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)

We report a patient with severe axial tardive dystonia who has had dramatic improvement for 4 years after treatment with the atypical antipsychotic drug clozapine (625 mg/day). Clozapine differs from conventional neuroleptics in that it has higher affinity for D1 and lower affinity for D2 dopamine receptors than do conventional antipsychotics, which are relatively selective D2 antagonists. We propose that repetitive stimulation of the D1 receptor by endogenous dopamine, resulting in sensitization of the D1-mediated striatal output in the presence of D2 receptor blockade, is a fundamental mechanism mediating tardive dyskinesia, including the dystonic type. According to this hypothesis, it is primarily the D1 antagonist action of clozapine that accounts for its inability to cause tardive dyskinesia as well as its therapeutic effect in tardive dystonia. Regardless of its mechanism of action, the sustained improvement observed in this case suggests that clozapine should be tried in cases of severe refractory tardive dystonia.
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PMID:Treatment of severe axial tardive dystonia with clozapine: case report and hypothesis. 796 12

We report the development of chronic painful oral or genital sensations in 11 patients with tardive akathisia, tardive dyskinesias, or tardive dystonia. In each case, the pain syndrome became a source of profound distress for the patient, overshadowing all other concurrent neuropsychiatric symptoms, and requiring treatment. Agents effective in treating tardive dyskinesia and tardive akathisia, such as catecholamine depletors, proved effective in reducing the painful sensations. Our observations support the concept of tardive pain as a complication of chronic neuroleptic exposure.
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PMID:Oral and genital tardive pain syndromes. 750 Nov 74

Clinical characteristics of 15 consecutively referred patients with tardive dystonia are reported. The onset of tardive dystonia occurred in all age groups and in both sexes, with some preponderance in men. There was considerable overlap with tardive dyskinesia and tardive akathisia. Six subjects reported past acute dystonia, and four had histories of essential tremor, suggesting a vulnerability to the development of dystonia.
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PMID:Clinical characteristics of 15 patients with tardive dystonia. 809

We describe a case of marked increases in serum creatine phosphokinase (CPK) associated with a dramatic exacerbation of tardive dyskinesia (TD). Chart review of eight additional patients with severe TD revealed three cases with mild CPK elevations. These cases suggest that TD, especially when accompanied by dystonia, may be associated with pathology of striated muscle.
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PMID:Serum creatine phosphokinase elevations in patients with tardive dyskinesia. 809 56

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

Eight Cebus apella monkeys were treated with haloperidol for 2 years. Five monkeys had developed mild oral tardive dyskinesia and all were primed for neuroleptic induced dystonia, thus serving as a model for both chronic and acute extrapyramidal side effects. In this model, the partial dopamine D2 receptor agonists SDZ HDC-912, SDZ HAC-911, terguride, (-)-3-(3-hydroxyphenyl)-N-propylpiperidine) ((-)-3-PPP) and SND 919 were tested for extrapyramidal side-effect liability. Their antipsychotic potential was also tested, using a dose of dextroamphetamine producing mild stereotypy and moderate motoric unrest. For comparison, the dopamine D2 receptor agonist, LY 171555 and antagonist, raclopride were used. In contrast to the other drugs tested, SDZ HAC-911 consistently reduced oral activity, P < 0.05 (at doses from 0.005 to 0.025 mg/kg). The relative dystonic potencies were raclopride > SDZ HDC-912 > SDZ HAC-911 = terguride. Neither (-)-3-PPP nor SND 919 produced dystonia, but had observable dopamine D2 receptor agonistic effects, (-)-3-PPP producing emesis at 1-4 mg/kg and SND 919 producing motoric unrest and stereotypy at 0.05-0.25 mg/kg. Comparing the antiamphetamine effects of the more antagonist-like drugs with raclopride, the relative potencies were terguride = SDZ HAC-911 > SDZ HDC-912 > raclopride. Comparing the antiamphetamine effects of the more agonist-like drugs with LY 171555, the relative potencies were SND 919 > (-)-3-PPP > LY 171555 in relation to motoric unrest, while neither (-)-3-PPP nor LY 171555 produced inhibition of stereotypy.
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PMID:Effects of several partial dopamine D2 receptor agonists in Cebus apella monkeys previously treated with haloperidol. 810 65

ADRs presenting as neurologic or psychic disturbances are rather frequent; therefore, it will not be possible to give a complete overview. Drug-induced extrapyramidal syndromes which are due to an interference of the drug or a drug metabolite with cerebral dopaminergic mechanisms in most instances are discussed in more detail. Neuroleptics are prominent in this group of preparations. Drug-induced Parkinsonism, acute dystonia, tardive dyskinesia and the neuroleptic malignant syndrome are the ADRs presented herein.
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PMID:[Drug side effects on the nervous system]. 810 59

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

Tardive dyskinesia (TD) has been associated with cognitive deficits, especially in older psychiatric patients on neuroleptic medication. This study investigated the relationship between presence of TD, organic brain dysfunction (OBD), and cognitive deficits in young psychiatric outpatients maintained on minimal doses of oral neuroleptics, with anticholinergics prescribed only on as-needed basis. Sixty-four patients, aged 20-39 years, were evaluated for the presence of abnormal movements, localizing and nonlocalizing physical signs, and deficits in memory, ability to shift, and sustained attention. Sixteen patients showed definite signs of TD. Significant associations were found between TD and OBD, and between cognitive deficits and OBD, but not between TD and cognitive deficits. Significant regression predictors of TD were the interaction between OBD and previous dystonia, as well as duration of neuroleptic treatment. These findings suggest that some potential risk factors for TD already identified in the literature also apply to younger patients with relatively shorter exposure to neuroleptics. However, the results indicate that the relationship between movement disorders and cognitive deficits may be more apparent in older patients.
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PMID:Organic brain dysfunction and cognitive deficits in young schizophrenic patients with tardive dyskinesia. 810 25


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