Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present here a case with various physical and neuropsychiatric symptoms caused by the administration of carbamazepine. The patient suffering from right ophthalmic neuralgia showed fever, eczema, erythema, lymphoadenopathy, eosinophilia, vomiting, headache, dizziness, nystagmus, and various mental disorders which consisted of emotional instability, personality change, delusions of reference and persecution, depressive state, and hyperventilation syndrome during the administration of carbamazepine. The physical symptoms in the present case were conformable to the side effect of carbamazepine. The mental disorders appeared in a few days from the start of carbamazepine administration and disappeared after the discontinuation of the administration of this drug without antipsychotic therapy and have never relapsed until now. The mental disorders and the physical symptoms were in parallel with their clinical course. This kind of mental disorders induced by carbamazepine has not yet been reported.
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PMID:Mental disorders induced by carbamazepine. 236 93

Trigeminal neuralgia, facial spasm, tinnitus, vertigo, and glossopharyngeal neuralgia are believed to be the symptoms complex of hyperactive dysfunction of the cranial nerve caused by vascular cross compression at the root entry (exit) zone of the appropriate nerve. Posterior cranial fossa approach for the neurovascular decompression was enhanced by Jannetta et al (1975). From their experiences of surgery, they emphasized that these symptoms were relieved by surgery. In this report, we will discuss the etiology of the disease, the neurotological examination, the angiographic findings, the operative findings and results in a series of 10 patients who have undergone neurovascular decompression. The series consisted of 4 cases with trigeminal neuralgia, 5 cases with facial spasm, and 1 case with paroxysmal tinnitus accompanied by facial spasm. The postoperative progress in these all patients was excellent and relieved of the symptoms. There was neither mortality nor any significant complication. We stress that the neurovascular decompression surgery is now well justified as the definite treatment for the trigeminal neuralgia and facial spasm, because the surgery can be performed easily and safely by the neurosurgeons. The indication of the neurovascular decompression for the acoustic nerve and glossopharyngeal nerve is still controversial. In our own case, tinnitus was paroxysmal and complicated with facial spasm, not synchronous with facial spasm, but with nystagmus. This selective synchronism between tinnitus and nystagmus is a particular feature of our clinical instance. This particular clinical experience may provide some highly significant suggestions in considering the applicability of neurovascular decompression to the acoustic nerve.
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PMID:[Surgical management of trigeminal neuralgia, hemifacial spasm, paroxysmal tinnitus and nystagmus by neurovascular decompression]. 667 36