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

Dystonia is a syndrome characterized by sustained muscle contraction, provoking twisting and repetitive movements or abnormal postures. It may be classified according to etiology, as idiopathic or symptomatic. We studied 122 Brazilian patients with a dystonic syndrome. Of these, 46 (37.7%) had symptomatic dystonia. The most frequent cause was tardive dystonia (34.8%) followed by perinatal cerebral injury (30.4%). Other causes were stroke (13.0%), encephalitis (6.5%) and Wilson's disease (4.3%). Cranial trauma, mitochondrial cytopathy and psychogenic, were the least frequent causes with one patient in each category. The etiology in two patients could not be established. Perinatal cerebral injury and postencephalitic dystonia were seen in the younger age group, while post-stroke and tardive dystonia were seen in the older age group.
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PMID:Symptomatic dystonia: clinical profile of 46 Brazilian patients. 142 47

Mumps virus is one of the most common causes of viral meningitis. Although brain involvement has been observed in a low proportion of children with mumps meningitis, a pure form of mumps encephalitis is extremely uncommon in the adult. A 23 year-old man presented with a rapidly evolving syndrome of cephalalgia , vomiting, mutism, disorders of gait, somnolence and dystonic movements. The electroencephalogram showed a diffusely slowed background activity. The CSF contained no cells, but the total protein concentration was elevated. The patient recovered without sequelae, but severe intellectual and motor disturbances persisted during more than a month. Serological studies showed an increase of blood IgM mumps-specific antibodies. We conclude that mumps encephalitis, although infrequent, should be considered among viral diseases that mimic herpes simplex encephalitis in the adulthood.
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PMID:[Mumps encephalitis in adulthood]. 205

We studied seven patients with AIDS or AIDS-related complex (ARC) and movement disorders. Three had hemichorea-ballismus, two had segmental myoclonus, one had postural tremor with dystonia, and one had paroxysmal dystonia. Besides the hyperkinesias, two patients had parkinsonism, and one had cerebral Whipple's disease. In two, the movement disorder preceded other evidence of AIDS; in three others, the diagnosis of AIDS was not considered until there was a movement disorder. The movement disorders were attributed to toxoplasmosis in four patients (one confirmed at autopsy), viral encephalitis, vacuolar myelopathy, and CNS Whipple's disease.
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PMID:Movement disorders and AIDS. 379 36

Acute catatonic syndrome is a condition that can be caused by a variety of metabolic, neurological, psychiatric, and toxic conditions, including neuroleptic malignant syndrome. Although ictal catatonia as a manifestation of non-convulsive status epilepticus has been described, reference to the occurrence of seizures in patients with acute catatonic syndrome is anecdotal. Twenty nine patients with acute catatonic syndrome were reviewed to identify patients with seizures after the onset of acute catatonic syndrome. Patients were divided into four diagnostic groups: affective (15), schizophrenic (eight), toxic (two), and organic (four). Seizures occurred in four patients (13.8%): two patients with dystonic seizures had viral encephalitis and schizophrenic disorder respectively; one patient with complex partial seizures had viral encephalitis and one patient with absence status had neuroleptic malignant syndrome. The results indicate the value of EEG in detection of epileptic activity in patients with acute catatonic syndrome, both at onset and in the course of such disturbance, particularly to provide a differential diagnosis between pseudo-seizures and neuroleptic-induced acute dystonia.
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PMID:Epileptic seizures in patients with acute catatonic syndrome. 796 25

Catatonia is a neuropsychiatric syndrome that may present a difficult diagnostic dilemma. Catatonic disorder due to general medical conditions must be considered in every patient with catatonic signs. Four patients with this disorder are presented. In these patients, general medical conditions associated with catatonic disorder included dystonia, HIV encephalopathy, progressive multifocal leukoencephalopathy, encephalitis, and renal failure. Three of these patients had multifactorial presentations of medical conditions or prior psychiatric disorders. A critical literature review concerning catatonia and associated nonpsychiatric medical conditions only infrequently supported causal relationships between organic factors and the development of catatonia. The majority of patients have multifactorial etiologies.
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PMID:Catatonic disorder due to general medical conditions. 804 33

A retrospective examination of lethargic encephalitis finds many parallels with neuroleptic effects. The encephalitis, like the neuroleptics, produced an acute continuum of cognitive disorders from emotional indifference through apathy and onto a rousable stupor. It also produced similar acute dyskinesias, including akinesia, akathisia, dystonia, oculogyric crises, and tremors. The encephalitis also caused similar chronic effects, including dementia and psychosis, and somewhat different persistent dyskinesias. The chronic motor and cognitive disorders, like those associated with the neuroleptics, were often delayed in onset. An acute, severe episode of lethargic encephalitis also finds a parallel in the neuroleptic malignant syndrome. These parallels are probably due to a common site of action in the basal ganglia. They provide a model for understanding many neuroleptic effects and alert us to the probability of persistent cognitive deficits, including dementia, from neuroleptic treatment.
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PMID:Parallels between neuroleptic effects and lethargic encephalitis: the production of dyskinesias and cognitive disorders. 810 24

We studied 53 patients (64% females) with static brain lesions who developed progressive movement disorders. Of these, 50 (94%) had dystonia, 17 (32%) tremor, eight (15%) parkinsonism, seven (13%) myoclonus, and three (6%) chorea. The precipitating insults included perinatal hypoxia/ischemia in 22 (42%), stroke in 12 (23%), head injury in eight (15%), encephalitis in eight (15%), and carbon monoxide poisoning, kernicterus, and radiation necrosis in one patient (2%) each. Among the 30 patients with initial insult occurring at age 2 years or younger (Infant group), distribution of dystonia at follow-up was focal in three (10%), segmental in eight (27%), unilateral in 10 (33%), and generalized in nine (30%). The mean latency between the original injury and onset of movement disorder was 25.5 +/- 16.7 years. Among the nine patients who developed dystonia after an insult occurring between ages 6 and 17 (Childhood group), the distribution of dystonia at follow-up was segmental in two (33%) and unilateral in seven (78%); the mean latency of dystonia onset was 4.9 +/- 7.8 years. Of the 14 patients in the Adult group (injury at age 25 or older), 11 developed dystonia, two developed parkinsonism, and one had carbon monoxide encephalopathy and parkinsonism. The distribution of dystonia in the 11 patients at follow-up was segmental in three (27%) and unilateral in eight (73%). The mean latency of movement disorder onset in the 14 patients of the Adult group was 2.5 +/- 4.9 years. No individuals in the Childhood or Adult groups became left-hand dominant; by comparison, nine of the 30 individuals in the Infant group became left-handed. In conclusion, brain injury at a young age is associated with a longer latency to onset of subsequent movement disorder, a greater tendency to development of generalized dystonia, and a greater probability of altered handedness. These tendencies may result from differences in age-related neuroplasticity.
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PMID:Delayed-onset progressive movement disorders after static brain lesions. 890 76

In 1954, when he was five years old, a patient suffered from encephalitis with a prolonged lethargic state. Following this episode, he presented a severe parkinsonian syndrome which was associated, after a few years, with an axial dystonia and stereotyped involuntary movements of the upper limbs. These abnormal movements were particular by their coordinated appearance, their rhythmicity and their relative slowness. Treatment with L-dopa suppressed all akinetic, dystonic and dyskinetic symptoms. At age of 40 years, all the akinetic, dystonic and dyskinetic symptoms reappeared after drug withdrawal. Cerebral computed tomography, magnetic resonance imaging and fluorodeoxyglucose positron emission tomography were normal. Fluorodopa positron emission tomography revealed a significant bilateral reduction of tracer accumulation in the posterior part of both putamen, similar to that observed in patients with idiopathic Parkinson's disease. In this patient, pharmacological tests revealed that effectiveness of L-dopa was abolished by administration of a D2 antagonist, and was fully reproduced by a D2 agonist. Clinical signs, pharmacological data and past-medical history strongly suggested a limited lesion of the zona compacta of substantia nigra induced by viral agression. This complex and progressive extrapyramidal syndrome had strong similarities with the lethargic encephalitis of Von Economo and its late symptoms. Other diseases associating akinesia and dyskinesia or dystonic phenomena, like dopa-sensitive dystonia and juvenile Parkinson's disease, are very unlikely. Thus, the persistance of sporadic forms of Von Economo's encephalitis could be discussed.
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PMID:[Parkinsonian syndrome and post-encephalitic stereotyped involuntary movements responsive to L-dopa]. 876 55

In 1954, at the age of 5 years, our patient had an encephalitic syndrome associated with a prolonged lethargic state. After this episode, he developed a severe parkinsonian syndrome that, after a few years, was associated with axial dystonia and stereotyped abnormal movements of the upper limbs. This complex and progressive extrapyramidal syndrome had many similarities to the encephalitis lethargica as described by von Economo. Results of cerebral computed tomography and magnetic resonance imaging were normal. Fluorodopa positron emission tomography showed a significant bilateral reduction of tracer accumulation in both putamen, similar to that observed in patients with idiopathic Parkinson's disease. However, in this patient, treatment with L-Dopa suppressed all akinetic, dystonic and dyskinetic symptoms. The effectiveness of L-Dopa was abolished by administration of a D2 antagonist and was fully reproduced by a D2 agonist. In conclusion, this patient presented a complex postencephalitic, extrapyramidal syndrome, with akinetic symptoms and involuntary movements. These symptoms appeared to be related to a limited lesion of the dopaminergic neurons of the zona compacta of the substantia nigra.
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PMID:Postencephalitic stereotyped involuntary movements responsive to L-Dopa. 886 99

Magnetic motor-evoked potential (MEP) study of patients with the syndrome of delayed posthemiplegic hemidystonia, hemiatrophy, and partial or hemi-seizures ('4-hemi' syndrome) has not been described. Among 35 patients investigated for posthemiplegic movement disorders from February 1988 to January 1995, seven showed '4-hemi' syndrome. Clinical work-up, magnetic resonance images (MRI) and/or computed tomography (CT) were performed in all. Transcranial MEP studies were done in five patients. The remote causes of '4-hemi' syndrome were neonatal stroke, trauma, and encephalitis in infancy. The dystonia may occur as long as a decade after the initial insult. MRI or CT showed destructive lesion in the contralateral putamen (five patients), caudate (four), thalamus (five), and atrophy of the contralateral hemisphere (five). Other associations were porencephalic cyst. Wallerian degeneration, and asymmetric compensatory ventriculomegaly. MEP showed abnormalities in the affected upper limbs in four of five patients. The abnormalities were reduced amplitude of the compound muscle action potential following cortical stimulations with or without temporal dispersion, and with or without prolongation of its latency. The peripheral motor conductions following cervical stimulations were normal. MEP abnormalities may not be related to the hemiatrophy and the size of brain lesion per se. The hemidystonia is static after the second decade of life, and it is often difficult to treat.
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PMID:The syndrome of delayed posthemiplegic hemidystonia, hemiatrophy, and partial seizure: clinical, neuroimaging, and motor-evoked potential studies. 888 90


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