Acute and Transient Psychotic Disorders: Newer Understanding.

Abstract

We review the ongoing research in the area of acute and transient psychotic disorders (ATPDs) with regard to their nosology, epidemiology, clinical description, genetics, and neurobiology, examining evidence for distinctiveness or otherwise of ATPDs. We further highlight the lacuna in research in ATPDs. Studies on ATPDs as defined in the ICD 10 have been reported from different parts of the world, more so from the developing countries. There is consistent evidence that there exist a group of ATPDs that occur more commonly among females, are often precipitated by stressful life events or exposure to physiological stresses like fever, child birth, are associated with well-adjusted premorbid personality, and show complete recovery in a short period. Although in some cases of ATPDs, there is symptomatic overlap with schizophrenic symptoms in the acute phase, they follow a completely different course and outcome, exhibit genetic distinctiveness, and do not share genetic relationship with schizophrenias or bipolar affective disorder (BPAD). Comparative studies on neurophysiology and neuroimaging in ATPDs and schizophrenias have demonstrated evidence of hyper arousal and hyper metabolism in ATPDs vs hypo arousal and hypo metabolism as noted in the P300 response and on FDG PET studies, respectively. Immune markers such as IL-6, TNF-alpha, and TGF-beta show higher levels in ATPDs as compared to healthy controls. Findings on the neurobiological mechanisms underlying ATPDs, so far, point towards significant differences from those in schizophrenia or BPAD. Although the studies are few and far between, nevertheless, these point towards the possibility of ATPDs as a distinct entity and underscore the need for pursuing alternate hypothesis such as neuro inflammatory or metabolic. Research on ATPDs is limited due to many reasons including lack of harmony between the ICD and DSM diagnostic systems and clinician biases. Available research data supports the validity of ATPDs as a distinct clinical entity. There is also evidence that ATPDs are different from schizophrenias or BPAD on genetic, neuroimaging, neurophysiological, and immunological markers and require further studies.