patients seem to have higher *

E-mail: [email protected]

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mortality rates from drug-induced metabolic dysfunctions or unhealthy life-styles, [11, 12, 13, 14] unnatural deaths due to lethal suicidal attempts prevalently occur in schizoaffective patients: approximately 10% of them actually die of suicide. [15, 16] A two-year, prospective, follow-up study investigating more than 900 patients at high risk for suicide also proved that the diagnosis of schizoaffective disorder plays a key-role among the main specific predictors of subsequent suicide-related events. [17] However, apart from the diagnosis, the presence of other concomitant specific social, behavioral, and clinical factors seems to be needed for increasing the frequency of deliberate self-harm in schizoaffective patients. They include: incomplete schooling, unfavorable life episodes during adolescence, history or current abuse at baseline of alcohol and/or illicit drugs, cigarette smoking, Other specific predictors of increased rates of suicidal deaths include number of lifetime suicide attempts, the number of hospitalizations in the previous 36 months to prevent suicide and, and, after hospital discharge, poor insight and non-compliance with medication. Finally, greater baseline scores on the InterSePT scale for suicidal ideation, the Covi Anxiety Scale, the Calgary Depression Scale, and the severity of extrapyramidal adverse effects have also been associated with high frequency of self-aggressive behaviors. [18, 19] Such results have been confirmed in a recent, 10-year, retrospective study by Shoval and colleagues. [20] Substance-user adolescent inpatients with schizophrenia or schizoaffective disorder seem to represent a subgroup of patents with peculiar clinical characteristics, as it is characterized by a specific relationship between alcohol and/or illicit drug abuse and suicidal attempts. In addition, these specific psychiatric populations are likely to show higher levels of aggression at hospital admission. Therefore, a further link between schizoaffective disorder associated with impulsive-aggressive personality traits and suicidality has been suggested. [21] Box 1. Predictors of an increased risk of suicide and suicide attempts in patients with schizoaffective disorder Unfavorable life episodes during adolescence Incomplete schooling History or current abuse at baseline of alcohol, tobacco, and/or illicit drugsrrrr Number of lifetime suicide attempts Number of hospitalizations in the previous 36 months to prevent suicide Young age and aggressive behaviors at hospital admission and/orimpulsive-aggressive personality traits Poor insight Severity of drug-induced extrapyramidal adverse effects Noncompliance with medication Greater baseline scores on: • the InterSePT scale, • the Covi Anxiety Scale, and the Calgary Depression Scale On a temporal dimension, the earliest 5 years following the occurrence of a first-episode psychotic disorder

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On a temporal dimension, the months following a first-episode psychotic disorder is a high-risk period for suicidal behaviors (14.5% of patients after a first psychotic episode display suicidal thoughts and attempts within the 5 years following diagnosis, and 2.4% die by suicide). [22] Predictors of an increased risk of either completed suicides and suicide attempts in schizoaffective patients are summarized in Box 1.

MATERNAL DEATHS DUE TO SUICIDE. NOT ONLY A POSTPARTUM DRAMA The World Health Organization defines “maternal deaths” all deaths occurring any time during pregnancy and up to 42 days after parturition. [23] Maternal deaths are additionally classified as: • • •

direct, resulting from obstetrical complications; indirect, resulting from a condition not directly related to obstetric cause but worsened by the pregnant status, such as cardiac disease; incidental, for which pregnancy is unlikely to have contributed significantly to the death).

An alternative classification of maternal death has been reported in Box 2. [24] When all maternal deaths within one year after delivery are considered, suicide is one of the four leading causes of maternal deaths overall (together with thromboembolisms, obesity, and cardiac events). [25, 26] For these reasons, maternal mortality associated with psychiatric illness remains a focus of high clinical interest also in the developed countries, where the rate of maternal deaths due to other conditions, such as poor antenatal care and malnutrition, have progressively been decreased during the last years. [27] Until now, however, epidemiological studies have been mainly focused on the increased risk of suicide during postpartum period. In the first year after birth, the suicidal risk increases 70-fold, and suicide is the leading cause of maternal death in the perinatal period (pregnancy to end of the first year postpartum), with the majority of suicides occurring with violent means. [28] The increase of the suicidal risk is one of the most significant clinical concern characterizing postpartum (puerperal) psychosis, the most severe perinatal psychiatric disorder. Puerperal psychosis shows relatively low incidence rates (cumulative incidence of bipolar disorder relapse: 0.03%; cumulative incidence of schizophrenic and schizoaffective disorder relapse: 0.07%). [29, 30] Clinical manifestations of postpartum psychosis include paranoid, grandiose, or bizarre delusions, denial of pregnancy, confused ideation, and grossly disorganized behavior that represent a dramatic changes from mothers’ previous functioning. [31] Despite manic episode is usually considered the most frequent acute psychotic event at postpartum onset, as it affects up to 35% of women with a history of bipolar or schizoaffective disorder, [32] conversely a number of epidemiological studies have suggested that postpartum episodes are almost exclusively depressive. [33] Puerperal psychosis is the only psychiatric illness included into the direct causes of maternal death, as the disease is deemed part of the typical pattern of obstetrical complications, whereas maternal deaths due

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to all the other psychiatric illness have been classified as incidental death. [34] Very recently, puerperal psychosis due to a relapse of bipolar disorder has been found to be associated with a genome-wide significant linkage observed on chromosome 16p13. [35] Conversely, until now possible genetic basis of puerperal psychosis due to acute relapse of schizoaffective disorder has been not investigated. Unfortunately, however, suicide is not uncommon during pregnancy and, especially, in teenage and unmarried mothers. [36] Epidemiological Australian data extracted by Austin and colleagues suggested that the vast majority of maternal suicidal deaths are due to psychiatric disorder and usually occur antenatally and, specifically, before week 20 of gestation. [37] An epidemiological U.S. study performed on a large database of the State of California showed that the cumulative incidence of suicide attempts during pregnancy is 4 per 10,000 pregnancies. [38] One of the best identifiers for pregnant women at risk for attempting suicide is substance abuse and it is well-known (as specified in Chapter 1) that alcohol and illicit drug use is common among the patients with schizoaffective disorder. Thus, it is not surprisingly that, whereas deaths by violent means characterize most of suicide in postpartum psychosis, women attempted suicide during pregnancy prevalently by ingestion of a liquid or a solid, primarily by drug (either licit or illicit) overdose followed by ingestion of corrosive poison. [39] Moreover, despite the rate of suicidal attempts in pregnancy seems to remain relatively small, on the other hand recent researches have demonstrated that, in pregnant women with history of psychiatric disorder, a percentage ranging from 13.1% to 33.0% of mothers may have suicidal ideation. [40] The rate of suicidal ideation in pregnancy is significantly associated with an unplanned pregnancy, as well as with current major depressive episode and comorbid anxiety disorder. [41] Hospital-based, cohort studies, and literature reviews have suggested that unplanned pregnancy, unemployment, difficult access to safe abortion service, intimate partner violence, previous experience of sexual assaults, and interpersonal conflicts also represent specific factors associated with an increased rate of maternal suicide attempts during pregnancy. [42, 43, 44, 45] Box 2. An alternative definition for maternal death (Pregnancy-associated death) Definition Pregnancy-associated death is the death of any woman, from any cause, while she is pregnant or within 1 calendar year of pregnancy termination, regardless of the duration and site of pregnancy Pregnancy-associated death include death as a result of complication of pregnancy itself, a chain of events initiated by the pregnancy, an unrelated medical condition in pregnancy, or a cause unrelated to pregnancy but within the pregnancy or within the first year after pregnancy Suicide during and after pregnancy is considered a subset of pregnancy-associated death

Proponent institution Maternal Mortality Study Group (Division of Reproductive Health at the Center of Disease Control and the American College of Obstetricians and Gynecologists)

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Specific social, relational, and psychiatric factors associated with an increased rate of maternal deaths are summarized in Box 3. Finally, it should be stressed that suicide attempts during pregnancy is associated with significantly higher rates of perinatal morbidity and mortality [increased rates of perinatal mortality have been recorded in women specifically requiring hospitalization after attempting suicide (see Box 4)]. Box 3. Specific social, relational, and psychiatric factors associated with an increased risk of maternal suicide in pregnancy Previous history of any serious psychiatric disorder Current major depressive episode Comorbid anxiety disorder History or current abuse at baseline of alcohol or illicit drugs Unwanted pregnancy Teenage Unmarried conditions Unemployment Difficult access to safe abortion services and family planning Interpersonal conflicts Intimate partner violence Previous personal experience of sexual assault

Box 4. Perinatal complications after maternal suicide attempts [38] Suicide attempts not requiring hospitalization Suicide attempts followed by hospitalization

Increased rates of: Respiratory distress syndrome Low birth weigh Increased rates of: Premature delivery Respiratory distress syndrome Neonatal death Infant death

THE SPECIFICITY OF SUICIDAL SPECTRUM IN PREGNANT WOMEN WITH SCHIZOAFFECTIVE DISORDER Among the symptoms which could characterize a psychotic and/or affective relapse, preventing the onset of suicidal ideation and behaviors is a clinical and ethical duty especially in pregnant patients with social and psychiatric personal history characterized by some or all features (specified above in the Chapter) associated with an increased risk of developing such psychopathological findings. In accordance with Shneidman, suicide may be identified as “a conscious act of selfinduced annihilation, best understood as a multidimensional malaise in a needful individual who defines an issue for which the suicide is perceived as the best solution”. [46] In any case, much has been written about the difficulties of providing adequate definitions for the complex symptomatological and behavioral pattern characterizing the suicidal spectrum. [47] Beyond the most widely accepted definitions related to suicide and

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summarized in Box 5, [48, 49] other several and crucial elements must be addressed to maximize the understanding of suicidality and provide accurate information to optimize intervention efforts in schizoaffective pregnant women. Despite the fact it has been stated that clinicians and researchers should carefully differentiate between low-lethality suicide attempts from those with high-lethality, [50] either psychopathological and social specificities of schizoaffective disorder must force clinicians to consider any suicidal expression shown by these patients as a signal of possible high-lethality suicide attempts. Indeed, suicide attempts among the individuals with schizoaffective disorder are often medically serious and associated with a high degree of intent. [51] The first specificity that requires to be highlighted is the peculiar symptomatological pattern characterizing the course of the disorder. Indeed, patients suffering from schizoaffective disorder, either bipolar o depressive type, are likely to show suicidal thoughts (which may lead to high-lethality suicide attempt or completed suicide) induced by psychotic symptoms which, in more than a few occasion, may complicate an underlying major depressive episode. [52] Despite command hallucinations seem to account for a relatively small percentage of these suicides, on the other hand suicidal ideation may be also complicated by other symptoms further increasing the risk of high-lethality suicide attempts in these patients, such as aggression, impulsiveness, hopelessness, and agitation. Box 5. The suicidal spectrum [47,48,49] Suicide

Death from injury, poisoning, or suffocation with evidence (either explicit or implicit) that the injury was self-inflicted and the person intended to die

Suicide attempt

A potential self-injurious behavior with a nonfatal outcome accompanied by evidence (either explicit or implicit) that the person intended at some level to die

Deliberate selfharm

Willful self-inflicting of painful, destructive, or injurious acts without intent to die

Lethality of suicidal behavior Suicidal ideation Suicidal intent

Objective danger to life associated witha suicide method or action

Thoughts of serving as the agent of one’s own death Subjective expectation and desire for a self-destructive act to end in deaths

The second specificity that needs to be stressed consists of the peculiar imbalance between risk and protective factors shown by this specific psychiatric population. Indeed, as specified in Boxes 1 and 3, schizoaffective women are likely to show some or all factors associated with an increased rate of suicidal activity, whereas factors playing an antisuicidal role in other psychiatric conditions seem conversely to be ineffective in protecting schizoaffective patients (see Box 6).

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Box 6. Factors associated with protective effect for suicide in general psychiatric population and causes which may lead to the annulment of this effect in schizoaffective pregnant woman Protective factors

Causes of annulment of theprotective effect in schizoaffective pregnant women

Pregnancy

• • •

Pregnancy often unplanned Psychiatric symptoms often undiagnosed in pregnancy

Children at home

•

Absence of protective effects during major depressive episodes Such episodes may especially complicate the course of pregnancy in schizoaffective patients who discontinue previous effective psychotropic drugs to avoid fetal exposure

•

Life satisfaction

• • •

High frequency of unfavorable life episodes during adolescence and early adulthood High frequency of incomplete schooling and unemployment

Positive social support

•

Pregnancy and maternity often occur in unmarried conditions Teenage schizoaffective patients often refuse social support because of wishing to continue their own unhealthy life-styles

•

THE USE OF ANTISUICIDAL DRUGS IN PREGNANCY Pregnancy, Mental Illness, and Psychotropic Drugs Women who die for suicide during pregnancy are unlikely to have previous episodes correctly identified and diagnosed. However, diagnosing and treating the pre-existing psychiatric disorder remains a central component of suicide prevention. [53, 54] Unfortunately, all women are likely to discontinue pharmacological regimens during pregnancy for fear of fetal anomalies, also because these mothers receive no adequate information for their pharmacological protective care. [55] However, the psychopharmacological approach is an indispensable tool for preventing fatal self-harming acts in this clinical condition. Thus, this specific communication from the physician to the vulnerable mother and her partner and family should be strongly promoted: sharing the objectives of the therapeutic project between the caregiver and the woman may be facilitated

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by the fact that patients with schizoaffective disorder show a relatively high insight into illness. [56] Therefore, pregnant patients suffering from severe psychiatric disorders (such as schizoaffective disorder) should be encouraged to continue effective drugs: in fact, if the mothers would privilege treatment discontinuation, the eventuality of experiencing symptoms severe enough to promptly reintroduce treatment with these medications seems to be ineluctable. [57] Also, the psychopharmacological approach represents an indispensable instrument for acquiring the maternal adherence to social interventions, psychological supports, and rehabilitative programs. [58] Regrettably, however, schizoaffective women who continue psychotropic drugs during pregnancy are often carelessly managed. Such women are likely to receive multiple medications during pregnancy; moreover, the dose of the medications that are prescribed do not change despite the changing metabolism occurring during the gestational period. This could be one of the reasons why up to 28% of these patients may require hospitalization for drug poisoning not related to drug abuse or suicidal acts due to psychiatric illness (poisoning incidents). [59]

The Relationship between Suicidality, Pregnancy, and Psychopharmacological Regimens Given this background, the necessity exists to carefully manage pregnant women with severe psychiatric disorders at high risk of suicidal behaviors with specific psychotropic drugs, [60] reducing as much as possible the risks of fetal structural major malformations and/or gestational metabolic complications (which may increase the rate of several fetal anomalies independent from the drugs). [61] Unfortunately, meta-analysis of randomized, controlled trials have generally not detected benefit for suicide or suicide attempts in studies on antidepressants or other psychotropic medications, perhaps due to the low base rate of suicidal behavior since reliance on spontaneous reporting underestimates rates of suicidal behavior. [62] However, patient population studies have reported lower suicide attempt rates in adult treated with antidepressant medication. [63] Among the newer antidepressant agents, the protective effect against suicide was strongest for SSRIs. [64, 65] Duloxetine seems to be also associated with the property to reduce the suicidal risk. [66] A general agreement also exists about the finding that clozapine may specifically reduce the suicidal risk in patients with schizoaffective disorder and other psychotic disorders. [67, 68, 69] Lithium is the psychotropic agent showing the greatest number of evidences of its intrinsic anti-suicidal activity, because long-term lithium therapy has been proven to decrease either frequency and lethality of self-aggressive acts. [70, 71, 72] Lithium could have antisuicidal properties possibly related to a specific anti-aggressive effect and, thus, besides the mood stabilizing properties of the medication, and also in patents not responding satisfactorily in terms of reduced number of bipolar or schizoaffective acute episodes. [73, 74, 75] However, most psychotropic drugs with suggested or proven antisuicidal properties have been associated with increased risks of fetal structural malformations (if used during the first trimester of pregnancy).

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Notwithstanding this severe safety limitation, pregnant women with schizoaffective disorder attempting suicide may often need psychopharmacological monotherapy or polypharmacotherapy (despite in other, less life-threatening clinical circumstances drugcombination must be considered inappropriate during early pregnancy). Indeed, in this situation the risk associated with the relapse of the maternal mental illness may outweigh the risk of fetal exposure. For this reason, if the woman has been diagnosed with suicidal ideation during early pregnancy, clinicians should investigated the possibility that the symptomatological relapse may be secondary to the discontinuation of previous effective drugs; in this case, clinical stabilization may be obtained by restoring the previous psychopharmacological regimen as soon as possible, and independently from the patient’s pregnant status. Indeed, pregnancy is not the best period for testing the efficacy of alternative medications. When the onset of suicidal ideation is due to the ineffectiveness of previous treatments or in drug-naïve patients, the choice of the best psychopharmacological option should derive from the psychopathological findings predominating the overall clinical picture of the pregnant woman. In the light of this background, the necessity exists to analyze and summarize published literature information on the teratogenic safety of lithium, SSRIs, duloxetine, and clozapine in order to identify the safest option to treat suicidal risk during early pregnancy. Further, in the following paragraphs we will also investigate the difficulties of managing the suicidal risk in schizoaffective patients during the last stages of pregnancy.

Lithium Lithium use during Pregnancy: General Considerations Lithium is in the FDA pregnancy category D. This means that lithium is known to be harmful to an unborn baby. However, lithium option should be privileged when psychiatric examination suggests that a decrease of the suicidal risk may be obtained by controlling dysphoria, impulsivity, and obtaining a mood stabilizing effect. One of the main concern regarding the clinical use of lithium during pregnancy is that its pharmacokinetics is altered during the gestational period. The glomerular filtration rate increases by 50% in early pregnancy and declines in late third trimester, thus returning to prepregnancy levels soon after parturition. [76] Hence, adjusting the lithium dose proportional to the oscillations of the glomerular filtration rate is needed, in order to maintain serum lithium concentrations within the therapeutic ranges during all stages of pregnancy. Lithium use during early pregnancy However, the teratogenic potential of lithium could have been overestimated in the past. Indeed, Ebstein’s anomaly (which, notably, can be corrected chirurgically) is rare, as it occurs once per 20 000 birth in the general population; during lithium pregnancy-exposure, the risk of this cardiac malformation may increase to 1/1000, thus remaining relatively infrequent. Literature data regarding the outcomes of lithium-exposed pregnancy have been summarized in Table 1.

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Salvatore Gentile Table 1. Maternal lithium use, fetal malformations and pregnancy outcomes

Study

Study’s methodology and sample size

Results

Schou , 1973

Retrospective study(n=118)

The following 9 cases of fetal malformations were observed: • 1 case of Coarctaction of aorta • 1 case of cardiac septal defect • 1 case of stenosis of aqueduct with hydrocephalus, spina bifida plus meningomyelocele, bilateral talipes equinovarus • 1 case of unilateral microtia • 1 case of mitral atresia • 2 case of Ebstein anomaly • 1 case of single umbilical artery plus bilateral hypoplasia of maxilla • 1 case of atresia of tricuspid valve

Park , 1980 Arnon et al, 1981 Long & Willis,1984 Steffelaar , 1991 Gültkein ,1994 Frankenburg & Lipinski, 1983 Källen & Tandberg, 1983 Jacobson , 1992

Case-report(n=1) Case-report(n=1) Case-report(n=2) Case-report(n=1) Case-report(n=1) Retrospective study(n=225) Retrospective study (n=59) Prospective study (n=148)

• • • • • •

Zalstein et al, 1990

Case-control study (n=59) Case-report(n=1) Case-report(n=1) Case-report(n=1)

Grover & Gupta, 2005 Khandelwal , 1989 Schou & Amdisen, 1970 Frassetto 2002 Nars & Picard, 1971 Von Brenndorff & Ertelt, 1978 Ang , 1990 Rane , 1978 Retamal & Cantillano, 2001 Kaufman & Okeva, 1985 Fries, 1970

• • •

Ebstein’s anomaly Tricuspid valve regurgitation 1 fcase of Ebstein’s anomaly Ebstein’s anomaly Ebstein’s anomaly 18 cases of cardiovascular malformations (6 of which were Ebstein’s anomaly) 11 cases of major malformations (no cases of Ebstein’s anomaly) 2 cases of neural tube defects 1 case of meromelia 1 case of Epstein’s anomaly None of the infants diagnosed with Ebstein’s anomaly were exposed in utero to lithium Anencephaly Stillbirth Auricular abnormalities

Case-report(n=1) Case-report(n=1) Case-report(n=1)

• • •

Congenital goiter Congenital goiter Thyroid toxicity

Case-report(n=1) Case-report(n=1) Case-report(n=1)

• • •

Polyhydramnios Hypoglycaemia Healthy outcome

Case-report(n=1)

•

Healthy outcome

Case-report(n=1)

•

Healthy outcome

• • • • •

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Table 2. Maternal paroxetine use and fetal major malformations Study

Study’s methodology and sample size

Daily Dose (mg)

Results

Unfred et al, 2001

Prospective cohort study (n=101)

N/A

No increased risks of major malformations

GSK, 2005

Prospective investigation (Manufacturer’s database) (n=527) Updated results from the previous prospective investigation (Manufacturer’s database) (n=717) Retrospective study(n=9170)

N/A

Increased risk of cardiac malformations (OR: 2.20; 95% CI: 1.34-3.63) No increased risks of major malformations

N/A

Diav-Citrin , 2005

Prospective controlled study(n=330)

N/A

Berard , 2006

Population-based registry study with 2 nested casecontrol arms (n=1403)

22.4

Bar-Oz , 2007

Meta-analysis

N/A

Increased risk of congenital malformations as a whole (AOR: 1.89; 95% CI: 1.20-2.98) Increased risk of cardiac malformations (RR: 3.96; 95% CI: 1.06-11.24) Increased risk of congenital malformation as a whole (Adj OR: 2.23; 95% CI: 1.19-4.17 ) Increased risk of cardiovascular malformations (Adj OR: 3.07; 95% CI: 1.00-9.42) Increased risk of cardiac malformations (OR: 1.72; 95% CI: 1.22-2.42)

GSK, 2005

Cole , 2007

Lithium Use during Late Pregnancy Late pregnancy exposure to lithium has been associated with perinatal unwanted events, mainly consisting of premature birth, macrosomia, floppy infant syndrome, and thyroid dysfunctions. [77, 78] Sporadic reports also describes cases of nephrogenic diabetes insipidus and lesions of cardiovascular, renal, and neuromuscular systems (see above). Finally, Newport demonstrated that the ratio of lithium concentrations in umbilical cord blood to maternal blood was uniform (mean: 1.05) across a wide range of maternal serum concentrations. [79] Significantly lower Apgar scores, longer hospital stays, and higher rates of central nervous system and neuromuscular complications were observed in infants with blood lithium concentrations higher than 0.64 meq/l. Clinicians should also take into account the risk of perinatal complications associated with exposure to lithium during late pregnancy. [80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, 101, 102, 103] General concerns and precautions regarding lithium utilization during pregnancy are available in Box 7.

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Salvatore Gentile Box 7. Lithium utilization during early and late pregnancy. General concerns and precautions

Early Pregnancy

Late Pregnancy

Whole pregnancy

•

Avoid lithium exposure or provide specific gynecologic and psychiatric surveillance

•

When therapy with lithium is deemed indispensable, analyses pros and cons of psychopharmacological treatment with the patient, her partner, and the familial setting

•

Foresee a strict cooperation between psychiatrist, pediatrician, and gynecologist

•

Consider however the opportunity to suspend lithium administration 24-48 hours before a scheduled Cesarean section or induction, or at the onset of labor in the event of spontaneous delivery

•

If therapy with lithium is deemed indispensable, make sure delivery happens in hospitals equipped with intensive nursery unit

•

Adjust the lithium dose proportional to the oscillations of the glomerular filtration rate, in order to maintain serum lithium concentrations within the therapeutic ranges. Indeed, an underdosed lithium treatment may expose the fetus to the toxic effect of the drug, without obtaining a maternal adequate psychopharmacological roofing

•

If it is possible, avoid concomitant treatments with drugs known as potentially increasing lithium toxicity

Table 3. Maternal fluoxetine use and fetal major malformations Study

Study’s methodology and sample size

Daily Dose (mg)

Results

Pastuszac , 1993 Goldstein , 1997

Prospective cohort study (n=128) Prospective investigation (Manufacturer’s register) (n=796) Prospective investigation (Swedish Medical Birth Registry) (n=516) Prospective controlled study (n=118) Prospective cohort study(n=228)

25.8±13.1

No increased risks of major malformations No increased risks of major malformations

Källen, 2004

Diav-Citrin , 2002 Chambers , 1996

N/A

N/A

No increased risks of major malformations

FLX vs PAR N/A

No increased risks of major malformations

25-28±10-15

Increased risk of minor anomalies (P=0.03)No increased risk of major malformations

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Table 4. Maternal fluvoxamine use and fetal major malformations Study Gentile, 2006 Edward, 1994

Study’s methodology and sample size Case-report (n=1) Retrospective analysis of prescription-event monitoring (n=31)

Daily Dose (mg) 200

Results

N/A

No cases of major malformations recorded

Birth of a healthy baby

Table 5. Maternal sertraline use and fetal major malformations Study Chambers etal, 1999

Study’s methodology and sample size Prospective investigation (U.S. database) (n=112)

Daily Dose (mg) N/A

Results No increased risks of major malformations

SSRIs and Duloxetine SSRIs and Duloxetine Use during Pregnancy: General Consideration SRI-monotherapy or SRI-lithium combination may be the most effective solutions in presence of severe depressive symptoms. Among the SRIs, the use of paroxetine during early pregnancy should be avoided (see Table 2 [104, 105, 106, 107, 108, 109, 110]). Indeed, the pregnancy category for paroxetine has been changed from C to D. Patients receiving paroxetine therapy who become pregnant or are currently in their first trimester of pregnancy should be warned of the potential risk to the fetus. Conversely, all the other SSRIs and duloxetine are still rated Category C. SSRIs and Duloxetine Use during Early Pregnancy Clinicians should consider fluoxetine as first-line agent because of the following reasons: a.

until now, fluoxetine has not been associated with an individual risk of increasing the rates of fetal structural malformations (see Table 3 [ 111, 112, 113, 114]). Moreover, the known number of healthy outcomes of fluoxetine-exposed pregnancies is significantly higher than that shown by fluvoxamine, citalopram, escitalopram, and duloxetine, so far also not or anecdotally associated with a suspect teratogenic potential (see Tables 4 to 7 [60, 116, 117, 118, 119, 120, 121, 122, 123]). b. Anecdotal reports suggest that sertraline may also have an its own teratogenic potential. [124] c. studies investigating collectively the teratogenic safety of SRIs (summarized in Table 8) have shown worrying results. However, information about the liability of SRIs as group to increase the teratogenic risk is of weak significance in clinical practice, as this information provides no useful data in order to assess the specific teratogenic risk (and its magnitude) potentially associated with the use of each drug of this class. [125, 126, 127, 128, 129, 130, 131, 132, 133, 134, 135, 136, 137, 138]

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Salvatore Gentile d. among the antidepressants not individually associated with increased rates of fetal anomalies, fluoxetine is unlikely to induce clinically relevant weight changes. [139] This aspect of safety is of great clinical relevance when using drugs during the gestational period, because excessive weight gain during pregnancy is per se associated with a higher incidence of gestational complications and poor pregnancy outcome.

Table 6. Maternal citalopram and escitalopram use and fetal major malformations Study

Study’s methodology and sample size

Drug and daily Dose (mg)

Results

Heikkinen , 2002

Prospective study(n=11)

CITRange: 2040

Sivojelezova , 2005 Gentile, 2006 Majewski, 2007 H. Lundbeck A/S Data on file, 2006

Prospective comparative study(n=125) Case-report(n=1) Case-report(n=1)

CITMedian: 0.345 mg/kg ESC20 ESCRange: 520 ESCN/A

Increased risk of neither poor pregnancy outcome nor neurodevelopmental delay monitored up to 12 months No increased risk of structural teratogenicity Birth of a healthy baby The baby showed total arhinia

Case-reports(n=129)

Some cases of fetal malformations were recorded, with no recurrent patterns of anomalies

Table 7. Maternal duloxetine use and fetal major malformations Study

Study’s methodology and sample size

Daily Dose (mg)

Results

Eli Lilly, 2005.Data on file

Case-reports(n=31)

N/A

No cases of fetal malformations were observed

Hudson , 2005

Accidental exposureduringplacebocontrolled trials (n=28)

N/A

No cases of fetal malformations were observed

SSRIs and Duloxetine Use during Late Pregnancy Despite concordant information exists suggesting the efficacy of a number of modern antidepressants in reducing the rates of either suicides and suicide attempts in psychiatric patients, several specific concerns should be highlighted regarding their use in schizoaffective women showing suicidal ideation and/or behaviors during the last stages of pregnancy. As regards duloxetine, no significant data are available bout its safe use during late pregnancy. However, a same-class drug (such as venlafaxine) has been associated with a high risk of inducing perinatal complications. [140]

Managing the Suicidal Risk in Pregnant Schizoaffective Women

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SSRIs also induce perinatal complications with relatively high frequency, as reviewed elsewhere. Among the SSRIs, paroxetine has been associated with the highest risk of inducing perinatal complications, mainly due to both toxic and withdrawal phenomena. [140] In fact, on the basis of extrapolation from adult SSRI-pharmacology, gestational exposure to SSRIs with short half-lives could lead to a neonatal withdrawal syndrome that occurs with declining levels; moreover, the potent inhibition of 5-HT reuptake and affinity for muscarinic receptors shown by paroxetine could render neonates with in utero exposure to the drug susceptible to both serotonin withdrawal and cholinergic overdrive. Finally, some neonates may experience acute paroxetine-induced toxicity. [141] Both toxic and withdrawal phenomena symptoms have been included under the definition of “Poor neonatal adaptation syndrome” (see Figure 1). However, I suggested the term “SRIinduced perinatal complications” to describe all perinatal unwanted events associated with late in utero exposure to SRIs, because the term “Poor neonatal adaptation” provides no specific information about the etiology of such neonatal events. [140] Further, these events may also be characterized by cases of poor obstetrical outcome, such as low birth weight and Apgar scores. [142] Moreover, other perinatal complications may occur that are not definitively attributable to withdrawal or serotoninergic overstimulation, such as Persistent Pulmonary Hypertension in the Newborn. [143] General concerns and precautions regarding the use of SSRIs and duloxetine during early and late pregnancy have been summarized in Box 8. Table 8. Summary of the studies evaluating collectively the reproductive safety profile of SRIs Study/Drugclass McElhatton ,1996

Kulin et al, 1998 Maschi et al, 2007 Ericson , 1999

Einarson & Einarson, 2005 Malm , 2005 Hendrick , 2003

Study design/Sample size

Drugs

Main study’s results

Prospective investigation of European Network of Teratology Information Service database (n=689) Prospective, multicentre, controlled cohort study (n=168) Prospective, controlled cohort study (n=200) Prospective investigation of the Swedish Medical Birth Registry (n=531) Meta-analysis of 7 studies (n=1774)

SSRIs and TCAs

No increased risks of major malformations

FVX, SER, PAR

No increased risks of major malformations

SSRIsTCAs

No increased risks of major malformations

SSRIs and other classes of antidepressants

No increased risks of major malformations

SSRIs and other classes of antidepressants SSRIs

No increased risks of major malformations

Population-based study (n=1782) Prospective review of obstetric and neonatal records (n=136)

SSRIs

No increased risks of major malformations No increased risks of major malformations

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Salvatore Gentile Table 8. (Continued)

Study/Drugclass

Study design/Sample size

Drugs

Main study’s results

Davis , 2007

Retrospective study (n=260)

SSRIs

Increased risk of eye malformations (RR and CI unspecified)

Wogelius, 2006

Population-based cohort study(n=1054)

SSRIs

Increased risk of major malformations for anytime exposure in early pregnancy (aRRs: 1.77; 95% CI: 0.73-4.32 )

Alwan , 2007

Ongoing, multisite, casecontrol study (n=9622)

SSRIs

Increased risk of omphalocele (OR: 2.8; 95% CI: 1.3-5.7) Increased risk of craniosynostosis (OR: 2.5; 95% CI: 1.5-4.0)) Increased risk of anencephaly (OR: 2.4; 95% CI: 1.1-5.1))

Alwan , 2007

Ongoing, multisite,casecontrol study (n=15,709)

SSRIs/NonSSRIs

Increased risk of sertralineassociated septal defects (OR: 2.0; 95% CI: 1.2-4.0) Increased risk of sertralineassociated omphalocele (OR: 5.7; 95% CI: 1.6-20.7) Increased risk of paroxetineassociated right ventricular outflow tract obstruction defects (OR: 3.3; 95% CI: 1.3-8.6)

Kállén, 2006

Prospective investigation (Swedish Medical Birth Register) (n=6896)

SSRIs NonSSRIs

Increased risk of paroxetineassociated cardiac septal defects (OR: 2.29; 95% CI: 1.28-4.09)

Clozapine Clozapine Use during Pregnancy: General Consideration The use of clozapine during early pregnancy should be discouraged. Indeed, despite its proven antisuicidal property, clozapine should be used during pregnancy only as last-line agent because of its poor reproductive safety profile (see Table 9 [144, 145, 146, 147, 148, 149, 150, 151, 152, 153, 154, 155, 156, 157, 157, 158, 159, 160]). In fact, although clozapine is the only SGAs rated Category B by the Food and Drug Administration (for incomprehensible reasons, however, whereas all the other SGAs are rated Category C) no information supports its safe use during early pregnancy.

Managing the Suicidal Risk in Pregnant Schizoaffective Women

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Poor neonatal adaptation syndrome (the definition includes symptoms due to either drug discontinuation and serotoninergic overstimulation)

¾ Respiratory distress ¾Hypoglycaemia ¾Jitteriness ¾Hyperbilirubinaemia ¾Lethargy ¾Hypo/Hypertonia ¾Poor feeding ¾Weak/Absent cry ¾Seizures ¾Increased risk of admission to intensive nursery units Figure 1. Symptoms included under the obsolete definition of “Poor neonatal adaptation syndrome”.

Box 8. Clinical utilization of SSRIs and duloxetine during early and late pregnancy. General concerns and precautions Early Pregnancy

Late Pregnancy

Avoid paroxetine exposure Provide specific gynecologic, and psychiatric surveillance Waiting for further reassuring information, avoid duloxetine exposure or provide specific gynecologic and psychiatric surveillance When therapy with a SSRI or duloxetine is deemed indispensable, analyze pros and cons of psychopharmacological treatment with the patient, her partner, and familial setting Foresee a strict cooperation between psychiatrist, pediatrician, and gynecologist Consider however the opportunity to suspend SSRI and duloxetine administration within the last month of pregnancy If SSRI/duloxetine treatment is deemed indispensable, make sure delivery happens in hospitals equipped with intensive nursery unit

Clozapine Use during Early Pregnancy Less than 200 babies exposed in utero to clozapine have been monitored, with 15 reported cases of fetal malformations. For most of these cases, no information is available about the kind of the malformation. Hence, it was not possible to analyze possible recurrent patterns of anomalies. Also, in some occasions the mothers took concomitant medications. Moreover, the use of clozapine during early pregnancy is likely to induce gestational metabolic complications (such as excessive weight gain and gestational diabetes). [161] Metabolic gestational complications may be associated not only with a higher incidence of fetal malformations, [162] but also with an increased rate of maternal deaths. [163] In

214

Salvatore Gentile

addition, gestational diabetes has been associated with an increased risk of developing breast cancer later in the life. [164] Unfortunately, almost all the other second-generation antipsychotics (SGAs) have also been associated with an increased incidence of gestational metabolic complications. Conversely, until now FGAs have not been associated with the risk of inducing such unwanted events in the pregnant women. Hence, if treatment with antipsychotic agents is deemed indispensable during the pregnancy of schizoaffective patients, clinicians should prefer first-generation antipsychotics (FGAs). [165]

Clozapine Use during Late Pregnancy Of note, reports on clozapine use during late pregnancy include cases of poor pregnancy outcomes and perinatal complications (ranging from transient floppy infant syndrome to retinopathy and severe neonatal hypoxemic encephalopathy). General concerns and precautions regarding the use of clozapine during pregnancy have been summarized in Box 9. Table 9. Clozapine and Pregnancy Study

Study’s methodology and sample size

Daily dose (mg)

Results

Lieberman & Case-series study (n=14) Safferman, 1992 Bazire, 2005 N/A (n=84)

N/A

No cases of major malformations were observed 8 cases of major malformations were observed No further clinical details available

Dev & Krupp, 1995

N/A

Data collectedretrospectively (n=80)

N/A

Barnas et al, Case-report(n=1) 50-100 1994 Gupta & Grover, Case-report(n=2 – 2 successive 200 in the first 2004 pregnancies ) case 100 in the second case Tényi & Trixler, Case-series N/A 1998 (n=6) Mendhekar et al, Case-report 100 2006 (n=1) Vavrusova & Case-report 100 Konikova, 1998 (n=1) Nguyen & Case-report 350 Lalonde, 2003 (n=2 – 2 successive pregnancies) Dickson & Case-report(n=1) 150-250 Hogg, 1998 Waldman & Case-report(n=1) N/A Safferman, 1993

5 cases of major malformations were observed No further clinical details available No cases of major malformations were observed No cases of major malformations were observed No cases of major malformations were observed Healthy outcome Atrial septum defect No cases of major malformations were observed No cases of major malformations were observed No cases of major malformations were observed

Managing the Suicidal Risk in Pregnant Schizoaffective Women Mendhekar et al, 2003 Rzewuska, 2000 Karakula et al, 2004 Stoner et al, 2004

215

Case-report(n=1)

75

Intrauterine death

Case-report(n=1) Case-report(n=1)

N/A 200

Case-report(n=2)

Infant’s retinopathy Hernia of the white linea and left testicle atresia No cases of major malformations were observed

350 in the first case 625 in the second case 300 No cases of major malformations were observed

Di Michele et al, Case-report (n=1) 1996

Box 8. Clozapine utilization during early and late pregnancy. General concerns and precautions Early Pregnancy

Avoid clozapine exposure or provide specific gynecologic, endocrinologic, and psychiatric surveillance When therapy with clozapine is deemed indispensable, analyze pros and cons of psychopharmacological treatment with the patient, her partner, and the familial setting

Late pregnancy

Foresee a strict cooperation between psychiatrist, pediatrician, and gynecologist Consider however the opportunity to suspend clozapine administration during the last month of pregnancy If therapy with clozapine is deemed indispensable, make sure delivery happens in hospitals equipped with intensive nursery unit

THE USE OF ELECTROCONVULSIVE THERAPY DURING PREGNANCY During the last 60 years, as clinical experience with ECT during pregnancy has accumulated, attitude towards its use have changed dramatically. In the past, ECT was considered contraindicated during pregnancy because animal studies suggested possible increases in the rate of pregnancy loss and abnormal maternal behaviors. [166] Subsequently, as growing cases of favorable outcome became available, pregnancy was included among the specific indications for the first-line use of ECT. [167] Until now, however, no prospective studies have been performed on women who needed ECT during pregnancy. In addition, as reviewed elsewhere, [168] some obstetrical, fetal, and perinatal unwanted events have been reported after ECT use during pregnancy. Two casereports with opposite outcome raised further concerns about the teratogenic safety of ECT use during various stages of pregnancy. [169, 170] For these reasons, it has been stated that ECT use in pregnancy should be limited to cases of pharmacologically-resistant severe depressive symptoms. [169] ECT-induced detrimental events complicating the progression of pregnancy are summarized in Table 10.

216

Salvatore Gentile Table 10. Detrimental events complicating progression and outcomes of ECT-exposed pregnancies. [168,169]

Detrimental event Maternal bleeding Other pregnancy complications Maternal abdominal pain Fetal structural malformations Fetal cardiac rhythm disturbance Miscarriage Premature birth Stillbirth/Neonatal death Perinatal complications Infant’s developmental delay

Number of cases 3 3 3 6 4 5 4 3 2 4

DISCUSSION Despite different pharmacological interventions have been proven to have power over suicidal tendency, only clozapine, lithium, and ECT have specifically demonstrated such a property in patients with schizoaffective disorder. Hence, in case of the onset or recurrence of suicidal tendency in pregnant schizoaffective women, the choice of intervention should be theoretically limited to these three options. As regards clozapine, however, the reproductive safety of this medication is impaired by the unclear teratogenic potential and its liability of inducing both gestational metabolic complications (which may increase the rates of maternal deaths and fetal anomalies independent of the drugs) and perinatal unwanted reactions. Conversely, despite lithium is associated with an increased rate of perinatal complications for maternal dosages within the therapeutic ranges, the structural teratogenicity of the drug may have been overestimated in the past. Moreover, lithium shows increasing evidence from randomized trials that the drug could reduce not only the rate of suicides but also the rate of mortality in general. [171] The antisuicidal property of lithium seems to be related to serotonin mediated reduction in impulsivity and unspecified benefit arising from the longterm monitoring provided during lithium therapy. [172] The suggested concern that, if lithium is prescribed, the potential toxicity in overdose should be taken into consideration when deciding on the quantity of lithium given with each prescription, is of legal, clinical, and ethical value only in United States and in other countries with similar methodology of drug prescription/dispensation on individual basis. In other countries, such as Italy and other European countries, the quantity of tablets is dispensed by pharmacists in accordance with the physician prescription but on the basis of fixed packages: thus, both clinicians and pharmacists are unable to provide the patients of doses below the toxic threshold. Hence, in case of lithium prescription, the drug-package should be cautiously kept by other family members accepting to administer the right daily dose of drugs to their relative. The safety of ECT during early and late pregnancy requires further confirmations. Moreover, merely expressed suicidal intents may relieve more rapidly with ECT than with psychopharmacological interventions. No specific data are available about potential ECT effectiveness in reducing suicidal behaviors too. Hence, in contrast with suggestion proposed

Managing the Suicidal Risk in Pregnant Schizoaffective Women

217

elsewhere, [173] for pregnant women showing a determined suicidal intent, ECT should be still considered a “last resort” position. Data on the efficacy of antidepressants in reducing suicidal behaviors are derived from patients with depressive or anxiety disorders; at the moment, no studies have investigated the anti-suicidal activity of such agents in schizoaffective patients. Nonetheless, SSRIs and duloxetine could be often useful because the eventuality of suicidal ideation and/or behavior not associated with depressed mood is rare in clinical practice. SSRIs could be also helpful in controlling associated-impulsive behaviors. Last but not least, SSRIs and duloxetine are relatively safe in overdose. However, some of these compounds have been associated with an increased risk of inducing fetal anomalies and all with an increased frequency of perinatal complications. For all these reasons, lithium should be considered as the first-line agent for reducing the risk of suicidal death in pregnant schizoaffective women with previous suicide attempts in anamnesis and/or with current psychopathological pattern including suicidal thoughts and/or suicidal plans. Figure 2 shows a flow-chart which details some suggestion for the use of antisuicidal psychotropics during pregnancy.

CONCLUSION Suicidal tendency may be not only the result of a psychiatric illness, but of concurrent underlying psychosocial factors too (above summarized in Box 3). For this reason, a comprehensive plan of service and supports, including specific social and psycho-educational programs, should be provided for all women with severe psychiatric disorders who become pregnant to prevent high-lethality suicide attempts. A proposal of the main tools which must be included in a comprehensive plan finalized to support these vulnerable mother is summarized below: • • • • •

•

•

Attenuate the stigma associated with mental illness, which may often lead to refuse psychiatric counseling. Help the patient to balance the risk of pregnancy exposure to drugs with the risks associated with the untreated psychiatric disorder. Reduce the access to highly lethal methods for attempting suicide. Offer adequate economic and health support. Investigate possible history of intimate partner violence and/or sexual assaults, and if present, provide the possibility to welcome these vulnerable mothers in specific protected houses, also to reduce the frequency of unhealthy life-styles such as poor antenatal cares and tobacco/illicit drug use. Discuss the difficulties to adhere to the life-style changes imposed by parenting with the mother, her partner, and the whole family, in order to identify supportive caregivers for the mother-infant pair. Facilitate social integration, especially for those women coming from disadvantaged community group.

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However, if a non fatal suicidal attempt occurs, either abruptly or following prevention failure, this situation represents primarily an obstetrical and medical/chirurgical emergency. Indeed, it is possible that the suicide attempt might have compromised the health of the mother-infant pair. Thus, these mothers should be admitted at intensive care units in order to receive immediate and optimal cares; moreover, specific obstetrical surveillance should be provided to investigate the repercussions of the maternal act on the fetus. After completing the management of possible life-threatening complications for both the mother and the fetus, the woman should be transferred to psychiatric care unit. Inpatient treatment should continue until her mental state and level of suicidality has stabilized. Finally, the above mentioned psychosocial task-force should be provided since during the first days of maternal hospitalization in order to support all the other family members, especially if they include other children. Indeed, offsprings of mothers reporting suicide attempts show a remarkably higher risk for suicidal thoughts and suicide attempts and a tendency toward suicide attempts at an earlier age. [174] Suicidal risk in patients who discontinued previous effective drugs

Recommence the previous effective therapy, avoiding pharmacological shift

Suicidal risk in drug-naïve patients

I STEPS Lithium monotherapy

Lithium monotherapy ineffectiveness

Shift to fluoxetine, conventional neuroleptics, or fluoxetine-conventional neuroleptic association

Lithium monotherapy partial effectiveness

VI. Add to lithium fluoxetine, conventional neuroleptics, or fluoxetine-conventional neuroleptic combination

Figure 2. A flow–chart for pharmacological management of suicidal risk in pregnant schizoaffective patients.

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[145] Bazire S. Psychotropic drug directory. Fivepin Limited, Salisbury (UK), 2005: 239. [146] Dev VJ, Krupp P. Adverse event profile and safety of clozapine. Rev Cont Pharmacother 1995; 6: 197-208. [147] Barnas C, Bergant A, Hummer M. Clozapine concentrations in maternal and fetal plasma, amniotic fluid, and breast milk [Letter]. Am J Psychiatry 1994; 151 (6): 945. [148] Gupta N, Grover S. Safety of clozapine in 2 successive pregnancies[Letter]. Can J Psychiatry 2004; 49 (12): 863. [149] Tényi T, Trixler M. Clozapine in the treatment of pregnant schizophrenic women[Hungarian]. Psichiatria Danubina 1998; 10: 15-8. [150] Mendhekar DN. Possible delayed speech acquisition with clozapine therapy during pregnancy and lactation[Letter]. J Neuropsychiatry Clin Neurosci 2007; 19 (2): 196-7. [151] Vavrusova L, Konikova M. Clozapine administration during pregnancy [Czechoslovakian]. Ceska Slov Psychiatr 1998; 94 (5): 282-5. [152] Nguyen HN, Lalonde P. Clozapine and pregnancy [French]. Encéphale 2003; 29 (2): 119-24. [153] Dickson RA, Hogg L. Pregnancy of a patient treated with clozapine. Psychiatr Serv 1998; 49: 1081-3. [154] Waldman MD, Safferman A. Pregnancy and clozapine [Letter]. Am J Psychiatry 1993; 150: 168-9. [155] Mendhekar DN, Sharma JB, Srivastava PK. Clozapine and pregnancy[Letter] J Clin Psychiatry 2003; 64 (7): 850. [156] Rzewuska M. Leczenie zaburzeá psychicznych. PZWL, Warszawa: 2000. [157] Karakula H, Szajer K, Śpila B. Clozapine and pregnancy. A case history. Pharmacopsychiatry 2004; 37: 303-4. [158] Stoner SC, Sommi Jr RW, Marken PA. Clozapine use in two full-term pregnancies[Letter]. J Clin Psychiatry 1997; 58 (8): 364-5. [159] Michele V, Ramenghi LA, Sabatino G. Clozapine and lorazepam administration in pregnancy[Letter]. Eur Psychiatry 1996; 11: 214. [160] Klys M, Rojek S, Rzepecka-Woźniak E. Neonatal death following clozapine selfpoisoning in late pregnancy. An unusual case-report. For Sci Int 2007; in press. [161] Gentile S. The clinical utilization of atypical antipsychotics in pregnancy and lactation. Ann Pharmacother 2004; 38 (7):1265-71. [162] Waller DK, Shaw GM, Rasmussen AS, Prepregnancy obesity as a risk factor for structural birth defects. Arch Pediatr Adolesc Med 2007; 161 (8): 745-50. [163] Caughey AB. Maternal mortality: more than a just anecdotal evidence. J Perinatol 2007; 27: 595-6. [164] Davson SI. Long-term risk of malignant neoplasm associated with gestational glucose intolerance. Cancer 2004; 100: 149-55. [165] Gentile S. Unpublished data. [166] Rosvold HE. The effects of electroconvulsive shock on gestation and maternal behavior. II. J Comprehens Psysiol Psychol 1949: 42: 207-19. [167] Consensus Conference. Electroconvulsive therapy. JAMA 1985; 254: 2103-8. [168] Miller LJ. Use of electroconvulsive therapy during pregnancy. Hosp Commun Psychiatry 1994; 45 (5): 444-50. [169] Pinette MG, Santarpio C, Wax JR, Blackstone J. Electroconvulsive therapy in pregnancy. Obstet Gynecol 2007; 110: 465-6.

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INDEX

A AA, 97, 129, 226 abdominal, 216 abnormalities, 94, 97, 99, 102, 103, 110, 206 abortion, 188, 200, 201 abstinence, 155, 157, 158, 161 AC, 85, 127, 219, 223 academic, 13, 17, 18, 21, 31, 125, 157, 182, 183, 187, 188, 190 academic performance, 187, 188 academics, 18, 21 access, xiii, 31, 61, 200, 201, 217 accommodation, 54, 60, 61, 62 accountability, 28 accuracy, 163, 169 acetylcholine, 99, 111 achievement, 195 action potential, 113 activation, 94, 100, 113 acute, xii, xiv, 3, 5, 10, 25, 33, 72, 90, 91, 93, 94, 98, 102, 105, 106, 107, 108, 111, 116, 124, 126, 127, 137, 149, 182, 184, 185, 199, 204, 211 acute schizophrenia, 107 AD, 130 ad hoc, 156 adaptation, 157, 173, 211, 213 addiction, 104 ADHD, 100 adjustment, x, 75, 92, 103, 153, 172 administration, 94, 158, 160, 163, 208, 213, 215, 222, 227 administrative, 183 adolescence, xii, xiii, 3, 36, 38, 45, 96, 102, 111, 123, 182, 187, 190, 198, 203 adolescents, 132, 179, 180, 220

adult, viii, 58, 101, 102, 109, 110, 181, 185, 204, 211, 222 adultery, 185 adulthood, xiii, 36, 38, 114, 197, 203 adults, 96, 128, 130, 139, 164 advocacy, 60, 61, 63 AE, 85, 133, 225, 226 AEP, 101 aetiology, 84 AF, 220 affective disorder, vii, viii, xiii, 1, 2, 3, 4, 5, 6, 7, 8, 9, 11, 12, 13, 15, 16, 19, 21, 22, 23, 24, 27, 28, 29, 30, 33, 34, 54, 58, 66, 69, 71, 81, 82, 84, 86, 87, 93, 96, 98, 103, 105, 106, 107, 108, 109, 116, 126, 129, 134, 137, 138, 146, 149, 150, 151, 181, 182, 196, 219, 222, 223 African American, 158 afternoon, 194, 195 age, x, xii, 71, 72, 75, 81, 98, 99, 100, 123, 124, 129, 133, 158, 159, 161, 164, 177, 182, 197, 198, 218 agent, 105, 202, 204, 209, 212, 217 agents, 92, 108, 204, 214, 217 aggregation, 108 aggression, 37, 41, 54, 100, 102, 198, 202 aggressive behavior, 198 aggressive personality, 198 aging, 38, 159 agranulocytosis, 226 aid, 62, 120, 126 air, 33, 176 air traffic, 176 AJ, 220, 223, 224 AL, 133, 134, 221 alcohol, 31, 110, 154, 159, 163, 176, 198, 200, 201 alcohol abuse, 163, 176 alcohol dependence, 110, 154

230

Salvatore Gentile

alcohol use, 176 alcoholics, 86 alcoholism, 90, 98, 177 algorithm, 95 alienation, 75 allele, ix, 70, 71, 74, 79, 80, 81, 82, 99 alleles, 70, 79, 80, 81 alpha, 98, 99, 172 alternative, 169, 199, 200, 205 alternatives, 186 Alzheimer, 96, 107, 121, 124, 131 AM, 132, 134, 222, 224 ambiguity, 11 ambivalence, 12, 34, 37 ambivalent, 12, 94, 164 ambulance, 48 American Psychiatric Association, 4, 6, 7, 24, 67, 115, 126, 141, 147 American Psychological Association, 8, 175 amniotic, 227 amniotic fluid, 227 amplitude, 97, 98, 99, 100, 110 Amsterdam, 131 amygdala, 114 analgesics, 94 anatomy, 128 anencephaly, 212, 224 anger, 37, 38, 42, 44, 53, 190, 193 anhedonia, xi, 154, 155, 157, 158, 160, 161, 164, 167, 173, 174, 177 animal models, 101, 106, 113 animal studies, 70, 215 annihilation, 201 anomalous, 163, 165 antagonism, 106 antagonist, 106, 111, 112 antagonists, 112 anterior cingulate cortex, 106, 110 antiapoptotic, 112 antibiotic, 95 antibiotics, 95 anticholinergic, 134 antidepressant, 84, 87, 96, 125, 193, 194, 204, 222, 226, 228 antidepressant medication, 125, 204, 226 antidepressants, 54, 184, 204, 210, 211, 217, 219, 221, 222, 225, 226 antinociception, 106 antioxidant, 104 antipsychotic, 11, 30, 49, 71, 85, 91, 93, 94, 95, 101, 106, 119, 125, 134, 149, 183, 184, 194, 214, 219 antipsychotic drugs, 71, 106, 149, 194

antipsychotics, 12, 48, 92, 94, 106, 112, 214, 219, 227 antisocial, 98, 110 antisocial personality, 98, 110 antisocial personality disorder, 110 anxiety, ix, 11, 19, 29, 41, 57, 75, 79, 81, 82, 85, 92, 96, 99, 141, 153, 156, 160, 172, 173, 175, 200, 201, 217, 222 Anxiety, 76, 105, 160, 198 anxiety disorder, 11, 57, 200, 201, 217 aorta, 206 APA, 115, 136 apathy, 157 aphasia, 117 apoptosis, 101, 113 apoptotic, 113 application, xiv, 25, 96, 124 AR, 84 argument, vii, 6, 50, 117, 154 aripiprazole, 106 arousal, 155 articulation, viii, 23 AS, 134, 222, 227 Asian, 16, 20, 21, 23, 50, 140, 158, 162 Asian countries, 20, 21 aspiration, 42, 62 assault, 41 assessment, 10, 22, 45, 73, 90, 91, 92, 102, 126, 130, 145, 147, 148, 176, 221, 222 assessment tools, 45 associations, 85, 107, 158, 159, 160, 165, 168, 171, 173 assumptions, 7, 10, 11 atmosphere, 40 ATP, 113 atresia, 206, 215 attacks, 117 attention, vii, 18, 28, 40, 70, 74, 77, 79, 93, 101, 107, 109, 113, 114, 119, 120, 124, 129, 130, 141, 145 attitudes, 15, 221 attribution, 40, 161 attribution bias, 40 atypical, 2, 92, 94, 125, 219, 227 audiology, 101 auditory evoked potential, 99, 111, 114 auditory evoked potentials, 111, 114 auditory hallucinations, xi, 36, 45, 52, 94, 107, 109, 117, 165, 173, 176 auditory stimuli, 114 Australia, 16, 20 authority, 11, 28, 58, 60, 188, 194 autonomy, 59

Managing the Suicidal Risk in Pregnant Schizoaffective Women averaging, 98 aversion, 160 avoidance, 42, 77, 173, 224 awareness, vii, xi, 33, 35, 43, 61, 138, 145, 154, 180 axons, 85

B babies, 213 back pain, 106 background noise, 98 banking, 32 bankruptcy, 186 barrier, 96 barriers, 64 base pair, 74 base rate, 169, 173, 204 basic needs, 54 basic research, 100 battery, 73, 102, 128, 132, 142, 159 Bax, 112 Bcl-2, 112 BD, 85, 130 BDNF, ix, 70, 74, 79, 80, 81, 82, 84, 86, 87 behavior, 6, 75, 76, 90, 91, 100, 122, 128, 148, 157, 171, 199, 202, 204, 217, 219, 221, 227 behaviours, 183 Beijing, 185 benefits, 64, 91 benign, 97, 116 benzodiazepine, 91 bible, 187 bilateral, 206 binding, 86, 91, 112 biochemical, vii, viii, 15, 16, 18, 19, 21, 28, 36, 55, 61, 101 biological, 65, 102, 117, 175 biological psychiatry, 117 biologically, 99 bipolar, viii, x, xii, 3, 4, 8, 11, 12, 30, 32, 33, 35, 40, 41, 42, 43, 45, 46, 47, 48, 49, 50, 53, 55, 57, 58, 66, 67, 69, 71, 85, 86, 87, 90, 92, 93, 94, 97, 98, 99, 100, 103, 105, 107, 108, 109, 110, 111, 116, 118, 123, 124, 125, 129, 133, 134, 136, 137, 146, 148, 149, 150, 161, 169, 170, 173, 174, 182, 183, 184, 197, 199, 202, 204, 219, 220, 223, 224 bipolar disease, 46 bipolar disorder, viii, xii, 4, 11, 12, 30, 33, 40, 41, 42, 47, 53, 55, 57, 58, 66, 69, 85, 86, 87, 90, 97, 103, 105, 107, 108, 109, 110, 111, 118, 123, 124, 125, 129, 133, 134, 136, 137, 146,

231

148, 149, 150, 161, 169, 170, 173, 174, 182, 199, 219, 223, 224 bipolar illness, xii, 90, 92, 93, 99, 109, 110, 170, 173 birth, 199, 201, 205, 207, 211, 216, 224, 226, 227 birth weight, 211 BIS, 159, 160 blame, 187 blaming, 36, 38, 44, 48 bleeding, 216 blood, 74, 90, 96, 101, 190, 207 blood pressure, 90 bonding, 188 borderline, 2, 7, 9, 98, 110, 139 borderline personality disorder, 110 boredom, xi, 153, 154, 155, 156, 157, 158, 159, 160, 161, 164, 165, 167, 168, 169, 170, 171, 172, 173, 174, 175, 176, 177 Boston, 131, 132 BP, 84, 90 brain, ix, 36, 55, 65, 70, 71, 84, 85, 86, 87, 96, 97, 98, 100, 101, 102, 106, 107, 109, 110, 112, 113, 117, 131, 134 brain activity, 106 brain development, 97, 113 Brazil, 139, 147 breakdown, 48, 64 breakfast, 194, 195 breast, 214, 227 breast cancer, 214 breast milk, 227 breastfeeding, 221, 222, 225 bribery, 190 Britain, 220 British, 25, 33, 39, 46, 50, 67, 149, 150, 175, 176 business, 186, 187, 188, 189, 190, 193 bypass, 125

C calcium, 101, 112 California, 115, 118, 126, 131, 200 Canada, 16, 20 cancer, 36 Cancer, 113, 227 capacity, xi, 73, 96, 99, 101, 133, 138, 146, 147, 156, 165, 167, 170, 171 cardiovascular, 206, 207 caregiver, 62, 203 caregivers, 60, 62, 185 cargo, 31 Caribbean, 197 case study, 157

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caspase, 113 caspases, 113 catalyst, 64, 156 catatonic, 3, 5, 71 categorization, 7 category b, 164 catholic, 32 cattle, 32 Caucasian, 158 causal attribution, 177 CB, 220 CD, 224, 225, 226 CE, 132, 134, 224 cell, 70, 101, 113, 161 cell death, 70, 101, 113 central executive, 120, 122, 132 central nervous system, 97, 112, 207 cerebral cortex, 112 cerebral ischemia, 112, 113 CG, 128 channels, 59 Chevron, 66 childbearing, 222 childbirth, 222 childhood, 35, 36, 38, 41, 45, 46, 64, 87, 95, 114, 123, 150, 187, 190 children, xiii, 96, 99, 100, 101, 102, 111, 113, 114, 179, 180, 187, 189, 218 China, v, xii, 32, 33, 44, 179, 180, 181, 182, 183, 184, 185, 195, 196, 197, 219 Chinese, viii, 31, 33, 39, 46, 50, 56, 58, 67, 183, 185, 195, 196 Chinese women, 33, 39 chloroform, 74 chlorpromazine, 90, 92 cholinergic, 211 chromosome, 70, 99, 109, 200, 221 chronic, 6, 7, 39, 71, 84, 90, 91, 94, 96, 102, 106, 108, 110, 112, 114, 134, 149, 167, 187, 188, 191 chronic illness, 187, 188, 191 chronic pain, 94 chronically ill, 96, 102 cigarette smoking, 198 citalopram, 209, 210 citizens, 39, 190 CL, 87, 219, 224 classes, 211 classical, vii, 21 classification, xii, 9, 71, 103, 108, 182, 199, 220 classified, 16, 199, 200

clients, viii, 3, 5, 7, 8, 10, 11, 12, 13, 21, 29, 37, 39, 47, 54, 55, 58, 59, 62, 64, 67, 148, 171, 183, 189, 190, 195 clinical, vii, viii, ix, x, xi, xii, 2, 5, 8, 9, 10, 15, 24, 25, 33, 36, 41, 66, 69, 70, 71, 72, 73, 75, 79, 80, 81, 82, 83, 84, 85, 93, 100, 102, 103, 104, 105, 107, 108, 109, 116, 118, 119, 122, 124, 126, 127, 132, 133, 137, 147, 148, 149, 153, 154, 155, 157, 159, 160, 161, 162, 163, 164, 171, 172, 181, 183, 198, 199, 201, 203, 205, 209, 210, 214, 215, 216, 217, 220, 221, 222, 223, 227 clinical depression, 36 clinical diagnosis, 2, 15, 103 clinical presentation, 69, 75, 83 clinical psychology, 119, 163, 171 clinical symptoms, ix, 70, 81, 83, 133, 137 clinical trial, 127, 137, 222 clinical trials, 137, 222 clinically significant, 92, 144, 164 clinician, 11, 12, 92, 136, 163 clinicians, vii, xiii, 12, 82, 91, 93, 101, 117, 121, 153, 154, 163, 171, 172, 173, 202, 205, 214, 216 clinics, xii, 57, 182, 183, 184 clozapine, 87, 93, 104, 105, 112, 134, 204, 205, 212, 213, 214, 215, 216, 222, 226, 227 cluster analysis, 138 clusters, 147, 164 CNS, 113, 219, 222 Co, xii, 96, 127, 181, 192, 193 cocaine, 91, 93, 96, 107 cochlear implant, 114 coding, 70, 99, 122, 132 co-existence, xii, 11, 14, 22, 23, 52, 181 cognition, x, xi, 37, 129, 130, 133, 134, 141, 150 cognitive, vii, ix, x, xi, 7, 10, 16, 21, 36, 40, 55, 70, 73, 74, 75, 79, 81, 82, 84, 86, 96, 109, 115, 116, 117, 118, 119, 120, 122, 123, 124, 125, 126, 130, 132, 133, 134, 136, 137, 138, 139, 141, 145, 146, 147, 148, 149, 150, 173, 175, 176 cognitive abilities, 118, 124 cognitive ability, x, 8, 118, 139 cognitive activity, 109 cognitive deficit, vii, 82, 123, 125, 126, 130, 133, 137, 146, 148 cognitive deficits, 82, 123, 125, 126, 130, 137, 146, 148 cognitive function, 16, 21, 55, 75, 82, 84, 116, 123, 124, 125, 132, 133, 134, 136, 138, 145 cognitive impairment, vii, 117, 136, 137, 138 cognitive models, 40

Managing the Suicidal Risk in Pregnant Schizoaffective Women cognitive performance, 86, 126, 150 cognitive perspective, 36 cognitive process, 122 cognitive test, 7, 125 cognitive therapy, 8 cognitive variables, 79 cohesiveness, 189 cohort, 129, 132, 200, 207, 208, 211, 212, 225 collaboration, 62 college students, xi, 155, 157, 160, 167, 169, 170, 172 colors, 123 communication, 203, 225 communities, 61, 62, 64 community, xiii, 15, 29, 31, 36, 57, 58, 59, 60, 61, 62, 63, 64, 72, 124, 133, 139, 142, 161, 172, 185, 217, 228 community support, 59 community-based, 161, 172 comorbidity, 69, 110 compensation, 192 competence, 11, 12, 42, 63 complementary, 60 complexity, 13, 93, 136, 158, 183 compliance, 57, 82, 162, 163, 166, 167, 169, 198 complications, 199, 201, 204, 207, 210, 211, 213, 214, 216, 217, 218, 226 components, 59, 64, 114, 120, 121, 124, 138, 176 composite, 158 composition, 113 compounds, 125, 217 computer, 111, 119 concentration, 6, 30 conception, 173 concordance, 96, 97, 108 Concrete, 150 conduct disorder, 97, 110 confidence, 169 confidentiality, 11, 13, 31, 182, 185 conflict, 185 confusion, vii, 5, 12, 13, 14, 15, 21, 41, 44, 48, 54, 55, 56, 63, 64, 182, 186, 190, 195 Congress, iv, 219 conjecture, 168, 172 connectivity, 128 conscientiousness, xi, 145 consciousness, 60 consensus, 31, 95, 123, 125, 182, 185 constitutional, 116 constraints, 43, 44, 156 construct validity, 116 consumers, 16, 21, 55, 60, 61, 62, 63 contempt, 41

233

content analysis, 17 continuing, 137 control, x, 5, 14, 40, 41, 44, 49, 56, 59, 60, 72, 75, 77, 79, 80, 81, 82, 86, 94, 98, 99, 104, 156, 163, 206, 207, 212, 224 control group, x, 72, 75, 79, 80, 81, 82, 98, 99 controlled, 34, 36, 40, 56, 63, 105, 106, 148, 193, 195, 204, 207, 208, 210, 211, 224, 225, 226 controlled trials, 204, 210 conviction, 156, 173 cooking, 189 Copenhagen, 25, 95 coping strategies, 64, 156, 172 coping strategy, 157 copyright, iv correlation, 158, 165, 166, 169, 174 correlation analysis, 158 correlation coefficient, 165 correlations, 114, 155, 164, 165, 172, 173 corrosive, xii, 200 corruption, 190, 193 cortex, 100, 112, 114 cortical, 36, 83, 100, 101, 104, 109, 111, 112, 113, 114, 117, 128 cortical neurons, 113 cost effectiveness, 196 counseling, 16, 18, 21, 31, 32, 39, 55, 57, 58, 185, 217 coupling, 104 covariate, 145, 170 coverage, 179 CR, 85, 127, 129, 133 crack, 93 craving, 155, 157, 161 creativity, 60 critical period, 102 criticism, 41, 176 cross-cultural, 139, 147 cross-cultural comparison, 147 cross-sectional, 136, 223 crying, 39, 136 CS, 132 CT, 135 cultural, vii, 21, 59, 176, 177, 183 culture, 154, 183, 195 currency, 163 cytochrome, 113

D DA, 85, 87, 129 daily living, 29, 36, 124, 133 D-amino-acid, 109

234

Salvatore Gentile

danger, 91, 202 data set, 222 database, 200, 207, 209, 211, 219 death, 14, 32, 38, 44, 45, 46, 63, 186, 197, 199, 200, 201, 202, 215, 216, 217, 219, 227 deaths, xii, 90, 197, 198, 199, 200, 201, 202, 213, 216, 220, 221 debt, 185, 187, 189, 190, 192 decision making, 59 decisions, 30, 60 declarative memory, 120 deconstruction, 124 defects, 206, 212, 226, 227 defense, 41, 104 defenses, 41 deficit, 116, 127, 128, 129, 130, 157 deficits, x, 10, 15, 40, 63, 111, 115, 117, 118, 119, 120, 121, 123, 124, 125, 126, 127, 129, 131, 133, 134, 135, 137, 147, 149, 150, 151 definition, 4, 9, 59, 70, 81, 108, 122, 155, 159, 200, 211, 213, 221 degree, xi, xiii, 9, 14, 32, 39, 41, 43, 44, 46, 48, 49, 51, 54, 64, 95, 113, 116, 118, 119, 125, 156, 158, 165, 167, 170, 171, 202 delinquent adolescents, 38 delinquents, 186 delivery, 30, 199, 201, 208, 213, 215 delusion, vii, 5, 6, 11, 12, 14, 28, 35, 39, 48, 49, 61, 63, 183, 189, 192, 193 delusions, 5, 6, 8, 11, 12, 34, 39, 48, 54, 61, 63, 67, 90, 93, 124, 136, 185, 186, 190, 192, 193, 199 demand, 37, 123, 179, 180 dementia, vii, 2, 23, 90, 93, 96, 116, 117, 121, 123, 128, 129, 133 demographic, 71, 72, 161, 162 demographic characteristics, 71, 72 demographics, 141 denial, 41, 42, 199 Denmark, 20 density, 100 Department of Health and Human Services, 31, 58, 59, 60, 61, 62, 63, 64 dependant, 91, 94, 99 depressants, 13, 14, 19, 30, 61 depressed, 4, 13, 14, 32, 33, 71, 90, 92, 94, 99, 102, 116, 118, 127, 130, 136, 150, 155, 156, 161, 163, 189, 192, 195, 217 depression, vii, ix, xi, 4, 5, 6, 14, 15, 33, 36, 37, 39, 41, 42, 46, 48, 49, 53, 59, 65, 67, 71, 75, 82, 86, 87, 90, 92, 93, 95, 96, 97, 98, 102, 105, 106, 107, 108, 110, 116, 118, 141, 156, 160,

162, 163, 165, 166, 167, 168, 170, 180, 186, 222 depressive disorder, vii, viii, ix, xii, 11, 12, 13, 30, 37, 47, 53, 55, 57, 58, 86, 105, 182, 183, 219, 228 depressive symptoms, 3, 48, 49, 50, 51, 52, 92, 107, 182, 188, 209, 215 desire, 202 desires, 44, 53, 54, 60 destruction, 38, 41 detection, 99 detention, 61, 186 developed countries, 32, 199 developmental delay, 216 developmental process, 188 DF, 85 DG, 128, 134, 222 DGGE, 87 DI, 133, 134 diabetes, 90, 207, 214 diabetes insipidus, 207 diagnostic, vii, ix, xiv, 5, 8, 9, 25, 45, 69, 71, 73, 81, 82, 83, 89, 90, 91, 92, 94, 95, 96, 97, 98, 100, 102, 103, 107, 116, 127, 131, 136, 137, 138, 139, 140, 145, 146, 147, 161, 169, 170, 174 Diagnostic and Statistical Manual of Mental Disorders, 24, 106, 126, 141, 147 diagnostic criteria, vii, 5, 8, 9, 71, 90, 96, 116, 140 dichotomy, ix, 93, 96, 108, 127, 163 differential diagnosis, 85, 94 differentiation, 34, 81, 148 diffusion, 2, 33, 34 digestion, 74 dignity, 30, 38, 60, 64, 192, 194 dipole, 114 disability, 94, 197 DISC1, 97, 109 discomfort, xi, 141, 146 discourse, 60, 153 discrimination, 63, 150 disease progression, 81 diseases, 71, 131 disorder, vii, viii, x, xi, xii, xiii, 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 18, 19, 21, 22, 23, 24, 27, 28, 29, 30, 31, 33, 35, 37, 40, 41, 42, 55, 58, 59, 60, 61, 62, 64, 65, 69, 71, 72, 83, 84, 85, 87, 90, 91, 93, 94, 95, 98, 99, 100, 102, 103, 105, 107, 108, 115, 116, 117, 118, 119, 120, 121, 123, 126, 127, 130, 135, 136, 137, 138, 139, 141, 142, 145, 146, 147, 148, 149, 150, 151, 155, 161, 169, 170, 173, 181,

Managing the Suicidal Risk in Pregnant Schizoaffective Women 182, 183, 185, 186, 190, 195, 196, 197, 198, 199, 202, 220, 222 dissatisfaction, 155, 161 dissociation, 35 distance learning, 32 distraction, 40 distress, 41, 82, 160, 165, 201 distribution, ix, 70, 79, 80, 81, 82, 94, 117 diurnal, 104 diversity, 53 division, 116 divorce, 185, 186, 187, 188, 190 dizygotic, 108 dizygotic twins, 108 DNA, 74, 113 doctor, 13, 14 dopamine, 91, 94, 104, 105, 106, 177 dopaminergic, 104 dopaminergic neurons, 104 doppler, 89 dosage, 14, 48, 56, 194, 225 DP, 131 draft, 123 dream, 32, 38, 54 drinking, 32 drug abuse, 198, 204 drug exposure, 93 drug treatment, 158, 228 drug use, 154, 158, 167, 200, 217 drug-induced, 198 drugs, xiii, 12, 19, 49, 56, 59, 101, 107, 112, 127, 176, 198, 201, 204, 205, 208, 210, 216, 217, 226 DSM, viii, x, 4, 6, 8, 9, 19, 23, 65, 69, 71, 84, 90, 91, 92, 93, 95, 96, 98, 103, 106, 107, 108, 115, 136, 140, 150, 176 DSM-II, 84, 107, 108, 140, 150, 176 DSM-III, 84, 107, 108, 140, 150 DSM-IV, x, 69, 71, 90, 91, 92, 95, 96, 98, 103, 107, 115, 136 duration, 3, 8, 72, 75, 81, 155, 157, 158, 160, 167, 169, 170, 177, 181, 182, 184, 200 duties, 64, 183 dysphoria, 205 dysregulated, x, 102 dysthymia, 92

E EA, 87, 132 early retirement, 195 eating, 168 economic, xiii, 217

235

education, 31, 58, 60, 61, 63, 64, 188 Education, 140 educational programs, 217 EEG, 83, 99, 103, 109, 110 efficacy, 92, 101, 107, 125, 205, 210, 217 ego, x, xi, 33, 37, 38, 39, 41, 42, 138, 139, 145, 146, 147 EI, 84 elderly, 84, 112, 124, 133, 149, 179, 180, 181, 196 Electroconvulsive Therapy, 215 electrodes, 99 electron, 101 electronic, iv electrons, 101 electrophoresis, 74 electrostatic, iv EM, 222, 223, 226 email, 135 emotion, 6, 40, 63, 65, 66, 67, 153 emotional, xi, 3, 34, 36, 38, 40, 43, 60, 97, 106, 141, 146, 179 emotional disorder, 97 emotions, 31 empathy, 186, 194 employees, 62, 145 employers, 63 employment, 54, 60, 62, 133, 139, 148, 150, 168, 186 employment status, 133 empowerment, 60, 195 encephalopathy, 214 encoding, 112, 121 encouragement, 36, 44, 45, 194 endogenous, 101, 160, 177 endophenotypes, 100, 148 energy, 40, 101 engagement, 40, 141, 158, 175 England, 128, 177 Enhancement, 106 environment, 11, 58, 153, 155, 156, 160, 161, 195 environmental, ix, 3, 47, 51, 99, 122, 158, 175 environmental change, 99 environmental conditions, 158 epidemiological, 70, 181, 199, 200 epidemiology, 21, 55 epilepsy, 90, 99, 103, 110, 179 episodic, 29, 119, 120, 124, 125, 145 episodic memory, 120, 145 equilibrium, 79 ERP, x, 98, 99 ERPs, 98

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Salvatore Gentile

ES, 87 escitalopram, 209, 210 ET, 128, 219 ethical, 201, 216 etiology, vii, viii, 1, 7, 13, 14, 16, 18, 19, 21, 22, 23, 27, 28, 29, 30, 55, 70, 111, 211 euphoria, 6 Eurocentric, 21 Europe, 90 European, 16, 20, 21, 23, 79, 83, 87, 105, 127, 148, 149, 150, 177, 211, 216, 219, 222, 225 evening, 32 event-related potential, 109, 110, 114 event-related potentials, 110 evidence, vii, ix, x, 81, 86, 89, 92, 94, 103, 109, 112, 114, 116, 117, 118, 123, 125, 128, 130, 137, 151, 154, 157, 163, 172, 202, 216, 221, 227 evoked potential, 114 evolution, 127 exaggeration, 155, 161 examinations, 116 excitement, 43, 105 excitotoxicity, 101, 112, 113 exclusion, 9, 72 executive function, 40, 73, 117, 119, 120, 122, 123, 124, 128, 131, 133, 142 executive functioning, 40, 120, 128, 133 executive functions, 73, 117, 119, 122, 124 exercise, 54, 59, 157 expert, iv, 91 explicit memory, 138 explosive, 100 exposure, xiii, 94, 96, 106, 157, 205, 207, 208, 211, 212, 213, 215, 217, 223, 224, 225, 226 external constraints, 156 extraction, 74 extrapolation, 211 extraversion, 75, 81 eye, 56, 99, 101, 212

F factorial, 147 failure, 37, 39, 95, 122, 136, 218 false, 34 familial, 72, 208, 213, 215 family, vii, x, xii, xiii, xiv, 5, 12, 13, 14, 25, 29, 31, 32, 35, 36, 39, 40, 46, 58, 60, 61, 62, 63, 67, 86, 90, 92, 95, 97, 99, 101, 103, 108, 109, 148, 164, 176, 182, 183, 184, 186, 187, 188, 189, 192, 201, 203, 216, 217, 218 family factors, 40

family history, xii, 182 family life, 189 family members, x, 63, 97, 216, 218 family planning, 201 family studies, vii, xiv, 5, 25, 67 family support, 60, 61 farming, 32 fat, 13 fatigue, 13, 38, 46, 185 faults, 14 FDA, 92, 127, 205 fear, 28, 44, 91, 153, 203 February, 127 fee, 32 feedback, 34 feeding, 104 feelings, xi, 2, 22, 30, 35, 37, 41, 42, 44, 45, 49, 54, 55, 56, 57, 58, 76, 154, 155, 156, 157, 158, 160, 161, 165, 167, 169, 171, 172, 186, 193 fees, 32, 182, 184, 186, 191, 193, 194 female prisoners, 176 females, xi, 46, 50, 71, 181 fetal, 203, 204, 205, 206, 207, 208, 209, 210, 213, 215, 216, 217, 225, 227 fetus, 208, 209, 218 fiber, 106 fibromyalgia, 91, 104 filtration, 205, 208 finance, 13, 59 first degree relative, 4, 96 first generation, 184 fitness, 138 fixation, 100 FL, 132 flexibility, 122, 132 flight, 4, 6, 172 flow, 217, 218 fluctuations, 106, 123 fluoxetine, 208, 209, 210, 224, 225 fluvoxamine, 209, 222, 225 fMRI, 94, 98, 100, 107 focusing, 29, 37, 64 food, 54, 142, 189 Food and Drug Administration, 212 Ford, 109, 110, 111 forgetting, x, 121 FP, 132 fragmentation, vii, 33, 34, 35, 36, 38, 39 France, 20 free radical, 101 free radicals, 101 free recall, 73, 121 Freud, vii, 33, 65, 100

Managing the Suicidal Risk in Pregnant Schizoaffective Women friendship, 62 frontal cortex, 84, 117 frontal lobe, 83, 126, 128 frontal lobes, 128 fruits, 73 frustration, 31, 34, 44, 62, 186, 189, 190, 191, 193, 195 FS, 133 fulfillment, 42, 91 fusion, 9

G G4, 9 gambling, 32, 35 games, 55, 56 GE, 127, 129, 222, 226 gel, 74 gene, ix, 70, 71, 83, 84, 85, 86, 87, 97, 109 general knowledge, 180 generalizability, 126 generation, 41, 101, 125, 214 genes, ix, 15, 70, 81, 83, 86, 87, 97, 109 genetic, v, vii, ix, 15, 21, 24, 28, 65, 69, 70, 81, 82, 83, 87, 94, 96, 97, 99, 102, 108, 109, 111, 119, 128, 130, 137, 147, 148, 200 genetic abnormalities, ix, 97 genetic factors, ix, 83 genetic marker, 97, 99 genetic susceptibility loci, x, 97 genetic testing, 94, 102 genetics, vii, viii, 16, 55, 70, 82, 96, 108, 111 Geneva, 25, 219, 220 genome, 200, 221 genotype, 70, 71, 74, 79, 80, 81, 82 genotypes, ix, 79, 80, 81, 83, 102, 149 geriatric, 87, 134 gestation, 200, 227 gestational diabetes, 213 gestures, 14 gift, 187 gifted, 130 girls, 39 GL, 128, 225 GlaxoSmithKline, 224 gliosis, 101 glucose, 227 glutamate, 101, 104, 112, 113 glutamatergic, 101, 111, 112 goal attainment, 40, 66 goal-directed, 104 goal-directed behavior, 104 goals, 8, 35, 59, 63, 74, 163

237

God, 188 goiter, 206, 224 gold, 89 gold standard, 89 government, iv, 125, 179, 192, 193 gray matter, 107 grouping, 116 groups, vii, viii, ix, x, xi, 2, 3, 5, 16, 36, 53, 60, 62, 75, 77, 79, 80, 81, 82, 92, 94, 95, 97, 98, 99, 101, 118, 135, 138, 139, 141, 142, 145, 146, 161, 169, 170, 184 growth, 61, 70, 99, 101, 156 Guangzhou, 185 guidelines, 221 guilt, 6, 37, 42, 44, 141, 190 guilty, 54, 188, 189 guns, 192 gut, 94 gynecologist, 208, 213, 215 gyrus, 107

H HA, 128 hallucinations, 3, 8, 11, 14, 34, 36, 39, 48, 51, 54, 61, 67, 90, 93, 94, 124, 136, 155, 157, 161, 165, 167, 176, 190, 192, 193, 202 Hallucinatory, 76 haloperidol, 91, 92, 104, 106, 108 happiness, 44 harbour, 38 hardships, viii, 10, 15, 27, 36, 45, 54, 61, 186, 189, 190, 192, 193 harm, ix, 10, 48, 55, 57, 91, 95, 183, 193, 198, 202 harmful, 205 Harvard, 149 hate, 37, 38, 190 HE, 130, 134, 227 head, 101, 125 healing, 31, 58, 63, 64 health, xiii, 19, 31, 58, 64, 176, 179, 180, 184, 194, 217, 218, 220, 222 health problems, 19, 220 health services, 179, 180 healthcare, 60 hearing, 34, 36, 39, 45, 49, 50, 52, 53, 55, 94, 100, 114, 162, 163, 165, 166 heart, 12, 32, 90, 187 heart failure, 90 hedonic, 157, 164, 176 height, 44, 101 helplessness, vii, 53

238

Salvatore Gentile

heredity, 4, 15 heritability, 83, 96, 97, 108 heterogeneity, 24, 118, 121, 124 heterogeneous, 94, 138, 155 heuristic, 116, 150 high risk, 102, 111, 198, 204, 210 high-risk, 99, 100, 111, 114, 199, 223 hip, 36 hippocampal, 86, 101, 113 hippocampus, 70, 112, 113, 128 Hispanic, 140, 158, 162 HK, 220 holistic, 3, 60, 61, 195, 196 homeless, 14 homogenous, 84 Hong Kong, 1, 27, 31, 48, 179, 196 hopelessness, 202 hormones, 19, 100 hospital, 7, 14, 33, 49, 55, 56, 57, 59, 60, 72, 182, 183, 184, 185, 188, 193, 194, 198, 207 hospital stays, 207 hospitalization, xiii, 8, 10, 14, 21, 27, 56, 57, 61, 62, 93, 182, 183, 184, 186, 193, 194, 201, 204, 218, 220 hospitalizations, 141, 198, 220 hospitalized, 32, 33, 45, 48, 57, 187 hospitals, xii, 32, 57, 95, 179, 182, 183, 184, 185, 186, 193, 195, 208, 213, 215 host, 154 hostility, 141, 154 household, 32 housing, 60, 141 HR, 86 human, 32, 37, 44, 54, 87, 96, 109, 111, 114, 137 human cerebral cortex, 111 human genome, 96, 137 human subjects, 114 humane, 194 humanistic perspective, vii humans, 94 Hungarian, 87, 227 husband, 39, 188, 189, 191 hydrocephalus, 206 hygiene, 193 hyperactivity, 75 hyperalgesia, 106 hypertension, 90 Hypertension, 211 Hypochondriasis, 73, 75, 77, 78 hypoplasia, 206 hypothalamic, 36 hypothesis, 6, 101, 105, 112, 130, 132, 161, 167

I iatrogenic, 91 ICD, xii, xiii, 8, 9, 19, 23, 24, 25, 66, 69, 107, 115, 182, 196, 220 id, 14, 34, 179 idealization, 41, 42 identification, 169 identity, 6, 11, 13, 63, 65, 185, 187, 190 imaging, 98, 107, 112 imaging modalities, 98 immigrants, 50 immunization, 96 impairments, x, 109, 125, 127, 129, 131, 137, 138, 141, 149, 150 impulsive, 198, 217 impulsiveness, 202 impulsivity, 160, 205, 216 in utero, 206, 211, 213, 223, 224, 226 in vivo, 86, 106 incentive, 172 incidence, 170, 199, 200, 210, 213, 223 inclusion, 63, 93, 159 income, 168 incomes, 184 incongruity, 5 independence, 59, 124 indices, 84 individual differences, 156 induction, 101, 208 industry, 138, 175 ineffectiveness, 205 inert, 14, 56, 193 inertia, 37 infancy, 38 infants, 206, 207, 225, 226 Infants, 223 infection, 95 inferiority, 6, 63 information processing, 40, 109, 110 informed consent, 74 ingestion, xii, 200 inheritance, 109, 149 inhibition, 113, 122, 123, 211 inhibitors, 226 inhibitory, 40 initiation, 70, 122 injection, 193 injuries, 117 injury, iv, 112, 113, 202 insane, 14, 56, 57, 63 insertion, 5 insight, 77, 198, 204

Managing the Suicidal Risk in Pregnant Schizoaffective Women insomnia, 6 instability, 102, 183 institutions, 59 instruments, 142, 153 insurance, 93, 184, 186 integration, 15, 58, 60, 61, 62, 66, 121, 138 integrity, 35, 36, 64 intelligence, 40, 42, 116, 120, 121, 131 intelligence tests, 121 intensity, 106, 154 intensive care unit, 218 intentions, 121, 145 interaction, 30, 34, 62, 65, 67, 86, 156 interactions, 109, 113 interference, 119 internal consistency, 164, 171 international, viii, 18, 20, 21, 23 International Classification of Diseases, 115 internet, 126 interpersonal conflict, 200 interpersonal conflicts, 200 interpersonal relations, 36, 142 interpersonal relationships, 142 interpretation, viii, 3, 10, 11, 23, 30, 46, 58, 94, 131, 132, 172, 173, 183 intervention, viii, 10, 11, 18, 62, 93, 99, 101, 115, 132, 202, 216, 221 interview, viii, 107, 141, 145, 153 interviews, 72 intestine, 190 intoxication, 9, 224 intracranial, 99 intrinsic, 156, 204 introversion, 73, 77, 79 intuition, 40 Investigations, 138 investment, 13, 32, 44 IP, 119 IQ, 140 IR, 133, 225 irritability, 136 IS, 224 isolation, 38, 186 Italy, xii, 20, 23, 197, 216

J JAMA, 219, 221, 223, 225, 226, 227 January, 219 Japanese, 85 Jefferson, 124, 133, 223 job satisfaction, 176 jobs, 32, 35, 61, 186

239

JT, 87, 228 judge, 45 judgment, 12, 77 Jun, 128, 129, 130, 133, 134, 149 justification, 93, 172

K Kant, 3, 23, 24, 27, 66 kappa, 95 karyotype, 97 ketamine, 101 KH, 87 King, 86, 87, 106 KL, 128, 220, 225, 226 knots, 91

L LA, xiii, 24, 84, 85, 126, 129, 133, 176, 219, 227 labeling, 13, 29, 37, 42, 53, 57, 91 labor, 31, 208 laboratory studies, vii, 5 labour, 31 lactation, 223, 225, 227 language, 60, 129 law, 14, 192 LC, 87, 133, 221 lead, viii, ix, 2, 29, 43, 44, 46, 47, 49, 52, 58, 59, 89, 102, 146, 167, 202, 203, 211, 217 leakage, 101 learning, 61, 119, 120, 121, 130, 131 learning task, 120 lesions, 207 liberation, 48 libido, 6 life satisfaction, xiii, 164 lifespan, 133 life-threatening, 205, 218, 221 lifetime, 92, 165, 170, 198 Likert scale, 145 limitation, 205 linear, 61, 133 linear model, 133 linear modeling, 133 linkage, 36, 44, 200, 221 links, 82, 94 lipid, 104 lipid peroxides, 104 listening, 30, 39, 109 literacy, 179

240

Salvatore Gentile

literature, viii, xiii, 15, 23, 82, 93, 94, 101, 102, 108, 117, 122, 124, 135, 138, 139, 141, 147, 149, 156, 169, 174, 200, 205, 219 lithium, x, 12, 86, 90, 92, 93, 96, 97, 101, 103, 105, 112, 113, 125, 134, 204, 205, 206, 207, 208, 209, 216, 217, 223, 224 Lithium, xiii, 90, 92, 94, 101, 105, 106, 113, 134, 184, 204, 205, 207, 208, 223, 224, 228 liver, 32 liver cancer, 32 LM, 225, 226 loans, 186, 192 local government, xii, 179 locus, 87, 97, 108 London, xiv, 33, 65, 66, 67, 103, 177, 220, 226 loneliness, 34, 44, 187 long period, 8, 12, 28, 29, 158, 160, 189 longitudinal studies, 100, 133 longitudinal study, 111 long-term, 73, 105, 116, 123, 125, 126, 149, 204, 216, 219, 223 long-term memory, 73 Los Angeles, 147 loss of appetite, 6 loss of control, 34, 35 losses, 46, 192 love, 30, 41, 49, 54, 185, 188, 189, 190, 194 low back pain, 104 lung, 187, 188 lying, 127, 146

M macrosomia, 207, 223 magnetic, iv, 99, 114 magnetic resonance, 114 magnetic resonance imaging, 114 magnetoencephalography, 111 Maine, 221 maintenance, 92, 122, 126, 159, 169 Maintenance, 176 major depression, 12, 84, 86, 92, 97, 109, 110, 136, 161, 169, 220 major depressive disorder, viii, 37, 54, 70, 84, 86, 87, 110, 182, 193, 222 maladaptive, 40, 172 malaise, 201 males, 39, 46, 50, 71, 110, 181 malignant, x, 90, 93, 95, 100, 101, 102, 103, 227 malnutrition, 199 Malta, 110 maltreatment, 56, 190 management, xii, 16, 107, 126, 218, 223

mania, 5, 28, 32, 33, 40, 41, 42, 43, 44, 45, 65, 72, 91, 92, 98, 102, 105 manic, viii, 2, 8, 9, 12, 23, 31, 32, 33, 34, 35, 36, 40, 41, 42, 43, 44, 45, 46, 48, 49, 50, 51, 52, 53, 54, 55, 56, 59, 63, 64, 65, 66, 71, 90, 95, 98, 102, 103, 105, 111, 116, 127, 137, 182, 199 manic episode, 8, 12, 31, 32, 33, 35, 36, 40, 41, 42, 43, 44, 45, 46, 48, 49, 50, 51, 52, 53, 54, 55, 56, 59, 63, 64, 95, 199 manic symptoms, 31, 48, 50, 51, 52, 53, 66 manic-depressive illness, 103 manic-depressive psychosis, 105 manipulation, 57, 120, 190 manpower, xii, 12, 183, 185, 196 mapping, 98 marginalization, 14 market, 13, 90 marriage, xi, 33, 39, 46, 145, 146, 185, 188, 189, 190 masking, 40, 129 mastery, 61 maternal, 199, 200, 201, 204, 205, 207, 208, 213, 215, 216, 218, 220, 221, 222, 224, 225, 227 matrix, 121, 166 maturation, 110, 114 maxilla, 206 meals, 32 meanings, 3, 56 measurement, 86, 133, 145, 176 measures, x, xi, xiii, 32, 74, 89, 96, 98, 99, 100, 102, 119, 120, 121, 124, 132, 139, 140, 141, 142, 145, 154, 155, 156, 157, 158, 159, 163, 164, 165, 170, 171 mechanical, iv medication, xii, 8, 10, 11, 12, 13, 14, 23, 28, 30, 55, 56, 60, 62, 90, 93, 111, 134, 141, 166, 169, 183, 184, 186, 192, 193, 194, 198, 204, 216, 220, 222, 223 medications, 10, 12, 13, 14, 29, 30, 56, 61, 63, 90, 91, 92, 93, 94, 95, 96, 101, 119, 124, 125, 134, 137, 163, 169, 183, 184, 192, 193, 195, 204, 205, 213 medicine, 49, 54, 89, 90, 101, 102, 105, 221 MEG, 99 melancholic, 110 memory, x, 40, 46, 73, 74, 79, 85, 101, 119, 120, 121, 122, 125, 129, 130, 131, 137, 138, 142, 148, 167, 187, 193 memory formation, 101 men, 72, 154, 158, 197 meningomyelocele, 206

Managing the Suicidal Risk in Pregnant Schizoaffective Women mental disorder, vii, 2, 9, 10, 11, 14, 55, 70, 196, 219 mental health, vii, xii, 31, 46, 58, 59, 60, 64, 65, 138, 179, 180, 182, 183, 196, 220 mental health professionals, 179, 182 mental illness, vii, viii, xi, xii, 3, 7, 8, 10, 11, 12, 13, 14, 15, 18, 22, 23, 29, 30, 33, 52, 54, 55, 56, 57, 58, 60, 62, 63, 67, 97, 100, 109, 111, 133, 145, 148, 155, 157, 161, 172, 179, 180, 181, 182, 185, 193, 194, 195, 197, 205, 217 mental retardation, 90, 181 mental state, 10, 11, 12, 14, 22, 23, 33, 49, 56, 194, 218 Merck, 219 messages, 65 meta analysis, 65 meta-analysis, 71, 107, 118, 120, 121, 122, 125, 130, 131, 134, 137, 150, 204, 222, 225, 226 metabolic, 91, 198, 204, 213, 216 metabolic dysfunction, 198 metabolic syndrome, 91 metabolism, 204 metaphor, 37 methionine, 70 Mexico, 89 mice, 97, 113 midbrain, 104 middle class, 188 middle-aged, 133 Minnesota, 72 mirror, 98 misconceptions, 132 misinterpretation, 5 missions, 54 MIT, 130 mitochondria, 113 mitochondrial, 113 mitral, 206 MK-80, 104, 112 ML, 87, 129, 221, 223, 226 MMT, 159 modality, 10, 56 modeling, 101, 111, 114 models, vii, 66, 69, 101, 117, 132, 149 moderators, 107 modulation, 104, 106, 107 molecular mechanisms, 112 momentum, 117 money, xi, 32, 35, 39, 100, 146, 187, 188, 189, 190, 192, 194 monograph, 103 monotherapy, 205, 209 Monozygotic, 108

241

monozygotic twins, 96, 97, 99, 109 mood, vii, viii, ix, xi, xii, 2, 3, 4, 8, 9, 11, 12, 13, 14, 19, 23, 28, 29, 30, 32, 35, 37, 38, 39, 41, 42, 43, 44, 45, 48, 49, 51, 52, 53, 54, 55, 56, 61, 63, 64, 69, 70, 87, 89, 90, 91, 92, 93, 94, 95, 96, 97, 101, 102, 105, 106, 112, 113, 116, 125, 127, 136, 141, 146, 149, 155, 156, 161, 165, 167, 168, 169, 181, 182, 183, 184, 189, 190, 193, 194, 204, 205, 217, 222, 228 mood change, ix mood disorder, vii, viii, x, xii, 2, 3, 8, 9, 14, 42, 69, 70, 87, 89, 90, 91, 92, 93, 94, 96, 101, 102, 103, 105, 106, 116, 127, 136, 155, 181, 182, 222, 228 mood swings, 4 morale, 36 morbidity, xiii, 4, 89, 201, 221, 222 morning, 6, 194 morphine, 106 morphometric, 107 mortality, xiii, 197, 199, 201, 216, 219, 220, 221, 222, 223, 227, 228 mortality rate, 198 mortgage, 13 mothers, xiii, 199, 200, 203, 204, 213, 217, 218, 220, 223, 226 motivation, 104, 117, 130, 134, 169 mouse, 85, 109 mouth, 32, 35 movement, 22, 65 mRNA, 71, 84 MS, 128, 224 multidimensional, 22, 116, 201 muscarinic receptor, 85, 211 mutant, 97 Mutual support, 62 MV, 84 myocardial infarction, 93, 100

N NA, 225 naming, 123 narcissism, xiv narcissistic, xiv, 42 nation, 176 national, 176, 181, 219, 222 natural, 40, 186, 187, 189, 190, 194 ND, 134 Nebraska, 86, 127, 129, 150 necrosis, 113 negative emotions, 153 negative mood, vii

242

Salvatore Gentile

negative reinforcement, 156 negativity, 99 neglect, viii, 23, 29, 30, 153, 221 neocortex, 70 neonatal, 113, 211, 213, 214, 221, 223 neonate, 224 neonates, 211 neoplasm, 227 nerve, 86, 110 nerve growth factor, 86 nervous system, 105 network, 32, 61, 62 neural network, 101 neuralgia, 106 neuroanatomy, 134 neurobiological, 100 neurobiology, 65, 106 Neurocognition, 125, 137 neurodegeneration, 112 neurodegenerative, 104 neurodegenerative disorders, 104 neurogenesis, 97 neuroimaging, 107 neuroimaging techniques, 107 neuroleptic, 84, 108, 113, 124, 125, 134, 150 neuroleptics, x, 90, 91, 96, 103, 137 neurological disease, 141 neurological disorder, 128 neurological injury, 122 neuromotor, 129 neuron death, 113 neuronal migration, 97 neurons, 70, 104, 112, 113 neuropathological, 128 neuropathology, 112, 117, 128 neuroplasticity, 70 neuroprotection, 101, 112, 113 neuroprotective, 101, 102 neuropsychological assessment, x, 124, 126, 134, 148 neuropsychological tests, 73, 110, 117, 119, 124 neuropsychology, 119, 122, 134 neuroscience, 117, 119, 120 neuroticism, 75, 81 neurotoxic, 90, 93, 101 neurotoxicity, 101, 102, 112 neurotoxins, 112 neurotransmission, 70, 106 neurotransmitters, 36 neurotrophic, ix, 70, 84, 85, 86, 87, 113 New England, 149 New Orleans, 176

New York, iii, iv, xiii, xiv, 24, 25, 65, 66, 67, 68, 98, 103, 127, 128, 129, 130, 132, 137, 148, 150, 153, 161, 196, 223 New Zealand, 20 NK, 106 NMDA, 101, 111, 112, 113 NMDA receptors, 101 N-methyl-D-aspartate, 106, 112, 113 noise, 98, 194 nomothetic approach, 139 non-clinical, 138, 154, 155, 157, 160, 164, 165, 173 non-clinical population, 155, 157, 164 non-institutionalized, x, 123 non-linear, 61, 195 norepinephrine, 36 normal, 8, 28, 30, 36, 46, 49, 61, 62, 63, 64, 75, 93, 97, 98, 99, 110, 114, 118, 125, 128, 129, 130, 138, 147, 155, 161, 164, 172, 173, 186, 195, 223 normal children, 46 normal development, 99 normalization, 125 norms, xi, 100, 102, 144, 145 North America, 103 Norway, 20 NOS, 96, 161, 166, 169 novelty, 153, 156, 157 NR2B, 113 nucleus, 91, 104 nucleus accumbens, 91, 104 nurse, 14, 39, 49, 56, 186, 193 nurses, 14, 49, 56, 193

O obesity, 19, 199, 220, 227 objectivity, 28 obligate, 101 obligation, 64 observations, 121 observed behavior, 90, 91 obsessive-compulsive, 71, 84 obsessive-compulsive disorder, 71, 84 obsolete, 213 obstruction, 212 occupational, 31, 124, 168 OCD, 98 olanzapine, 101, 105, 111, 134, 219, 222 older adults, 133 opiates, 160 opioid, 106 opioids, 154

Managing the Suicidal Risk in Pregnant Schizoaffective Women oppression, 14, 31, 45, 190 optimism, 125 OR, 74, 80, 81, 82, 207, 212 oral, 100 oral stage, 100 organic, 9, 71, 96, 117, 128 organism, 95 organization, 32, 39, 60 organizations, 44, 60, 62 orientation, 4, 9, 10, 33, 53, 60, 62, 185, 196 oscillations, 205, 208 outpatient, xii, 56, 57, 175, 182, 183, 184, 220 outpatients, 140 ownership, 190 oxidative, 112 oxidative stress, 112

P P300, 97, 98, 99, 100, 109, 110 p53, 112 PA, 222, 227 pain, 35, 89, 94, 100, 104, 106, 107, 216 palpation, 104 paper, 16, 18, 23, 92, 116, 180, 195 paradigm shift, 111 paradoxical, 106, 173 paranoia, 5, 34, 49, 194, 195 Paranoid Ideation, 160 paranoid schizophrenia, 11, 14, 56, 71, 90, 138 parenting, xiii, 217 parents, 41, 42, 100, 148, 183, 185, 186, 187, 189, 190, 194 Paris, 219 Parkinson, 86 parkinsonism, 108 paroxetine, 207, 209, 211, 212, 213, 224, 225 patents, 198, 204 pathogenesis, 65, 70 pathology, 71, 83, 104, 136, 144 pathophysiological, 128 pathophysiology, 84 pathways, 59, 100, 113 patient care, 126 patients, vii, ix, x, xi, xii, xiii, 2, 6, 7, 11, 12, 15, 19, 21, 49, 55, 56, 59, 60, 63, 67, 70, 71, 72, 73, 75, 76, 78, 79, 80, 81, 82, 83, 84, 86, 87, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, 101, 102, 104, 105, 106, 107, 108, 109, 110, 111, 112, 114, 116, 117, 118, 119, 120, 121, 122, 123, 124, 125, 126, 129, 130, 132, 133, 134, 135, 136, 137, 138, 139, 141, 145, 146, 147, 149, 154, 155, 157, 159, 160, 161, 163, 165,

243

167, 169, 170, 171, 172, 173, 175, 182, 183, 184, 197, 198, 199, 200, 201, 202, 203, 204, 205, 214, 216, 217, 218, 219, 220, 221, 222, 223, 225, 228 Paxil, 224 pay off, 185, 186, 190, 192, 194 PCR, 74 PD, 84, 129, 133, 134, 176 pediatric, 86, 101 pediatrician, 208, 213, 215 peer, 62, 63, 195 peer support, 62, 63, 195 peers, 34, 63, 64, 93 pendulum, 65 Pennsylvania, 65 peptide, 106 perception, 2, 29, 37, 57, 81 perceptions, 41, 45, 53, 58, 145 perfectionism, 37 performance, x, 28, 74, 75, 84, 110, 117, 118, 119, 120, 121, 122, 125, 126, 128, 130, 133, 138, 145, 146, 188 perinatal, xiii, 199, 201, 207, 210, 211, 214, 215, 216, 217, 220, 221, 223, 224, 226 permit, 122, 138 persecutory delusion, 108 persistent pulmonary hypertension of the newborn, 226 personal, viii, ix, 11, 13, 28, 29, 31, 34, 44, 47, 51, 63, 64, 182, 185, 192, 195, 201 personal accounts, 34 personal history, 201 personal hygiene, 64, 192 personal identity, 31, 182 personal responsibility, 63 personality, ix, 3, 5, 70, 72, 73, 75, 77, 78, 81, 82, 83, 84, 85, 98, 147, 148, 157 personality characteristics, ix personality dimensions, 75, 77 personality disorder, 3, 72, 83, 148 personality scales, 75 personality traits, 73, 75, 78, 82, 84, 157 PET, 94, 98, 106 PG, 86 pharmaceutical, 125 pharmaceutical industry, 125 pharmacists, 216 pharmacokinetics, 205 pharmacological, 203, 216, 218 pharmacology, 211 pharmacotherapy, 84, 95, 107 phencyclidine, 93, 112 phenol, 74

244

Salvatore Gentile

phenomenology, 136 phenotype, 81, 84, 108 phenotypes, 108, 109 pheochromocytoma, 91 Philadelphia, 65 phone, 12 phonological, 120 phosphorylation, 113 physical exercise, 186 physiological, 8, 187 physiology, 105 pig, 13 pilot study, 222 pituitary, 36 PL, 86 placebo, 101, 105, 111 placental, 223 planning, 39, 40, 122, 126 plasma, 104, 227 Platelet, 84 platelets, 86 play, 12, 61, 63, 70, 97, 101, 117, 173, 192 pleasure, 41, 42, 91, 157, 163, 167 PM, 83, 87 PMI, xi pneumonia, 95 point like, 163, 164 poison, xii, 200 poisoning, 202, 204, 227 polarity, 105 polarized, 3 police, 14, 91 policy makers, 60, 180 polyhydramnios, 224 polymorphism, ix, 10, 22, 23, 70, 71, 74, 80, 82, 83, 84, 85, 86, 87 polymorphisms, 79, 82, 84, 87 poor, 6, 32, 44, 89, 98, 136, 162, 163, 169, 179, 187, 189, 192, 193, 198, 199, 210, 211, 212, 214, 217 population, xii, 21, 23, 85, 86, 93, 100, 102, 113, 129, 157, 158, 160, 161, 169, 179, 180, 202, 203, 204, 205 positive correlation, xii positive reinforcement, 153, 156, 157, 167, 173 positive relation, 155 positive relationship, 155 positron, 86 positron emission tomography, 86 postmortem, 71, 85, 101, 109, 112 postpartum, xii, 199, 200, 220 Postpartum, 199, 220 postpartum period, 199

posttraumatic stress, 110 post-traumatic stress, 110 posttraumatic stress disorder, 110 post-traumatic stress disorder, 110 posture, 41 Potash, 127 poverty, 168, 190 power, 27, 30, 36, 45, 60, 67, 84, 186, 193, 195, 216 powers, 6 prediction, 25, 160, 169 predictor variables, 169 predictors, 104, 124, 133, 158, 160, 169, 198 pre-existing, 203 preference, 117 prefrontal cortex, 71, 104 pregnancy, xii, xiii, 187, 188, 189, 190, 199, 200, 201, 203, 204, 205, 206, 207, 208, 209, 210, 211, 212, 213, 214, 215, 216, 217, 221, 222, 223, 224, 225, 226, 227, 228 pregnant, xii, xiii, 188, 189, 199, 200, 201, 202, 203, 204, 205, 209, 214, 216, 217, 218, 221, 222, 223, 224, 225, 227 pregnant women, xiii, 200, 202, 203, 204, 205, 214, 217, 221, 222, 224, 225 premature death, 197 premature infant, 224 prematurity, 223 preparation, iv preservative, 122 pressure, 6, 57, 190 prestige, viii prevention, 93, 101, 102, 105, 203, 218, 219, 221, 222, 228 primacy, 130 principal component analysis, 84 private, 54 privation, 168 probability, 90, 93 probands, 96, 98, 99, 110, 137 problem solving, 67 procedures, 10 processing deficits, 111 prodrome, 101, 111 production, 113 productivity, xi, 146 prognosis, vii, 3, 4, 6, 7, 8, 23, 24, 90, 91, 93, 96, 123, 136 program, 135, 146, 159, 161 progressive, x, 70, 116, 124 promote, 32, 64, 70, 158 promoter, 86, 99 promoter region, 99

Managing the Suicidal Risk in Pregnant Schizoaffective Women property, iv, 187, 204, 212, 216 prophylactic, 90, 91, 105, 222 prophylactic agents, 105 prophylaxis, 105, 223 proposition, 34, 35, 37, 38, 39, 42, 43, 49, 51 prosthetics, 125 protection, 81, 113 protective factors, xiii, 202 protein, 93, 97, 109, 110, 113 proteins, 97, 101, 113 Prozac, 66, 225 pruning, 100, 101, 102, 111 PSD, 113 pseudo, 39, 42 psychiatric diagnosis, 97 psychiatric disorder, xii, xiii, 90, 128, 129, 148, 176, 197, 199, 200, 201, 203, 204, 217, 219, 222 psychiatric disorders, xii, 90, 128, 129, 148, 176, 197, 204, 217, 219, 222 psychiatric hospitals, 103 psychiatric illness, xiii, xiv, 25, 199, 204, 217, 222 psychiatric morbidity, 221 psychiatric patients, 176, 210 psychiatrist, 3, 6, 12, 13, 14, 21, 30, 44, 45, 48, 54, 55, 56, 71, 72, 91, 95, 163, 181, 183, 186, 193, 194, 208, 213, 215 psychiatrists, 13, 19, 30, 58, 59, 61, 74, 83, 94, 182, 183, 184, 193 psychiatry, 11, 65, 67, 89, 90, 91, 102, 134, 139, 182 psychic energy, 45 psychoactive, 9, 159 psychoanalysis, 153 Psychoanalysis, 66 psychodynamic perspective, 37 psychoeducational program, 185 psychogenic, 3, 117, 128 psychological, 54, 65, 75, 91, 128, 134, 138, 142, 153, 156, 188, 204 psychological functions, 134 psychologist, 73 psychologists, 10, 140 psychology, 32, 66, 130 psychometric properties, 176 psychopathology, 85, 87, 115, 126, 153, 154 psychopaths, 110 psychopharmacological, 203, 204, 205, 208, 213, 215, 216 psychopharmacology, 90, 147

245

psychoses, xiv, 2, 25, 70, 84, 87, 93, 103, 106, 112, 116, 117, 119, 124, 127, 136, 148, 149, 150 psychosis, vii, viii, ix, x, xii, xiv, 3, 4, 7, 9, 16, 19, 22, 23, 25, 30, 67, 69, 72, 76, 78, 79, 82, 83, 84, 86, 89, 90, 91, 92, 93, 94, 95, 96, 97, 99, 100, 101, 102, 103, 104, 109, 111, 114, 117, 119, 126, 127, 138, 146, 154, 163, 181, 182, 199, 200, 220, 221, 222 psychosocial, viii, xii, 10, 11, 16, 21, 31, 55, 61, 62, 106, 115, 116, 135, 137, 172, 183, 184, 190, 193, 195, 217, 218 psychosocial conditions, 193 psychosocial development, 172 psychosocial factors, 11, 217 psychosocial functioning, 116, 135, 137 psychosocial stress, 106, 195 Psychosomatic, 196 psychotherapy, 183, 184 psychotic, ix, 4, 12, 13, 19, 30, 33, 35, 49, 54, 55, 56, 67, 69, 72, 81, 83, 89, 90, 91, 92, 93, 94, 95, 96, 97, 100, 101, 102, 106, 107, 109, 113, 115, 116, 119, 126, 127, 128, 133, 136, 138, 139, 148, 149, 155, 157, 160, 161, 169, 176, 185, 198, 199, 201, 202, 204, 220, 222 psychotic states, 90, 128 psychotic symptoms, 54, 69, 90, 109, 115, 119, 136, 148, 149, 202 psychotropic drug, 203, 204 psychotropic drugs, 203, 204 psychotropic medications, 163, 167, 204 PTSD, 98 puberty, 97, 100 public, xii, 14, 186, 195, 197 publishers, xiv, 25, 67 puerperium, 224 punishment, 41 punitive, 42

Q quality of life, xi, 60, 107, 158, 160 Quality of life, 133 questionnaires, 73 quetiapine, 134

R RA, 128, 131, 133, 223, 227 radical, 104, 113 range, 28, 60, 69, 118, 119, 121, 154, 160, 161, 164, 169, 171, 207

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rat, 104, 106, 112, 113 rating scale, 170 ratings, ix, 72, 74, 75, 81, 82, 83, 136, 141, 145, 163, 170, 171 rationality, 60 rats, 112 RB, 84 RC, 85, 127, 219 reading, 120, 123, 142, 187, 194, 195 reality, 3, 34, 35, 41, 42, 46, 54, 61, 87, 90, 96, 99, 138, 147 reasoning, 137 recall, 73, 119, 120, 121, 131, 143 recalling, 73 receptors, 71, 84, 86, 91, 101, 106, 112 reciprocity, 156 recognition, 55, 121, 142, 145, 147 recovery, viii, xii, 2, 3, 4, 6, 7, 11, 22, 23, 25, 27, 30, 31, 32, 37, 53, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 103, 185, 186, 194, 196 recreation, 63 recreational, 31, 58, 59, 168, 184 recurrence, x, 92, 102, 103, 216 reduction, x, 98, 99, 100, 103, 125, 154, 216 redundancy, 158 reflection, 168 refractory, 91, 92, 105 Registry, 208, 211 regression, 35, 53, 160, 169 regression analysis, 160, 169 regular, 22, 56, 154, 163, 186, 194, 195, 223 regulation, 70, 84, 93 rehabilitate, 61 rehabilitation, viii, x, xi, xii, 1, 10, 11, 13, 15, 23, 29, 32, 53, 55, 57, 58, 59, 60, 61, 62, 102, 134, 135, 139, 141, 145, 146, 172, 179, 180, 181, 184, 185, 195 rehabilitation program, 139, 146 reimbursement, 93 reinforcement, 156, 167, 173 relapse, 40, 48, 50, 56, 65, 157, 184, 186, 192, 199, 201, 205 relapses, xii, 61, 181, 186, 195 relationship, 34, 35, 36, 41, 42, 47, 62, 85, 106, 107, 112, 115, 148, 155, 156, 158, 159, 160, 165, 167, 169, 173, 176, 185, 189, 190, 191, 198, 219 relationships, xi, 41, 62, 100, 109, 120, 124, 133, 145, 148, 155 relatives, 3, 40, 67, 72, 83, 85, 96, 97, 98, 99, 109, 111, 113, 119, 137, 150, 184, 194 relevance, 70, 108, 112, 126, 210

reliability, 95, 98, 104, 107, 145, 147, 163, 164, 171 Reliability, 107, 164 religious, 34, 67 religious belief, 34, 67 religious beliefs, 34, 67 remission, 4, 103, 137 renal, 90, 207 renal artery stenosis, 91 renal disease, 90 repair, 113, 189 reparation, 41 replication, 86, 141 reproduction, 131 research, vii, viii, 7, 15, 16, 17, 18, 20, 22, 23, 70, 90, 95, 97, 98, 99, 100, 101, 102, 103, 105, 111, 112, 116, 118, 119, 120, 122, 123, 124, 125, 130, 132, 133, 155, 156, 196, 222, 228 researchers, ix, 69, 71, 82, 96, 117, 121, 125, 136, 137, 138, 156, 157, 202 resilience, viii, 53, 190 resources, xii, 12, 59, 60, 120, 183, 184, 196 respiratory, 95 respiratory failure, 95 responsibilities, 14, 64, 189 restaurant, 31, 188, 189 restoration, 125 retardation, 77 retention, x, 121 retinopathy, 214, 215 retired, 186, 195 retirement, 194 RF, 86, 128, 134 rhythm, 40, 41, 66, 98, 216 rhythms, 66 risk, x, xii, xiii, 4, 86, 87, 90, 91, 92, 99, 101, 102, 105, 109, 124, 128, 137, 168, 173, 197, 198, 199, 200, 201, 202, 204, 205, 207, 208, 209, 210, 211, 212, 214, 217, 218, 219, 220, 221, 222, 223, 225, 226, 227, 228 risk benefit, 91 risk factors, 109, 137, 221 risks, xiii, 44, 91, 204, 207, 208, 209, 211, 217 risperidone, 106, 130, 134 RL, 226 RNA, 97 roadmap, 101 rodent, 113 Rouleau, 84 Royal Society, 226 RP, 130 rumination, 40 rural, 32, 182, 184

Managing the Suicidal Risk in Pregnant Schizoaffective Women rural areas, 182, 184 Russia, ix, 69 Russian, 69

S SA, ix, 69, 70, 71, 72, 75, 76, 77, 78, 79, 80, 81, 82, 83, 221, 224 sacrifice, 45 SAD, 94 sadness, 5, 38, 44, 49, 54 safety, xiii, 107, 205, 209, 210, 211, 212, 215, 216, 221, 227 salary, 187, 192 saliva, 187, 190 salt, 90 sample, xi, 71, 81, 84, 87, 94, 95, 107, 112, 118, 121, 135, 141, 142, 145, 146, 154, 155, 158, 159, 160, 161, 163, 164, 165, 168, 169, 170, 171, 172, 173, 206, 207, 208, 209, 210, 214 sampling, 84 sarin, 110 satisfaction, 41, 164, 168, 173, 203 savings, x, 32, 121, 131 schema, vii, 36, 38, 44 schemas, 40 schizoaffective disorder, vii, viii, ix, x, xi, xii, xiii, xiv, 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 17, 18, 19, 20, 21, 22, 23, 24, 25, 27, 28, 29, 30, 31, 32, 33, 34, 35, 37, 38, 42, 44, 46, 47, 51, 53, 54, 55, 57, 58, 59, 60, 61, 62, 63, 64, 66, 67, 82, 83, 84, 85, 89, 90, 93, 94, 95, 97, 99, 106, 107, 108, 115, 116, 117, 118, 119, 120, 121, 122, 123, 125, 126, 127, 129, 135, 136, 137, 138, 139, 140, 141, 145, 146, 147, 148, 149, 150, 155, 156, 161, 169, 170, 172, 173, 179, 180, 181, 182, 183, 184, 185, 186, 188, 190, 191, 193, 194, 195, 196, 197, 198, 199, 200, 202, 204, 205, 216, 219, 220, 222 schizophrenia, vii, viii, ix, x, xi, xii, xiii, xiv, 1, 2, 3, 4, 5, 6, 7, 8, 9, 11, 12, 13, 14, 15, 16, 19, 21, 22, 23, 24, 25, 27, 28, 29, 30, 33, 34, 35, 37, 44, 46, 47, 48, 50, 53, 54, 55, 57, 58, 59, 65, 66, 67, 69, 70, 71, 72, 76, 78, 79, 81, 82, 83, 84, 85, 86, 87, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, 101, 102, 103, 104, 105, 106, 107, 108, 109, 110, 111, 112, 113, 114, 115, 116, 117, 118, 119, 120, 121, 122, 123, 124, 125, 126, 127, 128, 129, 130, 131, 132, 133, 134, 135, 136, 137, 138, 139, 140, 141, 145, 146, 147, 148, 149, 150, 151, 155, 156, 160,

247

161, 169, 170, 172, 173, 180, 181, 182, 183, 196, 197, 198, 219, 220, 221, 222, 226 Schizophrenia, v, ix, xiii, 4, 6, 7, 8, 9, 14, 20, 24, 25, 33, 46, 47, 65, 66, 67, 68, 69, 73, 75, 77, 79, 85, 86, 87, 96, 106, 108, 109, 111, 117, 123, 125, 127, 129, 130, 132, 133, 138, 139, 140, 142, 143, 144, 146, 147, 148, 149, 150, 153, 169, 177, 180, 181 schizophrenic patients, 67, 71, 83, 86, 126, 128, 134, 138, 150, 176, 197 schizotypal personality disorder, 71 school, 32, 33, 35, 42, 46, 48, 56, 57, 62, 125, 183, 188 schooling, xiii, 32, 198, 203 science, 10 scientific, 93, 94, 139, 226 scores, ix, 72, 73, 74, 75, 77, 121, 122, 131, 141, 148, 158, 160, 164, 165, 167, 168, 170, 198, 207, 211 SD, 72, 76, 78, 79, 146, 158 SE, 89, 96, 134, 226 search, 15, 37, 65, 93, 96, 122 search engine, 15 searches, 37 searching, 51, 52, 61, 62 second generation, 119, 125, 138, 184 secondary schools, 57 secret, 188 secular, 53, 64 security, 14, 185, 191, 194 sedation, 91 seizure, 90 seizures, 103 selective attention, 40, 110, 119, 123 selective serotonin reuptake inhibitor, 225, 226 Self, xiv, 59, 63, 65, 66, 158, 176, 188, 189, 192, 194 self esteem, 42 self help, 60, 62 self image, 190, 195 self-care, 63 self-definition, 34 Self-Direction, 59 self-help, 65 self-identity, 34 self-monitoring, xi, 122, 145 self-regulation, 138 self-report, 136, 163, 165, 167, 173 semantic, 73, 95, 96, 120 semantics, 95, 96, 97 semi-structured interviews, 71 senile, 180 senile dementia, 180

248

Salvatore Gentile

sensitivity, xi, 60, 89, 113, 145, 146, 147, 164 sentences, 101 separation, 46, 74 septum, 214 series, x, 90, 91, 109, 116, 119, 121, 122, 123, 139, 140, 155, 160, 214 serotonergic, 70, 84, 85 serotonin, ix, 36, 70, 81, 84, 85, 86, 87, 211, 216, 226 Serotonin, 84, 86, 87 sertraline, 209, 212, 225 serum, 110, 205, 207, 208 services, iv, vii, x, xii, 16, 18, 21, 55, 59, 60, 61, 63, 148, 179, 180, 183, 185, 201, 220 severe stress, 192 severity, 90, 92, 93, 94, 95, 96, 97, 123, 124, 136, 146, 153, 154, 155, 161, 163, 167, 171, 198 sex, 54, 113, 177, 188, 197 sexual assault, 200, 201, 217 sexual assaults, 200, 217 Shanghai, 185, 196 shape, 122 shaping, 219 shares, 101 sharing, 62, 203 shock, 184, 227 shock therapy, 184 shoot, 192 short period, 43, 182 shortage, xii, 183 short-term, 73, 75 Short-term, 79 short-term memory, 73, 75 shoulder, 191 SI, 227 siblings, 110, 132, 137, 150, 185 side effects, 12, 56, 90, 93, 184, 193 sign, 49, 73, 89, 103, 119, 154 signal transduction, 105, 113 signaling, 70, 156 signs, 5, 56, 57, 63, 72, 136, 150, 171, 226 similarity, 156 Singapore, 103 single nucleotide polymorphism, 70 skills, 62, 122, 126, 133, 138, 172 sleep, 13, 41, 91, 92, 99, 189, 192, 194 sleeping pills, 194 smoke, 194 smoking, 99 SNP, 70 sociability, 154 social, xi, xiii, 3, 14, 29, 31, 33, 34, 39, 40, 41, 43, 45, 54, 58, 59, 60, 61, 62, 63, 67, 76, 77,

93, 113, 124, 129, 141, 142, 145, 146, 147, 148, 156, 170, 171, 172, 173, 174, 175, 183, 186, 187, 196, 198, 201, 202, 203, 204, 217 social activities, 63, 186 social adjustment, 93 social class, 113 social cognition, xi, 129, 142, 145, 146, 147 social context, 183 social environment, 43, 58 social factors, 173 social integration, xiii, 217 social learning, 62 social life, 29, 61 social network, 60 social problems, 170, 175, 187 social support, xiii, 203 social welfare, 39, 59 social withdrawal, 76 social work, 14, 33, 45, 67, 171 social workers, 45, 171 socially, 3 society, 59, 60, 61, 63, 64, 187, 190, 192, 193 solutions, 209 sorting, 122 South America, 16, 20, 21 SP, ix, 70, 71, 72, 75, 76, 77, 78, 79, 80, 81, 82, 83 SPA, ix, 70, 72, 75, 76, 77, 78, 79, 80, 81, 82, 83 Spain, 220 spatial, 120, 131, 137 specialists, 145 specificity, 89, 90, 103, 105, 202 spectra, 25, 66 spectrum, viii, 7, 9, 22, 23, 69, 70, 82, 87, 96, 136, 182, 201, 202 speech, 6, 94, 114, 117, 227 speech perception, 114 speed, 13, 35, 119, 121, 122, 125, 137, 138, 142, 145 spina bifida, 206 spiritual, 36 spirituality, 60 spontaneity, 76 sports, 59 sprouting, 85 SR, 85, 130, 225 SRIs, 209, 211, 226 stability, 44, 56, 57, 133, 145, 164, 196 stabilization, 91, 93, 96, 102, 103, 126, 205 stabilize, 91, 92, 93 stabilizers, x, 49, 56, 61, 96, 112, 113, 125, 184, 222

Managing the Suicidal Risk in Pregnant Schizoaffective Women stages, xiii, 37, 38, 41, 43, 45, 92, 94, 97, 100, 125, 137, 205, 210, 215 STAI, 73, 75, 79 standard deviation, 72, 76, 78, 79, 99 State Trait Anxiety Inventory, 73 statistics, 197 stenosis, 206 stereotypes, 5 stigma, 63, 217 stigmatization, 57 stigmatized, 57 stimulus, 98, 119, 120, 122 stimulus cards, 122 stock, 61 stomach, 14, 49, 56 storage, 120 strategies, 91, 102, 122, 153, 156, 219 stratification, 74 streams, 92 strength, 126, 145, 165, 194 stress, 3, 11, 47, 51, 64, 104, 177, 193, 195 stressful events, 40, 190 stressors, 219 striatum, 91, 104 stroke, 90, 187 students, 56, 57, 62, 176 subacute, 92, 95, 102 subgroups, 118, 128 subjective, viii, 11, 12, 16, 22, 29, 33, 35, 37, 38, 46, 47, 53, 54, 55, 56, 57, 58, 65, 67, 82, 93, 106, 156, 157, 160, 164, 165 subjective experience, viii, 11, 12, 16, 22, 29, 33, 35, 37, 38, 46, 47, 53, 54, 55, 57, 58, 65, 106, 156, 165 subjectivity, 37 substance abuse, 29, 49, 56, 147, 155, 161, 169, 173, 200, 220 substance use, xii, 96, 155, 158, 169, 174 substances, 159, 169 substitution, 49, 70 substrates, 119 subtraction, 73 suffering, xii, 14, 15, 35, 54, 197, 202, 204 suicidal, xii, xiii, 14, 31, 105, 186, 197, 198, 199, 200, 201, 202, 204, 205, 210, 216, 217, 218, 220, 221, 222, 228 suicidal behavior, 105, 199, 202, 204, 216, 217, 220, 221, 222, 228 suicidal ideation, xiii, 186, 198, 200, 201, 202, 205, 210, 217, 220 suicide, xii, xiii, 14, 16, 38, 92, 197, 198, 199, 200, 201, 202, 203, 204, 205, 210, 217, 218, 219, 220, 221, 222, 223

249

suicide attempts, xiii, 197, 198, 199, 200, 201, 202, 204, 210, 217, 218, 221, 222, 223 suicide rate, 92 superego, 37, 41, 42, 44, 53 superoxide, 101, 113 superoxide dismutase, 101 supervision, 194 supervisor, 13, 145, 194 supplements, 97 supply, 179 suppression, 51, 99, 111 surgical, 99 surveillance, 208, 213, 215, 218 survival, 34, 35, 54, 85 susceptibility, 71, 86, 95, 97, 99, 108, 153, 154, 156 Sweden, 219, 220 switching, 122 Switzerland, 219 symbols, 63 symptom, ix, 3, 5, 10, 23, 34, 37, 45, 48, 49, 51, 52, 53, 72, 82, 90, 92, 108, 147, 154, 155, 160, 163, 167, 171, 173 symptoms, vii, viii, ix, xi, xii, xiii, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 15, 16, 21, 22, 23, 27, 28, 29, 30, 31, 33, 34, 37, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 62, 63, 64, 65, 69, 71, 72, 75, 81, 82, 83, 84, 85, 86, 90, 92, 93, 94, 96, 100, 101, 103, 107, 116, 117, 123, 124, 126, 136, 137, 139, 141, 146, 147, 150, 160, 171, 173, 176, 181, 182, 183, 184, 186, 192, 201, 202, 203, 204, 211 synaptogenesis, 100, 111 syndrome, ix, xi, 69, 70, 71, 72, 76, 78, 79, 83, 85, 87, 90, 95, 96, 104, 116, 127, 136, 137, 147, 155, 161, 201, 207, 211, 213, 214 synthesis, 132 systematic, 156, 219, 228 systematic review, 219, 228 systems, 60, 63, 104, 117, 119, 120, 131, 207

T talipes equinovarus, 206 tardive dyskinesia, 91 targets, 115, 130, 134, 164, 180 task difficulty, 130 TE, 128, 134 teachers, 32, 57 teaching, 183 teenagers, 101 teens, 101

250

Salvatore Gentile

temperament, 3, 187 temporal, 94, 106, 109, 110, 112, 117, 160, 198, 199 temporal lobe, 94, 109, 110, 112, 117 teratogenic, xiii, 205, 209, 215, 216 test data, 94 test items, 164 test scores, 118, 121 testicle, 215 test-retest reliability, 111, 131 textbooks, 92 TF, 130 theoretical, vii, viii, 1, 33, 42, 43, 53, 58 theory, 91, 94, 130, 142, 148, 153 therapeutic, 96, 112, 203, 205, 208, 216, 225 therapists, 28 therapy, xiii, 10, 16, 18, 21, 66, 96, 105, 106, 134, 185, 204, 208, 209, 213, 215, 216, 222, 223, 224, 227, 228 thinking, 3, 37, 40, 48, 57, 75, 76, 115, 132, 141, 176, 187, 192 threatened, 14, 36, 190 threats, 186, 192 threshold, 113, 164, 216 thresholds, 113 thrombosis, 89, 103 thyroid, 207 time, 4, 8, 9, 10, 12, 16, 22, 23, 28, 29, 32, 33, 35, 36, 38, 39, 43, 44, 45, 46, 52, 54, 55, 56, 57, 61, 70, 71, 72, 81, 90, 92, 95, 96, 100, 101, 113, 120, 123, 136, 143, 145, 154, 156, 158, 159, 169, 174, 182, 183, 184, 185, 186, 188, 189, 191, 192, 194, 195, 197, 199 time frame, 100 tissue, 110 title, viii, 15, 17, 18 TJ, 87, 127 TM, 219 T-maze, 104 tobacco, 198, 217 Tokyo, 110 tolerance, 106, 172 Topiramate, 184 torture, 35 toxic, 66, 96, 102, 208, 211, 216 toxic effect, 208 toxicity, 206, 208, 211, 216, 223, 224 toxicology, 89, 154, 160 training, xii, 11, 28, 56, 57, 61, 125, 134, 146, 171, 182, 183, 185, 196 trait anxiety, 73 traits, ix, 75, 78, 79, 81, 83, 85, 198 trajectory, 92

trans, xiv, 66, 95 transcranial magnetic stimulation, 94, 107 transcription, 70 transformation, ix, 31, 42, 58, 96, 100, 101, 102 transition, 52 transitions, 176 translation, 121, 224 translocation, 109 transmission, 137 transparent, 81 transport, 101 trauma, 59 traumatic brain injury, 141 treatment-resistant, 130 trend, 20, 75, 81 trial, x, 92, 93, 97, 103, 111, 148, 220, 222 tricuspid valve, 206, 223 triggers, 40 trucks, 31 true/false, 163 trust, 30, 62, 189, 192 twins, 99, 106 typology, 120 tyrosine, 113

U ubiquitous, 153, 173 UK, 130, 220, 227 umbilical artery, 206 umbilical cord, 207 umbilical cord blood, 207 uncertainty, 116, 123 undifferentiated, x, 118, 138 unemployment, xiii, 91, 200, 203 uniform, 119, 207 unilateral, 206 United Kingdom, 16, 20, 21, 39, 50, 56, 220 United States, x, 7, 16, 20, 31, 90, 117, 147, 195, 196, 197, 216 university education, 183 UP, 145 urine, 154, 160, 187 URL, 219, 221 users, 169, 174

V validation, 82 validity, xiv, 24, 25, 69, 73, 77, 93, 95, 107, 108, 118, 136, 139, 146, 147, 148, 163, 164, 176 valine, 70

Managing the Suicidal Risk in Pregnant Schizoaffective Women values, 44, 54, 75, 89 variability, 84, 126, 164 variable, 167 variables, xi, 4, 5, 70, 74, 79, 146, 165, 169 variance, 99 variation, 86, 99, 104 variety of domains, 164 vein, 89, 103 venlafaxine, 210 ventricle, 111 ventricular, 212 verbal abuse, 188 verbal fluency, xi, 73, 142, 145, 146 victims, 110 vignette, 31 violence, 14, 31, 200, 201, 217, 221 violent, xii, 31, 190, 199, 200, 221 visual, xi, 40, 100, 109, 110, 119, 120, 121, 129, 131, 138, 142, 145, 146 visual memory, xi, 145, 146 visual processing, 109 visual system, 120 visuospatial, 120 vocational, x, 8, 135, 139, 140, 141, 146, 147, 148 vocational rehabilitation, x, 8, 135, 139, 140 voice, 36, 38, 39, 44, 45, 48, 49, 50, 52, 53, 54, 55, 56, 57, 60, 63, 119 vulnerability, xi, 92, 97, 98, 100, 102, 145, 147, 176

Washington, 24, 65, 67, 68, 106, 126, 134, 147, 175, 196, 219, 222 water, 188 Watson, 128 WCST, x, 122 weakness, 37, 101, 145, 154 wealth, 123, 190 weapons, 50, 190 weight changes, 210 weight gain, 101, 210, 213, 219 Weinberg, 79 wellness, 59, 64 WHO, 115, 220 Wisconsin, 122, 126, 128, 132, 143, 149 wisdom, 187 withdrawal, 2, 3, 5, 9, 29, 35, 76, 92, 95, 211 witnesses, 92 wives, 186, 189, 194 WM, 221 women, xii, xiii, 39, 46, 72, 158, 180, 189, 197, 199, 200, 201, 202, 203, 204, 210, 215, 216, 217, 220, 222, 223, 225, 227 wood, 35 work environment, 125 workers, 14 working memory, 40, 73, 79, 84, 97, 98, 119, 120, 122, 124, 126, 129, 130, 131, 137, 142 workplace, xi, 145 World Health Organization, 7, 9, 25, 115, 126, 197, 199, 219, 220 writing, 117, 186

W Y walking, 195 war, 55, 182, 184

251

yield, 102, 121, 141, 158 young adults, 3, 176