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)

Photosensitivity has proved to be a useful model to study the acute effects of experimental antiepileptic drugs (AEDs). The photosensitivity range is usually diminished or even abolished after administration of a known or experimental AED. An increase in photosensitivity, an unexpected reaction, was found in four photosensitive epileptic patients after oral ingestion of 500, 100, or 50 mg of Org 6370. Moreover, the three patients receiving doses of 100 and 500 mg reported nausea, dizziness, restlessness, and an increase in spontaneous epileptic seizures (myoclonus and in one patient a generalized tonic-clonic convulsion). The side effects coincided with peak Org 6370 serum levels. Our findings indicate that in the photosensitivity model experimental drugs with proven anticonvulsant properties in animals may increase rather than decrease the degree of patient photosensitivity. Photosensitive patients may represent a special subgroup of epileptic patients and therefore need to be classified as such.
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PMID:Preliminary assessment of the efficacy of Org 6370 in photosensitive epileptic patients: paradoxical enhancement of photosensitivity and provocation of myoclonic seizures. 173 47

Ceftazidime, a beta-lactamase-stable, third-generation cephalosporin, is widely used for the treatment of serious gram-negative infections. Neurotoxicity has rarely been associated with the drug; however, two of our patients developed ceftazidime-induced neurotoxicity that produced confusion, disorientation, agitation, generalized weakness, and myoclonus. In both patients these symptoms cleared with either discontinuation or reduction of the dosage of ceftazidime. This emphasizes the importance of adjusting the dosage of ceftazidime in patients with renal insufficiency.
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PMID:Neurotoxicity associated with ceftazidime therapy in geriatric patients with renal dysfunction. 192 20

The baboon Papio papio develops a nonepileptic myoclonus 20 to 30 min after i.m. benzodiazepine injection. It is characterized by bilateral jerks involving mainly the neck and the trunk, by the absence of any correlative EEG paroxysmal discharge, and by its facilitation during movement or agitation. This myoclonus resembles the intention myoclonus of human patients as seen, for example, after anoxia. We found in experiments on 10 adolescent baboons that atropine alone induced the myoclonus for several hours, that physostigmine completely antagonized the benzodiazepine-induced as well as the atropine-induced myoclonus, and that the peripherally acting cholinergic antagonist, methyl-QNB, and agonist prostigmine had no action on the myoclonus, suggesting that the benzodiazepine-induced myoclonus in this species depends on a strong depression of the central cholinergic system by benzodiazepine. The benzodiazepine-induced myoclonus was mediated by benzodiazepine receptors as it was blocked by the specific benzodiazepine receptor antagonist, Ro 15-1788, which did not block atropine-induced myoclonus; latency to myoclonus after benzodiazepine was longer than after atropine. These facts suggest that benzodiazepines, by an as yet unknown mechanism, induce a depression of the cholinergic system which in turn leads to the development of myoclonus. Finally, the benzodiazepine-induced myoclonus of the baboon can be considered as a good model for testing drugs that act on the muscarinic cholinergic system and also for testing benzodiazepine-acetylcholine interactions.
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PMID:Stimulus-sensitive myoclonus of the baboon Papio papio: pharmacological studies reveal interactions between benzodiazepines and the central cholinergic system. 307 7

The restless legs syndrome is generally benign but is occasionally associated with anemia, metabolic disorder, or polyneuropathy. Leg restlessness with disruptive nocturnal myoclonus has been described as a sleep disorder. We report two patients with complex partial and secondarily generalized seizures, who developed restless legs while taking methsuximide and phenytoin. They had no evidence of metabolic disturbance or neuromuscular disease, although one patient had fragmented sleep and disruptive myoclonus on polysomnography, and leg restlessness subsided with change of antiepileptic drugs. These symptoms could reflect transient alteration in peripheral nerve function not evident by examination or electrophysiologic studies, sleep disturbance by antiepileptic drugs or the effects of temporal lobe seizure foci on perception of the physiologic state of nerves and muscles.
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PMID:Restless legs with antiepileptic drug therapy. 314 64

The analgesic meperidine has been reported to produce signs of central nervous system excitation in human beings. To determine the relationship between signs and symptoms of central nervous system excitation and plasma levels of meperidine and normeperidine, we studied 67 patients receiving meperidine for the relief of postoperative or chronic pain. In 48 patients, excitatory effects ranging from mild nervousness to tremors, twitches, multifocal myoclonus, and seizures were directly correlated with accumulation of normeperidine in plasma. Evidence of compromised renal function occurred in only 14 of the 48 symptomatic patients, suggesting that renal dysfunction may contribute to but is not the sole factor in the accumulation of normeperidine or its relation to adverse neurological signs. In a second study we surveyed mood alterations in 47 patients receiving meperidine and 29 receiving other narcotic analgesics for postoperative pain. The repeated administration of meperidine was associated with adverse alterations in various elements of mood (e.g., apprehension, sadness, restlessness).
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PMID:Central nervous system excitatory effects of meperidine in cancer patients. 618 75

Etomidate has been studied in two groups of patients. In Group 1, 50 patients received etomidate 100 micrograms/kg/minute with fentanyl and a muscle relaxant, ventilation being with air and oxygen (50%). The technique gave a smooth, pleasant induction with all patients asleep within 2 minutes. The incidence of pain on infusion was 6% and of myoclonus 6%. Cardiovascular changes were minimal, the most common finding being persistent tachycardia. The mean recovery time was 9.1 minutes. There was no incidence of awareness, recall, or thrombophlebitis, but a 20% incidence of nausea and vomiting. In Group 2, 20 patients received the same dosage of etomidate to supplement spinal anaesthesia for lower abdominal surgery. The technique worked most satisfactorily, with patients falling quietly to sleep within 2-3 minutes with no hiccoughs, coughing or laryngospasm. Six patients exhibited myoclonus, one being severe. In no case did myoclonus interfere with the operation. The cardiovascular system remained stable in all patients. Mean recovery time was 16.1 minutes (range 3-38 minutes). Twitching and restlessness were the main complications during recovery.
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PMID:Etomidate infusion. Its use in anaesthesia for general surgery. 686 59

We studied the clinical features, blood levels of cyclosporine, and neuroimaging findings in 46 patients with cyclosporine neurotoxicity after liver transplantation. The clinical presentation of cyclosporine neurotoxicity was characterized by tremulousness and restlessness in all patients and was associated with acute confusional state and psychosis in 20 patients, seizures in eight, speech apraxia or action myoclonus speech in three, and cortical blindness in two. In 35 patients, cyclosporine neurotoxicity occurred during IV treatment. Neuroimaging studies showed only minor white matter abnormalities in two patients despite dramatic clinical presentations, including speech difficulties, seizures, and cortical blindness. In only 19 of 31 patients (61%) did trough levels of cyclosporine suggest neurotoxicity. Neurologic findings were reversible in all patients after cyclosporine was withheld and then given in lower dosage. In three patients, substituting FK 506 did not result in neurotoxicity.
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PMID:Neurotoxicity in liver transplant recipients with cyclosporine immunosuppression. 750 Nov 41

A minority of patients treated with serotonergic agents develop a fulminant and potentially life-threatening illness characterized by changes in mental status, restlessness, myoclonus, hyperreflexia, tremor, shivering, incoordination, hyperthermia, diaphoresis and diarrhea. This condition of serotonergic hyperstimulation is called the "serotonin syndrome". The author describes an adverse response in a patient given fluoxetine and lithium. A 61-year-old woman presented to casualty exhibits nearly all of the diagnostic criteria proposed by Sternbach [17].
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PMID:[A case of serotonin syndrome]. 756 25

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


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