Introduction Reversible cerebral vasoconstriction syndromes (RCVS) compromise a group of disorders characterized by prolonged but reversible vasoconstriction of the cerebral arteries. RCVS has been reported to occur in various clinical settings and although the pathophysiology remains unclear, a disturbance in the regulation of cerebral vascular tone has been the prevailing hypothesis. We report a case of ipsilateral reversible cerebral vasoconstriction following carotid stenting. To our knowledge, this is the first report of RCVS following carotid stenting in the literature.
Case report/imaging findings A 49-year-old female with a past medical history of hypertension, hyperlipidemia, and migraines underwent carotid angioplasty/stenting for a symptomatic 70%–80% left internal carotid artery origin stenosis at our institution. Although the procedure was uncomplicated, the patient complained of a significant constant left frontal headache post-stenting. Serial CT head and CTA neck studies however, revealed a patent left carotid stent with no evidence of in-stent stenosis, thrombosis, or intracranial hemorrhagic complications and the patient was discharged. The patient returned to the ED 14 days later due to transient ischemic episodes of right upper and lower extremity weakness and right facial numbness. Interestingly, these symptoms occurred 1 day after commencing new antihypertensive therapy and an associated resolution of her headache. MR brain studies demonstrated 2–3 punctuate foci of restricted diffusion in the left fronto-parietal lobe consistent with acute infarcts. Brain MR perfusion studies revealed an elevated mean transit time and mild compensatory increase in relative cerebral blood volume suggesting autoregulatory vasodilation. Although subsequent CTA head and neck studies re-demonstrated stent patency with no residual stenosis, there was suspicion of irregularity in the distal intracranial vasculature of the left anterior intracranial circulation, and left posterior cerebral artery, prompting a cerebral angiogram. Cerebral angiogram results confirmed diffuse segmental narrowing in the distal intracranial vasculature of the left anterior, middle, and posterior cerebral arteries. This finding was restricted to the left hemisphere. The vasoconstriction resolved immediately following the administration of intra-arterial verapamil and a repeat MR perfusion showed near complete normalization. The patient's neuorologic symptoms did not recur although her headache had returned during the IA verapamil administration. The patient was placed on 120 mg verapamil daily and discharged. Upon follow-up, the patient continued to suffer from persistent headaches, which were partially resolved with verapamil. Subsequent CTA/MRP studies; however, demonstrated complete reversal of the left-sided vasoconstriction.
Conclusion The mechanism by which carotid revascularization procedures precipitate cerebral vasoconstriction is not well understood; however, a direct mechanical relationship is suggested based on the observation of ipsilateral vasospasm in 4 of the reported carotid endarterectomy cases in addition to our endovascular case. It has been postulated that severe ICA stenosis may lead to chronic cerebral hypoperfusion and a disturbance of cerebral vessel autoregulation. Following revascularization of the carotid artery, a relative hyperperfusion state may induce an accentuated vasoconstrictive response in susceptible individuals and actually lead to symptomatic hypoperfusion. The presence of headache correlated well with our patient's cerebral perfusion status.
Competing interests None.
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