title: Delayed emergence of striatal dopaminergic hyperactivity after anterolateral ischemic cortical lesions in humans; evidence from turning behavior.
abstract: To test the hypothesis that striatal dopaminergic hyperactivity in humans may be an aftermath of anterior cortical ischemic insults, we utilized earlier observations that in several species, including humans with hemiparkinson's disease, asymmetric striatal dopaminergic activity results in spontaneous asymmetric turning away from the hemisphere with higher dopaminergic activity. In this study, electronic monitoring showed that, compared to normal controls, outpatients with old frontal and inferior-parietal cortical strokes exhibit a marked tendency to turn away from the side of the lesion. This delayed ipsilateral neglect suggests a delayed emergence of lasting ipsilateral striatal dopaminergic hyperactivity after unilateral anterolateral cortical insult in humans. Old ischemic insults to anterolateral cortical areas could be one etiological mechanism in human brain disorders that are associated with cortical dysfunction and delayed subcortical dopamine hyperactivity.
authors.affiliation: Department of Psychiatry, Veterans Administration Medical Center, San Diego, CA.
authors.forename: H S
authors.initials: HS
authors.lastname: Bracha
authors.forename: P D
authors.initials: PD
authors.lastname: Lyden
authors.forename: S
authors.initials: S
authors.lastname: Khansarinia
mesh_terms: D000368:Aged; D002540:Cerebral Cortex / Q000098:blood supply*; D002544:Cerebral Infarction / Q000503:physiopathology*; D003342:Corpus Striatum / Q000503:physiopathology*; D004292:Dominance, Cerebral / Q000502:physiology*; D006801:Humans; D008297:Male; D009043:Motor Activity / Q000502:physiology; D009949:Orientation / Q000502:physiology; D010302:Parkinson Disease, Secondary / Q000503:physiopathology; D011954:Receptors, Dopamine / Q000502:physiology*; D013239:Stereotyped Behavior / Q000502:physiology*
chemical_list: D011954:Receptors, Dopamine