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Query: UMLS:C0013421 (dystonia)
 8,418 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical and experimental evidence suggests that alpha methylparatyrosine (AMPT), an inhibitor of tyrosine hydroxylase, can potentiate the effects of other dopamine antagonists. We therefore treated patients having various forms of dystonia and chorea with tetrabenazine (TBZ), and then added AMPT to determine if further improvement could be obtained. Side effects of both drugs were common, and they often necessitated withdrawal of the drug. Patients with Huntington's chorea and tardive dyskinesia were improved by TBZ. They obtained additional benefit from the combination of AMPT and TBZ. The results in the dystonia patients were disappointing with both drugs. Although a small number of patients did improve, and short- and long-term remissions occurred in a few, most patients with dystonia were not benefited by either drug.
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PMID:Alpha methylparatyrosine and tetrabenazine in movement disorders. 613 Aug 39

There are at least four phenomenologically different types of movement disorders that fall under the rubric of tardive dyskinesia: a) classical TD which is choreatic in speed of movement and stereotypic in pattern, b) tardive akathisia, c) withdrawal emergent syndrome, which presents as true chorea and d) tardive dystonia which presents with dystonic movement and postures. This paper reviews the main treatments of tardive dyskinesia. The drugs utilized have been considered according to their mechanism of action.
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PMID:[Treatment of tardive dyskinesia caused by neuroleptics]. 614 88

Tardive dyskinesia (TD) consists of persistent involuntary movements that are due to antipsychotic drug treatment. Prevention depends on accurate psychiatric diagnosis and use of antipsychotics only for specific indications. Little is known about what antipsychotic drug regimens affect the risk of TD. Clinical subtypes of TD may exist. Tardive dystonia differs from oral choreic TD in its clinical phenomenology, epidemiology, and clinical pharmacology. Another possible subtype, persistent motor restlessness, seems also distinguishable in its phenomenology and epidemiology. Both of these forms of TD can be disabling, whereas typical oral TD often is not. Although TD may spontaneously remit more often than was once believed, it nevertheless is often persistent. No current therapy is universally effective.
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PMID:Tardive dyskinesia: current clinical issues. 614 18

Brains from Cebus Apella monkeys have been mapped biochemically using a cryo-section technique which enables exact micro-dissectioning of tissue. Two neurotransmitters; noradrenaline (NA) and gamma-amino-butyric acid (GABA) were measured by gas chromatography-masspectrometry technique. In addition biochemical markers reflecting metabolic activity in the dopamine (homovanillic acid, HVA, 3, 4-dihydroxyphenylacetic acid, DOPAC), serotonin (5-hydroxyindoleacetic acid, 5-HIAA), noradrenaline (4-hydroxy-3-methoxy-phenylglycol, HMPG), acetylcholine (choline acetyltransferase, CAT) and GABA (glutamic acid decarboxylase, GAD) transmitter systems were assayed. The distribution of these transmitter markers roughly corresponded to earlier studies in other non-human primates, whereas similar studies on the human brain generally show lower concentrations and enzyme activities. One monkey exposed to severe stress immediately before death deviated from the normal animals with regard to HVA, 5-HIAA, GAD and GABA. For the study of neuroleptic drugs, and notably their neurological side-effects, Cebus Apella monkeys have turned out to be particularly useful. In our laboratory we have employed this species of monkey to develop a model for acute dystonia and tardive dyskinesia (Gunne and Barany 1976, 1979, Barany et al. 1979). As a first step in the topological mapping of brain neuro-chemistry in these animals we here present data from normal monkeys, not treated with neuroleptics. During the ongoing project there was an unplanned "stress experiment" in one monkey, which had a nightly fight with a cage partner and had to be sacrificed the morning after due to severe wounds. The present communication describes a method for obtaining well-defined samples from monkey brains and presents the data on homovanillic acid (HVA), 3.4-dihydroxyphenylacetic acid (DOPAC), 5-hydroxyindoleacetic acid (5-HIAA), noradrenaline (NA), 4-hydroxy-3-methoxy-phenyl glycol (HMPG), choline acetyltransferase (ChAT), glutamic acid decarboxylase (GAD), and gamma-amino-butyric acid (GABA) in discrete regions from 7 drug-naive control monkeys. Also data from the stressed animal are presented.
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PMID:Discrete regional distribution of biochemical markers for the dopamine, noradrenaline, serotonin, GABA and acetylcholine systems in the monkey brain (Cebus Apella). Effects of stress. 615 Jun 1

Excluding surgical procedures, this article focuses on clinical pharmacotherapeutic approaches to treatment of parkinsonism and tremor, chorea, dystonia, tic, and tardive dyskinesia.
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PMID:Involuntary movement disorders. 623 89

The clinical pharmacological, and neuroradiological observations in six patients with spontaneous blepharospasm-oromandibular dystonia (Meige's) syndrome are recorded. This group consisted of five males and one female, mean age at onset being 50.3 years. The duration of symptoms ranged from three months to 12 years, three patients having had symptoms for over four years. The dyskinesia was arrhythmic and asymmetrical in the orbicularis oculi and masseter muscles electrophysiologically. Pharmacological studies evinced no consistent response to parenteral physostigmine, no response to oral levodopa and no significant improvement in the dyskinesia following oral haloperidol. Lumbar air encephalogram was done in five patients, and showed frontal cortical atrophy without ventricular dilation in three. It is concluded that Meige's syndrome is a distinct nosological entity, and that physostigmine test is unlikely to be helpful in the differential diagnosis from neuroleptic-induced tardive dyskinesia. Neurotransmitter imbalance in the basal ganglia in this disorder remains to be established, and at present there is no satisfactory drug treatment for this progressively disabling movement disorder.
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PMID:Meige's syndrome: clinical, pharmacological and radiological observations. 627 56

Twenty-nine patients with tardive dyskinesia (n = 20) or related syndromes [spontaneous dyskinesia (n = 3), levodopa-induced dyskinesia (n = 3), tardive dystonia (n = 3)] were treated with clonidine. Clinical effects of this drug were observed for up to 4 years. Seventy-five percent of patients showed at least moderate improvement, and in 50% of patients, full resolution occurred. In most cases, patients received concomitant medications, including neuroleptics and benzodiazepines. Two patients received clonidine alone, and dyskinesia was only minimally improved; however, when bromocriptine was added, prompt improvement occurred on this combined regimen. On the basis of these findings, we suggest that not only receptor supersensitivity of dopaminergic neurons but also involvement of noradrenergic neurons is important in the pathophysiology of tardive dyskinesia and related syndromes.
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PMID:Clonidine therapy for tardive dyskinesia and related syndromes. 648 98

The descriptive aspects of all types of movement disorders and their related syndromes and terminologies used in the literature are reviewed and described. This comprises the features of (a) movement disorders secondary to neurological diseases affecting the extrapyramidal motor system, such as: athetosis, chorea, dystonia, hemiballismus, myoclonus, tremor, tics and spasm, (b) drug induced movement disorders, such as: akathisia, akinesia, hyperkinesia, dyskinesias, extrapyramidal syndrome, and tardive dyskinesia, and (c) abnormal movements in psychiatric disorders, such as: mannerism, stereotyped behaviour and psychomotor retardation. It is intended to bring about a more comprehensive overview of these movement disorders from a phenomenological perspective, so that clinicians can familiarize with these features for diagnosis. Some general statements are made in regard to some of the characteristics of movement disorders.
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PMID:Clinical features of movement disorders. 662 43

Persistent signs of oral dyskinesia (tongue protrusion and facial grimacing) had developed as a result of earlier chronic treatment with neuroleptics in a Cebus apella monkey. When this animal was given single doses of any classical neuroleptic, a transient deterioration of dyskinesia occurred, preceded by a temporary abolishment of dyskinesia sometimes with an attack of acute dystonia. Fluphenazine (5-25 micrograms/kg) causes dose-related deteriorations of dyskinesia. Six different drugs were tested on this monkey for their capacity to elicit aggravation of dyskinetic signs: three antihistamines (brompheniramine, promethazine, diphenhydramine) and three dopamine D2 receptor antagonists (sulpiride, tiapride, metoclopramide). High doses of promethazine and diphenhydramine (5 mg/kg) induced a temporary alleviation of dyskinesia, possibly through sedation. All three D2 receptor antagonists precipitated signs of acute dystonia at some dose levels, but out of the test drugs only metoclopramide caused deterioration of dyskinetic symptoms. According to the present results only metoclopramide stands out as a drug with an inherent propensity to cause tardive dyskinesia.
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PMID:Application of a primate model for tardive dyskinesia. 684 25

Concurrent administration of lithium (Li) significantly attenuates the dopamine (DA) depleting effects of reserpine and tetrabenazine, but does not change alpha-methyl-p-tyrosine (AMPT) induced DA depletion in rat brain. This effect of Li is probably mediated, in part, by inhibiting the magnesium-dependent binding of both reserpine and tetrabenazine to their specific receptor sites. Such interaction between these drugs may attenuate the beneficial effects of tetrabenazine and reserpine on patients with tardive dyskinesia or tardive dystonia who are treated concurrently with lithium for their psychiatric disorder.
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PMID:Lithium attenuates dopamine depleting effects of reserpine and tetrabenazine but not that of alpha methyl-p-tyrosine. 686 53


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