Background Reversible vasoconstriction syndrome has been described as an important cause of cerebral arteriopathy and/or vasoconstriction, with non-aneurysmal SAH recently being noted as a more common presentation that previously recognized. No standardized treatment exists and serious complications such as ischemic stroke have been reported. Although distal segmental narrowing is typical, proximal vessel occlusions have been reported.
Case Report A 43-year-old female marathon runner presented to an outside hospital following a thunderclap headache with initial negative head CT and lumbar puncture. 1 week later after worsening headache and nausea, a repeat head CT revealed right frontal intraparenchymal hematoma. A CT angiogram revealed right carotid terminus occlusion and scattered diffuse segmental narrowings. She was treated with steroids and nimodipine. Following progression of symptoms including left hemi-inattention, she was transferred to our facility and found to have a large right parietal infarct, subarachnoid hemorrhage along the right frontal cortex and multifocal moderate to severe segmental stenoses. Her NIH stroke scale was 16. Based on our experience with intra-arterial verapamil for the treatment of aneurysmal subarachnoid hemorrhage, she was taken to angiography where confirmation of multifocal proximal and distal segmental vascular narrowing was made and intra-arterial verapamil was given: 5 mg in the right internal carotid artery, 20 mg in the left internal carotid artery and 10 mg in the left vertebral artery. Immediate clinical improvement was appreciated despite modest angiographic changes. Daily transcranial Doppler studies were performed, along with induced hypertension and monitoring of central venous pressure. Systemic verapamil and high dose steroids were also administered. She returned to the angiography suite four times in the next 5 days week for clinical symptoms (left arm weakness, agitation and confusion) or elevated transcranial Doppler studies and was found to have a similar and recurrent pattern of vasospasm. She received similar intra-arterial treatment at each angiogram, again with clinical and angiographic improvement. At the time of discharge, the patient's left sided weakness and cognitive deficits had resolved but she suffered from residual left hemi-inattention.
Conclusion We describe a patient with severe, medical-treatment refractory RCVS who demonstrated clinical and radiographic response to repeated treatment with intra-arterial vasodilator therapy.
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