Objective: Acquired pendular nystagmus occurs mainly in multiple sclerosis (MS) and focal brainstem lesions. In the later case, it is part of the syndrome of oculopalatal tremor. Even though pathophysiology of acquired pendular nystagmus has been clearly characterized experimentally in both etiologies, there is a persisting ambiguity in clinical literature, which leads one to consider both clinical conditions as a common entity. The objective of our work was to compare in a prospective study clinical features, eye movement recording, and functional consequences of acquired pendular nystagmus in 14 patients with oculopalatal tremor and 20 patients with MS.
Methods:Besides complete neurologic evaluation, evaluation of visual function, 3-dimensional eye movement recording, and functional scores of the Visual Function Questionnaire were recorded.
Results:One patient with oculopalatal tremor and 15 patients with MS disclosed signs of optic neuropathy. The nystagmus in the oculopalatal group showed significant larger mean amplitude (8 deg vs 1 deg), higher mean peak velocity (16 deg/s vs 6 deg/s), lower mean frequency (1-3 Hz vs 4-6 Hz), and larger asymmetry and irregularity of ocular oscillations compared to the MS group. The vision-specific health-related quality of life was more deteriorated in the oculopalatal tremor group than in the MS group.
Conclusions:This study emphasizes the need to consider acquired pendular nystagmus in MS and oculopalatal tremor as 2 different clinical entities. This is of particular importance regarding the future evaluation of potential specific effects of pharmacologic agents. Pendular nystagmus corresponds to an enduring to and fro eye oscillation without resetting quick phases. The most common causes of acquired pendular nystagmus (APN) are multiple sclerosis (MS) and focal brainstem lesions. In the later case, APN arises as a feature of the oculopalatal tremor (OPT) syndrome. OPT develops weeks, months, or even years after a single brainstem or cerebellar lesion, 1-3 in most cases a hemorrhagic stroke. It results in synchronized low-frequency tremor of the eyes and palate or other orofacial motor territories and is associated with an hypertrophic degeneration of the inferior olivary nucleus (ION), 2 leading to T2 hypersignal on MRI.1 This condition is triggered by interruption of the GuillainMollaret triangle.
2,4Even though both etiology and clinical aspects appear different in APN associated with MS or OPT, 5 many neurologists are not familiar with the distinct pathogenesis and characteristics of nystagmus in these 2 syndromes. Furthermore, some pharmacologic studies and nystagmus treatment reviews did not differentiate their results according to the underlying etiology. 6 -10 In this study, we aimed to compare clinical features, eye movement recordings, and functional consequences of APN in patients with MS or OPT. The main objective was to emphaFrom the INSERM U1028,