Behavioral and Cognitive Changes Following Thalamic and Basal Ganglionic Lesions

Abstract

Subcortical small lesions involving the thalamus, caudate, and globus pallidus disrupt corticosubcortical circuits, resulting in cognitive dysfunction. Disruption of the frontosubcorticaI circuits leads to cognitive impairment with striking frontal lobe features, and disruption of the memory-related circuits leads to amnesia. Specific vascular lesions cause characteristic neurobehavioral syndromes: the syndrome of left polar thalamic artery territory infarction features amnesia accentuated for verbal materials, as compared with nonverbal ones, and emotional and motivational deficits; the syndrome of bilateral paramedian thalamic artery territory infarction features sudden onset of coma or confusion followed by a persistent amnesia of varying severity, with or without language impairment and frontal lobe dysfunction; and caudate or pallidal lesions lead to behavioral and cognitive changes including abulia, apathy and depression in some patients, and disinhibition, hyperactivity, and inattention in others. These components are often the features of vascular dementia, and ischemic lesions in those strategic sites are often found in patients with vascular dementia. Studies of subcortical strategic lesions involving the neural circuits provide an important clue, for understanding of vascular dementia. The effects of discrete ischemic subcortical lesions in the thalamus and basal ganglia on the neural circuits can be documented with high-resolution MR imagings and functional brain imaging.