E-009 Reversible cerebral vasoconstriction syndrome following carotid artery stenting
E-009 Reversible cerebral vasoconstriction syndrome following carotid artery stenting
复制标题
E-009 颈动脉支架置入术后可逆性脑血管收缩综合征
DOI：
10.1136/neurintsurg-2012-010455c.9
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发表时间：
2012
影响因子：
4.8
通讯作者：
M. Hurley
中科院分区：
文献类型：
--
作者：
M. Soltanolkotabi;S. Ansari;B. Patel;A. Shaibani;M. Hurley
可逆性脑血管收缩综合征（RCVS）是一组以脑动脉持续但可逆的血管收缩为特征的疾病。据报道，RCVS发生在各种临床环境中，尽管病理生理学尚不清楚，但脑血管张力调节障碍一直是流行的假设。我们报告一例颈动脉支架置入术后发生同侧可逆性脑血管收缩的病例。据我们所知，这是第一个报告的RCVS后，颈动脉支架在文献中。病例报告/影像学发现一名49岁女性，既往有高血压、高脂血症和偏头痛病史，在我院接受颈动脉血管成形术/支架植入术治疗症状性70%-80%左颈内动脉起始部狭窄。尽管手术并不复杂，但患者主诉支架植入后持续左额叶头痛。然而，系列CT头部和CTA颈部研究显示左颈动脉支架通畅，没有支架内狭窄、血栓形成或颅内出血并发症的证据，患者出院。14天后，患者因右侧上肢和下肢无力和右侧面部麻木的短暂性缺血发作返回艾德。 有趣的是，这些症状发生在开始新的抗高血压治疗后1天，并伴随头痛消退。 脑部磁共振检查显示左侧额顶叶有2-3个点状弥散受限病灶，符合急性梗死。脑MR灌注研究显示平均通过时间升高，相对脑血容量轻度代偿性增加，提示血管自动调节舒张。尽管随后的CTA头颈部研究再次证明支架通畅，无残余狭窄，但怀疑左侧前颅内循环和左侧大脑后动脉的远端颅内血管不规则，提示进行脑血管造影。脑血管造影结果证实左大脑前、中、后动脉远端颅内血管系统弥漫性节段性狭窄。这一发现仅限于左半球。血管收缩后立即解决动脉内维拉帕米和重复MR灌注显示接近完全正常化。患者的神经系统症状没有复发，尽管在维拉帕米IA给药期间头痛复发。患者每日接受120 mg维拉帕米治疗并出院。 随访时，患者持续头痛，维拉帕米部分缓解。然而，随后的CTA/MRP研究显示左侧血管收缩完全逆转。结论颈动脉血管重建术引起脑血管收缩的机制尚不清楚;但是，根据4例颈动脉内膜切除术病例以及我们的血管内病例中同侧血管痉挛的观察，提出了直接的机械关系。伊卡严重狭窄可能导致慢性脑灌注不足和脑血管自动调节障碍。颈动脉血运重建后，相对高灌注状态可能会引起易感个体的血管收缩反应加重，实际上会导致症状性低灌注。头痛的出现与我们病人的脑灌注状态密切相关。竞争利益无。
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.