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

Several clinical and experimental findings suggest that abnormal serotonin (5-HT) function may be involved in movement disorders such as dystonia, and it was proposed that selective 5-HT1A receptor antagonists may be of benefit in treating such disorders. In the present study, the novel, highly selective and silent 5-HT1A receptor antagonist (+)-WAY-100135 (N-tert-butyl-3(4-(2-methoxyphenyl)piperazin-1-yl)-2-phenylprop ionamide) was tested in an inbred line of Syrian hamsters with generalized dystonia, i.e. a frequent movement disorder in humans. In order to demonstrate that WAY-100135 acts as a 5-HT1A receptor antagonist in the hamster, the drug was shown to antagonize the behavioural syndrome induced by 8-hydroxy-2-(di-n-propylamino)tetralin. When administered at 5-HT1A receptor antagonistic doses in dystonic hamsters, (+)-WAY-100135 dramatically aggravated the dystonic attacks. The data thus suggest that, in contrast to previous theoretical proposals, 5-HT1A receptor antagonists provide no novel therapeutic approach to involuntary movement disorders such as dystonia.
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PMID:The novel selective and silent 5-HT1A receptor antagonist (+)-WAY-100135 aggravates dystonic movements in a mutant hamster model. 802 48

Dystonia, a movement disorder resulting from dysfunction of the basal ganglia and thalamus, has not been described during the acute post-traumatic period after severe traumatic brain injury. We reported three patients who developed early onset dystonia after sustaining severe closed head injuries. The first patient went on to complete resolution of the dystonia; the second patient improved and had minimal residual dystonia that did not limit function; and the third patient became frankly agitated at which time the dystonic features became difficult to track. In contrast, delayed onset dystonia after traumatic brain injury has been reported to be relatively persistent. All of our patients also presented with autonomic instability. Because injuries that cause damage to the basal ganglia and thalamus may also affect the nearby hypothalamus, both dystonic posturing and autonomic instability may result.
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PMID:Early onset dystonia following traumatic brain injury. 805 95

The objective of this study was to determine the putative risk factors for the development of tardive dystonia (TDt) in contrast with tardive dyskinesia (TD). Fifteen TDt patients seen in the Movement Disorders Clinic were compared with 2 groups of 15 TD controls each. The first control group was drawn from the Clinic and matched with the TDt cases for severity, using degree of dysfunction as the matching variable. The second control group comprised mild TD cases drawn from a separate study of drug-induced movement disorders in chronic schizophrenia and were matched for age and sex with the TDt cases. A number of demographic, treatment-related, diagnosis-related and historical variables suggested in the literature were examined. Most risk factors for TDt that have been suggested by previous studies were not supported. The first control group was significantly older than the TDt cases. The TDt patients had a more frequent past history of acute drug-induced dystonia and of postural tremor prior to the onset of the mental illness, although only the former reached statistical significance. The results suggested that TDt and TD do not differ in most putative risk factors, although the small sample size increases the likelihood of a type II error. It is inconclusive on the role of young age and male sex as risk factors. TDt cases may, however, be individuals vulnerable to the development of dystonia, with neuroleptics probably bringing out such a vulnerability. This finding needs to be examined in larger studies.
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PMID:Risk factors for tardive dystonia: a case-control comparison with tardive dyskinesia. 810 38

We report two case histories of previously healthy patients who both developed persistent dyskinetic syndromes (spasmodic torticollis and cranial dystonia, respectively) following the intake of norpseudoephedrine (NPE) as an appetite suppressant. The symptoms took a chronic course even after NPE intake was discontinued. Similar drug-induced dyskinesias have been described for amphetamine and neuroleptic drugs. This side effect has, however, not yet been reported for NPE, which is pharmacologically related to amphetamine. One of the patients may also have had multiple sclerosis. Structural lesions in the basal ganglia area might predispose the development of such a movement disorder. The potential relationship between NPE intake and the development of dyskinesia is discussed. Appetite suppressants, often taken without the neurologist's knowledge, may be the cause of dyskinetic syndromes.
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PMID:Dyskinesias possibly induced by norpseudoephedrine. 816 19

The effects of R-(+)-HA-966 ((+)-3-amino-1-hydroxypyrrolid-2-one), a low-efficacy partial agonist of the glycine modulatory site of the NMDA receptor complex, were studied in an inbred line of Syrian golden hamsters with generalized dystonia, a frequent movement disorder in humans. The effects of R-(+)-HA-966 were compared with those of D-cycloserine, a glycine/NMDA receptor ligand with higher intrinsic activity. R-(+)-HA-966, 30-60 mg/kg i.p., potently reduced the severity of dystonic attacks in the mutant hamster model of dystonia without inducing any behavioural adverse effects. D-Cycloserine did not exert antidystonic activity at i.p. doses of 10-40 mg/kg, which might be due to its much higher intrinsic activity at the glycine site. The data indicate that the antidystonic effect of (+)-HA-966 is related to antagonism of NMDA receptor-mediated excitatory neurotransmission.
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PMID:The glycine/NMDA receptor ligand (+)-HA-966 but not D-cycloserine has potent antidystonic efficacy in a genetic animal model of dystonia. 822 2

The use of botulinum-A toxin will be described in two conditions--the extrapyramidal syndrome of dystonia and the pyramidal deficit, spasticity. There is no cure for dystonia and its cause is unknown. Drug therapy is unpredictable and dose-limiting side effects frequently occur with little or no alleviation of symptoms. Spasticity of adductor muscles in the lower limbs causes profound disability and major nursing problems in patients with chronic disorders of the pyramidal tract. As in the case with dystonia, drug therapy is unsatisfactory. At the UBC Movement Disorders Clinic treatment with botulinum-A has been applied to over 400 patients since 1985. The results of the first studies using this treatment in spasmodic torticollis (the most common form of focal dystonia) and spasticity (in late stage multiple sclerosis) will be discussed. As well the effects of long term treatment will be addressed. Botulinum-A toxin is approved treatment for strabismus, blepharospasm and hemifacial spasm. Approval for its use in other focal dystonias is anticipated. The very nature of the agent used for treatment requires that patients be well prepared and reassured before they undergo their first treatment. There is a wide gulf between the patients' preconceived notions about the treatment and reality.
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PMID:Local treatment of dystonia and spasticity with injections of botulinum-A toxin. 827 87

Movement disorders have been coined for diseases characterized by excessive and abnormal movements occurring in a conscious patient. Movement disorders are frequent among neurologic and psychiatric patients. They have a behavioral, or psychiatric, component. Movement disorders are mostly associated with disordered function in the basal ganglia, brain stem, and cerebellum. Such diseases are characterized by the occurrence of involuntary movement. This paper describes general concept of movement disorder, and shows classification by WHO (1991) and by Joseph, AB. and Young, RR. (1992). The classification of WHO includes I. Extrapyramidal movement disorders: 1) Parkinson disease, 2) Secondary parkinsonism, 3) Other degenerative diseases of the basal ganglia, 4) Dystonia, and 5) Other extrapyramidal and movement disorders. II. Behavioral and emotional disorders with onset usually occurring in childhood and adolescence: 1) Hyperkinetic disorders, 2) Tic disorders, and 3) others.
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PMID:[Movement disorders--concept and grand classification]. 827 55

Athetosis is a peculiar involuntary movement resulting from pathologic involvement of the basal ganglia. Although mechanism of this movement is still far from established, athetosis is clinically differentiated from chorea and dystonia. The purpose of this article is to review and summarise the classification of this involuntary movement disorder. This movement disorder is classified into double athetosis, chorea-athetosis, unilateral athetosis and pseudo-athetosis. The double athetosis is featured by increased muscle tonus and irregular small amplitude movement, which appears the most frequently in patients of cerebral palsy. In chorea-athetosis, irregular abnormal movement is more prominent and larger than double athetosis. This type of movement appears commonly in patients other than cerebral palsy. Unilateral and pseudo-athetosis are derived not from disturbance of the basal ganglia but from impared sensory pathways of the deep sensation due to cerebro-vascular lesion. Stereotactic VL-thalamotomy is effective to relieve increased muscle tonus but not to decrease involuntary movement.
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PMID:[Athetosis]. 827 61

The effects of the atypical neuroleptic clozapine were studied in an inbred line of Syrian golden hamsters with generalized dystonia, i.e. a frequent movement disorder in humans. The effects of clozapine were compared with those of the classical neuroleptic, haloperidol. Clozapine, 7.5-20 mg/kg i.p., potently reduced the severity of dystonic attacks in the mutant hamster model, but induced marked sedation at these doses. Lower doses were ineffective. Haloperidol, 0.5 mg/kg i.p., significantly reduced the severity of dystonia without marked sedation. The finding that clozapine possesses antidystonic potency similar to that of haloperidol in a genetic model of dystonia might suggest that this atypical neuroleptic is an effective alternative in the treatment of dystonic patients who respond to neuroleptics, particularly because of the clinical evidence that clozapine is almost devoid of extrapyramidal adverse effects.
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PMID:The atypical neuroleptic, clozapine, exerts antidystonic activity in a mutant hamster model. Comparison with haloperidol. 828 96

Cranial dystonia is normally considered as a pure movement disorder. Sensory symptoms have not received much attention, but we found ill-defined pain, discomfort, distortion of sensory modalities, 'phantom' kinetic or postural sensations in the orofacial areas subsequently involved by the dyskinesia in all of 11 consecutive patients, preceding by weeks or months the motor syndrome. Physicians were often mislead, initially making diagnoses such as trigeminal neuralgia, dental problems, sicca syndrome, chronic conjunctivitis, glossitis or stomatitis. The patients reported that the orofacial movements were at first willingly performed in order to decrease the discomfort which was felt in these facial areas before the movements finally escaped voluntary control and became socially disturbing. We suspect that the sensory symptoms, for which no objective substrate could be found, and which were always reported before and in the exact location of the subsequent dyskinesia, could be the earliest manifestation of an evolving process in cranial and perhaps other focal dystonias.
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PMID:Sensory symptoms in cranial dystonia: a potential role in the etiology? 833 60


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