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)

The effects of intracerebroventricular (i.c.v.) or systemic injections of Met- or Leu-enkephalin, beta-endorphin, FK 33.824 (D-Ala2, MePhe4, Met(O5)-ol-enkephalin) and of morphine and naloxone have been studied in baboons, Papio papio, which spontaneously show photically induced epileptic responses. Animals were chronically implanted with epidural or deep recording electrodes and a cannula in one lateral ventricle, and tested whilst seated in a primate chair. In some animals the natural syndrome was enhanced by the prior administration of DL-allylglycine, 100--200 mg/kg, i.v. Met- or Leu-enkephalin, 1--10 mg, i.c.v., did not lead to any manifest focal or generalized seizure discharges. Nor did it lead to any consistent enhancement or reduction of photically induced myoclonic responses (as tested 5--10 min after injection). beta-Endorphin, 0.1--0.5 mg, i.c.v., did not enhance or impair photically induced myoclonic responses. FK 33.824, 0.1--0.5 mg, i.c.v., depressed respiration and slowed EEG background rhythms for 9--15 h. This was associated with a loss of myoclonic responses to photic stimulation. These effects were reversed for 20--40 min following the injection of naloxone, 1 mg/kg i.m. A depression of respiration and a slowing of EEG rhythms was seen beginning 5--20 min after FK 33.824, 2 or 4 mg/kg, i.v. The higher dose also abolished photically induced myoclonic responses. Naloxone, 1 mg/kg, definitively reversed these effects. Morphine, 5--10 mg i.c.v., tended to increase the latency to onset of generalized myoclonus during photic stimulation. Myoclonic responses were delayed or diminished after morphine, 5 mg/kg, i.m. Naloxone, 1--2 mg/kg i.m., reversed this effect. Naloxone, 0.2--5.0 mg/kg i.m., alone, did not significantly modify photically induced myoclonus, either in animals of low or high initial responsiveness, or in those pretreated with allylglycine.
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PMID:Effects of opiate-like peptides, morphine, and naloxone in the photosensitive baboon, Papio papio. 22 24

To evaluate the safety and possible efficacy of high-dose naloxone for the treatment of acute cerebral ischemia, 38 patients received a loading dose of 160 mg/m2 over 15 minutes followed by a 24-hour infusion at the rate of 80 mg/m2/hr. Nausea and/or vomiting were common side effects. Naloxone was discontinued in seven patients (because of hypotension in one, bradycardia and hypotension in two, myoclonus in one, focal seizures in two, and hypertension in one); all seven patients responded to treatment and no permanent sequelae to naloxone were noted. Twelve of the 38 patients showed early neurologic improvement (by completion of the naloxone loading dose). However, there was no correlation between such a loading dose response and clinical outcome at 3 months. Our experience suggests that naloxone is safe at the dose used, but data for efficacy are inconclusive.
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PMID:High-dose intravenous naloxone for the treatment of acute ischemic stroke. 233 51

The neuropharmacologic profile of intraperitoneally injected harmala alkaloids and related beta-carbolines was evaluated in the rat. All drugs induced central effects (convulsions, catalepsy, or altered startle), but only harmaline and harmine were tremorogenic at low doses. Methoxylation of the carboline 7 position was requisite for this effect. Coadministration of harmaline (but not harmine) and 5-hydroxytryptophan (tryptamine or m-chlorophenyl-piperazine) induced a lethal convulsive myoclonic syndrome which could not be evoked by either drug separately. Compared with the myoclonic-serotonergic syndrome evoked by 5-hydroxytryptophan in rats with 5.7-dihydroxytryptamine lesions, harmaline+5-hydroxytryptophan-treated rats displayed more continuous and greater axial myoclonic jerks and some postural differences. Clorgyline or tranylcypromine but not pargyline could be substituted for harmaline. The harmaline syndrome was blocked by the benzodiazepine agonists, physostigmine and verapamil. The harmaline+5-hydroxytryptophan syndrome was blocked by drugs acting at benzodiazepine receptors (CL 218,872 greater than ethyl-beta-carboline-3-carboxylate, clonazepam, diazepam, Ro 15-1788, pentobarbital), and baclofen. Naloxone, benztropine, quipazine, and apomorphine had partial effects, and calcium channel blockers prevented death but did not prevent convulsions. 5-Hydroxytryptamine antagonists were poor blockers, although cyproheptadine and ketanserin significantly reduced mortality. Phenobarbital was more effective than other anticonvulsants. Lesion studies suggested a role for monoaminergic neurons and the inferior olive in the expression of the harmaline+5-hydroxytryptophan syndrome. These data describe a complex convulsive myoclonic syndrome that is behaviorally related to but pharmacologically distinct from the serotonin syndrome, which may be useful in studying serotonergic-benzodiazepine interactions in the pathophysiology of myoclonus.
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PMID:Harmala alkaloids and related beta-carbolines: a myoclonic model and antimyoclonic drugs. 349 51

Regional anesthesia, especially epidural anesthesia, rarely causes involuntary movement Here we present a case of a patient who demonstrated myoclonus-like involuntary movement of the lower limbs during continuous infusion of ropivacaine, fentanyl, and droperidol through the thoracic epidural catheter. This movement disappeared when the epidural infusion was stopped, but reappeared when the epidural infusion was restarted. Naloxone did not eliminate the movement The patient was thereafter discharged uneventfully. This case and other reports in the literature suggest that involuntary movement associated with regional anesthesia is rare and self-limiting. However, careful consideration should be given to exclude other, potentially dangerous complications.
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PMID:[Involuntary Movement of Bilateral Lower Limbs Caused by Epidural Anesthesia: A Case Report]. 2748 62