Mokri B, Silbert P L, Schievink W I, Piepgras D G
Department of Neurology, Mayo Clinic and Mayo Foundation, Rochester, MN 55905, USA.
Neurology. 1996 Feb;46(2):356-9. doi: 10.1212/wnl.46.2.356.
Cranial nerve palsy was present in 23 of 190 consecutive adult patients (12%) with spontaneous dissection of the extracranial internal carotid artery. Ten patients (5.2%) had a syndrome of lower cranial nerve palsies (with invariable involvement of cranial nerve XII with or without additional involvement of cranial nerves XI, X, and IX), seven (3.7%) had palsy of cranial nerve V, and five (2.6%) had a syndrome of ocular motor palsies. Palsy of cranial nerve VIII and ischemic optic neuropathy occurred in one patient each. Three patients had dysgeusia without other cranial nerve involvement, presumably due to involvement of the chorda tympani nerve. Headache or face pain (often unilateral) was present in 83% of patients. Other associated manifestations were cerebral ischemic symptoms, bruits, or oculosympathetic palsy. In one patient, cranial nerve palsy was the only manifestation of internal carotid artery dissection, and in another patient, the disease presented only as a palsy of cranial nerve XII and oculosympathetic palsy. In six patients, a syndrome of hemicrania and ipsilateral cranial nerve palsy was the sole manifestation of internal carotid artery dissection. Cranial nerve palsy is not rare in internal carotid artery dissection. Compression or stretching of the nerve by the expanded artery may explain some but not all of the palsies. An alternative mechanism is likely interruption of the nutrient vessels supplying the nerve.
在190例连续性成年颅外段颈内动脉自发性夹层患者中,23例(12%)出现颅神经麻痹。10例(5.2%)出现下颅神经麻痹综合征( invariably累及 XII 颅神经,可伴有或不伴有 XI、X 和 IX 颅神经的额外受累),7例(3.7%)出现 V 颅神经麻痹,5例(2.6%)出现动眼神经麻痹综合征。VIII 颅神经麻痹和缺血性视神经病变各有1例患者出现。3例患者出现味觉障碍但无其他颅神经受累,推测是由于鼓索神经受累所致。83%的患者出现头痛或面部疼痛(通常为单侧)。其他相关表现为脑缺血症状、血管杂音或眼交感神经麻痹。1例患者,颅神经麻痹是颈内动脉夹层的唯一表现,另1例患者,该病仅表现为 XII 颅神经麻痹和眼交感神经麻痹。6例患者,偏头痛和同侧颅神经麻痹综合征是颈内动脉夹层的唯一表现。颅神经麻痹在颈内动脉夹层中并不罕见。扩张的动脉对神经的压迫或牵拉可能解释部分而非全部麻痹情况。另一种机制可能是供应神经的营养血管中断。