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.