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)

Three patients with hemichorea and ten with dystonia of vascular origin are reported. Five were secondary to ischemic infarcts, two to lacunar infarcts, three to intraparenchymal hematoma, and in the remaining three the type of lesion could not be determined. The patients with chorea, as opposed to those with dystonia, presented abruptly immediately after the stroke, and had a regressive evolution and good therapeutic response. The type of dyskinesia was not useful to identify the precise localization of the lesion or to determine its nature. In addition, in 5 patients multiple lesions were found and 5 had release of archaic reflexes or cortical atrophy in CT; this shows the importance of the overall functional impairment and focal lesions in the genesis of dyskinesia. There were sensory deficits in 7 patients. In 2 patients lesions were not found in the CT in spite of the presence of previous hemiparesis; this suggests that this technique has limitations to discover focal cerebral lesions in patients with focal or hemicorporal dyskinesia.
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PMID:[Abnormal movements of vascular origin]. 263 96

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

Lacunar infarcts in the basal ganglia are known to cause various movement disorders, such as chorea, focal dystonia, and hemichorea-hemiballismus. We report here a case of putaminal lacunar infarction which presented with "painful tonic spasms" of the contralateral limbs. This consisted of paroxysmal brief, painful, flexor contractures of the upper, and occasionally the lower limb. These were not focal seizures but were controlled with carbamazepine, which has been used for the "painful tonic spasms" well-associated with multiple sclerosis. The putaminal infarct we describe is probably related to a lupus anticoagulant and systemic lupus erythematosus.
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PMID:Painful tonic spasms caused by putaminal infarction. 381 Jul 37

Reports of 62 cases with a movement disorder associated with a focal lesion in the thalamus and/or subthalamic region were analyzed. Thirty-three cases had a lesion confined to the thalamus. Sixteen cases had a thalamic lesion extending into the subthalamic region and/or midbrain. Thirteen cases had a lesion in the subthalamic region or a subthalamic lesion extending into the midbrain. Nineteen cases with dystonia, 18 with asterixis, 17 with ballism-chorea, three with paroxysmal dystonia, and five with clonic or myorhythmic movements have been described. No case with isolated tremor has been described. In 53 cases with unilateral thalamic or subthalamic lesions, all but one with bilateral blepharospasm (associated with right posterior thalamic, pontomesencephalic, and bilateral cerebellar lesions) had dyskinesias in the limbs contralateral to the lesion. The other nine cases had bilateral paramedian thalamic lesions; seven developed bilateral dyskinesias, and the remaining two had unilateral dyskinesias. Regarding the 19 patients with dystonia, the two with bilateral blepharospasm had thalamic and upper brainstem lesions, and one with hemidystonia and torticollis had a subthalamic lesion. The other 16 patients all had a unilateral thalamic lesion with contralateral dystonia (10 hemidystonia, five focal dystonia affecting a hand and/or and one segmental dystonia involving face, arm, and hand). The exact location of the thalamic lesion was mentioned in 10 cases; the posterior or posterolateral thalamus was involved in six and the paramedian thalamus in four. These areas are more posterior or medial to the ventrolateral and ventroanterior thalamic nuclei, which receive pallido-thalamic and nigro-thalamic afferents. Two cases developed dystonia immediately after thalamotomy, and one case developed it 4 days after head trauma. The others initially had a hemiplegia and developed dystonia 1-9 months after the acute insult. Fifteen of the 17 patients with chorea had a unilateral lesion in the subthalamic nucleus or subthalamic region (eight due to infarcts, one to hemorrhage, five to mass lesions, and one to multiple sclerosis). All had contralateral hemichorea or hemiballism. One other case had bilateral chorea of the hands and tongue due to paramedian thalamic infarction. Another case with generalized chorea and thalamic atrophy was complicated by stereotaxic surgery. Thirteen of the 18 cases with asterixis had lesions confined to the thalamus. Eight were associated with thalamotomy, and five others had a stroke (four infarction and one hemorrhage) affecting the contralateral thalamus.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Movement disorders following lesions of the thalamus or subthalamic region. 799 Aug 45

Stroke-related nonepileptic transient dyskinesias are rare, and the site of ischemia remains often undetermined. Five cases out of 47 consecutive thalamic infarcts (10.6 per cent) are reported. Patients presented with monochorea (1 case), hemiballism-hemichorea (2 cases), choreoathetosis (1 case with subsequent arm painful dystonia and hand tremor), and asterixis (1 case). Magnetic resonance imaging demonstrated that the subthalamic nucleus was spared in all cases. Transient dyskinesias occurred at any time in the course of infarction (as a warning sign in 1 case, as an associated symptom in 3 cases, or during recovery in 1 case). Moreover, this study suggests that: 1) transient dyskinesias are mainly related to thalamic ischemic injury, and 2) small vessels disease is the main etiology.
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PMID:[Transient involuntary movement disorders and thalamic infarction]. 830 59

Seven patients with dyskinesia due to cerebrovascular lesions are described. They presented hemichorea, hemiballism and focal dystonia; the site(s) of the lesion responsible, as defined by MRI (magnetic resonance imaging) or CT (computerized tomography) scan were the putamen, the caudatus, the thalamus and the subthalamic body of Luys. Data of similar cases in the literature are reviewed with reference to the location of the responsible lesions, which can aid in predicting the outcome of illness or prescribing treatment.
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PMID:Dyskinesia of vascular origin. Clinical data and response to therapy in 7 cases. 861 18

The symptomatic and functional outcomes of a series of 14 patients with disabling and medically refractory hemiballism who were treated with functional stereotactic surgery are reported. Seven (50%) of the 14 patients had concomitant hemichorea. To relieve the hyperkinesia, the 14 patients underwent a total of 15 stereotactic operations (one patient had a second stereotactic procedure). Combined lesions in the contralateral zona incerta and the base of the ventrolateral (oroventral) thalamus were applied in 13 instances. The zona incerta was reached by means of a movable chord electrode to obviate the need for repeated puncture. In two instances the medial pallidum was used as the stereotactic target. Hemiballism was abolished or considerably improved in 13 (93%) of 14 patients in the immediate postoperative phase. Residual dyskinesia was evaluated using the hemiballism/hemichorea outcome rating scale. Long-term follow-up review was available for 13 of the 14 patients (mean follow-up period 11 years). Persistent improvement in the hemiballism was found in 12 of these 13 patients: seven patients (54%) were free of any hyperkinesia and five patients (39%) had minor residual and predominantly hemichoreic hyperkinesia. One of the 13 patients presented with a probable psychogenic movement disorder at long-term follow-up examination. Persistent morbidity, most likely related to the operative intervention, was detected in three of the 13 patients; this included mild hemiparesis and dystonia. Functional disability was assessed using the Huntington's Disease Activities of Daily Living scale. The patients' preoperative mean value of 83% of maximum disability was reduced to a mean of 30% observed at long-term follow-up review (p < 0.001). The residual disability exhibited in most older patients was associated with cardiovascular disease. The authors compare their findings with the results of 44 cases reported previously. The authors contend that functional stereotactic surgery should be considered in patients with persistent, medically refractory hemiballism.
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PMID:Functional stereotactic surgery for hemiballism. 875 57

Reports of 9 cases with hand dystonia due to stroke are described. The site of the lesion was found to be parietothalamic in 1 patient, posterolateral thalamic in 5 patients, dorsal thalamic in 2 patients and medial thalamic in 1 patient as defined by computerized tomography or magnetic resonance imaging. In addition to the hand dystonia, hemiballism was noted in 1 case, hemichorea in 2 cases, action tremor in 3, anxiety in 3 and pain in 2 cases. The time lapse from the stroke to the manifestation of dystonia was 1 month to 2 years.
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PMID:Lesion localization in developing poststroke hand dystonia. 969 39

A series of six patients with movement disorders associated with cerebral arteriovenous malformations (AVM) is reported. The AVMs were classified according to the Spetzler-Martin classification as grade V (one patient), grade IV (four patients), and as grade III (one patient). One patient had action-induced hemidystonia caused by a contralateral frontoparietal AVM which compressed the putamen and was supplied partially by enlarged lenticulostriate arteries. Two patients presented with unilateral cortical tremor associated with contralateral high-frontal cortical/subcortical AVMs sparing the basal ganglia. Another patient developed hemidystonia and hemichorea-hemiballism after bleeding of a contralateral temporooccipital AVM and subsequent ischemia. Two patients had focal dystonia after thalamic and basal ganglia hemorrhage from AVMs. Five patients were operated on. The movement disorder was abolished in one patient postoperatively. Different mechanisms were identified that are relevant for the development of AVM-related movement disorders: mass effect, diaschisis, local parenchymal altered cerebral blood flow, and hemorrhagic or ischemic structural lesions.
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PMID:Cerebral arteriovenous malformations and movement disorders. 1046 3

A 12-month-old boy with acute onset hemichorea and dystonia following a gastroenteritis has abnormal signal intensities of his basal ganglia on brain magnetic resonance imaging (MRI). A rigorous laboratory investigation is successful in diagnosing his rare condition. A discussion of the differential of abnormal basal ganglia on MRI is presented to help illustrate this case.
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PMID:Acute onset of chorea and dystonia following a febrile illness in a 1-year-old boy. 1052 42


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