Abnormal connectivity between PFC and thalamus linked to cognitive impairment in schizophrenia
A new neuroimaging study from the Woodward Lab found that individuals with schizophrenia show reduced anatomical connectivity between the prefrontal cortex (PFC) and thalamus, and that this reduction is related to cognitive impairment. Executive cognitive functions, including working memory, cognitive flexibility, and inhibition, are impaired in schizophrenia. Executive functions rely on coordinated information processing between the PFC and thalamus, particularly the mediodorsal (MD) nucleus. Communication between the PFC depends on the integrity of structural white matter tracts connecting these two brain regions. This raises the possibility that anatomical connectivity between the PFC and MD thalamus may be: 1) reduced in schizophrenia; and 2) related to deficits in executive function. To test these hypotheses, 45 healthy subjects and 62 individuals with a schizophrenia spectrum disorder underwent diffusion-weighted imaging (DWI), a type of MRI scan capable of measuring white matter connectivity, and completed a battery of neuropsychological tests. We found that white matter connectivity between the thalamus and PFC was reduced in schizophrenia and correlated with impaired working memory. In contrast to reduced PFC-thalamic connectivity, thalamic connectivity with somatosensory and occipital cortices was increased in schizophrenia. The results are consistent with models implicating dysrupted PFC-thalamic connectivity in the pathophysiology of schizophrenia and mechanisms of cognitive impairment. PFC-thalamic anatomical connectivity may be an important target for procognitive interventions. Further work is needed to determine the implications of increased thalamic connectivity with sensory cortex.