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114. Thalamocortical anatomical connectivity in schizophrenia and psychotic bipolar disorder
Anatomical connectivity between the prefrontal cortex (PFC) and thalamus is abnormal in schizophrenia. Overlapping phenotypes, including clinical symptoms and deficits in PFC-dependent cognitive functions, as well as shared genetic risk, suggest dysrupted thalamocortical anatomical connectivity may extend to psychotic bipolar disorder. We tested this hypothesis and examined the impact of illness stage (i.e. early stage, chronic) to determine if trajectories of thalamocortical anatomical connectivity differ between psychotic disorders. Diffusion-weighted imaging data was collected on 70 healthy individuals and 124 people with a psychotic disorder (schizophrenia spectrum=75; psychotic bipolar disorder=49). Anatomical connectivity between major divisions of the cortex, including PFC, and thalamus was quantified using probabilistic tractography and compared between groups using region-of-interest (ROI) and voxel-wise analyses. ROI analyses revealed reduced thalamus-PFC anatomical connectivity in schizophrenia (p=.015, Cohen’s d=.40) and psychotic bipolar disorder (p=.032, Cohen’s d=.41). Voxel-wise analysis localized the reduction to left mediodorsal thalamus. Reduced PFC-thalamic connectivity was present in both chronic (n=62) and early stage psychosis (n=62) with no evidence of differential progression between schizophrenia and psychotic bipolar disorder. These findings suggest that thalamus-PFC dysfunction is a shared feature of both schizophrenia and psychotic bipolar disorder that emerges early in the course of psychosis and remains relatively stable.