Cases reported "Myoclonus"

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1/7. Methylbromide intoxication: a case report.

    This work focuses on the neurophysiological features in a patient with action myoclonus and mental deterioration following methylbromide intoxication. The patient is a 28-year-old man, without respiratory distress or exposure to other toxics. myoclonus improved with polytherapy (clonazepam, 5-HT, carbidopa, GABA). The neurophysiological and neuropsychological evidence in this patient suggests a possible double site of action of methylbromide at cortical and subcortical levels.
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2/7. Pathological findings in a case of hypoxic myoclonus treated with 5-hydroxytryptophan and a decarboxylase inhibitor.

    A 72-year-old woman suffered a respiratory arrest following intoxication with barbiturates. Her examination 27 months after the anoxic incident revealed involuntary jerks of trunk and limb muscles triggered by willed movements. On a regimen of 1 g L-5-HTP and 100 mg l-alpha-methyldopa hydrazine (carbidopa), action myoclonus disappeared completely. This medication had to be discontinued because of a regressive hysterical reaction. Two months later, she was found unconscious; resuscitation efforts were unsuccessful. autopsy showed death was caused by choking on food. Coronal slices of the cerebral hemispheres and transverse section of the brainstem and cerebellum revealed no lesion. No evidence of hypoxic damage could be demonstrated in the cerebral cortex, hippocampus, striatum, pallidum, subthalamus, thalamus, or other diencephalic structures. In the caudal half of the midbrain tegmentum, a marked astrocytic reaction of some duration was encountered in the lateral parts of the supratrochlearis nucleus, the lateral subnucleus of the mesencephalic gray, and the immediately adjacent cuneiform and subcuneiform nuclei. In the former nucleus, sites of presumed nerve cell disintegration were found, but the neuronal populations of this nucleus and of the other raphe nuclei were well maintained. The other brainstem structures and the cerebellum were normal. Our neuropathological findings suggest that hypoxic myoclonus (a) does not seem to be explained by demonstrable neuronal loss in motor structures, such as cerebellum, thalamus, or basal ganglia and (b) does not appear to be causally related to a detectable reduction in the serotonin-containing neurons of the brain but rather to a functional derangement of anatomically intact serotonergic pathways originating perhaps from other, as yet unidentified, damaged neuronal structures.
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3/7. A case of lithium intoxication with downbeat vertical nystagmus.

    lithium carbonate has recently been used in the treatment of manic diseases. However, since the marginal range between therapeutic and toxic doses is very narrow, close attention should be paid to the development of adverse reactions in its application. Lithium intoxication is manifested by neurological symptoms. Neurotological tests were performed on a patient with lithium intoxication that occurred in the course of psychiatric treatment of mania. The observed sequelae included marked downbeat vertical nystagmus and truncal ataxia. The main lesions in the present case were considered to be located in the cerebellum. Close observation, including neurotological tests, is of greatest importance because in cases of lithium intoxication the development of cerebellar as well as brainstem disorders must not be overlooked.
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keywords = intoxication
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4/7. Postmortem studies on posthypoxic and post-methyl bromide intoxication: case reports.

    In two cases of action myoclonus following hypoxic or shock encephalopathy, neuropathological examination disclosed mild or moderate scattered changes involving thalamus, griseum centrale mesencephali, and nucleus centralis superior. Other areas were affected only in one of these cases (striatum, nucleus subthalamicus or hippocampus, nuclei pontis, and cerebellar cortex). In another case (an alcoholic patient), the changes, which involved only corpus mamillare and thalamus, were those of Wernicke-Korsakoff encephalopathy. In one case of oscillatory myoclonus following septic shock, there were marked cerebellar changes involving deep nuclei and mild abnormalities in the thalamus and inferior olive. The last case of action myoclonus following acute methyl bromide intoxication was characterized by marked changes in the inferior colliculi and moderate or mild abnormalities of thalamus, griseum centrale mesencephali, nucleus centralis superior, nucleus reticularis tegmenti pontis, nuclei pontis, and dentatus. The findings are compared with the data of seven previously reported neuropathological examinations in action myoclonus following hypoxic encephalopathy.
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5/7. carbamazepine intoxication with negative myoclonus after the addition of clobazam.

    We report a case a carbamazepine (CBZ) intoxication with negative myoclonus that occurred 4 weeks after clobazam (CLB) had been added to a stable regimen of CBZ and topiramate (TPM). Both CBZ and CBZ-epoxide (CBZ-E) blood levels were elevated, and the symptoms resolved quickly when CBZ dosage was reduced and CLB discontinued. CLB was reintroduced a year later with the patient's consent, and the time course of the interaction was studied: CBZ and CBZ-E levels increased slowly over 12 days. The interaction is thus probably related to the progressive increase in Nor-CLB.
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6/7. carisoprodol-induced myoclonic encephalopathy.

    CASE REPORT: A 39-year-old man ingested 35 g carisoprodol. He developed agitation, tachycardia, myoclonus, and coma. The blood carisoprodol was 71 micrograms/mL; the meprobamate was 26 micrograms/mL. DISCUSSION: carisoprodol overdose is thought to induce simple central nervous system depression. This case demonstrates a severe overdose with symptoms more consistent with myoclonic encephalopathy. A review of cases presenting to the san francisco Division of the california Poison Control System during 1997 suggests that carisoprodol is more commonly associated with agitation and bizarre movement disorders than the current literature suggests. The pharmacology and potential mechanisms of toxicity are discussed. CONCLUSION: Agitation, hypertonia, and a myoclonic encephalopathy may be seen with significant carisoprodol intoxication.
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7/7. A neuropathological case-study of myoclonus epilepsy.

    A 28-year-old male of progressive myoclonus epilepsy was reported, who had showed a gradual progression in myoclonus, mental retardation and cerebellar symptoms, and had been treated with a large dosage of diphenylhydantoin. Neuropathologically, slight degenerative changes of the cerebrl cortex, especially in the IV layer, the external pallidum, and the dentate and olivary nuclei were observed. The most obvious change was diffuse reduction of Purkinje's and granular cells in the cerebellum. A congenital cyst was found with surrounding gliosis in the central tegmental tract of the pons. A significant relationship between myoclonus and the cyst was proposed, and furthermore, influences of diphenylhydantoin intoxication on the clinicopathological development of myoclonus epilepsy were emphasized.
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ranking = 0.2
keywords = intoxication
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