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)

5-Hydroxytryptophan (5-HTP) induces a characteristic behavioural syndrome of altered motor activity with muscle jerking in guinea pigs. Myoclonic jerking occurs synchronously in forelimbs and hindlimbs and is associated with a stereotyped electromyographic (EMG) pattern of a burst of activity lasting 40-50 msec in active muscles, followed by silence lasting 50-70 msec, followed by a further variable period of muscle activity. Such myoclonus may be induced also by the administration of L-tryptophan plus a monamine oxidase inhibitor (MAOI), or by agents acting as serotonin (5-HT) receptor agonists. The 5-HTP-induced syndrome is antagonised by a central decarboxylase inhibitor (NSD-1035) and by agents which block 5-HT receptors (methysergide and cyproheptadine). 5-HTP-induced jerking is abolished below the level of a spinal cord transection, but persists in decerebrate animals. No electroencephalographic (EEG) changes are seen preceding the muscle jerks. The clinical significance of this animal model of myoclonus is discussed.
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PMID:5-hydroxytryptophan-induced myoclonus in guinea pigs. A physiological and pharmacological investigations. 30 85

Post-hypoxic intention myoclonus successfully treated by long-term administration of the combination of 5-hydroxytryptophan and carbidopa is described. Persistent euphoria and diarrhoea were essential side effects. Methysergide (12 mg/day) blocked the therapeutic effect, indicating a specific serotoninergic function of precursor loading with 5-hydroxytryptophan. Tryptophan (8 g/day) had no effect on the myoclonus suggesting a reduced tryptophan hydroxylase activity. Plasma concentrations of 5-hydroxytryptophan in the range of 10--30 micromoles per liter were obtained during maintenance therapy with 900 mg 5-hydroxytryptophan per day in combination with 150 mg carbidopa per day.
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PMID:Post-hypoxic intention myoclonus treated with 5-hydroxy-tryptophan and an extracerebral decarboxylase inhibitor. 30 27

5-Hydroxytryptophan has been found to be beneficial when administered alone or in combination with extracerebral aromatic amino acid decarboxylase inhibitors for therapeutic purposes in various disorders in which myoclonus is prominent. In five subjects the effect of decarboxylase inhibitors on the accumulation and elimination of 5-hydroxytryptophan in plasma was studied. The plasma concentrations of 5-hydroxytryptophan were increased about ten fold by pretreatment with the decarboxylase inhibitors, carbidopa and benserazide. Half-lives of 2.2--3.0 hrs. were obtained following oral administration of a single dose of 5-hydroxytryptophan with or without pretreatment. In one subject the half-life of 5-hydroxytryptophan in plasma increased to 5.5 hrs. during long-term treatment with carbidopa.
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PMID:The effects of aromatic amino acid decarboxylase inhibitors on plasma concentrations of 5-hydroxytryptophan in man. 30 71

Intracisternal injection of 5,7-dihydroxytryptamine (5,7-DHT) following treatment with desmethylimipramine induced development of behavioral supersensitivity to the intraperitoneally administered serotonin precursor 5-hydroxytryptophan (5-HTP) in the mouse. This behavioral syndrome, characterized by tremor and muscle twitches (myoclonus), showed a clear dose-response relationship with 5,7-DHT as well as with 5-HTP. Mice lesioned with a low dose of 5,7-DHT (20 micrograms) or a placebo were treated repeatedly with a protein synthesis inhibitor, sycloheximide (45 mg/kg, s.c., every 12 h for up to 10 days). This treatment resulted in a reversible decrease of cerebral protein synthesis varying between 70 and 20% with time between treatments. The myoclonic response to 5-HTP in animals pretreated with 5,7-DHT and by cycloheximide showed a decrease in intensity within 24 h when evaluated quantitatively by an electronic activity monitor, the results of which were confirmed by direct observation. Cycloheximide also exerted a similar, though smaller, effect following full development of sensitivity to 5-HTP over 10 days. These effects may de mediated by inhibition of rapidly turning over serotonin receptor proteins, although their interpretation is somewhat obscured by possible toxic effects of cycloheximide.
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PMID:Inhibition of 5,7-dihydroxytryptamine-induced supersensitivity to 5-hydroxytryptophan in mice by treatment with cycloheximide. 31 Mar 31

p,p'-DDT (100 to 600 mg per kilogram orally) produced spontaneous and stimulus-sensitive myoclonus in mice and rats. Drugs that enhance brain serotonergic activity reduced p,p'-DDT-induced myoclonus, and serotonin antagonists invariably aggravated this syndrome. p,p'-DDT-treated rats had increased concentrations of 5-hydroxyindoleacetic acid (5-HIAA) in seven regional areas, but serotonin was increased only in the midbrain and cerebellum. We postulate that p,p'-DDT-induced myoclonus may be causally related to blockage of serotonin receptors or inhibition of serotonin release into the synapse, resulting in functional deficiency of this neurotransmiter at the receptor site.
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PMID:p,p'-DDT-induced neurotoxic syndrome: experimental myoclonus. 31 46

The effects of rapid intracarotid injection of 20 to 100 mg of sodium amobarbital were studied in three patients with bilateral myoclonic status epilepticus due to Jakob-Creutzfeldt disease, sequelae to anoxic encephalopathy, and hepatic coma, respectively. In each instance, the drug produced prompt abatement of clonic jerks contralaterally and attenuation of electroencephalographic epileptiform discharges ipsilaterally. These results suggest that the cerebral cortex actively participates in the elaboration of certain types of bilateral myoclonus in human beings.
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PMID:Electrographic and clinical effects of intracarotid sodium amobarbital on bilateral myoclonic status epilepticus. 32 84

Serial EEG studies and full neuropathological investigations (optic and electronic microscopy of biopsy and necropsy material) were carried out on two patients: 1. A 68-year-old man: development in two and a half months of Creutzfeldt-Jakob's disease signalled by early clinical and EEG changes and confirmed by associated spongiosis of the triad characteristic of Alzheimer's disease, which was unexpected in this case. 2. A 43-year-old man: first phase of four years of progressive deterioration, followed by an encephalopathic syndrome with myoclonus developing in twelve months. The serial EEG studies showed discontinuous periodic paroxystic activity from the start of the second phase of the disease, although the first biopsy still showed nothing but the signs of Alzheimer's disease. A fortnight later, a second biopsy revealed ultrastructural microspongiosis. Examination of necropsy material confirmed the extensive association of the characteristic images of the two processes. On the basis of these two case studies and some similar cases published in the literature, the authors discuss the possible etiological links between these two diseases and stress the importance of the EEG and cerebral biopsy for the purposes of differential diagnosis. (Acta neurol. belg., 1977, 77, 202-212).
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PMID:[Association of Alzheimer's disease and Creutzfeldt-Jakob's disease (author's transl)]. 33 54

Since the advent of intensive care units the number of cases of posthypoxic action or intention myoclonus has greatly increased. This has given rise to renewed research into the physiopathology and therapy of the disease. The latent effective treatment is based on derivatives of benzodiazepine, and especially L-5-hydroxytryptophan, administered with or without an inhibitor of peripheral decarboxylase. The disadvantages of these compounds, associated with their secondary effects, make our fortuitous discovery of the effectively curative action of piracetam doubly valuable.
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PMID:[Therapeutic effect of piracetam in a case of posthypoxic action myoclonus (author's transl)]. 34 25

The disorders of ocular motility seen in association with brainstem or cerebellar disorders may point to rather specific anatomical or pathological correlations. Pontine gaze palsy reflects involvement of the pontine paramedian reticular formation. Internuclear ophthalmoplegia signifies a lesion in the medial longitudinal fasciculus. Skew deviation may result from a lesion anywhere in the posterior fossa. Ocular bobbing typically results from a pontine lesion. The Sylvian aqueduct syndrome is characteristic of involvement in the upper midbrain-pretectal region, usually a pinealoma. Cerebellar lesions may be manifested by gaze paresis, skew deviation, disturbances of saccadic or smooth pursuit movements, ocular myoclonus, or several characteristic forms of nystagmus. Familiarity with these disorders may be of great help to the physician dealing with a patient with a possible posterior fossa lesion.
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PMID:Abnormal ocular motility with brainstem and cerebellar disorders. 34 6

A patient with postanoxic action myoclonus (Lance-Adams syndrome) was severely disabled with this movement disorder. Valproate sodium was administered orally, with complete resolution of the myoclonus. This favorable response has been maintained for two years. Excessive yawning, the only side effect encountered, was dose related and was abolished with the addition of pimozide to the drug regimen.
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PMID:Postanoxic action myoclonus (Lance-Adams syndrome) responding to valproate. 36 91


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