Psychedelics, empathogens, and psychostimulants produce increased connectivity between the thalamus and sensorimotor areas of the brain, a pattern similar to that observed in individuals with psychotic disorders. This suggests a shared neural mechanism across these substances and certain psychiatric conditions, linking altered thalamocortical communication to changes in perception and behavior.
Classic psychedelics and acute psychosis share overlapping disruptions in brain connectivity, particularly involving the thalamus and its connections to cortical regions. Both states exhibit hyperconnectivity between the thalamus and sensorimotor cortices, linked to altered perceptions and hallucinations. Psychosis also shows hypoconnectivity between the thalamus and prefrontal cortices, associated with cognitive disturbances. These patterns of thalamocortical dysconnectivity extend to cortico-striato-pallido-thalamo-cortical circuitry. The review synthesizes neuroimaging and neuropharmacological evidence to highlight shared and distinct neurophysiological changes, suggesting clinically relevant parallels that may inform future research on perception and cognition.
Earlier cannabis initiation among people with recent-onset psychosis is associated with more severe positive symptoms and greater gray matter volume in a cerebellar network previously linked to schizophrenia. This cerebellar volume increase correlates with lower volume in an insula-temporal-frontal network also implicated in schizophrenia. The findings suggest that early cannabis use may alter the developmental trajectory of specific brain networks, increasing later psychosis risk.