Gresty M A, Ell J J, Findley L J
J Neurol Neurosurg Psychiatry. 1982 May;45(5):431-9. doi: 10.1136/jnnp.45.5.431.
Investigations were made of 16 patients with acquired pendular nystagmus and a further 32 cases reported in the literature were reviewed. Amongst our own patients two thirds had multiple sclerosis, almost one third a cerebrovascular accident or angioma and two had optic atrophy with squint. The nystagmus took forms which could be monocular or binocular, conjugate or disconjugate and could involve movements about single or multiple axes. Spectral analysis was used to characterise the amplitude and frequency of the movements and to estimate the degree of relationship (coherence) between movements of the two eyes or between movements of one eye about several axes. The oscillations ranged in frequency from 2·5 Hz to 6 Hz, with typical amplitudes between 3° and 5°. In a given patient all oscillations, regardless of plane, were highly synchronised. Somatic tremors of the upper limb, face and palate associated with the nystagmus were often at similar frequencies to the eye movement. The other ocular signs common to all our patients were the presence of squint with failure of convergence. Most patients also had skew deviation or internuclear ophthalmoplegia or both. The major oculomotor systems, that is, saccades, pursuit, optokinetic and vestibulo-ocular reflexes could be intact. It is inferred that the mechanism responsible for the pendular nystagmus lies at a level which is close to the oculomotor nuclei so that it can have monocular effects but is not part of the primary motor pathways. It is possible that this mechanism normally subserves maintenance of conjugate movement and posture of the eyes. The periodicity of the nystagmus is likely to arise from instability in a certain type(s) of neurone, for the associated somatic tremors have similar characteristics and yet involve very different neuronal muscular circuitry. Prognosis for cessation of the nystagmus is poor. In five patients with multiple sclerosis it was suppressed by intravenous hyoscine with, however, unacceptable subsequent side effects.
对16例获得性摆动性眼球震颤患者进行了研究，并对文献中报道的另外32例病例进行了回顾。在我们自己的患者中，三分之二患有多发性硬化症，近三分之一患有脑血管意外或血管瘤，2例患有伴有斜视的视神经萎缩。眼球震颤的形式可以是单眼或双眼的、共轭或非共轭的，并且可以涉及围绕单个或多个轴的运动。频谱分析用于表征运动的幅度和频率，并估计双眼运动之间或一只眼睛围绕几个轴的运动之间的相关程度（相干性）。振荡频率范围为2.5赫兹至6赫兹，典型幅度在3°至5°之间。在给定患者中，所有振荡，无论平面如何，都高度同步。与眼球震颤相关的上肢、面部和腭部的躯体震颤频率通常与眼球运动相似。我们所有患者共有的其他眼部体征是存在斜视且集合功能障碍。大多数患者还存在斜向偏斜或核间性眼肌麻痹或两者皆有。主要的眼球运动系统，即扫视、追踪、视动和前庭眼反射可能是完整的。据推测，导致摆动性眼球震颤的机制位于接近眼球运动核的水平，因此它可以产生单眼效应，但不是初级运动通路的一部分。这种机制可能正常情况下有助于维持双眼的共轭运动和姿势。眼球震颤的周期性可能源于某种类型神经元的不稳定性，因为相关的躯体震颤具有相似的特征，但涉及非常不同的神经肌肉回路。眼球震颤停止的预后很差。在5例多发性硬化症患者中，静脉注射东莨菪碱可抑制眼球震颤，但随后出现了不可接受的副作用。
