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The inadequacy of the simple neurodevelopmental model
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premorbid level and functioning, estimated premorbid intelligence, pregnancy and birth complications, and selected CT variables. Minor physical anomalies are found in a range of functional psychoses. There may be overlap between the various genes that predispose to psychiatric illness (especially in males) and those genes that predispose to developmental instability. Compared to non-dysmorphic patients with functional psychoses, those patients with minor physical anomalies required more frequent and longer admissions.
ON ASSESSING AND TREATING NEGATIVE SYMPTOMS Alexander L. Miller*, Dawn I. Velligan, Roderick Mahurin, James W. Maas
Department of Psychiatry, The University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78284-7792, USA There are important conceptual differences between negative and positive symptoms of schizophrenia, This presentation will identify these differences and explore their implications for clinicians and researchers. Assessment of negative symptoms is primarily by clinical observation and is heavily reliant on the observer's judgment about "normal" behaviors under the conditions of observation. Identification of positive symptoms is typically based on patient self-report and the symptoms rarely fall in the continuum of "normal" behaviors. The goal of treatment of positive symptoms is their absence, whereas the goal of treatment of negative symptoms is the presence of "normal" levels of functional attributes. Negative symptoms may represent deficits of motivation and/or learning, whereas positive symptoms are extant and not dependent on learned skills, other than language, for their expression. To adequately evaluate negative symptoms, clinicians must learn to take the sociocultural perspective of the patient, independent of their own. Testing the efficacy of treatments for negative symptoms is made complex by the possibility that both the motivation and the skills to express the deficient behaviors may need to be enhanced. Researchers need to learn how to measure each of these components, to identify the barriers to rehabilitation of negative symptom patients.
THE INADEQUACY OF THE SIMPLE NEURODEVELOPMENTAL MODEL R.M. Murray
Institute of Psychiatry, Denmark Hill, London SE5 8AF, UK Since the mid 1980s, the neurodevelopmental model of schizophrenia has become widely accepted. In its simple formulation, this states that the cause is a fixed early brain lesion where behavioural expression is modified by the stage of brain maturation. However, there are major deficiencies in this
"Doomed from the Womb" model. Firstly, none of the, supposedly developmental, cytoarchitectonic changes have yet been replicated. Secondly, there is no plausible explanation for the delayed age of onset, in particular for late onset schizophrenia. Thirdly, many schizophrenics, especially females, show no evidence of abnormal development. Fourthly, the model does not explain the genetic overlap with affective psychosis. Fifthly, the model does not take into account the effect of adult risk factors such as drug abuse and adverse life events. Two other models appear more plausible. (A) A multifactorial model in which schizophrenia results from the accumulation of risk factors until a critical threshold for psychosis is crossed; neurodevelopmental deviance is but one of these risk factors. (B) A heterogeneity model in which there are at least three types of schizophrenia (a) a severe early onset neurodevelopmental form common in males; (b) a relapsing and remitting type with much in common with affective psychosis; (c) a late onset type associated with degenerative brain disease.
THE RELATION OF NEUROMOTOR DYSFUNCTION WITH SYMPTOM RATINGS AND CORTISOL RESPONSE IN SCHIZOPHRENIA-SPECTRUM, PERSONALITY DISORDERED SUBJECTS C.S. Neumann*, E.F. Walker
Department of Psychology, Emory University, Atlanta, GA 30322, USA Prior research has indicated that neuromotor problems (e.g., dyskinesia, motor overflow) are associated with schizophrenia and schizophrenia-spectrum disorders (e.g., Schizotypal Personality Disorder). The present study explored the relation of neuromotor dysfunction with symptom ratings and cortisol response in personality disordered subjects. A computerized neuromotor assessment, designed as a choice reaction time task, was used to obtain indices of motor functioning. Using pressure sensitive response buttons, measures of motor overflow were obtained. Motor overflow was assessed with a bimanual condition and was indexed by the change in applied pressure in the non-responding hand. In support of prior research, we found that heightened motor overflow was associated with higher saliva cortisol levels. The pattern of findings is consistent with previous reports linking dyskinesias with negative symptoms and heightened cortisol in schizophrenic patients. Implications for theories of neuropathophysiology of schizophrenia symptoms are discussed.
BALL EXPERIMENTS I N 32 C A T A T O N I C PATIENTS: DEFICITS OF INTERNAL INITIATION AND VOLUNTARY GENERATION OF MOVEMENTS G. Northoff*, J. Wenke, W. Krill, B. Pflug
Department of Psychiatry, University of Frankfurt, 60528 Frankfurt~Main, Germany
premorbid level and functioning, estimated premorbid intelligence, pregnancy and birth complications, and selected CT variables. Minor physical anomalies are found in a range of functional psychoses. There may be overlap between the various genes that predispose to psychiatric illness (especially in males) and those genes that predispose to developmental instability. Compared to non-dysmorphic patients with functional psychoses, those patients with minor physical anomalies required more frequent and longer admissions.
ON ASSESSING AND TREATING NEGATIVE SYMPTOMS Alexander L. Miller*, Dawn I. Velligan, Roderick Mahurin, James W. Maas
Department of Psychiatry, The University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78284-7792, USA There are important conceptual differences between negative and positive symptoms of schizophrenia, This presentation will identify these differences and explore their implications for clinicians and researchers. Assessment of negative symptoms is primarily by clinical observation and is heavily reliant on the observer's judgment about "normal" behaviors under the conditions of observation. Identification of positive symptoms is typically based on patient self-report and the symptoms rarely fall in the continuum of "normal" behaviors. The goal of treatment of positive symptoms is their absence, whereas the goal of treatment of negative symptoms is the presence of "normal" levels of functional attributes. Negative symptoms may represent deficits of motivation and/or learning, whereas positive symptoms are extant and not dependent on learned skills, other than language, for their expression. To adequately evaluate negative symptoms, clinicians must learn to take the sociocultural perspective of the patient, independent of their own. Testing the efficacy of treatments for negative symptoms is made complex by the possibility that both the motivation and the skills to express the deficient behaviors may need to be enhanced. Researchers need to learn how to measure each of these components, to identify the barriers to rehabilitation of negative symptom patients.
THE INADEQUACY OF THE SIMPLE NEURODEVELOPMENTAL MODEL R.M. Murray
Institute of Psychiatry, Denmark Hill, London SE5 8AF, UK Since the mid 1980s, the neurodevelopmental model of schizophrenia has become widely accepted. In its simple formulation, this states that the cause is a fixed early brain lesion where behavioural expression is modified by the stage of brain maturation. However, there are major deficiencies in this
"Doomed from the Womb" model. Firstly, none of the, supposedly developmental, cytoarchitectonic changes have yet been replicated. Secondly, there is no plausible explanation for the delayed age of onset, in particular for late onset schizophrenia. Thirdly, many schizophrenics, especially females, show no evidence of abnormal development. Fourthly, the model does not explain the genetic overlap with affective psychosis. Fifthly, the model does not take into account the effect of adult risk factors such as drug abuse and adverse life events. Two other models appear more plausible. (A) A multifactorial model in which schizophrenia results from the accumulation of risk factors until a critical threshold for psychosis is crossed; neurodevelopmental deviance is but one of these risk factors. (B) A heterogeneity model in which there are at least three types of schizophrenia (a) a severe early onset neurodevelopmental form common in males; (b) a relapsing and remitting type with much in common with affective psychosis; (c) a late onset type associated with degenerative brain disease.
THE RELATION OF NEUROMOTOR DYSFUNCTION WITH SYMPTOM RATINGS AND CORTISOL RESPONSE IN SCHIZOPHRENIA-SPECTRUM, PERSONALITY DISORDERED SUBJECTS C.S. Neumann*, E.F. Walker
Department of Psychology, Emory University, Atlanta, GA 30322, USA Prior research has indicated that neuromotor problems (e.g., dyskinesia, motor overflow) are associated with schizophrenia and schizophrenia-spectrum disorders (e.g., Schizotypal Personality Disorder). The present study explored the relation of neuromotor dysfunction with symptom ratings and cortisol response in personality disordered subjects. A computerized neuromotor assessment, designed as a choice reaction time task, was used to obtain indices of motor functioning. Using pressure sensitive response buttons, measures of motor overflow were obtained. Motor overflow was assessed with a bimanual condition and was indexed by the change in applied pressure in the non-responding hand. In support of prior research, we found that heightened motor overflow was associated with higher saliva cortisol levels. The pattern of findings is consistent with previous reports linking dyskinesias with negative symptoms and heightened cortisol in schizophrenic patients. Implications for theories of neuropathophysiology of schizophrenia symptoms are discussed.
BALL EXPERIMENTS I N 32 C A T A T O N I C PATIENTS: DEFICITS OF INTERNAL INITIATION AND VOLUNTARY GENERATION OF MOVEMENTS G. Northoff*, J. Wenke, W. Krill, B. Pflug
Department of Psychiatry, University of Frankfurt, 60528 Frankfurt~Main, Germany