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前庭眼反射缺陷伴内侧纵束病变。

Vestibulo-ocular reflex deficits with medial longitudinal fasciculus lesions.

机构信息

Institute of Clinical Neuroscience, Royal Prince Alfred Hospital, Missenden Road, Sydney, NSW 2050, Australia.

Brain and Mind Research Institute, University of Sydney, 94 Mallett St, Sydney, NSW 2050, Australia.

出版信息

J Neurol. 2017 Oct;264(10):2119-2129. doi: 10.1007/s00415-017-8607-8. Epub 2017 Sep 6.

Abstract

The medial longitudinal fasciculus (MLF) is the final common pathway for all conjugate adducting horizontal eye movements, as well as for the vertical-torsional vestibulo-ocular reflex (VOR). MLF lesion causes adduction paresis of ipsilesional (adducting) eye with dissociated nystagmus of contralesional (abducting) eye-the well-known clinical syndrome of internuclear ophthalmoplegia (INO). We measured the VOR stimulation and also any catch-up saccades, from individual semicircular canal (SCC) evoked by the head impulse test (HIT), using head and binocular 3-dimensional scleral search coils in 27 multiple sclerosis (MS) patients, 8 with unilateral, 19 with bilateral INO. In unilateral INO, VOR gain (normal >0.90) from ipsilesional lateral SCC stimulation was 0.48 for the adducting eye and 0.81 for the abducting eye; 0.61 from contralesional anterior SCC stimulation and only 0.29 from contralesional posterior SCC stimulation. In bilateral INO, there were VOR gain deficits from all six SCCs: lateral SCC gains were asymmetrically reduced to 0.45 in the adducting eye and 0.66 in the abducting eye; anterior SCC gain was 0.48 and posterior SCC gain was only 0.19. Horizontal VOR versional dysconjugacy between adducting and abducting eyes at 0.66 was less severe than horizontal catch-up saccade versional dysconjugacy (0.44); normal >0.80. Unexpected partial preservation of horizontal VOR with greater catch-up saccade impairment from the adducting than abducting eye suggests that the ascending tract of Deiters (ATD), an extra-MLF pathway, also mediates the horizontal VOR, but not adducting horizontal saccades. Vertical VOR deficits will produce vertical oscillopsia with any vertical head movement and measurement of the vertical VOR could help with the diagnosis and quantitative evaluation of MLF lesions in suspected MS. Horizontal VOR deficits and catch-up saccade versional dysconjugacy in INO will cause gaze instability and horizontal oscillopsia during active horizontal head movements.

摘要

内侧纵束(MLF)是所有共轭内收水平眼球运动以及垂直扭转前庭眼反射(VOR)的最终共同途径。MLF 损伤导致同侧(内收)眼球内收无力,对侧(外展)眼球分离性眼球震颤-众所周知的核间眼肌麻痹(INO)临床综合征。我们使用头部冲击测试(HIT)刺激单个半规管(SCC),测量了来自 27 名多发性硬化症(MS)患者的 VOR 刺激和任何代偿性扫视,8 名单侧,19 名双侧 INO。在单侧 INO 中,同侧外侧 SCC 刺激引起的 VOR 增益(正常> 0.90)为内收眼的 0.48 和外展眼的 0.81;对侧前 SCC 刺激的 0.61 和对侧后 SCC 刺激的仅 0.29。在双侧 INO 中,所有六个 SCC 都存在 VOR 增益不足:外侧 SCC 增益不对称地降低到内收眼的 0.45 和外展眼的 0.66;前 SCC 增益为 0.48,后 SCC 增益仅为 0.19。0.66 时内收和外展眼之间的水平 VOR 矢状失共轭比水平代偿性扫视矢状失共轭(0.44)轻;正常> 0.80。与代偿性扫视相比,内收眼的水平 VOR 有部分保留而代偿性扫视损伤更大,这表明 Deiters 上升束(ATD)是 MLF 以外的额外通路,也介导水平 VOR,但不介导内收性水平扫视。垂直 VOR 不足会导致任何垂直头部运动时出现垂直摆动性眼球震颤,测量垂直 VOR 有助于诊断和定量评估疑似 MS 中的 MLF 损伤。INO 中的水平 VOR 不足和代偿性扫视矢状失共轭会导致主动水平头部运动时注视不稳定和水平摆动性眼球震颤。

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