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)

The effects of three-week daily intrastriatal 45 mcg GABA, 5 and 15 mcg picrotoxin and 5 bicuculline microinjections in rats were investigated. The inhibition of avoidance conditioning in shuttle box was registered in first days of GABA microinjection; stereotyped behaviour and paradoxal freezing in further GABA effects were developed. After the short orofacial dyskinesia as the acute picrotoxin effects, the choreo-myoclonic limb jerks, with the distinct generalization stage were observed. Picrotoxin dose increasing in toxic convulsive status results. No any dystonia, but strong avoidance conditioning inhibition in all three weeks of bicuculline treatment were observed only. The novel functional and controlled model of choreo-myoclonic hyperkinesis is proposed. The role of the striatal GABA system in human neuro-motor dyskinesias were discussed.
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PMID:[Myoclonic hyperkinesis induced by repeated administration of picrotoxin into rat neostriatum]. 805 87

The St. Hans Rating Scale (SHRS) is a multidimensional rating scale for the evaluation of neuroleptic-induced hyperkinesia, parkinsonism, akathisia and dystonia. This scale and the Abnormal Involuntary Movement Scale (AIMS) were tested by 7 raters (2 experienced, 2 less experienced and 3 totally inexperienced) in 30 psychiatric patients with tardive dyskinesia (TD). The test was performed 3 times in the same patients: 1) live evaluation during a video recording, 2) evaluation 2 weeks later from the videotape, and 3) evaluation after another 2 weeks from the same videotape. The intrarater reliability was high in the experienced group (0.91-0.96 for SHRS hyperkinesia scale, 0.80-0.84 for AIMS, and 0.82-0.97 for SHRS total parkinsonism). No significant changes occurred from live to video evaluation. The interrater reliability coefficient for the experienced group was also high: 0.89-0.95 for the SHRS hyperkinesia scale, 0.76-0.85 for the AIMS scale and 0.95-0.98 for the SHRS parkinsonism scale. The less experienced and the inexperienced raters had coefficients for intra- and interrater reliability that were 0.10 and 0.20 lower, respectively. The SHRS parkinsonism scale had a high construct validity, as determined by the homogeneity coefficients of Cronbach (0.82) and Loevinger (0.43). The corresponding coefficients for the hyperkinesia scales were low, in agreement with the individual distribution of TD (only about 50% present extremity dyskinesia and less than 25% facial, head and trunk dyskinesia, independent of the severity of the syndrome). Finally, convergent validity was found between the SHRS hyperkinesia scale and AIMS and divergent validity between all of the other scales.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The St. Hans Rating Scale for extrapyramidal syndromes: reliability and validity. 809 78

Buspirone, an azospirone compound, is a nonsedative anxiolytic that has achieved wide usage since its introduction in 1987. Although relatively free of side-effects, there have been several instances of dyskinesia and dystonia associated with the use of buspirone. We report two patients with persistent movement disorders that developed after prolonged treatment with the drug. One patient developed a lasting problem of cervical-cranial dystonia and tremors after treatment with buspirone at a dosage of 40 mg/day for several weeks. Another, receiving 30 mg/day for 6 weeks, experienced an exacerbation of preexisting spasmodic torticollis and tardive dyskinesia as well as the onset of involuntary phonations. As shown by these and other examples, buspirone poses the risk for inducing or exacerbating several types of movement disorders.
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PMID:Persistent movement disorders induced by buspirone. 810 69

A group of four monkeys was rendered parkinsonian with the toxin MPTP. They were then treated chronically with L-DOPA/benserazide 50/12.5 mg/kg given orally daily for 2 months. This dose produced a striking antiparkinsonian effect, but all animals manifested dyskinesia. A series of agents acting primarily on neurotransmitters other than dopamine were then tested in combination with L-DOPA to see if the dyskinetic movements would be modified. Several drugs, including clonidine, physostigmine, methysergide, 5-MDOT, propranolol, and MK-801, markedly reduced the dyskinetic movements but at the cost of a return of parkinsonian symptomatology. However, yohimbine and meperidine reduced predominantly the dyskinetic movements. Baclofen was also useful in one monkey against a more dystonic form of dyskinesia. Atropine converted the dystonic movements into chorea.
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PMID:Effect of nondopaminergic drugs on L-dopa-induced dyskinesias in MPTP-treated monkeys. 810 50

Forty-one patients with Parkinson's disease and severe dyskinesias were analyzed retrospectively to determine if some general principles would emerge to aid physicians handling this complication of treatment. Dyskinesia type (high dopa chorea [HDC], low dopa chorea [LDC], high dopa dystonia [HDD], and low dopa dystonia [LDD]) predicted response to treatment and whether or not levodopa dose reduction would benefit dyskinesias without producing unacceptable "offs." High dopa chorea improved best but at the expense of increased "off" time, followed by LDD, HDD, and LDC. Levodopa reduction was an acceptable strategy in ameliorating HDC and LDD only. Adjunctive therapy benefited all dyskinesia types, although the majority of patients (12/17) helped by selegiline had LDD or LDC. Generally, low doses of dopamine agonists were helpful (bromocriptine < 20 mg/day; pergolide < 2 mg/day). When adding adjunctive therapy (except for selegiline or controlled-release carbidopa/levodopa), concomitant reduction in daily dose of levodopa was not an effective strategy to decrease dyskinesias. Serial trials of multiple drug regimens are useful in these patients.
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PMID:An analysis of treatment options and outcome in patients with Parkinson's disease and severe dyskinesias. 814 65

Because intramuscular injections of type A botulinum toxin (btx) are effective for idiopathic spasmodic torticollis, they were administered to 3 patients who had neck movements as their only manifestation of tardive dystonia. Each improved, with a decrease in involuntary movement and reduction in pain. None had either systemic or local side effects. Although expensive, btx treatment is recommended for involuntary neck movements of tardive dystonia but not yet for the classic buccolingual dyskinesia.
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PMID:Use of botulinum toxin injections for spasmodic torticollis of tardive dystonia. 814 37

The authors discuss the results of long-term follow-up, clinical and paraclinical examination, including electropolysomnography, of a female patient with a rare neurological syndrome, paroxysmal dystonia. The disease runs with frequent episodes of dyskinesia during slow-wave sleep. Diagnostic and treatment issues are also covered.
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PMID:[Hypnogenic paroxysmal dystonia]. 816 Apr 95

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

We report a case of juvenile Parkinson's disease which initially presented as bulbar incoordination at the age 12. The condition was characterized by dystonia of the upper extremities. The patient was a 14-year-old female. The patient's main symptoms were bulbar dysfunction. Resting and action tremor, akinesia, stooped posture, distortion of the trunk, dystonia of the upper extremities, oculogyric crisis, and impairment of the postural reflex were seen. The bulbar symptoms were considered to be attributable to circumoral uncoordination. Although L-dopa decarboxylase inhibitors were markedly effective in alleviating these symptoms, an adverse reaction due to the agent was observed as the form of oral dyskinesia. Since the changes in blood concentration of L-dopa after administration of the agent was clearly reflected in the surface electromyogram, we concluded that this diagnostic procedure is useful in evaluating the therapeutic efficacy of L-dopa.
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PMID:[Juvenile Parkinson's disease initially presenting as bulbar incoordination: a case report]. 818 82

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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