Thömke Frank, Urban Peter P, Marx Jürgen J, Mika-Grüttner Annette, Hopf Hanns C
Neurologische Universitätsklinik, Johannes-Gutenberg Universität, Langenbeckstr. 1, 55101 Mainz, Germany.
J Neurol. 2002 Nov;249(11):1556-62. doi: 10.1007/s00415-002-0894-y.
Small brainstem infarctions are increasingly recognized as a cause of isolated ocular motor and vestibular nerve palsies in diabetic and/or hypertensive patients. This raises the question whether there are also isolated 7(th) nerve palsies due to pontine infarctions in patients with such risk factors for the development of cerebrovascular diseases.
Over an 11-year-period, we retrospectively identified 10 diabetic and/or hypertensive patients with isolated 7(th) nerve palsies and electrophysiological abnormalities indicating pontine dysfunction. All patients had examinations of masseter and blink reflexes, brainstem auditory evoked potentials, direct current electro-oculography including bithermal caloric testing, and T1- and T2-weighted MRI (slice thickness: 4-7 mm).
Electrophysiological abnormalities on the side of the 7(th) nerve palsy included delayed masseter reflex latencies (4 patients), slowed abduction saccades (4 patients), vestibular paresis (2 patients), and abnormal following eye movements (2 patients). Electrophysiological abnormalities were always improved or normalized at re-examination, which was always associated with clinical improvement. MRI revealed an ipsilateral pontine infarction in 2 patients. Another 2 had bilateral hyperintense intrapontine lesions, and one an ipsilateral cerebellar infarction.
Simultaneous improvement or recovery of abnormal clinical and electrophysiological findings strongly indicated that both were caused by the same actual pontine lesions. A 7(th) nerve palsy may be the only clinical sign of a pontine infarction in diabetic and/or hypertensive patients. Such mechanism may be underestimated if based on MRI only.
小脑干梗死越来越被认为是糖尿病和/或高血压患者孤立性动眼神经和前庭神经麻痹的一个病因。这就引出了一个问题，即对于有脑血管疾病发生风险因素的患者，是否也存在因脑桥梗死导致的孤立性面神经麻痹。
在11年的时间里，我们回顾性地确定了10例患有孤立性面神经麻痹且伴有提示脑桥功能障碍的电生理异常的糖尿病和/或高血压患者。所有患者均接受了咬肌反射和瞬目反射检查、脑干听觉诱发电位、包括冷热试验的直流电眼震图检查，以及T1加权和T2加权MRI（层厚：4 - 7毫米）。
面神经麻痹侧的电生理异常包括咬肌反射潜伏期延长（4例患者）、外展扫视减慢（4例患者）、前庭功能减退（2例患者）以及跟踪眼动异常（2例患者）。复查时电生理异常总是得到改善或恢复正常，且这总是与临床改善相关。MRI显示2例患者同侧脑桥梗死。另外2例有双侧脑桥内高信号病变，1例有同侧小脑梗死。
临床和电生理异常表现同时改善或恢复强烈表明两者是由同一实际脑桥病变引起的。面神经麻痹可能是糖尿病和/或高血压患者脑桥梗死的唯一临床体征。如果仅基于MRI，这种机制可能被低估。
