Abstract:The nosological status of schizoaffective disorders remains controversial. Twin studies are potentially valuable for investigating relationships between schizoaffective-mania, schizoaffective-depression and other psychotic syndromes, but no such study has yet been reported. We ascertained 224 probandwise twin pairs (106 monozygotic, 118 same-sex dizygotic), where probands had psychotic or manic symptoms, from the Maudsley Twin Register in London (1948–1993). We investigated Research Diagnostic Criteria schizoa… Show more
“…Individuals with schizoaffective mania may have broad aetiological factors that increase risk of both schizophrenia and bipolar disorder and/or the co-occurrence of relatively specifi c aetiological factors for schizophrenia and bipolar disorder. The same twin analysis was also consistent with schizoaffective depression being due to co-occurring elevated liability to schizophrenia and depression, but with less elevation of liability to mania (Cardno et al, 2012 ).…”
Section: Family and Twin Studies Of Schizoaffective Disorder(s)supporting
confidence: 52%
“…Further twin analysis of the manic and depressive subtypes of schizoaffective disorder in the same sample was consistent with schizoaffective mania being due to co-occurring elevated liability to schizophrenia, mania, and depression (Cardno et al, 2012 ), at least in terms of familial/genetic aetiological factors. Individuals with schizoaffective mania may have broad aetiological factors that increase risk of both schizophrenia and bipolar disorder and/or the co-occurrence of relatively specifi c aetiological factors for schizophrenia and bipolar disorder.…”
Section: Family and Twin Studies Of Schizoaffective Disorder(s)mentioning
“…Individuals with schizoaffective mania may have broad aetiological factors that increase risk of both schizophrenia and bipolar disorder and/or the co-occurrence of relatively specifi c aetiological factors for schizophrenia and bipolar disorder. The same twin analysis was also consistent with schizoaffective depression being due to co-occurring elevated liability to schizophrenia and depression, but with less elevation of liability to mania (Cardno et al, 2012 ).…”
Section: Family and Twin Studies Of Schizoaffective Disorder(s)supporting
confidence: 52%
“…Further twin analysis of the manic and depressive subtypes of schizoaffective disorder in the same sample was consistent with schizoaffective mania being due to co-occurring elevated liability to schizophrenia, mania, and depression (Cardno et al, 2012 ), at least in terms of familial/genetic aetiological factors. Individuals with schizoaffective mania may have broad aetiological factors that increase risk of both schizophrenia and bipolar disorder and/or the co-occurrence of relatively specifi c aetiological factors for schizophrenia and bipolar disorder.…”
Section: Family and Twin Studies Of Schizoaffective Disorder(s)mentioning
“…Even bipolar disorder with psychosis and schizophrenia, the two major and ostensibly distinct psychosis categories, do not “breed true” (10,11). There is overlap in susceptibility genes and phenotypes across bipolar disorder with psychosis and schizophrenia (12–14) and considerable similarity between different psychotic disorders on symptoms, illness course, cognition, psychophysiology and neurobiology (15–26).…”
Objective
Clinical phenomenology remains the primary means for classifying psychoses despite considerable evidence that this method incompletely captures biologically meaningful differentiations. Rather than relying on clinical diagnoses as the gold standard, this project drew on neurobiological heterogeneity among psychosis cases to delineate subgroups independent of their phenomenological manifestations.
Method
A large biomarker panel (neuropsychological, stop signal, saccadic control, and auditory stimulation paradigms) characterizing diverse aspects of brain function was collected on individuals with schizophrenia, schizoaffective disorder, and bipolar disorder with psychosis (N=711), their first-degree relatives (N=883), and demographically comparable healthy subjects (N=278). Biomarker variance across paradigms was exploited to create nine integrated variables that were used to capture neurobiological variance among the psychosis cases. Data on external validating measures (social functioning, structural magnetic resonance imaging, family biomarkers, and clinical information) were collected.
Results
Multivariate taxometric analyses identified three neurobiologically distinct psychosis biotypes that did not respect clinical diagnosis boundaries. The same analysis procedure using clinical DSM diagnoses as the criteria was best described by a single severity continuum (schizophrenia worse than schizoaffective disorder worse than bipolar psychosis); this was not the case for biotypes. The external validating measures supported the distinctiveness of these subgroups compared with clinical diagnosis, highlighting a possible advantage of neurobiological versus clinical categorization schemes for differentiating psychotic disorders.
Conclusions
These data illustrate how multiple pathways may lead to clinically similar psychosis manifestations, and they provide explanations for the marked heterogeneity observed across laboratories on the same biomarker variables when DSM diagnoses are used as the gold standard.
“…One traditional method for resolving such uncertainties, family history studies, has not provided decisive support for any of these positions : first-degree relatives of schizo-affective patients have variously been found to show elevated rates of schizophrenia, affective disorder or both illnesses (Coryell & Zimmerman, 1988 ;Maier et al 1993 ;Kendler et al 1995 ;Laursen et al 2005). Similarly, examples of all forms of psychotic disorder are seen among the monozygotic co-twins of patients with schizo-affective disorder (Cardno et al 2012).…”
Background. Schizo-affective disorder has not been studied to any significant extent using functional imaging. The aim of this study was to examine patterns of brain activation and deactivation in patients meeting strict diagnostic criteria for the disorder.Method. Thirty-two patients meeting Research Diagnostic Criteria (RDC) for schizo-affective disorder (16 schizomanic and 16 schizodepressive) and 32 matched healthy controls underwent functional magnetic resonance imaging (fMRI) during performance of the n-back task. Linear models were used to obtain maps of activations and deactivations in the groups.Results. Controls showed activation in a network of frontal and other areas and also deactivation in the medial frontal cortex, the precuneus and the parietal cortex. Schizo-affective patients activated significantly less in prefrontal, parietal and temporal regions than the controls, and also showed failure of deactivation in the medial frontal cortex. When task performance was controlled for, the reduced activation in the dorsolateral prefrontal cortex (DLPFC) and the failure of deactivation of the medial frontal cortex remained significant.Conclusions. Schizo-affective disorder shows a similar pattern of reduced frontal activation to schizophrenia. The disorder is also characterized by failure of deactivation suggestive of default mode network dysfunction.
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