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)

Idiopathic orofacial dyskinesia, also called Brueghel's syndrome, blepharospasm-oromandibular dystonia, and Meige dystonia, is characterized by involuntary facial movements. Since this disorder can be difficult to distinguish from tardive dyskinesia, we have generated a neuropharmacologic profile of Meige dystonia. Symptoms were improved by antagonists of both dopamine and acetylcholine and worsened by the cholinergic agonist physostigmine, consistent with a hypothesis of relative excess in both dopamine and acetylcholine neuronal activities. Since tardive dyskinesia is hypothesized to be characterized by dopamine excess and acetylcholine deficiency, a physostigmine infusion may help differentiate these two disorders by exacerbating Meige dystonia but improving tardive dyskinesia.
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PMID:Pharmacologic characteristics of Meige dystonia: differentiation from tardive dyskinesia. 717 19

Extrapyramidal syndromes have been described after administration of phenytoin and primidone. Although asterixis, dystonia, and tremor have been described with carbamazepine (Tegretol), there is no report of orofacial dyskinesia. We report a case in which a dose-related lingual-facial-buccal extrapyramidal reaction occurred in association with carbamazepine intoxication.
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PMID:Carbamazepine-induced orofacial dyskinesia. 719 14

Methlyphenidate is one of two stimulant drugs used in the management of the Hyperkinetic Reaction in children. It has been known to have side effects such as dyskinesia, but this case details the emergence of dystonia and dyskinesia when the simultaneous use of methylphenidate and a phenothiazine was followed by withdrawal of the phenothiazine. It is postulated that the use of phenothiazine resulted in a post-synaptic supersensitivity which precipitated dystonia and dyskinesia when phenothiazine was withdrawn and methylphenidate reinstituted. It is also suggested that the phenothiazine dopamine-blocking action may necessitate the use of larger quantities of stimulant in order to produce the desired effect.
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PMID:Methylphenidate, neuroleptics and dyskinesia-dystonia. 737 Sep 9

The progress of 178 patients with Parkinson's disease who began treatment with levodopa between November 1969 and December 1972 is reviewed after six years. One hundred and twenty-five patients showed an initial improvement of their individual total disability scores exceeding 25 per cent, but after six years of sustained treatment only 37 patients still obtained similar benefit. By 1978 only five patients had maintained their initial improvement compared to 69 patients after two years therapy; however, 47 patients were still better than before treatment. The overall mortality ratio--the ratio of observed to expected death rate--for all the patients was 1.45:1. In those patients who unable to tolerate levodopa for longer than two years the ratio was 2.38:1; in those who were able to tolerate sustained medication, life expectancy was normal (ratio of 0.91:1 for males and 1.14:1 for females). Involuntary movements were the commonest complication of treatment. Three main types were distinguished. Peak dose dyskinesias, beginning 20 to 90 minutes after an oral dose and most severe midway through the inter-dose period, affected 80 per cent of patients. Early morning and end-of-dose dystonia occurred in 20 per cent of patients and biphasic dyskinesia--two distinct episodes of involuntary movements within each inter-dose period--was the least common pattern affecting 3 per cent of patients. Involuntary movements increased in frequency and severity as treatment continued. End-of-dose deterioration ('wearing-off' effect of individual doses) occurred in 65 per cent of patients: unpredictable oscillations in motor performance (the 'on-off' phenomenon) unrelated to the time and dosage of levodopa, occurred in 10 per cent. Psychiatric side effects included toxic confusional states, visual pseudohallucinations and paranoid psychoses and constituted the most frequent reason for stopping medication. Forty (22 per cent) of the patients had suffered severe depression before the onset of disease and levodopa had no sustained antidepressant effect in this group. After six years of treatment with levodopa, 32 per cent of the patients had unequivocal dementia.
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PMID:The impact of treatment with levodopa on Parkinson's disease. 746 63

A woman and her son had progressive dystonia and chronic insomnia at 32 and 19 years of age respectively. Levodopa was markedly effective at low dose both for dystonia and insomnia without dyskinesia over a 5-year follow-up period.
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PMID:[L-dopa-responsive dystonia: 2 familial cases of adult onset with sleep disorders]. 748 95

We prescribed a solution of levodopa-carbidopa and ascorbic acid (LCAAS) to 21 Parkinsonian patients with motor complications. Eight patients continued the treatment for a mean period of 16.8 months, experiencing substantial increases in the number of hours with good functional capacity. Bothersome symptoms such as dystonia and akathisia in off periods disappeared in all cases in which they had been present and LCAAS was tolerated (in 6 of the 8 patients who continued in the study and in 4 who abandoned treatment late). Intake of other anti-Parkinsonian drugs was reduced. Thirteen patients abandoned the study, citing exacerbation of biphasic dyskinesia as the main reason. We conclude that LCAAS is a useful therapy in some Parkinsonian patients whose motor complications are not managed with conventional drug treatment. Screening of patients is probably of utmost importance to ensure that LCAAS is not administered to patients who already suffer intense biphasic dyskinesia.
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PMID:[Treatment of complicated Parkinson disease with a solution of levodopa-carbidopa and ascorbic acid]. 754 11

We report a family with autosomal dominant type hereditary juvenile dystonia-parkinsonism in which eight members in three generations exhibited parkinsonism, sleep benefit, marked efficacy of levodopa, wearing-off phenomenon, and dopa-induced choreic dyskinesia. However, one case showed mainly dystonic movement that worsened after administration of levodopa. The patients in this family showed neck dystonia, such as torticollis and retrocollis, in addition to foot dystonia and other dystonic movement, such as frequently lifting the thigh. From the family history and clinical findings, these patients are considered to have a specific form of hereditary dystonia-parkinsonism.
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PMID:A family with hereditary juvenile dystonia-parkinsonism. 756 30

Neuroleptic treatment frequently induces movement disorders, the tardive dyskinesias. These are frequently seen in the orobuccolingual region. Although the beginning of neuroleptic treatment can cause acute dystonia and breathing difficulty, chronic neuroleptic treatment has only rarely been shown to affect the laryngeal musculature. Laryngeal abnormal movements were assessed in 12 patients receiving chronic neuroleptic treatment who showed orobuccolingual abnormal movements. The Abnormal Involuntary Movement Scale was systematically assessed in all patients. Clinical examination revealed that 8 had speech disorders, 8 had breathing difficulties, and 5 had swallowing disorders. Laryngeal endoscopy showed that 10 of the patients had intermittent partial obstruction of the glottis, due to repetitive abnormal adduction of the vocal cords. Percutaneous electromyography of the thyroarytenoid muscles showed spontaneous irregular and prolonged muscular contractions, while the patients were at rest and when speaking. The patients were not aware of these movements. In view of this finding, laryngeal dyskinesia should be considered and studied as a possible side-effect of chronic neuroleptic use.
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PMID:Laryngeal tardive dyskinesia. 759 77

Although the gene defect responsible for Huntington disease (HD) has recently been identified, the pathogenesis of the disease remains obscure. One potential mechanism is that the gene defect may lead to an impairment of energy metabolism followed by slow excitotoxic neuronal injury. In the present study we examined whether chronic administration of 3-nitropropionic acid (3-NP), an irreversible inhibitor of succinate dehydrogenase, can replicate the neuropathologic and clinical features of HD in nonhuman primates. After 3-6 weeks of 3-NP administration, apomorphine treatment induced a significant increase in motor activity as compared with saline-treated controls. Animals showed both choreiform movements, as well as foot and limb dystonia, which are characteristic of HD. More prolonged 3-NP treatment in two additional primates resulted in spontaneous dystonia and dyskinesia accompanied by lesions in the caudate and putamen seen by magnetic resonance imaging. Histologic evaluation showed that there was a depletion of calbindin neurons, astrogliosis, sparing of NADPH-diaphorase neurons, and growth-related proliferative changes in dendrites of spiny neurons similar to changes in HD. The striosomal organization of the striatum and the nucleus accumbens were spared. These findings show that chronic administration of 3-NP to nonhuman primates can replicate many of the characteristic motor and histologic features of HD, further strengthening the possibility that a subtle impairment of energy metabolism may play a role in its pathogenesis.
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PMID:Chronic mitochondrial energy impairment produces selective striatal degeneration and abnormal choreiform movements in primates. 762 78

Determinations of biopterin (BP), homovanilic acid (HVA), glutamic acid (GTA), and glutamine (GT) levels in cerebrospinal fluid (CSF) obtained through a lumbar tap were performed in 20 parkinsonian patients in different stages of evolution and without medication. In patients with motor symptoms not related to Parkinson's disease (dystonia, dyskinesia and essential tremor) (n = 4). In 7 other neurological patients subjected to spinal tap for diagnostic procedures neurotransmitters were also determined and taken as control groups. In 14 of the patients with Parkinson's disease, the symptoms were evaluated using conventional scales (UPDS, NYPDS, NWPDS, Schwab and England, and Hoehn and Yahr scale). The amplitude and the frequency of tremor were quantitatively evaluated through a single plane accelerometer Grass SP-1, akinesia was measured through reaction time to auditory stimuli, and rigidity through the speed of lineal movement. Evaluations were performed with the patient not on any medication for 1 week and repeated 1 h after the intake of 250 mg of 200/50 L-dopa/carbidopa preparation (Sinemet) and on a different day after the intake of biperiden (Akineton) 6 mg/day. Differences in neurotransmitter or metabolites levels between Parkinson's disease and control groups were determined through an independent Student's t test. Correlation between severity of symptoms in the scales and for each individual symptom measured through the quantitative tests and the levels of neurotransmitters in CSF were evaluated through the Pearson correlation analysis test. Modifications in the motor performance after administration of Sinemet and Akineton, and the levels of neurotransmitters were indirectly determined. RESULTS. (1) There were significant differences between the levels of BP and GT in patients with Parkinson's disease and control groups, (2) lower GTA levels correlated with more severe rigidity and akinesia, and with the best response to the administration of L-dopa and may be an important marker for prognosis, and (3) lower levels of GT correlated with least akinesia, but not with tremor, which may indicate that the akinesia depends on other biochemical abnormalities besides dopamine depletion.
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PMID:Neurotransmitter levels in cerebrospinal fluid in relation to severity of symptoms and response to medical therapy in Parkinson's disease. 763 Oct 94


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