Schizoaffective disorder was first described by J. Kasanin in 1933, since then its nosology remains a matter of controversy. We aim to add further neurobiological findings to this debate.Memory and executive function were tested in 22 acutely ill schizoaffective patients; they also underwent fMRI scanning during performance of the n-back working memory test. The same measures were obtained after they had been in remission for ≥2 months. 22 matched healthy individuals were also examined.Compared to controls, acute schizoaffective patients showed reduced activation in the DLPFC and also a failure of deactivation in the medial frontal cortex (1).In clinical remission, schizomanic patients showed an improvement of memory but not of executive function, while schizodepressive patients did not change in either domain. All schizoaffective patients in clinical remission showed memory and executive impairment compared to the controls. On fMRI, acutely ill schizomanic patients had reversible frontal hypo-activation when compared to clinical remission, while activation patterns in ill and remitted schizodepressive patients were similar. The whole group of schizoaffective patients in clinical remission showed a failure of de-activation in the medial frontal gyrus compared to the healthy controls. There was evidence for memory improvement and state dependent changes in activation in schizomanic patients across relapse and remission (2).The results demonstrate that schizoaffective disorder is characterized by medial frontal failure of deactivation and hence default mode network dysfunction (3), which is present during both active illness and remission suggesting that it is a trait factor for the disorder.
Objectives: Functional brain activity has been only studied marginally in schizoaffective disorder (SAD), a disorder whose nosological status is controversial. The present study investigated the prefrontal cortex (PFC) activity of schizomanic patients during performance of a working memory task. Method: 13 schizoaffective patients, with current schizomanic episode (Young> 18); and 26 sex-and age-matched healthy controls underwent functional magnetic resonance imaging (fMRI) while performing baseline, 1-back and 2-back versions of the n-back task. Linear models were used to obtain maps of activations and deactivations in the groups. Results: During performance of the n-back task, controls showed activation in a cluster of frontal areas and de-activation in the medial orbitofrontal and anterior cingulate cortex. The SAD patients showed significantly less activation in prefrontal areas than the controls. They also showed a marked failure to deactivate in medial frontal cortex. The SAD patients' impaired task performance was associated with both reduced activation of the dorsolateral PFC and reduced de-activation of the medial frontal areas. Conclusions: Schizomanic patients show failure of activation in a network of cortical regions, and also a failure to deactivate the ventromedial PFC and anterior cingulate cortex. This latter area corresponds to the one of the components of the ´default mode network´. This pattern of abnormality is similar to that found by our group to characterise schizophrenia (failure to activate and failure to deactivate), but different from that which characterises manic patients (failure to deactivate only).
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