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)

Tardive dyskinesia (TD) is a consequence of chronic neuroleptic therapy. It is an irregular stereotyped movement disorder that is usually choreic in appearance, and is subject to temporary volitional control. Dystonia, akathisia, and tics are uncommon variants of the classic tardive syndrome. Characteristic clinical features including amelioration by action, augementation by distraction, partial volitional suppressibility, and lack of subjective distress help differentiate TD from other movement disorders such as resting tremor, Huntington's disease, spontaneous dyskinesias, and abnormal movements accompanying psychiatric illnesses.
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PMID:Recognition and differential diagnosis of tardive dyskinesia. 257 70

Unlike tardive dyskinesia (TD) which is much better known by clinicians, tardive dystonia is a more recently recognised complication of neuroleptic use. It refers to chronic dystonia related to the use of neuroleptic drugs and may be an even more disabling condition than TD. This article reviews its epidemiology, clinical features and treatment aspects, and suggests that it should be separated from TD as a distinct entity.
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PMID:Tardive dystonia. 257 73

Two patients developed difficulties in eyelid opening following long-term neuroleptic treatment of more than 6-8 years. Tardive dyskinesia and dystonia apart from the face were not found in either case. The symptoms fluctuated in their severities on a daily basis and were easily aggravated by various stimuli, e.g., stress, walking, reading and watching television. Electromyographic studies of their faces clearly indicated that the symptoms resulted from spontaneous blepharospasm and were analogous to idiopathic Meige's syndrome. Therefore, the patients' difficulties in opening their eyes were considered to be the so-called drug-induced Meige's syndrome and/or facial tardive dystonia. It must be stressed that this syndrome is extremely distressing to patients and is a severe complication accompanying a long-term neuroleptic treatment.
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PMID:Meige's syndrome during long-term neuroleptic treatment. 257 1

We measured four monoamine metabolite levels in CSF before and after probenecid administration to normal controls and to patients with Huntington's disease (HD), dystonia, and tardive dyskinesia. We identified differences only for the dopamine metabolite homovanillic acid (HVA), which showed increased baseline values and decreased turnover in normal aging, but decreased baseline values and normal turnover in HD. These results suggest that dopamine neurons are linked both to normal aging and to HD and that CSF HVA studies can distinguish differences in the functioning of dopamine neurons in normal aging and HD.
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PMID:CSF monamine metabolites in movement disorders and normal aging. 267 3

The face is prominently or exclusively involved in several involuntary movement disorders, called "facial dyskinesias," in addition to the common buccolingual form of tardive dyskinesia. This review describes the appearance of the most frequently occurring facial dyskinesias: chorea, dystonia, tremor, and tics. Some new treatments are discussed.
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PMID:Facial dyskinesias. 266 10

Clozapine has had a uniquely favorable motor system side effect profile since its initial evaluations. This has been convincingly corroborated by many double blind, single blind, and open studies treating acute and chronic psychosis. The acute extrapyramidal syndromes of dystonia, akathisia and parkinsonism infrequently occur, whereas these syndromes develop in up to 75% of patients receiving traditional neuroleptics. Tardive dyskinesia can be suppressed with higher doses of clozapine given over extended periods. However, an antipsychotic effect can be achieved in many patients at doses below the dyskinesia suppressing level. There is no established causative relationship between clozapine and tardive dyskinesia, but there is a theoretical basis that this may occur. Preliminary data suggest clozapine has mild antiparkinsonian effects as well as efficacy in controlling dopamine agonist-induced psychosis without aggravating parkinsonism. A much wider use of clozapine will further characterize the magnitude of differences compared to other neuroleptics, and identify additional indications for this special compound.
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PMID:Clozapine: neuroleptic-induced EPS and tardive dyskinesia. 268 32

Metoclopramide, a dopamine-2 receptor antagonist used for various gastrointestinal disorders, may cause or exacerbate a variety of extrapyramidal movement disorders. To draw attention to the frequent occurrence of metoclopramide-induced movement disorders, we identified and studied 16 patients who had been exposed to this neuroleptic. The average age at onset was 63 years (range, 24 to 85 years), and women outnumbered men 3 to 1. Tardive dyskinesia was the most common movement disorder (n = 10 [63%]). Five patients had metoclopramide-induced parkinsonism, 1 patient had tardive dystonia, and 1 patient had akathisia. The average duration of exposure prior to onset of movement disorders was 12 months (range, 1 day to 4 years). Therapy was continued for an average of 6 months (range, 1 day to 2 years) after the onset of symptoms, reflecting clinical nonrecognition of the movement disorder and its relationship to metoclopramide. To prevent persistent and disabling movement disorders, long-term use of metoclopramide should be avoided, and patients should be carefully observed for potential neurologic reactions.
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PMID:Metoclopramide-induced movement disorders. Clinical findings with a review of the literature. 268 75

Voluntary suppressibility of abnormal movements is helpful in the classification of movement disorders because this ability appears to be a common component of tics. However, there has been no systematic study of voluntary suppressibility in other movement disorders. We have therefore assessed 146 patients with tremors and dyskinetic disorders as to their ability to suppress movements by mental concentration. Patients were videotaped while trying to stop their movements, and the length of time they could suppress their abnormal movements was recorded. One hundred percent (10 of 10) of patients with tics could suppress movements for an average of 2.5 min. Two percent (1 of 50) of essential tremor patients could suppress the tremor, and the tremor of 24% (12 of 50) was made worse by mental concentration. Eighty percent (4 of 5) of neuroleptic-induced tremor could be improved mentally. Seventy percent (35 of 50) of patients with parkinsonian tremor could voluntarily diminish their tremor for an average of 48 s. Fifty percent (8 of 16) of chorea (tardive dyskinesia, Huntington's disease, postencephalitic) was reduced. Dystonia was suppressible in 20% (3 of 15). It is concluded that movement disorders besides tics can be voluntarily suppressed and that suppressibility should not be used to classify movement disorders. Tics, however, are easier to suppress and can be suppressed for a longer time.
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PMID:Volitional control of involuntary movements. 273 7

Continuous administration of haloperidol, sulpiride, or cis-flupenthixol, but not of domperidone or apomorphine, to Wistar rats for up to 3 weeks caused an increase in spontaneous purposeless chewing movements. Treatment with physostigmine and pilocarpine, but not neostigmine, for up to 3 weeks increased chewing, whilst scopolamine decreased chewing. Metergoline and cyproheptadine, but not quipazine, increased chewing after only 1 and 7 days but not thereafter. Chewing was not altered following treatment with compounds acting on GABA or noradrenaline systems or by a range of non-neuroleptic agents inducing dystonia in man. The enhancement of chewing induced by neuroleptic and cholinomimetic drugs was reduced by acute treatment with scopolamine, and reverted to control levels following drug withdrawal. Neuroleptic-induced purposeless chewing in Wistar rats appears to be primarily influenced by cerebral dopamine and acetylcholine function and may resemble acute dystonia, rather than tardive dyskinesia.
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PMID:Pharmacological characterisation of spontaneous or drug-associated purposeless chewing movements in rats. 285 1

The role of neuroleptics in causing the tardive dyskinesia syndrome is controversial. To properly assess the contribution of drugs as the etiology of dyskinesias, the effects of aging, the natural history of psychosis, and characteristics of spontaneous dyskinesias must be considered. Though the buccolinguo-masticatory triad is seen more often in tardive than in spontaneous dyskinesias, these two disorders have many symptoms in common. Other dyskinesias, such as idiopathic and tardive dystonia or tardive Tourette's syndrome and dyskinesias in untreated schizophrenia, are poorly understood. Chronic neuroleptic treatment may only precipitate TD in those already predisposed to develop such movement disorders. Tardive dyskinesia is not a unique movement disorder, but rather spans several clinical and epidemiological phenomena which must be considered in a balanced evaluation of how much of the permanent dyskinesias should be attributed to neuroleptic drugs.
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PMID:Is tardive dyskinesia a unique disorder? 286 Jun 61


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