Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027066 (myoclonus)
 4,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1 The physiological, biochemical and pharmacological features of alpha-chloralose-induced myoclonus in the guinea-pig have been studied. 2 EMG bursts in muscles jerking in chloralose-induced myoclonus are long, and are not time-locked to any cortical event recorded in the EEG, although they are evoked by auditory or peripheral nerve stimuli. 3 The efferent conduction velocity down the spinal cord of the signals generating the EMG bursts is fast but the afferent conduction velocity up the cord for stimulus-evoked jerks is slow, in distinction to the reverse characteristics of the spino-bulbo-spinal relfex arc. 4 alpha-Choralose did not cause any consistent change in 5-hydroxytryptamine (5-HT) or 5-hydroxyindoleacetic acid levels in any brain area, nor did it alter 5-HT turnover as judged by the depletion of 5-HT after p-chlorophenylalanine pretreatment. 5 Pretreatment of animals with drugs that increase brain 5-HT action (L-tryptophan with a monoamine oxidase inhibitor, or 5-hydroxytryptophan), or antagonize the action of 5-HT (cyproheptadine) did not abolish or obviously increase chloralose-induced myoclonus. 6 Chloralose-induced myoclonus is not similar to 5-HT-sensitive reticular reflex myoclonus in man.
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PMID:Observations on chloralose-induced myoclonus in guinea-pigs. 615 35

Eleven patients with long-standing progressive myoclonus epilepsy, PME, and age- and sex-matched epileptic controls received L-tryptophan (L-Trp) 100 mg/kg body weight combined with carbidopa in addition to their usual anticonvulsant regimen. During six weeks of the trial an improvement in activities of daily living and a decrease of action myoclonus was noted in the PME patients. The frequency of seizures compared with the past year decreased significantly in the PME patients, but not in the epileptic controls. Changes in the EEGs of the PME patients were scant, but a slight decrease was noted in myoclonic spikes. Both plasma Trp and platelet 5-HT increased significantly and at least as much as in epileptic controls. 5-HIAA and HVA concentrations in the CSF of the PME patients increased significantly during the trial. The results support previous findings concerning Trp treatment in PME, and longer trials with Trp + carbidopa could be of value in this disease.
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PMID:L-tryptophan-carbidopa trial in patients with long-standing progressive myoclonus epilepsy. 617 51

Since p,p'-DDT-induced myoclonus is ameliorated by serotonin agonists and aggravated by serotonin antagonists, the effect of p,p'-DDT on serotonin metabolism in rat brain was examined. p,p'-DDT (600 mg/kg intragastrically) elevated plasma tryptophan as well as tryptophan and 5-hydroxyindoleacetic acid concentrations in all seven regional areas of the brain assayed. Serotonin levels were elevated only in the midbrain and cerebellum of p,p'-DDT-treated rats. p,p'-DDT increased serotonin turnover in the medulla and midbrain. p,p'-DDT had no effect on the transport of 5-hydroxyindoleacetic acid out of the central nervous system, serotonin uptake and release from nerve terminals, or serotonin receptor binding in the brain. The findings in this study do not support a brain serotonin deficiency hypothesis as the explanation for the response of p,p'-DDT-induced myoclonus to serotonin agonists.
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PMID:p,p'-DDT-induced alterations in brain serotonin metabolism. 617 20

L-5-Hydroxytryptophan (5HTP) (with or without carbidopa pretreatment), L-tryptophan (plus pargyline pretreatment), or tryptamine (plus pargyline pretreatment) all induced dose-dependent myoclonus in guinea pigs. At the time of maximal behavioural response animals were killed for determination of brain indoleamine content. Administration of 5HTP (50-200 mg/kg) to naive guinea pigs, or of 5HTP (20-80 mg/kg) to carbidopa- (25 mg/kg 1 hr previously) pretreated animals, markedly elevated brain 5-hydroxytryptamine (5HT) concentrations but depressed whole brain tryptamine content. L-Tryptophan (50-200 mg/kg) administration to pargyline- (75 mg/kg 30 min previously) pretreated animals also increased cerebral 5HT levels. L-Tryptophan (200 mg/kg plus pargyline), elevated whole brain tryptamine content. Administration of tryptamine (40 mg/kg) to pargyline-pretreated guinea pigs caused a small increase in brain 5HT levels, but markedly elevated cerebral tryptamine content. 5HT appears to be the indoleamine mainly responsible for 5HTP-induced myoclonus but tryptamine predominates in tryptamine-induced myoclonus. Both 5HT and tryptamine may contribute to myoclonus induced by L-tryptophan.
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PMID:Alterations in brain 5HT and tryptamine content during indoleamine-induced myoclonus in guinea pigs. 619 24

A patient with chronic manic-depressive illness developed generalized myoclonus and spontaneous ocular oscillations after a single 2 gm dose of L-tryptophan. She had been pretreated with both a tricyclic antidepressant and a monoamine oxidase inhibitor. The involuntary movements gradually disappeared within 24 hours after the drugs were discontinued. Electrooculographic recording 7 hours after onset of the abnormal eye movements revealed square-wave jerks and hypometric voluntary saccades. Pursuit as well as optokinetic and vestibular slow phases were normal except for superimposition of the square-wave jerks. Repeat recording 24 hours later was entirely normal.
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PMID:Myoclonus and ocular oscillations induced by L-tryptophan. 705 33

The serotonin syndrome has increasingly been recognised in patients who have received combined serotonergic drugs. This syndrome is characterised by a constellation of symptoms (confusion, fever, shivering, diaphoresis, ataxia, hyperelflexia, myoclonus or diarrhoea) in the setting of the recent addition of a serotonergic agent. The most common drug combinations causing the serotonin syndrome are monoamine oxidase inhibitors (MAOIs) and serotonin selective reuptake inhibitors (SSRIs), MAOIs and tricyclic antidepressants, MAOIs and tryptophan, and MAOIs and pethidine (meperidine). This syndrome is caused by excess serotonin (5-hydroxytryptamine; 5-HT) availability in the CNS at the 5-HT1A-receptor. There may also be some interaction with dopamine and 5-HT2-receptors. This syndrome probably has a low incidence, even among patients taking these drug combinations, and there is likely to be some other as yet unidentified inciting factor causing some patients to develop a full serotonin syndrome. Because fatalities and severe complications have accompanied the serotonin syndrome, the previously described drug combinations should be used cautiously or not at all. The serotonin syndrome is usually mild and, if managed with drug withdrawal and supportive therapy, generally improves within hours. Patients who develop hyperthermia should be treated aggressively with external cooling and paralysis. Methysergide and cyproheptadine appear to be useful adjuncts in treating the serotonin syndrome.
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PMID:The serotonin syndrome. Implicated drugs, pathophysiology and management. 757 68

We describe a patient treated with trazodone, isocarboxazid, and methylphenidate hydrochloride who developed confusion, agitation, poor concentration, rigidity, myoclonus, involuntary movements, orthostatic hypotension, and hyperreflexia. CK was normal, and the syndrome resolved spontaneously over 12 hours. The serotonin syndrome occurs following the use of serotomimetic agents (serotonin reuptake inhibitors, tricyclic and tetracyclic antidepressants, tryptophan, 3,4-methylenedioxy-methamphetamine, dextromethorphan, meperidine, S-adenosylmethionine) alone or in combination with monoamine oxidase inhibitors. It is characterized by various combinations of myoclonus, rigidity, hyperreflexia, shivering, confusion, agitation, restlessness, coma, autonomic instability, low-grade fever, nausea, diarrhea, diaphoresis, flushing, and rarely, rhabdomyolysis and death.
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PMID:Serotonin syndrome. 785 15

There is a new, potentially fatal disorder that is infrequently reported. The apparent rareness may be because of a lack of recognition of the syndrome or its predisposing factors. Fluoxetine (Prozac, Dista Products Co, Division of Eli Lilly Co, Indianapolis, IN), sertraline (Zoloft, Roerig Division, Pfizer Inc, New York, NY), and paroxetine (Paxil, SmithKline Beecham Pharmaceuticals, Philadelphia, PA) belong to a new class of antidepressant medication: the serotonin reuptake-inhibitors (SRIs). The relative safety profile of the SRIs has led to their widespread use. However, a syndrome of excessive serotonergic activity, the "serotonin syndrome" (SS), has recently been recognized. It is characterized by changes in mental status, hypertension, restlessness, myoclonus, hyperreflexia, diaphoresis, shivering, and tremor. A high index of suspicion is required to make the diagnosis in these acutely ill patients. The most common agents implicated in SS are the monoamine oxidase inhibitors in combination with L-tryptophan or fluoxetine. A case of a patient with significant peripheral vascular disease who developed SS while taking paroxetine and an over-the-counter cold medicine is reported. There have been no prior reports of this interaction. Discontinuation of the offending agents, sedation, and supportive care are the mainstays of treatment. The interactions of serotonin with platelets and vascular endothelium are also discussed.
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PMID:The serotonin syndrome associated with paroxetine, an over-the-counter cold remedy, and vascular disease. 766 67

Twenty-one patients with disabling spontaneous, reflex, or action myoclonus due to various causes, who had shown apparent clinical improvement on introduction of piracetam, entered a placebo-controlled double-blind crossover trial of piracetam (2.4-16.8 g daily). All but one patient had electrophysiological evidence of cortical myoclonus. Patients were randomly allocated to a 14-day course of piracetam followed by identical placebo, or placebo followed by piracetam. Nineteen patients received piracetam/placebo in addition to their routine antimyoclonic treatment (carbamazepine, clonazepam, phenytoin, primidone, sodium valproate, or tryptophan plus isocarboxazid, alone or in combination) and two received piracetam/placebo as monotherapy. All patients were rated at the end of each treatment phase using stimulus sensitivity, motor, writing, functional disability, global assessment, and visual analogue scales. Ten of the 21 patients had to be rescued from the placebo phase of the trial because of a severe and intolerable exacerbation of their myoclonus. No patients required rescue from the piracetam phase of the double-blind trial. When the 21 patients were considered together, there was a significant improvement in motor, writing, functional disability, global assessment, and visual analogue scores during treatment with piracetam compared with placebo. The total rating score also improved significantly with piracetam, by a median of 22%. Piracetam, usually in combination with other antimyoclonic drugs, is a useful treatment for myoclonus of cortical origin.
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PMID:Effectiveness of piracetam in cortical myoclonus. 841 9

In animals the occurrence of a behavioural syndrome consisting of hyperactivity, stereotyped movements and increase of temperature has been induced by MAOIs, 5-HT precursors (L-tryptophan) and 5-HT reuptake inhibitors. Most of these manifestations were specifically blocked by a pretreatment with an inhibitor of serotonin synthesis. In humans, the association of myoclonus, diarrhea, confusion, hypomania, agitation, hyperreflexia, shivering, incoordination, fever and diaphoresis, when patients are treated with serotoninergic agents, could constitute a "serotonin syndrome". Such cases of serotonin syndrome were reported after treatments with L-tryptophan, MAOIs, serotonin reuptake inhibitors and tricyclics alone or in association. The authors prospectively evaluated all the "serotonin-related" symptoms in 38 depressed inpatients fulfilling DSM III-R criteria of major depression. 16 (42%) out of 38 patients presented at least one symptom of serotonin syndrome. In 14 cases tremor and myoclonus occurred simultaneously and 10 patients presented at the same time tremor, myoclonus, diaphoresis and shivering. Except for two patients, symptoms were transient, lasted less than one week and disappeared with the pursuit of the treatment. Most often, serotonin syndrome thus corresponds to a reaction induced by a combination of serotoninergic agents at high dosages. In very rare cases, a toxic and potentially fatal interaction can occur between MAOIs, tricyclics and selective serotonin reuptake inhibitors at therapeutic dosages. Serotonin syndrome also provides an heuristic model of the putative mode of action of antidepressants. Serotonin-related symptoms are the physical and objective expression of the antidepressant-induced increase in serotonin. The specificity of serotonin-related syndrome also needs to be discussed since most of the symptoms, such as tremor and diaphoresis, are not in all cases related to an increase in serotonin.
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PMID:[The serotonin syndrome: review of the literature and description of an original study]. 852 62


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