Department of Neurology, Seoul National University College of Medicine, Seoul National University Bundang Hospital, 300 Gumi-dong, Bundang-gu, Seongnam, Gyeonggi-do, 463-707, Korea.
J Neurol. 2014 Mar;261(3):480-9. doi: 10.1007/s00415-013-7221-7. Epub 2013 Dec 31.
Even though trigeminovestibular connections are well established in animals, mastication-induced dizziness has been described only as a vascular steal phenomenon in humans. We determined induction or modulation of nystagmus in two index patients with mastication-induced vertigo, 12 normal controls, and 52 additional patients with peripheral (n = 38, 26 with vestibular neuritis/labyrinthitis and 12 with Meniere's disease) or central (n = 14, 11 with Wallenberg syndrome, two with cerebellar infarction, and one with pontine infarction) vestibulopathy during their acute or compensated phase. Both index patients developed mastication-induced vertigo after near complete resolution of the spontaneous vertigo from presumed acute unilateral peripheral vestibulopathy. The nystagmus and vertigo gradually built up during mastication and dissipated slowly after cessation of mastication. Brain MRI and cerebral angiography were normal in these patients. Mastication did not induce nystagmus in normal controls. However, mastication induced nystagmus in five (24 %) of the 21 patients without spontaneous nystagmus (SN) but with a previous history of a vestibular syndrome, and either increased (21/31, 68 %) or decreased (7/31, 23 %) the SN in almost all the patients (28/31, 90 %) with SN. Mastication may induce significant vertigo and nystagmus in patients with a prior history of acute vestibulopathy. The induction or modulation of nystagmus by mastication in both peripheral and central vestibulopathies supports trigeminal modulation of the vestibular system in human. The gradual build-up and dissipation suggest a role of the velocity storage mechanism in the generation of mastication-induced vertigo and nystagmus.
尽管在动物中已经确立了三叉神经 - 前庭连接,但咀嚼引起的头晕仅在人类中被描述为血管盗血现象。我们在两名因咀嚼引起眩晕的索引患者、12 名正常对照者和 52 名患有外周(n = 38,26 例前庭神经炎/迷路炎和 12 例梅尼埃病)或中枢(n = 14,11 例 Wallenberg 综合征、2 例小脑梗死和 1 例脑桥梗死)前庭病变的患者中,确定了咀嚼诱导的眼球震颤的诱导或调制,这些患者处于急性或代偿期。两名索引患者在假定的单侧急性外周前庭病变的自发眩晕基本完全缓解后,均出现咀嚼诱导的眩晕。咀嚼时眼球震颤和眩晕逐渐增强,咀嚼停止后缓慢消散。这些患者的脑 MRI 和脑血管造影均正常。正常对照者咀嚼时不会引起眼球震颤。然而,21 名无自发性眼球震颤(SN)但有前庭综合征病史的患者中有 5 名(24%)在咀嚼时诱导出眼球震颤,并且几乎所有有 SN 的患者(28/31,90%)的 SN 要么增加(21/31,68%),要么减少(7/31,23%)。咀嚼可能会引起急性前庭病变史患者明显的眩晕和眼球震颤。咀嚼在外周和中枢前庭病变中诱导或调制眼球震颤支持三叉神经对前庭系统的调制。眼球震颤的逐渐增强和消散提示速度储存机制在咀嚼诱导的眩晕和眼球震颤的产生中起作用。