以动眼神经麻痹为先兆的颈内动脉夹层:1例报告及文献复习。

Ahmad Nizam, Hussam A Yacoub, James S McKinney
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引用次数: 9

摘要

急性动眼神经麻痹通常由微血管疾病或压迫性病变和动脉瘤引起,但很少与缺血性大血管疾病相关。我们报告一例颅内外颈内动脉(ICA)夹层预示着CN III型麻痹并复习相关文献。病例报告:一名24岁的右撇子男子,2天前出现右侧虚弱并呕吐。第二天,家人发现他的左眼向外倾斜,瞳孔增大,眼睑下垂。入院当天,他因右侧无力跌倒。他的神经学检查显示有明显的失语,左第三神经麻痹,右侧同义性偏盲和右侧偏瘫伴半感觉缺陷。脑磁共振成像显示左侧大脑中动脉急性缺血性梗死,无肿块效应。磁共振血管造影显示左颅外大脑内动脉(ICA)夹层,颈远端和颅内ICA段无血流。他接受了左侧半脑减压切除术,部分改善了他的缺陷。讨论:由ICA疾病引起的动眼神经麻痹是一种罕见的疾病,但在狭窄、闭塞和剥离的病例中也有报道。这很可能是由于供血神经的动脉中继发的低流量或微栓塞引起的CN III灌注不足。有胎儿大脑后动脉存在的ICA患者发生CN III型麻痹的风险更高。结论:急性动眼神经麻痹伴瞳孔受累值得深入研究。当常规检查不能明确病因时,应考虑颅外颈动脉病理检查。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Internal carotid artery dissection heralded by an oculomotor nerve palsy: case report and literature review.

Introduction: Acute oculomotor nerve (CN III) palsies are commonly attributed to microvascular disease or compressive lesions and aneurysms, but may rarely be associated with ischemic large vessel disease. We report a case of an extracranial internal carotid artery (ICA) dissection heralded by CN III palsy with review of the relevant literature.

Case report: A 24-year-old right-handed man presented with right-sided weakness preceded by vomiting 2 days earlier. The following day, the family noted his left eye to be deviated outward with enlarged pupil and droopy eyelid. On the day of admission, he had a fall owing to right-sided weakness. His neurological examination revealed significant aphasia, left third nerve palsy, right homonymous hemianopsia, and right-sided hemiplegia with hemisensory deficits. A brain magnetic resonance image showed an acute ischemic infarct in the left middle cerebral artery distribution without mass effect. Magnetic resonance angiogram showed a left extracranial internal cerebral artery (ICA) dissection with absence of flow within the distal cervical and intracranial ICA segments. He underwent a decompressive left hemicraniectomy with partial improvement in his deficits.

Discussion: Oculomotor nerve palsy as a result of ICA disease is a rare entity but has been reported in cases of stenosis, occlusion, and dissection. It is likely to be caused by hypoperfusion of CN III secondary to low flow or microembolism in the arteries feeding the nerve. The risk of CN III palsy in patients with ICA disease is higher in the presence of a fetal posterior cerebral artery.

Conclusions: Acute oculomotor nerve palsies with pupillary involvement warrant thorough investigation. When routine work-up fails to elucidate an etiology, extracranial carotid pathology should be considered.

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