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模仿急性外周前庭病的脑桥病变

Pontine lesions mimicking acute peripheral vestibulopathy.

作者信息

Thömke F, Hopf H C

机构信息

Department of Neurology, University of Mainz, Germany.

出版信息

J Neurol Neurosurg Psychiatry. 1999 Mar;66(3):340-9. doi: 10.1136/jnnp.66.3.340.

Abstract

OBJECTIVES

Clinical signs of acute peripheral vestibulopathy (APV) were repeatedly reported with pontine lesions. The clinical relevance of such a mechanism is not known, as most studies were biased by patients with additional clinical signs ofbrainstem dysfunction.

METHODS

Masseter reflex (MassR), blink reflex (BlinkR), brainstem auditory evoked potentials (BAEPs), and DC electro-oculography (EOG) were tested in 232 consecutive patients with clinical signs of unilateral APV.

RESULTS

Forty five of the 232 patients (19.4%) had at least one electrophysiological abnormality suggesting pontine dysfunction mainly due to possible vertebrobasilar ischaemia (22 patients) and multiple sclerosis (eight patients). MassR abnormalities were seen in 24 patients, and EOG abnormalities of saccades and following eye movements occurred in 22 patients. Three patients had BlinkR-R1 abnormalities, and one had delayed BAEP waves IV and V. Clinical improvement was almost always (32 of 34 re-examined patients) associated with improvement or normalisation of at least one electrophysiological abnormality. Brain MRI was done in 25 of the 44 patients and confirmed pontine lesions in six (two infarcts, three inflammations, one tumour).

CONCLUSIONS

Pontine dysfunction was suggested in 45 of 232 consecutive patients with clinical signs of APV on the basis of abnormal electrophysiological findings, and was mainly attributed to brainstem ischaemia and multiple sclerosis. The frequency of pontine lesions mimicking APV is underestimated if based on MRI established lesions only.

摘要

目的

急性外周前庭病变(APV)的临床体征曾多次被报道与脑桥病变有关。由于大多数研究受到伴有脑干功能障碍其他临床体征患者的影响,这种机制的临床相关性尚不清楚。

方法

对232例连续出现单侧APV临床体征的患者进行了咬肌反射(MassR)、瞬目反射(BlinkR)、脑干听觉诱发电位(BAEP)和直流电眼震图(EOG)检测。

结果

232例患者中有45例(19.4%)至少有一项电生理异常,提示脑桥功能障碍,主要原因可能是椎基底动脉缺血(22例)和多发性硬化(8例)。24例患者出现MassR异常,22例患者出现扫视和跟踪眼动的EOG异常。3例患者出现BlinkR-R1异常,1例患者BAEP波IV和V延迟。临床改善几乎总是(34例复查患者中的32例)与至少一项电生理异常的改善或恢复正常相关。44例患者中有25例进行了脑部MRI检查,其中6例证实有脑桥病变(2例梗死、3例炎症、1例肿瘤)。

结论

根据异常电生理结果,232例连续出现APV临床体征的患者中有45例提示脑桥功能障碍,主要归因于脑干缺血和多发性硬化。如果仅基于MRI确定的病变,模仿APV的脑桥病变发生率被低估。

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