Intra-Arterial Verapamil for Managing Intracranial Giant Cell Arteritis

Introduction/Purpose Giant Cell Arteritis (GCA) rarely involves the intracranial vasculature; when it does, the disease course is often aggressive and refractory to conventional therapies, even with optimal medical management. We report a case of refractory intracranial GCA successfully managed with intra‐arterial verapamil, illustrating its potential utility in improving cerebral perfusion in this challenging clinical scenario. Results/Case description A 66‐year‐old woman presented with acute, painless monocular vision loss in the left eye accompanied by headache. Initial evaluation revealed >90% stenosis of the bilateral extracranial internal carotid arteries and a small left frontal cerebral infarction. The vision loss was initially attributed to anterior ischemic optic neuropathy. Neuroimaging also demonstrated severe intracranial atherosclerosis. She underwent left carotid endarterectomy and was started on dual antiplatelet therapy. Due to associated temporal tenderness and pain, GCA was suspected. Despite normal erythrocyte sedimentation rate (ESR) and C‐reactive protein (CRP) levels, oral prednisone was initiated empirically. GCA was confirmed on temporal artery biopsy.The patient returned with recurrent thunderclap headaches and new onset left homonymous hemianopsia. Neuroimaging revealed an acute infarction in the right occipital lobe. CT angiography demonstrated progression of multifocal intracranial stenoses, raising a strong suspicion for intracranial GCA. Rheumatology recommended high‐dose intravenous methylprednisolone followed by tocilizumab. Despite aggressive immunosuppressive therapy, the patient's neurological status deteriorated. Follow‐up imaging revealed new infarctions in the left temporoparietal region. Catheter‐based cerebral angiography confirmed diffuse, multifocal segmental narrowing consistent with severe intracranial vasculitis. To improve cerebral perfusion, intra‐arterial verapamil was administered, with 20 mg infused into the left internal carotid artery (ICA) and 10 mg into the right common carotid artery over 10 minutes each. Follow‐up angiography demonstrated moderate improvement in vessel caliber and anterograde flow across previously stenotic segments of the middle cerebral artery (MCA) and anterior cerebral artery (ACA). Discussion Intracranial involvement in GCA is rare and frequently resistant to standard immunosuppressive therapies. Arterial vasoconstriction in GCA has been hypothesized to result from an inflammatory cascade that promotes smooth muscle cell (SMC) proliferation and intimal hyperplasia, ultimately leading to luminal narrowing. This pathophysiological mechanism may explain the observed response to intra‐arterial verapamil in our case, as calcium channel blockers exert vasodilatory effects by modulating vascular SMC tone. Conclusion This case highlights the potential use of intra‐arterial verapamil as a targeted vasodilatory intervention in the management of refractory intracranial GCA. Further studies are warranted to explore its efficacy and define its role within the broader treatment algorithm for intracranial GCA.