The notion of cortical reorganisation in psychosis
Poster A87, Monday, October 8, 11:30 am - 1:00 pm, Essex Ballroom
LENA PALANIYAPPAN1; 1University of Western Ontario
One of the few well-replicated features of schizophrenia is the demonstration of neuroanatomical abnormalities affecting cortical and subcortical grey matter (GM). The 2 predominant theories of psychotic disorders - neurotoxic and neurodevelopmental views - are largely built on the reported GM changes. When taking a critical view of reported GM changes in the literature, we find that 1. Contrary to the popular belief, pre-psychotic GM changes are surprisingly limited in space and magnitude. Instead, the greatest reduction in GM immediately follows the first psychotic episode (temporal constraint) 2. These post-psychotic GM changes have certain spatial predilections that are surprisingly non-specific to psychosis (spatial constraint) 3. GM increase must be co-occuring with GM loss (topological constraint) 4. GM changes scarcely, if ever, relate to the clinical course of psychosis (outcome constraint). When we consider all of these constraints together, we are left with very few parsimonious explanations for the anatomical course of schizophrenia. In this talk, I put forward the view that the GM changes in schizophrenia may not represent a deficit or decompensation process per se. A substantial amount of the observed GM changes are likely to be the result of a distributed, nevertheless inefficient, cortical reorganization response. Distributed cortical reorganization occurs as a part of a universal response to provocation. In this context, we should not be surprised that antipsychotic agents exaggerate this compensatory reorganization and intensify GM reduction.
Topic Area: First Episode Psychosis