Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013421 (dystonia)
 8,418 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

3-Nitropropionic acid (3-NPA)--a suicide inhibitor of succinate dehydrogenase--is a widely distributed plant and fungal neurotoxin known to induce a damage to basal ganglia, hippocampus, spinal tracts and peripheral nerves in animals. Recent reports from Northern China indicate that 3-NPA is also likely to be responsible for the development of putaminal necrosis with delayed dystonia in children after ingestion of mildewed sugar cane. This article discusses the role of 3-NPA in the causation of the disease in China, its neurotoxic effects in animals and the potential role for this compound as a probe of selective neuronal vulnerability.
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PMID:3-Nitropropionic acid-exogenous animal neurotoxin and possible human striatal toxin. 178 16

A 39-year-old man showed a combination of severe parkinsonism and progressive dystonia following attempted suicide with sodium cyanide. Computed tomography (CT) scan showed bilateral lucencies in the putamen and external globus pallidus. The topography of lesions on CT scan closely correlated with the pathological findings described in a previous report of cyanide-induced parkinsonism. This is the first reported case of cyanide intoxication with delayed-onset dystonia.
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PMID:Clinical and CT scan findings in a case of cyanide intoxication. 273 10

Forty-seven railroad workers who were exposed to polychlorinated phenols, including dioxin (TCDD), during 1979 while cleaning up the chemical spillage following damage to a tank car filled with these chemicals were followed medically for the subsequent 6 years. Two committed suicide. The initial neurological complaints included a sense of fatigue and muscle aching, both of which have been reported in other individuals following dioxin exposure. On detailed neurological examination in December, 1985, 24 of 45 had dystonic writer's cramp and/or other action dystonias of the hands. None of the involved individuals had a family history of dystonia, and all 24 dated the onset of the dystonia to the first 2 to 3 years subsequent to their toxic exposure. The dystonias varied in severity but were usually mild. No other types of dystonic involvement were recognized. Thirty-five of the 45 individuals also manifested postural and terminal intention tremor which resembled benign essential tremor. None of the involved individuals had a family history of tremor, and all 35 of those affected dated the onset of the tremor to some time subsequent to their toxic exposure. Forty-three of 45 patients had histories and findings suggestive of peripheral neuropathy. This is the first report relating any type of dystonia to prior dioxin exposure and the first report relating action dystonia, such as dystonic writer's cramp, and postural/terminal intention tremor, to toxic exposure of any type.
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PMID:Dystonia and tremor following exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin. 284 55

Psychic distress is often expressed in the form of physical pain or disease, but the converse also occurs. Illnesses with an organic aetiology are sometimes misdiagnosed as psychogenic. We describe three patients who developed rare forms of acute drug-induced dystonia when treated with antipsychotic drugs. All three cases were initially misdiagnosed as "hysteria" because the patients had psychiatric illnesses and because the symptoms were bizarre and became worse when the patients became very anxious. Furthermore, if the patients were helped to relax the symptoms disappeared for a moment. One of the patients developed dystonia 24 hours after ingestion of 750 mg tetrabenazine in an attempt at suicide. Another patient who had HIV/AIDS developed severe dystonia after receiving only 2 mg haloperidol by mouth. The clinical presentation, treatment, and possible mechanisms of the pathophysiology of acute drug-induced dystonia are briefly reviewed.
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PMID:[Drug-induced dystonia misinterpreted as hysteria]. 864 96

Neuroleptics were the first modern class of pharmacotherapeutic agents available for the treatment of schizophrenia. Although they were effective in reducing florid psychotic symptoms, up to 90% of treated individuals subsequently developed extrapyramidal symptoms (EPS) (akathisia, dystonia, or parkinsonism), and about 20% developed tardive dyskinesia (TD). When clozapine became commercially available for treatment-resistant and treatment-intolerant (i.e., prone to EPS and TD) schizophrenic individuals, it became apparent that an antipsychotic need not induce motor side effects to be efficacious in reducing the symptomatology of schizophrenia. Sociodemographic, behavioral, and clinical predictors of TD are useful in identifying a subset of schizophrenic individuals who would benefit from treatment with clozapine, the prototype atypical antipsychotic whose efficacy and motor side effect profile are superior to those of chlorpromazine. This favorable motor side effect profile of clozapine contributes to improved patient outcomes by reducing noncompliance, substance abuse, and suicide, resulting in improved quality of life and savings on health care costs.
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PMID:Effects of clozapine therapy in schizophrenic individuals at risk for tardive dyskinesia. 954 36

A 14-year-old female attempted suicide by ingesting the organophosphate methyl parathion. A severe acute poisoning developed with the characteristic symptomatology: muscarinic, nicotinic and neurologic, as well serum cholinesterase activity decreased 88%. An extrapyramidal syndrome appeared suddenly nine days after the onset with ocular and buccal crisis, neck and trunk dystonic movements, and hypertonia and tremors. The patient improved with the administration of i.v. diphenhydramine. Other causes of toxic extrapyramidalism and organophosphate intermediate syndrome were discarded. Although an absolute causal relationship of the transient extrapyramidal symptomatology to the organophosphate exposure cannot be clearly established in this case, we speculate a possible delayed inhibition of the dopaminergic receptors in the substantia nigra and the basal ganglia.
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PMID:[Acute methyl parathion poisoning with extrapyramidal manifestations not previously reported]. 1020 15

Olanzapine, a new atypical antipsychotic drug, has been prescribed in the treatment of schizophrenia and psychotic mood disorders for approximately 2.3 million patients worldwide. Considering the increase in olanzapine prescriptions and the increased risk of suicide in this patient population, the number of reported cases of olanzapine overdose may be expected to increase. This report describes the clinical course and serum concentrations in a patient who consumed an olanzapine overdose (800 mg). Profound central nervous system depression and tachycardia without arrhythmia occurred within 2 hours after the ingestion. Additional clinical findings (ie, fever, mutism, agitation, dystonia, akathisia, elevated creatine kinase, and increased leukocyte count) were similar to those of neuroleptic malignant syndrome. After intubation, gut decontamination, and supportive care, the patient recovered and was discharged.
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PMID:Olanzapine overdose with serum concentrations. 1042 35

A toxin produced by legumes of the genus Astragalus and Arthrinium fungi, 3-NPA is a suicide inhibitor of succinate dehydrogenase and causes acute encephalopathy and late onset dystonia. It has been suggested that dopamine (DA) toxicity plays a role in 3-NPA induced brain damage. In order to simulate natural conditions of toxicant intake, adult, male, Sprague-Dawley rats were exposed to 3-NPA weekly for 24-h periods at 10 and 20 mg/40 ml in drinking water. This dosing regimen continued for 3 months with animals from both high and low dose groups sacrificed at the end of each month. Dopamine and its metabolites, 3,4-dihydroxylphenylacetic acid (DOPAC) and homovanillic acid (HVA), were assessed by HPLC-EC in the frontal cortex (FC) and caudate nucleus (CN). Increases of DA concentration were seen in both low and high dose groups in the CN after 1 and 3 months of dosing and in the FC after 2 months of exposure. An increase in DA turnover was observed in the CN of the high dose group following 2 months of dosing. Data suggest an activation of the dopaminergic system after long-term, intermittent exposure to 3-NPA. The production of radical oxygen species associated with DA metabolism may contribute to 3-NPA-induced neurotoxicity.
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PMID:Dopamine toxicity following long term exposure to low doses of 3-nitropropionic acid (3-NPA) in rats. 1090 28

Organophosphate poisonings are not uncommon, and are the leading cause of death in suicide patients in Taiwan. Acute cholinergic crisis caused by the inhibition of synaptic acetylcholinesterase is the major manifestation of organophosphate poisoning and may cause death within minutes. Delayed neurotoxicities include intermediate syndrome and delayed polyneuropathy have also been described. However, these symptoms may not characterize the complete picture of organophosphate poisoning. Among the 633 patients ever admitted to our hospital with organophosphate poisoning, three patients were found exhibiting impermanent neuromuscular dysfunction, including blepharoclonus, oculogyric crisis, intermittent dystonia, rigidity, and tremor, with two of them developing mask face, dyskinesia and akathisia later, following acute cholinergic crisis. The symptoms appeared within 4 days with the duration ranging from 25 days to 2 months. Other causes of the extrapyramidal syndrome noted on these patients have been excluded, and we consider the extrapyramidal syndrome a possible neurotoxic manifestation of organophosphate poisoning, which is transient, needs no treatment, and may be missed because of the critical condition, in a minority of patients. The mechanism remains to be identified, but may be related to the impediment of the function of acetylcholinesterase to modify nigrostriatal dopaminergic system, which is independent of hydrolyzing acetylcholine. More detailed observation for organophosphate poisoned patients and more studies for the biological functions of acetylcholinesterase including the influence on the nigrostriatal dopaminergic system are needed.
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PMID:Acetylcholinesterase inhibition and the extrapyramidal syndrome: a review of the neurotoxicity of organophosphate. 1157

A patient with severe postanoxic dystonia and bilateral necrosis of the basal ganglia, who was confined to a wheelchair, underwent bilateral ventralis oralis anterior deep brain stimulation (Voa-DBS) after 6 weeks of unsuccessful bilateral pallidal DBS (GPi-DBS). After 4 months of high intensity Voa-DBS, cognitively unimpaired, he showed major improvement in dystonia, became ambulant, but committed suicide. Brain examination confirmed the correct location of the electrodes in GPi and Voa on both sides.
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PMID:Postanoxic generalized dystonia improved by bilateral Voa thalamic deep brain stimulation. 1180 66


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