Spontaneous opening and closing of both eyes usually occurs in the normal awake state, unless a deliberate and voluntary attempt is made to open only one eye. We present a rare case of a male patient who was unable to open both eyes simultaneously after bilateral posterior cerebral artery infarction. He was able to close both eyes voluntarily. However, he was unable to keep both eyes open simultaneously and either the right or left eye remained closed. Upon a verbal command to open both eyes, the opened eye closed and the contralateral eye opened. When the closed eye was forced open, the opened eye closed. We thus presented a case of right-left dissociation of voluntary eyelid opening following bilateral posterior cerebral artery infarction, which was treated with botulinum toxin type A injection. Differential diagnosis to other movement disorders of the eyelids was discussed.
To evaluate the pathophysiological mechanism of hemifacial spasm (HFS), we performed electrophysiological examinations, such as supraorbital nerve stimulation with orbicularis oris muscle recording and lateral spread tests, after suppressing the patient's central nervous system by administering intravenous diazepam.
Six patients with HFS were recruited. Supraorbital nerve stimulation with orbicularis oris muscle recording and the lateral spread test were performed, followed by intravenous application of 10 mg diazepam to achieve facial motor neuron suppression. Subsequently, we repeated the two electrophysiological experiments mentioned above at 10 and 20 minutes after the patients had received the diazepam intravenously.
Orbicularis oris muscle responses were observed in all patients after supraorbital nerve stimulation and lateral spread tests. After the diazepam injection, no orbicularis oris muscle response to supraorbital nerve stimulation was observed in one patient, and the latencies of this response were evident as a slowing tendency with time in the remaining five patients. However, the latencies of the orbicularis oris muscle responses were observed consistently in all patients in the lateral spread test.
Our results suggest that ectopic excitation/ephaptic transmission contributes to the pathophysiological mechanisms of HFS. This is because the latencies of the orbicularis oris muscle responses in the lateral spread test were observed consistently in the suppressed motor neuron in our patients.
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