Watson, S.

Introduction/Purpose Diabetic striatopathy (DS) is a rare neurologic complication of poorly controlled diabetes mellitus characterized by hemichorea/hemiballism and distinctive basal ganglia imaging abnormalities, most commonly T1 hyperintensity in the putamen or caudate nucleus. Emerging evidence suggests that DS may coexist with acute ischemic stroke, particularly in the context of intracranial atherosclerotic disease (ICAS), complicating both diagnosis and management. The pathophysiological interplay between chronic hyperglycemia and impaired regional perfusion is postulated to increase basal ganglia vulnerability to metabolic and ischemic injury, leading to the characteristic clinical and radiological features of DS. This case report aims to highlight the clinical course, diagnostic evaluation, and management of a patient presenting with DS and stroke secondary to ICAS. Materials/Methods A 68‐year‐old female with hypertension, hyperlipidemia, and newly diagnosed diabetes presented with a one‐month history of left arm choreiform movements, episodic dizziness, and blurred vision. Movements correlated with hyperglycemia (home blood glucose in the 400s) and resolved with dietary modification and improved glycemic control. Initial MRI revealed right M1 segment MCA occlusion with multiple subacute‐chronic infarcts in the right MCA territory and T1 hyperintensity in the right putamen, suggestive of DS. CT angiography head and neck demonstrated distal right M1 severe stenosis vs occlusion with distal reconstitution, atherosclerotic calcification in the right carotid siphon, and severe stenosis in the right V4 segment and left AICA. Laboratory evaluation showed LDL 103 mg/dL and HbA1c 10.7%. Cardioembolic evaluation with echocardiography, transcranial doppler, and prolonged cardiac monitoring was unremarkable. The patient was managed with dual antiplatelet therapy (aspirin and clopidogrel for 90 days, then aspirin monotherapy), high‐intensity statin, and intensive glycemic control per current consensus guidelines for ICAS and DS. Results The patient's involuntary movements resolved with improved glycemic control, consistent with DS. Follow‐up imaging at three months demonstrated interval resolution of right lentiform nucleus edema and enhancement, with residual mild T1 hyperintensity and curvilinear susceptibility artifact. No new infarcts were identified; prior right MCA territory infarcts appeared subacute/chronic. Persistent right distal M1 MCA stenosis was noted. The cessation of choreiform movements with normalization of blood glucose and the radiological evolution of basal ganglia changes supported the diagnosis of DS in the context of ICAS. Aggressive medical management, including dual antiplatelet therapy and statin, was implemented per American Heart Association (SAMMPRIS) recommendations for symptomatic ICAS. The patient remained neurologically stable without recurrent stroke or movement disorder. Conclusion This case illustrates the complex interplay between chronic hyperglycemia and intracranial atherosclerotic disease in the pathogenesis of both stroke and diabetic striatopathy. The combination of metabolic and vascular insults likely increases basal ganglia susceptibility to injury, manifesting as DS and ischemic stroke. Recognition of this association is critical for accurate diagnosis and optimal management, as DS may herald imminent cerebrovascular events. Aggressive risk factor modification and guideline‐directed medical therapy are essential for secondary prevention in ICAS, while glycemic control remains the cornerstone of DS management. Further research is needed to elucidate the mechanistic links and refine therapeutic strategies for these overlapping entities.