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Query: UMLS:C0027066 (myoclonus)
 4,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two patients are reported with palatal myoclonus, progressive ataxia, and dysarthria, unresponsive to treatment with trihexyphenidyl or L-5-hydroxytryptophan. MRI showed enlargement of the inferior olives in one patient, consistent with the pathology usually associated with palatal myoclonus. The syndrome of progressive ataxia and palatal myoclonus should be distinguished from other ataxias and degenerations that affect the brainstem and cerebellum. Pathology and specificity of site of the lesions are distinctive.
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PMID:Syndrome of palatal myoclonus and progressive ataxia: two cases with magnetic resonance imaging. 402 58

In male Swiss mice, muscimol produced myoclonic jerks. A 3 mg/kg (i.p.) dose induced this response in all of the mice tested and the peak response of 73 jerks per min was observed between 27 and 45 min. Increasing the brain serotonin levels by the administration of 5-hydroxytryptophan (80-160 mg/kg) in combination with a peripheral decarboxylase inhibitor resulted in an inhibition of the muscimol effect. However, in a similar experiment l-dopa (80-160 mg/kg) was without effect. In doses of 3-10 mg/kg, the serotonin receptor agonist MK-212 caused a dose-dependent blockade of the response of muscimol. Of the benzodiazepines, clonazepam (0.1-0.3 mg/kg) was found to be several fold more potent than diazepam (0.3-3 mg/kg) in blocking the myoclonic jerks. While (-)-baclofen (1-3 mg/kg) proved to be an effective antagonist of muscimol, its (+)-isomer (5-20 mg/kg) lacked this property. Considering the fact that 5-HTP and the benzodiazepines have been found to be beneficial in the management of clinical myoclonus, the muscimol-induced myoclonus seems to be a satisfactory animal model that may prove useful for the development of new drug treatments for this condition. Our present study indicated the possible value of MK-212 and (-)-baclofen in the management of clinical myoclonus.
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PMID:Serotonergic drugs, benzodiazepines and baclofen block muscimol-induced myoclonic jerks in a strain of mice. 611 80

Tryptamine (1-320 mg/kg) evoked only slight muscle jerking in naive guinea-pigs but, in animals pretreated with pargyline (75 mg/kg; 1 hr previously), tryptamine induced a dose-dependent (6-160 mg/kg) myoclonus. The myoclonus induced by tryptamine (40 mg/kg) plus pargyline (75 mg/kg) was differentially inhibited by the indoleamine receptor antagonists, methergoline (5 mg/kg) which was more potent than methysergide (10 mg/kg), mianserin (10 mg/kg) which was more potent that cyproheptadine (10 mg/kg) and propranolol (20 mg/kg) which was more potent than cinanserin (10 mg/kg). This rank order of potency differed from that observed for the order of potency of these drugs in inhibiting the myoclonus induced by L-5-hydroxytryptophan (5HTP) plus carbidopa in guinea-pigs (Luscombe, Jenner and Marsden, Neuropharmacology, 1981), perhaps indicating involvement of pharmacologically distinct indoleamine receptors. Manipulation of presynaptic function of 5-hydroxytryptamine (5HT) by tryptophan hydroxylase inhibition with p-chlorophenylalanine to produce depletion of cerebral 5HT, or by an L-tryptophan load to elevate 5HT in brain, suggested that the functional integrity of serotonergic neurones is required for the expression of myoclonus induced by tryptamine plus pargyline. A range of blockers of 5HT re-uptake did not alter the jerking produced by tryptamine (40 mg/kg) in guinea pigs pretreated with pargyline (75 mg/kg; 1 hr previously), or the threshold myoclonus induced by a smaller dose of tryptamine (10 mg/kg; plus pargyline 75 mg/kg). It is suggested that myoclonus induced by tryptamine in guinea pigs pretreated with pargyline involves activation of post-synaptic indoleamine receptors by tryptamine by a mechanism which requires intact presynaptic function of 5HT.
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PMID:Tryptamine-induced myoclonus in guinea-pigs pretreated with a monoamine oxidase inhibitor indicates pre- and post-synaptic actions of tryptamine upon central indoleamine systems. 613 Apr 89

Certain benzodiazepines (BZs) like lorazepam, diazepam or clonazepam induce myoclonus jerks in photosensitive and non-photosensitive baboons. Papio papio, which are not accompanied by EEG paroxysmal discharges (type B). The effect of the selective BZ antagonist R0 15-1788 was evaluated in this myoclonus. Ro 15-1788 completely blocked type B myoclonus without decreasing the level of vigilance in the two types of baboons, and reversed the antiepileptic action of the BZs in the photosensitive ones, permitting the reappearance of myoclonus following EEG paroxysmal discharges (type A). L-5-hydroxytryptophan and progabide also blocked type B myoclonus, but the blockade was only transiently effective and was always accompanied by slight drowsiness.
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PMID:Differential effects of the benzodiazepine antagonist Ro 15-1788 on two types of myoclonus in baboon Papio papio. 613 45

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

Postanoxic myoclonus was first accepted as being related to a dysfunction of the ventrolateral thalamic nucleus. Several stereotaxic studies have invalidated this hypothesis. The neurochemical approach, in particular the measure of 5-hydroxyindolacetic acid in the cerebrospinal fluid, has opened new theoretical and therapeutic possibilities involving serotoninergic pathways. A typical case is presented who improved markedly under a combined therapy with 5-hydroxytryptophan and a decarboxylase inhibitor. A review of the pathogenesis and therapeutic approach to postanoxic myoclonus is presented.
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PMID:Postanoxic myoclonus. Treatment of a case with 5-hydroxytryptophane and a decarboxylase inhibitor. 616 57

Some types of intention myoclonus respond to serotonin precursor therapy (e.g., L-5-hydroxytryptophan, L-5HTP). Fluoxetine, a specific serotonin (5HT) uptake blocker, was found to have no antimyoclonic effect when administered by itself to four patients with intention myoclonus. However, in two patients with intention myoclonus responsive to L-5HTP and carbidopa, fluoxetine reduced the required dose of L-5HTP to approximately one-third, with greater antimyoclonic activity, decreased side effects, and reduction in platelet 5HT and plasma 5-hydroxyindoleacetic acid and L-5HTP concentrations. These findings further support the hypothesis that some forms of intention myoclonus are caused by a deficiency of brain 5HT, and suggest that the addition of fluoxetine to L-5HTP and carbidopa may improve antimyoclonic therapy.
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PMID:Fluoxetine in the treatment of intention myoclonus. 618 99

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

From a family with essential familial myoclonus, 150 members in eight generations were studied. Twenty-five of them suffered from myoclonus of varying severity. The findings in routine examinations of blood, urine and cerebrospinal fluid, EEG and skull radiographs were normal. Therapeutic trials did not produce lasting satisfactory results. The most promising results were obtained with 5-hydroxytryptophan therapy. Haloperidol worsened the symptoms, while alcohol produced a striking improvement. It is suggested that serotoninergic neurons in the brain could be involved in the triggering of essential myoclonus.
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PMID:Essential familial myoclonus. 619 10

Six patients with myoclonus were given 0.1-0.15 mg lisuride i.v. All patients had stimulus-sensitive myoclonus and an increased size of somatosensory evoked potentials, and in three there was electrophysiological evidence of a cortical event time-locked to the jerks. All subjects showed a considerable diminution of spontaneous, action- and stimulus-evoked jerking. Lisuride has potent central dopaminergic and serotonergic actions. Administration of the dopamine agonists levodopa or apomorphine had no effect on myoclonic jerking in any of the six patients. Detailed pharmacological analysis of the myoclonus in one patient showed that levodopa, apomorphine, and haloperidol had no effect, and that haloperidol did not prevent the therapeutic action of lisuride. 5-Hydroxytryptophan abolished the myoclonus, and methysergide prevented the beneficial effect of lisuride, although it did not alter spontaneous myoclonus. These observations suggest that lisuride improves some types of reflex, stimulus-sensitive cortical myoclonus by a serotonin agonist action.
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PMID:Cortical reflex myoclonus responds to intravenous lisuride. 641 86


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