Abstract
Although see-saw nystagmus has been reported in multiple sclerosis (MS) (1), there is no previous report of a patient presenting with this finding. A 33-year-old woman reported a 2-day history of oscillopsia. She had no other neurologic or systemic symptoms. On examination, the eyes were aligned with full ductions. The patient had characteristic pendular see-saw nystagmus that increased on left gaze. The velocity of the nystagmus was equal in both directions. The OD ascended and intorted, whereas the OS descended and extorted; then the OD descended and extorted, whereas the OS ascended and intorted. Otherwise, the ophthalmologic and neurologic examination was unremarkable. Total blood count, erythrocyte sedimentation rate, glucose, urea, electrolytes, and a collagen vascular disease profile were normal. Lumbar puncture revealed a normal opening pressure and cerebrospinal fluid formula, but isoelectric focusing showed three positive IgG oligoclonal bands; none was detected from a simultaneous serum sample. Brain magnetic resonance imaging showed a linear area of signal change in white matter adjacent to the body of left lateral ventricle (Fig. 1A) and in the deep white matter of the left frontal lobe (Fig. 1B). The combination of clinical, cerebrospinal fluid, and imaging findings suggested a diagnosis of multiple sclerosis.FIG. 1: A. Axial T2-weighted magnetic resonance imaging shows linear high signal in the white matter adjacent to the body of the left lateral ventricle (arrow). B. Coronal FLAIR magnetic resonance imaging shows high signal in the deep white matter of the left frontal lobe (arrow).The exact mechanism of see-saw nystagmus is still not known. Its frequent association with chiasmal and parasellar lesions initially led to speculation that see-saw nystagmus was related to a disturbance in visual input. Recent evidence suggests that see-saw nystagmus is caused by dysfunction of the rostral brainstem (2). A disturbance in the interstitial nucleus of Cajal, a small collection of neurons located adjacent to medial longitudinal fasciculus in the midbrain tegmentum, is often implicated (2). Soupramanien Sandramouli, FRCS, FRCOphth Hani T. Benamer, MRCP, PhD Mark Mantle, MRCP, FRCR Randhir Chavan, MS Wolverhampton and Midland Counties Eye Infirmary and Departments of Neurology and Radiology; New Cross Hospital; Wolverhampton, England; E-mail: [email protected]
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