Lesion Topography and Etiology of Post‐Stroke Apathy After Basal Ganglia Infarction: A Retrospective Observational Case Series

Background Apathy and depression frequently occur after stroke and may impair functional recovery. While post‐stroke depression is typically managed pharmacologically, apathy is mainly addressed through rehabilitation, and differentiating abulia‐related apathy from depression‐associated apathy is often difficult in routine practice. The association between basal ganglia lesion topography and the etiology of post‐stroke apathy remains unclear. Methods This hypothesis‐generating retrospective observational case series reviewed 516 consecutive patients with ischemic stroke and identified 13 patients with infarctions predominantly involving the basal ganglia who developed apathy during the subacute phase. Apathy was evaluated using the Vitality Index. Abulia was clinically defined by impaired behavioral initiation and persistence, and depression was assessed using the Patient Health Questionnaire‐2. Lesion distribution was categorized by basal ganglia subregions. Given the small sample size, only descriptive comparisons were performed. Results Depression occurred in three patients, abulia in three, and both conditions in one. All patients with abulia without depression had isolated globus pallidus infarction, with symptoms evident from the acute phase. In contrast, anterior striatal involvement (caudate nucleus and/or anterior putamen) was more frequently associated with depression. Posterior putaminal or small basal ganglia infarcts tended to present with apathy alone. Conclusions Isolated globus pallidus infarction suggests a potential association with abulia without depression, whereas anterior striatal lesions are more closely linked to depression. Recognition of lesion topography may provide preliminary insights into clinical differentiation and guide appropriate multidisciplinary management after stroke.