Poststroke language outcomes vary widely and are inadequately explained by lesion location alone.
Structural network disruption informed by neurotransmitter receptor distribution revealed key roles of serotonergic (5-HT1a, 5-HT2a) and dopaminergic (D1) systems in language impairment.
Neurotransmitter-driven connectome damage explained additional variability in language deficits beyond traditional clinical factors.
Findings support a novel neurochemical network framework for understanding poststroke aphasia with potential, though preliminary, implications for targeted interventions.
