A case of opsoclonus.
Motoyuki Hashiba, Jun Hondo, Shunkichi Baba
Abstract
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Motoyuki Hashiba, Jun Hondo, Shunkichi Baba
Abstract
Open-access reader
The patient was a 22-year-old male student who developed dizziness and unsteadiness of gait. Neuro-otological examination two weeks later showed transient spontaneous down beat nystagmus, rotary nystagmus on bilateral gaze, and rebound nystagmus. The cold caloric test was normal, and the OKP showed a slightly irregular pattern under high speed stimulation. The pursuit movements of the eyes were slightly saccadic. He also had truncal ataxia without dysmetria of the extremities and no other neurologic abnormalities. Cerebro-spinal fluid was clear with no cells and a protein level of 38 mg/ 100 ml. CT scan was normal. Three weeks after onset, rotary gaze nystagmus and rebound nystagmus were absent. He developed intermittently irregular oscillations of the eyes with horizontal, vertical, and rotary components (opsoclonus) with oscillopia. He had no myoclonuc jerks elsewhere. His opsoclonus was precipitated by hyperextension of the neck and by vibration applied to the neck muscles. We observed that the caloric response at this time was suppressed intermittently by the opsoclonus, but the OKP was normal with DP toward the left. Five months after onset, he did not complain of dizziness, but opsoclonus persisted. CAG and VAG were performed but showed no abnormality. The opsoclonus precipitated by hyperextension of the neck disappeared 12 months after onset. The neuro-otological examinations of patients with opsoclonus are discussed. In our patient, opsoclonus was the only type of nonnystagmic abnormal ocular movements (NAOMs). We could not observed other NAOMs; ocular dysmetria, flutter-like oscillations of eyes, ocular myoclonus and lightning eye movements. Opsoclonus is caused by different abnormality in ocular control system from the other NAOMs.
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The patient was a 22-year-old male student who developed dizziness and unsteadiness of gait. Neuro-otological examination two weeks later showed transient spontaneous down beat nystagmus, rotary nystagmus on bilateral gaze, and rebound nystagmus. The cold caloric test was normal, and the OKP showed a slightly irregular pattern under high speed stimulation. The pursuit movements of the eyes were slightly saccadic. He also had truncal ataxia without dysmetria of the extremities and no other neurologic abnormalities. Cerebro-spinal fluid was clear with no cells and a protein level of 38 mg/ 100 ml. CT scan was normal. Three weeks after onset, rotary gaze nystagmus and rebound nystagmus were absent. He developed intermittently irregular oscillations of the eyes with horizontal, vertical, and rotary components (opsoclonus) with oscillopia. He had no myoclonuc jerks elsewhere. His opsoclonus was precipitated by hyperextension of the neck and by vibration applied to the neck muscles. We observed that the caloric response at this time was suppressed intermittently by the opsoclonus, but the OKP was normal with DP toward the left. Five months after onset, he did not complain of dizziness, but opsoclonus persisted. CAG and VAG were performed but showed no abnormality. The opsoclonus precipitated by hyperextension of the neck disappeared 12 months after onset. The neuro-otological examinations of patients with opsoclonus are discussed. In our patient, opsoclonus was the only type of nonnystagmic abnormal ocular movements (NAOMs). We could not observed other NAOMs; ocular dysmetria, flutter-like oscillations of eyes, ocular myoclonus and lightning eye movements. Opsoclonus is caused by different abnormality in ocular control system from the other NAOMs.
Key concepts: Opsoclonus, Dysmetria, Nystagmus, Medicine, Saccadic masking, Audiology, Ataxia, Eye movement