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瓦伦贝格外侧延髓综合征视觉-前庭相互作用期间的动眼神经功能障碍。

Oculomotor disturbances during visual-vestibular interaction in Wallenberg's lateral medullary syndrome.

作者信息

Waespe W, Wichmann W

机构信息

Department of Neurology, University Hospital of Zürich, Switzerland.

出版信息

Brain. 1990 Jun;113 ( Pt 3):821-46. doi: 10.1093/brain/113.3.821.

Abstract

Transient and lasting oculomotor disturbances during visual-vestibular interaction are described in 9 patients with Wallenberg's lateral medullary syndrome. In all patients magnetic resonance imaging (MRI) demonstrated a single focal area of pathological signal intensity in the (dorso)-lateral medulla suggesting infarction. In 2 of these 9 patients and in 3 further patients with no medullary signs, the infarction involved the cerebellar territory of the posterior inferior cerebellar artery (PICA). Acutely, all patients with Wallenberg's syndrome (except 1) had saccadic lateropulsion and spontaneous nystagmus in light with the horizontal fast component beating to the contralateral normal side. The velocity of the slow drift to the side of the lesion was dependent on eye position and induced a characteristic asymmetry of the visually and vestibularly elicited slow eye movements. In most patients smooth pursuit, optokinetic nystagmus and visual suppression of the vestibulo-ocular reflex were still impaired when this spontaneous drift was minimal or absent. The oculomotor disturbances in patients with and without cerebellar infarction are compared. The following conclusions are made. (1) The spontaneous drift that is dependent on eye position is mostly created by 'ocular lateropulsion', that is, a tonic bias within the oculomotor system which may have several sources. (2) The abnormalities and asymmetries of oculomotor responses during visual-vestibular stimulation cannot solely be explained by this spontaneous drift and its interaction with otherwise normal eye movements. Instead, structures and pathways are damaged in Wallenberg's syndrome which mediate visual and/or motor signals important for the cerebellar control of visually-guided slow eye movements. (3) Damage to these pathways occurs in the lateral medulla, as the MRI findings show that in most patients the cerebellum is rarely involved, but no definite conclusion can be made as to which of the fibres travelling in the inferior peduncle to the cerebellum may be interrupted.

摘要

9例患有延髓外侧综合征(Wallenberg综合征)的患者出现了视觉 - 前庭相互作用期间的短暂和持续性眼球运动障碍。所有患者的磁共振成像(MRI)均显示延髓(背)外侧有单个局灶性病理信号强度区域,提示梗死。在这9例患者中的2例以及另外3例无延髓体征的患者中,梗死累及小脑后下动脉(PICA)的小脑区域。急性期,所有患有Wallenberg综合征的患者(除1例)在光照下均有眼球跳动性侧推和自发性眼球震颤,水平快速成分向对侧正常侧跳动。向病变侧的缓慢漂移速度取决于眼位,并导致视觉和前庭诱发的缓慢眼球运动出现特征性不对称。在大多数患者中,当这种自发漂移最小或不存在时,平稳跟踪、视动性眼球震颤以及前庭眼反射的视觉抑制仍受损。对有和没有小脑梗死的患者的眼球运动障碍进行了比较。得出以下结论:(1)依赖于眼位的自发漂移主要由“眼球侧推”产生,即眼球运动系统内的一种紧张性偏差,其可能有多种来源。(2)视觉 - 前庭刺激期间眼球运动反应的异常和不对称不能仅由这种自发漂移及其与其他正常眼球运动的相互作用来解释。相反,Wallenberg综合征中一些结构和通路受损,这些结构和通路介导对视觉引导的缓慢眼球运动的小脑控制很重要的视觉和/或运动信号。(3)这些通路的损伤发生在延髓外侧,因为MRI结果显示大多数患者的小脑很少受累,但对于下行至小脑的下脚中哪些纤维可能中断,尚无明确结论。

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