Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of fusaric acid 150-450 mg daily on tardive dyskinesia and mental state was studied in 15 chronic psychogeriatric patients. The patient's previous drug treatment was maintained unchanged during the experiment. Fusaric acid significantly relieved oro-facial dyskinesia, tremor, and rigidity, and it improved the mental state of the patients (BPRS). Akathisia was exacerbated, but this change was not significant. Akinesia and anxiety were not altered.
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PMID:Effect of fusaric acid on tardive dyskinesia and mental state in psychogeriatric patients. A pilot study. 33 75

In a double-blind crossover placebo controlled trial the effectivity of piracetam in neuroleptic-induced extrapyramidal side effects was confirmed. 40 psychotic patients treated with neuroleptics in an average daily dose equal to 600 mg of chlorpromazine were included in this study. Akathisia, tremor, muscle rigidity and dyskinesia were evaluated on a 4-point scale. The patients were randomly divided into two subgroups--40 g of piracetam or placebo from identic ampoules were given i.v. with a crossover readministration after 60 min. The intensity of the extrapyramidal side effects was evaluated at 30-min intervals during 2 h. Piracetam was proved to be significantly effective in both subgroups, the onset of its action being between 30 and 60 min after i.v. administration. Possible interpretations of the observed piracetam effectivity are considered. Further trials with piracetam in neurologic complications during neuroleptic treatment, tardive dyskinesia included, are suggested.
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PMID:Effect of piracetam on extrapyramidal side effects induced by neuroleptic drugs. 612 31

This case report describes a schizophrenic patient who developed akathisia and tremor following neuroleptic pharmacotherapy with fluphenazine decanoate. The patient also suffered from familial (benign essential) tremor. The patient's neuroleptic-induced extrapyramidal side effects were not relieved by anticholinergic antiparkinson drugs or by phenobarbital. The patient was started on propranolol 10 mg b.i.d. She was also started on diazepam 5 mg t.i.d. for anxiety. The diazepam dose was held constant and propranolol was gradually increased to 40 mg q.i.d. The patient's extrapyramidal symptomatology gradually resolved over the course of one month, during which time the propranolol dose was being steadily increased. Propranolol also effectively controlled her familial tremor. After nine months as an outpatient, during which time the patient was neuroleptic-free, she developed psychotic decompensation for which she was treated with thiothixene. Akathisia or tremor did not develop, possibly because the patient was taking propranolol simultaneously. Propranolol may be useful for treating neuroleptic-induced akathisia. This requires systematic investigation with open and controlled trials.
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PMID:Case report of propranolol (Inderal) pharmacotherapy for neuroleptic-induced akathisia and tremor. 613 28

Neuroleptic-induced extrapyramidal side effects (EPS) were evaluated in 92 patients treated with clozapine for the first time and 59 patients treated with haloperidol followed in a drug monitoring program. Side effects were measured by the Columbia University Rating Scale, the Simpson Dyskinesia Scale and the Hillside Akathisia Scale. The cumulative incidence rate for tremor was found to be 24.4% in the clozapine group and 39.3% in the haloperidol group. This did not amount to a statistically significant group difference. Bradykinesia was observed in 21.8% of the patients treated with clozapine and in 47.7% of the patients of haloperidol (P = 0.011). In the clozapine group the akathisia incidence rate was 5.6%, whereas haloperidol patients showed a higher rate of 31.7% (P = 0.005). Our results show higher incidence rates of tremor and bradykinesia during clozapine treatment than previous studies. We conclude that clozapine is not entirely free of EPS, but they are usually less severe and of a different quality than side effects induced by typical antipsychotics.
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PMID:Extrapyramidal side effects of clozapine and haloperidol. 759 22

FK506 is a macrolide immunosuppressant agent used in solid organ and bone marrow transplantation and for autoimmune disorders. FK506 is reported to have a number of neuropsychiatric side effects, including anxiety and tremor. Because FK506 was implicated in causing akathisia in a case report, we did a prospective, cross-sectional study of 25 renal transplant recipients to determine whether akathisia occurred and/or had a relationship to FK506 plasma levels. The Symptom Checklist-90-R, Hamilton Anxiety (HAM-A), and Akathisia Rating (ARS) scales were administered. Higher FK506 plasma levels correlated with higher HAM-A scores. ARS scores did not correlate with FK506 plasma levels; however, when FK506 plasma levels were divided into "high" (> or = 0.9 ng/mL) and "low" (< 0.9 ng/mL) groups, total ARS and HAM-A scores were significantly higher in the "high" group. We discuss implications of these findings as well as management.
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PMID:Prospective study of FK506 side effects: anxiety or akathisia? 887 43

Akathisia is characterized by subjective discomfort and motor restlessness. The motor hyperactivity can express itself by frequent changes of posture, constant limb shaking or restless pacing. If symptoms of akathisia are severe, treatment becomes extremely complicated and patients may even become suicidal as seen in the case described here. In the literature, different forms of akathisia are distinguished (Barnes and Braude, 1985): the acute form of neuroleptic-induced akathisia (recent onset, related to an increase in antipsychotic drug dose), pseudoakathisia (motor signs but no subjective symptoms), and chronic or tardive akathisia. The acute form of akathisia is well known and described (Zubenko et al., 1984a,b). In a retrospective analysis of clinical features and therapeutic trials for tardive akathisia, Burke et al. (1989) showed that almost all of the 52 cases developed this chronic form after an average of 4.5 yr following neuroleptic drug initiation, 34% even within 1 yr. Twenty-six of the patients who were able to stop taking dopamine antagonists still had symptoms of akathisia persisting for 0.3-7 yr (mean = 2.7 yr).
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PMID:Treatment of tardive akathisia with clonidine: a case report. 1128 83

Predictors for the development of tardive dyskinesia (TD) have been studied extensively over the years, yet there are few studies of predictors of the course of TD after it has developed. Moreover, few studies have examined predictors of the course of other extrapyramidal side effects (EPS) in patients maintained on neuroleptics. The purpose of this study was to determine which modifiable variables are important in the prediction of EPS in patients with persistent TD over a period of as long as 2 years. One hundred fifty-eight patients enrolled in the Veterans Affairs Cooperative Study 394 were included in this study. A linear mixed-effects (LME) analysis to estimate the Abnormal Involuntary Movement Scale score (for TD severity), Simpson-Angus Scale (for parkinsonism severity), and Barnes Akathisia Scale at any given time after intake assessment was performed. The severity of each of the TD and EPS outcomes at any given visit was predicted by their respective baseline severity scores. Additional predictors of a favorable course of TD included lower doses of antipsychotic medications and use of anticholinergic medications. Other predictors of a favorable course of EPS included younger age and the use of atypical antipsychotic medication (for rigidity) and the use of anticholinergic medication (for tremor). These findings indicate that clinician-modifiable factors related to medication usage can influence the outcome of TD and EPS in patients with persistent TD.
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PMID:Treatment predictors of extrapyramidal side effects in patients with tardive dyskinesia: results from Veterans Affairs Cooperative Study 394. 1191 Feb 66

Data from a published double-blind randomized trial comparing olanzapine versus haloperidol in acute mania were used to address the response and tolerability of Latin American patients. Primary efficacy end point was the remission rate (Young Mania Rating Scale score <or=12 and Hamilton Depression Rating Scale score of <or=8). Patients were analyzed on an intent-to-treat basis. The mean modal doses (milligrams per day) were similar in Latin American (OL) (14.2; n = 51) and white (OC) (15.1; n = 120) patients treated with olanzapine, and in Latin American (HL) (7.1; n = 48) and white (HC) (8.5; n = 113) patients treated with haloperidol. At week 6, remission rates were similar among the OL and HL patients (64.7% vs. 68.8%) but were higher in the OC than in HC (49.2% vs. 32.7%; P = 0.012). Significantly more HL than OL patients experienced extrapyramidal symptoms such as akathisia and tremor. Tremor was significantly higher in HL than in HC patients, whereas a significant increase in the Barnes Akathisia Scale and Abnormal Involuntary Movement Scale scores was observed in HC versus HL. Somnolence and weight gain were significantly higher in OL than in OC patients, and more OL and OC patients experienced weight gain in comparison with the HL and HC groups, respectively. The incidence of nonfasting glucose levels above normal levels did not statistically differ between groups. In conclusion, in contrast to our findings among white patients, the Latin American patients who have acute mania did not differ in overall response to olanzapine or haloperidol. The pattern of adverse events differed between treatment groups. Prospective clinical trials in Latin American bipolar populations are justified.
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PMID:Outcomes for Latin American versus White patients suffering from acute mania in a randomized, double-blind trial comparing olanzapine and haloperidol. 1741 34

Quetiapine is an atypical antipsychotic agent with well established efficacy and tolerability in the acute and maintenance treatment of adults with schizophrenia. The extended-release formulation of quetiapine (quetiapine XR) was developed to provide more convenient once-daily administration, as well as allowing simple and rapid dose escalation, with the aim of improving compliance (known to be a substantial issue in patients with schizophrenia). In several short-term clinical trials, oral quetiapine XR 400-800 mg once daily was generally effective across a range of symptoms in the acute treatment of schizophrenia. As a long-term maintenance treatment, quetiapine XR prevented relapse in patients with stable disease, with significantly longer times to relapse in patients treated with quetiapine XR compared with placebo. Quetiapine XR was generally well tolerated in clinical trials. According to pooled results from three 6-week trials, events occurring in >or=5% of quetiapine XR recipients with an incidence>or=2-fold that seen in placebo recipients were dry mouth, somnolence and dizziness. A generally low incidence of extrapyramidal symptoms (EPS) is seen in quetiapine XR recipients. The most common potentially EPS-associated adverse events seen with quetiapine treatment were akathisia, restlessness and tremor. Rates of worsening of Simpson-Angus Scale and Barnes Akathisia Rating Scale scores were not dissimilar among quetiapine XR, quetiapine immediate release and placebo.
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PMID:Quetiapine extended release: in schizophrenia. 1932 May 34