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)

Of 125 patients with neuroleptic (dopamine blocking) drug-induced movement disorders who had been referred to a specialized clinic to differentiate the predominant movement disorder, 63% had tardive dyskinesia, 30% had parkinsonism, 24% had dystonia, 7% had akathisia, and 2% had isolated tremor. Two or more movement disorders coexisted in 31 patients (25%). Functional disability was more severe in patients with akathisia than in other patients. Women outnumbered men at a ratio of 4:1, except for tardive dystonia which affected both sexes equally. The average at onset was 56 years (range, 13 to 87); 69 patients (55%) had onset of movement disorder in the sixth decade. While tardive dystonia was distributed relatively evenly in all age groups, almost a third of patients with parkinsonism had it in the eighth decade. Haloperidol was implicated in 47 patients (37%), followed by amitriptyline/perphenazine in 30%, thioridazine in 27%, and chlorpromazine in 20%. Metoclopramide-induced movement disorders were found in 10 (8%). Most patients (101 or 81%) had history of psychiatric illnesses, but of these only 44 had psychosis. Neuroleptic drugs had been prescribed for 33 patients (26%) who had gastrointestinal problems. It is important to recognize and differentiate various drug-induced movement disorders because such differentiation has pathophysiologic and therapeutic implications. Many patients could have been treated with less potent drugs.
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PMID:Neurologic approach to drug-induced movement disorders: a study of 125 patients. 197 59

Metoclopramide, a dopamine-2 receptor antagonist used for various gastrointestinal disorders, may cause or exacerbate a variety of extrapyramidal movement disorders. To draw attention to the frequent occurrence of metoclopramide-induced movement disorders, we identified and studied 16 patients who had been exposed to this neuroleptic. The average age at onset was 63 years (range, 24 to 85 years), and women outnumbered men 3 to 1. Tardive dyskinesia was the most common movement disorder (n = 10 [63%]). Five patients had metoclopramide-induced parkinsonism, 1 patient had tardive dystonia, and 1 patient had akathisia. The average duration of exposure prior to onset of movement disorders was 12 months (range, 1 day to 4 years). Therapy was continued for an average of 6 months (range, 1 day to 2 years) after the onset of symptoms, reflecting clinical nonrecognition of the movement disorder and its relationship to metoclopramide. To prevent persistent and disabling movement disorders, long-term use of metoclopramide should be avoided, and patients should be carefully observed for potential neurologic reactions.
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PMID:Metoclopramide-induced movement disorders. Clinical findings with a review of the literature. 268 75

Sixty-four patients treated with cisplatin-containing regimens were entered into a randomized, double-blinded study examining the antiemetic efficacy of metoclopramide with and without lorazepam for control of cisplatin-induced emesis. Metoclopramide was administered to all patients at 2 mg/kg, intravenously, 30 minutes before chemotherapy and 1.5, 3.5, and 5.5 hours posttreatment. Patients randomized to receive combined antiemetic therapy were administered lorazepam at 2 mg/m2 (maximum, 4 mg dose) intravenously, 30 minutes before chemotherapy. Those patients not receiving lorazepam were given normal saline placebo. Degree of nausea and number of vomiting episodes were recorded on a data flow sheet with a visual analogue scale. Drug toxicities were evaluated before each administered dose. Patients receiving both metoclopramide and lorazepam experienced significantly less vomiting episodes (P less than 0.05) and nausea (P less than 0.01) when compared to patients given metoclopramide alone. Forty-four percent of those receiving the combined therapy reported no nausea or vomiting episodes compared to only 22% receiving metoclopramide alone. Sedation was significantly more common in patients receiving lorazepam (88%) as opposed to patients receiving only metoclopramide (43%), P less than 0.01. Amnesia was seen in 25% receiving lorazepam. No significant difference in diarrhea, dystonia, or disinhibition was observed between the two arms. The authors conclude that the combination of lorazepam and metoclopramide was superior to metoclopramide alone in the prevention of cisplatin-induced nausea and vomiting, with sedation and amnesia more commonly observed in the combined regimen.
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PMID:Metoclopramide versus metoclopramide and lorazepam. Superiority of combined therapy in the control of cisplatin-induced emesis. 291 33

Metoclopramide (Paspertin) was infused intravenously in the high doses of 1.75, 3.5, 7.0, and 14 mg/kg body wt. per treatment cycle as antiemetic therapy for cisplatin-induced emesis (363 cycles, 25-120 mg/m2). The antiemetic potency of metoclopramide increased in a log linear manner, giving from 40% to 95% protection against emesis. Gastrointestinal motility showed a similar increase, i.e. diarrhoea. In contrast, the extrapyramidal reactions, namely akathisia, rigidity and acute dystonia, did not show a dose-dependent increase in frequency and remained constant over the dose range of 3.5-14 mg/kg per cycle. The results suggest increasing benefit of metoclopramide treatment with increasing doses of the drug.
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PMID:Improved benefit/risk ratio of higher-dose metoclopramide therapy during cisplatin-induced emesis. 407 27

Five Cebus apella monkeys with persistent neuroleptic-induced dyskinesia were given a single dose of sulpiride (20 mg/kg i.m.). The dyskinesia was reduced in all five although four developed attacks of acute dystonia which had to be reversed by anticholinergic medication in three animals. In one monkey the administration of classic neuroleptics had earlier been shown to induce a typical sequence of events. First there was a similar reduction of dyskinesia as seen in the other monkeys, 1-2 days later there was noticed a rebound deterioration lasting for several days. Metoclopramide 0.5 mg/kg, caused such a rebound effect (for 2 days), whereas sulpiride did not.
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PMID:Effects of sulpiride on persistent neuroleptic-induced dyskinesia in monkeys. 614 86

We compared acute effects of single intravenous administrations of metoclopramide (40 mg) and placebo in a double-blind crossover study involving 81 patients with tardive dyskinesia. Metoclopramide produced significantly greater reduction in mean total Abnormal Involuntary Movement Scale score as well as in ratings for six of the seven body areas, when compared with placebo. On adjusting each patient's metoclopramide response for his or her placebo response, we found that 35 of the 81 patients had 50% or greater placebo-corrected improvement. There were no apparent clinical differences between metoclopramide responders and nonresponders. Administration of 60 mg of metoclopramide to 15 patients produced greater improvement in tardive dyskinesia as compared with 40 mg; the incidence of acute dystonia, however, jumped from 10% with 40 mg to 33% with 60 mg.
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PMID:Effects of intravenous metoclopramide in 81 patients with tardive dyskinesia. 717 60

A familial study of 13 Ashkenasy Jewish patients suffering from torsion dystonia (TD) of various origin, was carried out using clinical observation and determination of serum dopamine-beta-hydroxylase (DBH) activity. None of the following criteria: Jewish origin, dominant trait, slow progression and axial topography are specific for an elevated serum DBH activity. A significantly high serum DBH activity was found in TD patients and their relatives compared with controls, particularly in the childhood onset group. Intravenous injection of 20 mg Metoclopramide (MP) did not change serum DBH activity in 12 patients and 17 relatives. In one patient with symptomatic dystonia and two of her maternal relatives (from different fathers) serum DBH activity increased after i.v. injection of MP. In these three cases the serum DBH activity doubled and tripled. It is suggested that the MP induced elevation of serum DBH activity in relatives of TD patients indicates a genetic disposition.
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PMID:Serum dopamine beta hydroxylase activity and metoclopramide provocative test in torsion dystonia. 735 23

Metoclopramide is a dopamine antagonist that is widely used in gastroesophageal disease and chemotherapy-induced emesis in the paediatric population. It is also prescribed in nausea and vomiting caused by respiratory tract infections and enteritis in practice. The primary side-effect of the drug is extrapyramidal reactions with incidences as high as 25% in children. We report two cases, one of which was referred to our emergency department as encephalitis and the other as tetany, but which were just acute dystonic reactions caused by metaclopramide, even though the patients had used the drug in the recommended dosages. The adverse effects of the drug can be seen at normal doses. These dystonic reactions caused by metaclopramide can easily be confused with other diseases, because dystonia is not seen frequently in paediatric practice whatever the cause.
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PMID:Metoclopramide induced dystonia in children: two case reports. 1589 43

Metoclopramide, the only drug approved by the FDA for treatment of diabetic gastroparesis, but used off-label for a variety of other gastrointestinal indications, has many potentially troublesome adverse neurologic effects, particularly movement disorders. In this article, we comprehensively review the indications and side effects of metoclopramide, and describe some common pitfalls and strategies to minimize the medicolegal risks to the prescribing physician. Metoclopramide accounts for nearly a third of all drug-induced movement disorders, a common reason for a malpractice suit. The entire spectrum of drug-induced movement disorders, ranging from subtle to life-threatening, can ensue from its use; akathisia and dystonia are generally seen early in the course of metoclopramide-induced movement disorders, whereas tardive dyskinesia and parkinsonism seem to be more prevalent in chronic users. Female sex, age and diabetes are the major risk factors for metoclopramide-induced movement disorders. It is therefore incumbent on gastroenterologists and other prescribing physicians to become familiar with the adverse neurologic effects associated with the use of metoclopramide, and to take appropriate preventive and defensive measures.
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PMID:Drug Insight: from disturbed motility to disordered movement--a review of the clinical benefits and medicolegal risks of metoclopramide. 1651 48

Metoclopramide is a dopamine receptor antagonist that is used to treat diabetic gastroparesis, chemotherapy-induced nausea, and migraines. It is known to cause extrapyramidal side effects such as tardive dyskinesia, parkinsonism, dystonia, and akithisia, but not chorea. We describe a patient who presented with choreiform movements shortly after the administration of intravenous metoclopramide. Her work-up for secondary causes of chorea was otherwise negative and her symptoms abated with the administration of oral quetiapine and intravenous diazepam.
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PMID:Acute chorea associated with metoclopramide use. 1712 36


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