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Acute thalamic esotropia

Cerebrovascular and Neuro-ophthalmology Services, Department of Neurology, St. Louis University School of Medicine, St. Louis, MO.

Three men developed acute esotropia, stupor, and impaired upward gaze. Vestibulo-ocular stimulation showed that the adducted eye remained immobile while the fellow eye responded normally. The alteration of consciousness, the long-tract neurologic signs, and the esotropia quickly resolved. Upgaze paresis and brief bursts of convergence-retraction nystagmus were the major residual signs. Imaging techniques demonstrated lesions of the contralateral posterior thalamus in each patient. Several mechanisms are proposed to explain the acute esotropia. Impairment of monocular projections in the contralateral posterior thalamus could disinhibit neurons in the oculomotor complex, or ischemia of inputs to neurons involved with vergence control in the midbrain could result in tonic activation of the medial rectus. The clinical and radiographic findings are consistent with infarction in the territory of penetrating branches of the basilar-communicating (mesencephalic) artery. Embolism to the top of the basilar artery is presumed to be the precipitating event.

Address correspondence and reprint requests to Dr. C.R. Gomez, Cerebrovascular Disease Service, Department of Neurology, 3660 Vista, # 305, St. Louis, MO 63110.

Presented in part at the thirty-ninth annual meeting of the American Academy of Neurology, New York, NY, April 1987.

Received November 18, 1987. Accepted for publication in final form April 28, 1988.

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