| dc.description.abstract | Objectives: The onset of psychosis is often preceded by prodromal signs and symptoms. The precise neurobiological changes and time course underlying the prodromal phase are not yet known and have been studied intensively by several research centers. The aim of this review was to summarize the findings from the various structural MRI studies in order to investigate potential neurobiological markers preceding the onset of a first psychotic episode in individuals at increased risk of developing psychosis.
Methods: We conducted a search using the electronic database PubMed to identify publications on structural neuroimaging in subjects at risk of developing psychosis. Three approaches were used to search for studies, which investigated neurobiological precursors of psychosis. Clinical high risk studies are based on help-seeking individuals who come to a clinic because of the experience of prodromal symptoms. Familial liability of psychotic disorders is a second approach that investigates subjects with affected family members. The third approach studies patients with a genetic disorder (Klinefelter syndrome or velo-cardio-facial syndrome). As psychosis normally occurs at young adulthood and prodromal symptoms occur up to five years before that, the neurobiological changes underlying the prodromal phase should be identifiable during adolescence. Therefore, we restricted the search by only including studies that concentrated on adolescents at risk for psychosis (mean age range of 10-24 years).
Results: A total of 50 studies using structural MRI met inclusion criteria and were included for this review. Across the three high risk approaches, the majority of studies predominantly found gray matter decreases in various brain regions for the high risk subjects as compared to healthy controls, and for the at risk subjects who subsequently developed psychosis as compared to at risk subjects who did not. There is a great variety in brain regions that are found to be reduced, although the most frequently observed is a smaller total brain for the at risk subjects. Further frequently reported reduced brain volumes were found for the prefrontal cortex, the superior temporal lobe and the anterior cingulate gyrus.
Conclusions: In this review, despite methodological limitations and inconclusive results, we tentatively postulate that structural GM reductions in prefrontal cortex, superior temporal gyrus and anterior cingulate cortex could be regarded as precursors for the onset of psychosis. | |
