Abstract 305: Cyclical nightmare, Recurrent basilar occlusion culminating in locked‐in syndrome

Background Basilar artery occlusion (BAO) is a rare but devastating cause of stroke, representing only 1% of cases but with mortality rates up to 95% if untreated. Diagnosis is often delayed due to nonspecific symptoms, which may range from dizziness to quadriplegia. Management remains challenging; recent trials support endovascular treatment (EVT), though with risks of complications and hemorrhage. Data on recurrent BAO resistant to multimodal therapies are especially limited. We present a patient with recurrent BAO and complete recovery between events, whose final episode resulted in locked‐in syndrome. Case: A 68‐year‐old man presented with sudden left arm and leg ataxia, right facial droop, and mild dysarthria (NIHSS 4). Initial CT was negative, and IV thrombolysis was administered. Hours later, symptoms worsened (NIHSS 17) and CTA revealed basilar occlusion. Mechanical thrombectomy (TICI 3c) was performed, followed by dual antiplatelet therapy. MRI showed a small left pontine infarct. Stroke workup was unrevealing, and he was discharged on dual antiplatelets and statin, returning to work without deficits. Outpatient CTA demonstrated improvement in basilar stenosis. Platelet testing revealed aspirin non‐responsiveness, so he remained on clopidogrel monotherapy. Three months later, he re‐presented with dysarthria, severe ataxia, and left‐sided weakness (NIHSS 6). CTA showed persistent basilar occlusion with progression. IV thrombolysis was given, but no EVT was pursued. MRI revealed right pontine and multifocal left pontine infarcts. Cilostazol was added, and he was discharged NIHSS 0, with mRS 2 on follow‐up. Four months later, he presented with generalized weakness, dysarthria, and gait impairment (NIHSS 5). CTA showed near‐occlusive basilar stenosis. IV thrombolysis was administered, but NIHSS rapidly worsened to 13, with plegia, dysconjugate gaze, and obtundation. EVT was not attempted due to chronicity and near‐total occlusion. MRI demonstrated bilateral pontine infarction with hemorrhage. He became locked‐in, with only vertical gaze and blinking. During hospitalization, extensive deep vein thromboses were discovered in both lower and upper extremities, and he was transitioned to long‐term anticoagulation. Discussion Basilar occlusions can be devastating as they are associated with locked‐in syndrome. Current studies have shown a benefit of thrombectomy in BAOs, but the best management remains uncertain, especially in relation to recurrent thrombosis when both medical and surgical avenues have been exhausted. This case highlights the difficulty of treating BA stenosis in that, even after successful recanalization, BAO can recur despite maximal medical therapy with multiple platelet inhibition strategies. It questions the efficacy of antiplatelet strategies alone for preventing recurrent basilar artery occlusion and may suggest that other strategies (anticoagulation or a combination of antiplatelet with anticoagulation) may be needed to prevent BAO.