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Patients with Stroke Confined to Basal Ganglia Have Diminished Response to Rehabilitation Efforts

From the Department of Neurology, Cornell University Medical College, The Burke Rehabilitation Center, White Plains, NY.
Received May 17, 1996. Accepted in final form June 25, 1996.
Address correspondence and reprint requests to Dr. Bruce T. Volpe, Department of Neurology, Cornell University Medical College, The Burke Rehabilitation Center, 785 Mamaroneck Ave, White Plains, NY, 10605.

Prediction of the functional outcome for patients with stroke has depended on the severity of impairment, location of brain injury, age, and general medical condition.This study compared admission and discharge functional outcome (Functional Independence Measure, FIM) and deficit severity (Fugl-Meyer, F-M) scores in a retrospective study of patients with similar neurologic impairments: homonymous hemianopia, hemisensory loss, and hemiparesis. CT-verified stroke location was the independent variable: cortical (n = 11), basal ganglia and internal capsule (normal cortex and thalamus, n = 13), or combined (cortical, basal ganglia, and internal capsule, n = 22). By 3 months on average after stroke, all groups demonstrated significantly improved motor function as measured by F-M scores. Patients with cortical lesions had the least CT-imaged damage and the best outcome. Patients with combined lesions and more extensive brain injury had significantly higher FIM scores (p < 0.05) than patients with injury restricted to the basal ganglia/internal capsule. Patients with basal ganglia/internal capsule injury were more likely to have hypotonia, flaccid paralysis, and persistently impaired balance and ambulation performance. While all patients had a comparable rehabilitation experience, these results suggest that patients with stroke confined to the basal ganglia and internal capsule benefited less from therapy. Isolated basal ganglia stroke may cause persistent corticothalamic-basal ganglia interactions that are dysfunctional and impede recovery.

NEUROLOGY 1997;48: 95-101

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