Guidetti D, Pisanello A, Giovanardi F, Morandi C, Zuccoli G, Troiso A
Divisione Neurologica, Azienda Ospedaliera Santa Maria Nuova, Viale Risorgimento 80, 42100 Reggio Emilia, Italy.
J Neurol Sci. 2001 Mar 1;184(2):203-7. doi: 10.1016/s0022-510x(01)00440-3.
Cranial nerve palsy in internal carotid artery (ICA) dissection occurs in 3--12% of all patients, but in 3% of these a syndrome of hemicranias and ipsilateral cranial nerve palsy is the sole manifestation of ICA dissection, and in 0.5% of cases there is only cranial nerve palsy without headache. We present two cases of lower cranial nerve palsy. The first patient, a 49-year-old woman, developed left eleventh and twelfth cranial nerve palsies and ipsilateral neck pain. The angio-RM showed an ICA dissection with stenosis of 50%, beginning about 2 cm before the carotid channel. The patient was treated with oral anticoagulant therapy and gradually improved, until complete clinical recovery. The second patient, a 38-year-old woman, presented right hemiparesis and neck pain. The left ICA dissection, beginning 2 cm distal to the bulb, was shown by ultrasound scanning of the carotid and confirmed by MR angiogram and angiography with lumen stenosis of 90%. Following hospitalisation, 20 days from the onset of symptoms, paresis of the left trapezius and sternocleidomastoideus muscles became evident. The patient was treated with oral anticoagulant therapy and only a slight right arm paresis was present at 10 months follow-up. Cranial nerve palsy is not rare in ICA dissection, and the lower cranial nerve palsies in various combinations constitute the main syndrome, but in most cases these are present with the motor or sensory deficit due to cerebral ischemia, along with headache or Horner's syndrome. In the diagnosis of the first case, there was further difficulty because the cranial nerve palsy was isolated without hemiparesis, and the second case presented a rare association of hemiparesis and palsy of the eleventh cranial nerve alone. Compression or stretching of the nerve by the expanded artery may explain the palsies, but an alternative cause is also possible, namely the interruption of the nutrient vessels supplying the nerve, which in our patients is more likely.
颈内动脉(ICA)夹层导致的颅神经麻痹在所有患者中的发生率为3% - 12%,但其中3%的患者仅表现为偏侧头痛和同侧颅神经麻痹综合征,0.5%的病例仅有颅神经麻痹而无头痛。我们报告两例下颅神经麻痹病例。首例患者为一名49岁女性,出现左侧第十一和第十二颅神经麻痹及同侧颈部疼痛。血管磁共振成像显示颈内动脉夹层,狭窄率为50%,起始于颈动脉管前方约2厘米处。患者接受口服抗凝治疗后逐渐好转,直至临床完全康复。第二例患者为一名38岁女性,表现为右侧偏瘫和颈部疼痛。颈动脉超声扫描显示左侧颈内动脉夹层,起始于球部远端2厘米处,磁共振血管造影和血管造影证实管腔狭窄率为90%。症状出现20天后住院时,左侧斜方肌和胸锁乳突肌麻痹明显。患者接受口服抗凝治疗,随访10个月时仅遗留轻微右臂麻痹。颅神经麻痹在颈内动脉夹层中并不罕见,各种组合的下颅神经麻痹构成主要综合征,但在大多数情况下,这些麻痹伴有因脑缺血导致的运动或感觉障碍,以及头痛或霍纳综合征。在首例病例的诊断中,由于颅神经麻痹孤立存在且无偏瘫,诊断存在进一步困难;而第二例病例表现为偏瘫与仅第十一颅神经麻痹的罕见组合。扩张的动脉对神经的压迫或牵拉可能解释这些麻痹,但也可能存在另一种原因,即供应神经的营养血管中断,在我们的患者中这种情况更有可能。