Abstract

Neurological manifestation of metronidazole toxicity include neuropathy and encephalopathy. We report a 67-year-old man with progressive painful paresthesias involving all the four limbs of 3 weeks' duration before admission. He had been treated with metronidazole and cephalosporin for 10 weeks for a hepatic abscess. Five weeks after the symptom onset, he complained of dysarthria and limb ataxia. Magnetic resonance imaging revealed signal abnormalities in the splenium of the corpus callosum and bilateral dentate nuclei. A few hours after brain imaging, the patient exhibited excessive diaphoresis and fluctuation in blood pressure, which resolved within several hours after discontinuation of metronidazole. Whereas his speech returned to near normal within approximately 1 week, a burning sensation was not completely relieved, even 6 months after discharge.

Pure trigeminal motor neuropathy is characterized by trigeminal motor weakness without signs of trigeminal sensory or other cranial nerve involvement. We describe a 63-year-old woman with progressive weakness and atrophy of the left masticatory muscles. She had no sensory disturbance. The diagnosis of pure trigeminal motor neuropathy was made on the basis of clinical and electrophysiologic studies. Magnetic resonance imaging of the brain revealed enhancement of the enlarged mandibular branch of the trigeminal nerve coursing through the left foramen ovale. Our observations suggest that pure trigeminal motor neuropathy can be induced by a tumor.

Isolated peripheral facial and abducens nerve palsy could theoretically be caused by a caudal pontine infarction, but as far as we know, there has been no published case history which has demonstrated this point. We describe the cases of two hypertensive patients who showed combined peripheral facial and abducens nerve palsy without other neurologic symptoms or signs. Other than hypertension, there was no identifiable etiology. Magnetic resonance imaging demonstrated compatible isolated ipsilateral ischemic infarction of the caudal tegmental pons. The present cases indicate that a well-placed small pontine infarction can cause isolated peripheral facial and abducens nerve palsy.

No abstract