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Laurence Jasse, Alain Vighetto, Sandra Vukusic, Denis Pelisson, Laure Pisella, Caroline Tilikete; Unusual mechanism of monocular oscillopsia. Journal of Vision 2008;8(6):644. doi: 10.1167/8.6.644.
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Among neuro-ophthalmologic manifestations of multiple sclerosis (MS), eye movement (EM) disorders are frequent. Internuclear ophthalmoplegia (INO), isolated ocular-motor palsy, gaze-evoked nystagmus and pendular nystagmus are the most frequently reported EM disorders. Pendular nystagmus is characterized by involuntary to-and-fro oscillation of eyes, usually horizontal and conjugate. Monocular nystagmus has only been reported in the abducting eye of INO. We present two cases of monocular oscillopsia (MO) due to an unusual monocular nystagmus of pendular aspect. The first patient is a 40 year-old woman who experienced partially regressive VI nerve paresis as the first manifestation of relapsing-remitting MS. She complained of right eye paroxysmal oscillopsia. Neuro-ophthalmologic examination revealed normal visual acuity, visual field, contrast and colour discrimination. EM examination showed right esotropia and monocular horizontal tremor of right eye, triggered by abduction. There was no paresia or slowing of left adducting eye. EM recording showed a 5 Hz, 3° amplitude tremor of right eye, induced by abduction. The second patient is a 42 year-old woman whose initial complaint was MO of adducting left eye. EM examination showed left INO, with slowing of adduction and jerk nystagmus of the abducting eye in right-sided gaze. There was also a monocular horizontal tremor of adducting left eye. She lately developed acute left-sided optic neuritis. Recent EM recording showed a persisting 6 Hz, 2° amplitude tremor of adducting left eye. MO is usually reported either as a sign of posterior or anterior INO, or as a peripheral paroxysmal disorder such as superior oblique myokimia. These mechanisms can not explain our two cases which are both triggered by a specific eye position and disclose a paresia in the same eye direction. Different mechanisms are discussed: paroxysmal manifestations due to peripheral hyperexcitability or evolution of a central monocular paresia.
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