Case Report: Dual Antiplatelet in Capsular Warning Syndrome

Abstract

Background: Capsular warning syndrome (CWS) is defined as a recurrent stereotype transient lacunar syndrome without cortical symptoms. However, to date, there is limited literature proposed on the definitive treatment options for the prevention of persistent stroke in cases of capsular warning syndrome. Aim: The aim of this case report is to address dual antiplatelet therapy as a treatment choice in CWS to prevent progressive stroke. Case presentation: A 56-year-old man with several comorbidities experienced recurrent periods of limb weakness and dysarthria lasting 5 -20 minutes with a complete resolution of symptoms in between. The fluctuating episodes lasted for 72 hours followed by a persistent minor stroke. A gadolinium-enhanced MRI scan of the brain revealed a right basal ganglia infarct. He was treated with dual antiplatelet, and his functional outcome was favourable at 90 days post stroke. Conclusion: Dual antiplatelet may be a beneficial therapeutic option in CWS in improving functional outcomes in the early neurological deficit and decreasing the clinical fluctuation.

Capsular warning syndrome and its clinical awareness and therapeutic approach: two case reports and a systematic review of the literature

“…The absence of cortical signs is due to the confined injury of the internal capsule, or in some cases, vascular damage in the pons, midbrain, or thalamus ( 1 , 44 ). Pure motor hemiparesis affecting the face, arm, and leg with normal speech is a characteristic of CWS ( 4 ). Our two cases showed this clinical presentation that evolved into hemiplegia, even after treatment with DAT, and one of them after super selective intra-arterial nimodipine infusion into the left lenticulostriate arteries.…”

“…Its exact underlying mechanism remains unknown; nonetheless, small perforating artery disease has been described as the most common cause ( 3 ). Atherosclerosis ( 2 ), artery-to-artery microemboli ( 1 ), and intermittent hemodynamic changes secondary to structural arterial changes or blood pressure fluctuations ( 4 , 5 ) have also been suggested as potential mechanisms.…”