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

Four patients are described who sustained comparatively minor peripheral injury, the affected area soon becoming the site of segmental dystonia. The movement disorder developed as the symptoms from the injury subsided, and except for the recent trauma, no cause for the dystonia was apparent; litigation was not an issue for any patient. It is suggested that on rare occasions peripheral trauma results in the development of dystonia. Since injury never involved the head, the role of the spinal dopaminergic system and the relevance of pain from the injury are discussed in considering possible underlying mechanisms.
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PMID:The relationship of peripheral trauma and pain to dystonia. 403 15

Two patients developed either blepharospasm or blepharospasm-oromandibular dystonia following chronic therapy with chlorpromazine, haloperidol, or thioridazine. In one patient, appearance of the movement disorder was associated with neuroleptic withdrawal, and in the other patient, the movement disorder began while neuroleptic therapy continued. Because of the age of one patient and the severe intermittent psychosis in the other, these Meige-like symptoms were attributed to chronic neuroleptic use rather than to spontaneously occurring Meige syndrome. The symptoms occurring as part of a tardive dyskinesia suggest that dopaminergic mechanisms play a role in idiopathic Meige syndrome.
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PMID:Meige syndrome (blepharospasm-oromandibular dystonia) after long-term neuroleptic therapy. 611 44

It has been reported that intraventricular injection of chlorpromazine methiodide (CPZMI), a quaternary ammonium derivative of chlorpromazine, in rats induces abnormal, twisting postures which may serve as an experimental model of the human movement disorder dystonia. We have shown elsewhere that the behavior induced by intraventricular CPMZI is identical to what has been called "barrel rotation," first observed to follow intraventricular injection of somatostatin (SRIF), which consists of twisting about the long axis, with repetitive lateral rolling. The suitability of barrel rotation, induced by CPZMI or SRIF, as an experimental model for dystonia depends on its physiologic basis. Human dystonia is clinically not a convulsive phenomenon. SRIF-induced barrel rotation has been reported to be associated with epileptiform activity recorded by the electroencephalogram (EEG). The purpose of this study was to investigate EEG activity during CPZMI- and SRIF-induced rotation. We found that CPZMI barrel rotation was not associated with epileptiform activity in cortex, amygdala, or hippocampus, and contrary to prior reports, neither was SRIF rotation. Both CPZMI and SRIF injected in high doses could induce epileptiform activity, but this was associated with clonic motor phenomena and not barrel rotation. We conclude that electroencephalographic criteria do not exclude either CPZMI- or SRIF-induced rotation as models for movement disorders, but their validity as such requires further study.
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PMID:Electroencephalographic studies of chlorpromazine methiodide and somatostatin-induced barrel rotation in rats. 613 Sep 62

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

A unilateral microinjection of adrenocorticotropin 1-24 in the rat brainstem in the region of the locus ceruleus resulted in postural asymmetry and movement disorder that resembled human dystonia, the severity and duration (2 to 3 days) being dose-dependent. These results show for the first time that neuropeptides in the brainstem may modulate posture and movement, and they suggest that some forms of movement disorder such as dystonia may be due to a disordered regulation of postural and locomotor mechanisms by adrenocorticotropin 1-24.
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PMID:Postural asymmetry and movement disorder after unilateral microinjection of adrenocorticotropin 1-24 in rat brainstem. 628 33

The evaluation, diagnosis, and treatment of involuntary hyperkinetic movements can be a difficult challenge. A thorough history, including past and present drug use, and a complete physical, neurological, and psychiatric examination, accompanied by appropriate laboratory tests, are often necessary to make the correct differential diagnosis of dyskinesias. Movement disorders in psychiatric patients are usually related to neuroleptic medicines. Extrapyramidal syndromes related to starting these drugs include dystonia, akathisia, and parkinsonism, whereas dyskinesia occurs late in the course of the treatment. Involuntary movements may, however, be idiopathic, be caused by many other drugs, or occur as part of psychoses, hereditary neurodegenerative diseases, or other medical illnesses.
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PMID:The differential diagnosis of tardive dyskinesia. 694 30

Fibroblasts provide a source of living cells that can be obtained easily from humans and used to evaluate inherited differences in the activities of enzymes important in neurotransmitter and drug metabolism. Here, we describe biochemical characteristics of catechol-O-methyltransferase (COMT, EC 2.1.1.6) activity in homogenates of cultured human skin fibroblasts. Many properties of the enzyme, including apparent affinity for dihydroxybenzoic acid and S-adenosyl methionine, optimal pH and (Mg++), and inhibition by Ca++, are similar to those reported in lysates of human erythrocytes. Culture and assay conditions have been established for optimal and reproducible measurement of COMT activity in individual fibroblast lines. In 16 control lines, COMT activity ranged from 115 to 263 pmol/min/mg protein with a mean of 181 pmol/min/mg protein. Enzyme activity did not vary with the age or sex of the donor. The COMT activities in fibroblasts from eight patients with dystonia musculorum deformans, an inherited movement disorder of unknown etiology, were not significantly different from controls. Monoamine oxidase (MAO, EC 1.4.3.4) type A activity was measured in 12 lines from patients with dystonia, and values did not differ significantly from age- and sex-matched controls. We conclude that inherited variation in activity of these two catabolic enzymes is not sufficient to explain alterations in monoamine metabolism described in this disorder.
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PMID:Catechol-O-methyltransferase activity in cultured human skin fibroblasts from controls and patients with dystonia musculorum deformans. 729 45

One third of a patient population with idiopathic parkinsonism was found to suffer from debilitating, painful dystonic movements of the lower extremities. The prevalence of this involuntary movement disorder was found to be positively correlated with the duration of dopaminergic treatment, but it also occurred occasionally in untreated persons. We suggest that the "dystonic foot response of parkinsonism" is a distinct clinical entity that has no localizing value in frontal lobe disorders and is associated with extrapyramidal disease. This disorder, though exacerbated by dopaminergic therapy, also differs from well-accepted dopaminergic side-effects and does not predictably respond to manipulation of antiparkinsonian medications. Although the precise pathophysiology of this movement disorder is unknown, its response to baclofen therapy suggests that neurotransmitter systems other than cholinergic or dopaminergic ones may be implicated.
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PMID:Dystonic foot response of Parkinsonism. 735 17

Of 842 consecutive patients with movement disorders seen over a 71 month period, 28 (3.3%) were diagnosed as having a documented or clinically established psychogenic movement disorder. Tremor was most common (50%) followed by dystonia, myoclonus, and parkinsonism. Clinical descriptions of various types are reviewed. Clinical characteristics common in these patients included distractability (86%), abrupt onset (54%), and selective disabilities (39%). Distractability seems to be most important in tremor and least important in dystonia. Other diagnostic clues included entrainment of tremor to the frequency of repetitive movements of another limb, fatigue of tremor, stimulus sensitivity, and previous history of psychogenic illness. On examination, 71% had other psychogenic features. Over 60% had a clear history of a precipitating event and secondary gain and 50% had a psychiatric diagnosis (usually depression). Twenty five per cent of patients presented with combined psychogenic movement disorder and organic movement disorder; 35% resolved and this subgroup had a shorter duration of disease than those who are unresolved. Psychogenic movement disorder represents an uncommon diagnosis among patients with movement disorders. The ability to make a diagnosis rests on the presence of a multitude of clinical clues and therapeutic action should be taken as early as possible.
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PMID:Psychogenic movement disorders: frequency, clinical profile, and characteristics. 756 21

Movement disorders (MD), other than tremor, associated with multiple sclerosis (MS) occur infrequently. We report 14 new cases of whom nine had dystonia, three parkinsonism, and two had myoclonus. We also reviewed 135 such cases from the literature. From an analysis of the individual MDs and the site of the lesions described, we conclude that paroxysmal dystonias (tonic spasms), ballism/chorea, and palatal myoclonus can be caused by demyelinating lesions. Parkinsonism, dystonia, and other types of myoclonus, however, often appear to be coincidental.
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PMID:Movement disorders in multiple sclerosis. 938 76


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