Rosiglitazone-Induced Proptosis

Comment. Ocular neuromyotonia affects the extraocular muscles either individually or in combination, causing episodic diplopia that develops either spontaneously or after gaze in the direction of action of the affected muscle. Electromyography suggests a neurogenic basis for the movements. The tonic contractions are thought to result from the spontaneous discharge of unstable neurons, which are transmitted to adjacent neurons by ephaptic transmission. Consistent with the theory of axonal instability, membranestabilizing agents such as carbamazepine are effective. To our knowledge, this is the first report of a patient whose ocular neuromyotonia was caused by a stroke, as well as the first in which the responsible lesion was intramedullary. Our patient’s lesions were predominantly contralateral to the side of his neuromyotonia, with only 1 small lesion at the ipsilateral mesodiencephalic junction. While we cannot determine which, if any, of his lesions caused the neuromyotonia of his right eye, we note that his lesions spared the nuclei and intramedullary fascicles of the right third nerve. We conclude that ocular neuromyotonia can result from purely intramedullary lesions, without the involvement of the lower motor neuron.