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)

Elective cardioversion is a short procedure performed under general anesthesia for the treatment of cardiac dysrhythmias. Selection of the anesthetic agent is important, because a short duration of action and hemodynamic stability are required. Forty-four patients scheduled for elective cardioversion in the coronary care unit were studied prospectively. All patients were randomly assigned, according to the last digit of their clinical record number, to receive one of the four anesthetic agents studied: group 1, 12 patients who received 3 mg/kg of sodium thiopental; group 2, 10 patients who received 0.15 mg/kg of etomidate; group 3, 12 patients who received 1.5 mg/kg of propofol; and group 4, 10 patients who received 0.15 mg/kg of midazolam. All patients also received 1.5 micrograms/kg of fentanyl 3 minutes before induction. All four drugs provided satisfactory anesthesia for cardioversion and there were no major complications. Midazolam produced a more prolonged duration of effect and more interindividual variability. Propofol was associated with hypotension and a higher incidence of apnea, and its duration of action was similar to that of etomidate or thiopental. Etomidate produced myoclonus and pain on injection; however, it was the only agent that did not decrease arterial blood pressure. Thiopental reduced blood pressure but otherwise seemed an appropriate anesthetic for this procedure. In conclusion, all four anesthetic agents were acceptable for cardioversion, although their pharmacological differences suggest specific indications for individual patients.
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PMID:Anesthesia for elective cardioversion: a comparison of four anesthetic agents. 176 20

We describe a 37-year-old man with spinal segmental myoclonus characterized by symmetric, rhythmic contractions of the abdomen with a frequency ranging between 100 and 150/min. The combination of sodium valproate and L-5-hydroxytryptophan was useful to control the myoclonus. We comment on the possible role of the serotonergic system in this syndrome.
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PMID:Spinal myoclonus: successful treatment with the combination of sodium valproate and L-5-hydroxytryptophan. 201 15

Within generalized epilepsy, the syndrome of epilepsy with myoclonic absences is considered as intermediate between idiopathic and symptomatic forms. This syndrome is characterized by developing in childhood with a male predominance. Critical EEG shows paroxysms of PO at 3 Hz, and in the polygraphic recording rhythmic 3 Hz myoclonus is observed with a strict correspondence between EEG spike and myoclonus. The response to therapy is generally poor, and 18% develop generalized symptomatic epilepsy. We report 3 patients with epilepsy with myoclonic absences and good outcome, to emphasize the importance of a precise diagnosis by means of the polygraphic recording of the attack, the fact the association of sodium valproate and ethosuximide is the most useful therapy and, finally, the possibility that some patients with epilepsy with myoclonic absence may develop Janz's juvenile myoclonic epilepsy.
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PMID:[Epilepsy with myoclonic absences]. 212 43

Posthypoxic action myoclonus is usually associated with impaired serotonin (5-HT) neurotransmission but in some patients 5-HT precursors aggravate and 5-HT blockers improve action myoclonus. We studied a 65-year-old man who presented with action myoclonus following a prolonged episode of moderate hypoxia and severe hypercarbia. The myoclonus increased with 5-hydroxytryptophan (5-HTP) 1,200 mg/day plus carbidopa 300 mg/day and sodium salt of valproic acid (SVA) 800 mg/day, and improved with 1 mg of clonazepam (CNZ) in an intravenous bolus. Biochemical analysis of the cerebrospinal fluid (CSF) prior to any drug therapy did not reveal abnormalities in the levels of homovanillic acid (HVA) and methoxyhydroxyphenylglycol (MHPG) but 5-hydroxyindoleacetic acid (5-HIAA) levels were elevated in comparison with controls (33 versus 21 ng/ml). SVA therapy produced a moderate increase and 5-HTP plus carbidopa a threefold elevation of 5-HIAA in CSF and marked aggravation of action myoclonus. Methysergide (3 mg/day) totally suppressed myoclonus and decreased CSF 5-HIAA to undetectable levels. Methysergide also reduced CSF tryptophan to 40% of baseline levels. Discontinuation of methysergide and substitution by placebo was followed by reappearance of myoclonus. A partial and incomplete spontaneous remission of symptoms took place 7 months after the asphyxic episode. Action myoclonus and enhanced 5-HT neurotransmission may be present in patients in which acidosis reverses the effects of hypoxia on 5-HT neurotransmission.
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PMID:Clinical, biochemical, and pharmacological observation in a patient with postasphyxic myoclonus: association to serotonin hyperactivity. 245 56

Ten patients with severe disabling myoclonus were treated with clonazepam, sodium valproate, primidone and piracetam alone, or in different combinations. Electrophysiological assessment indicated a cortical origin for the myoclonus in every case. Considerable improvement of myoclonus was achieved with combinations of these drugs in all patients, but this was not possible with monotherapy. In one patient two drugs were necessary (clonazepam and piracetam); in the others more than two drugs were required. The combination of sodium valproate, clonazepam and primidone (3 patients), or piracetam, clonazepam and primidone (3 patients), or the four drugs together (3 patients) was necessary to provide substantial relief of myoclonus. Such polytherapy generally was tolerated well. The benefits of treatment continued for more than 1 year in all cases, although progressive underlying pathology often caused other increasing disability.
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PMID:The treatment of severe action myoclonus. 249 99

A new baboon model was used to investigate the therapuetic effect of sodium valproate on the high pressure neurologic syndrome (HPNS). A hyperbaric chamber was used to achieve environmental pressures of 61 ATA, over a 5-h period. Eight animals underwent two compressions, a control and a valproate-treated compression (half the animals had valproate on the first compression). Mild signs of HPNS (e.g., paw and limb tremor) were first observed at approximately 20 ATA. More severe signs (e.g., whole body tremor, myoclonus, and vomiting) were observed above 40 ATA. Sodium valproate was administered during the compression phase and for 2 wk previously. It was effective at the higher pressures above 41 ATA in reducing the severity of the signs of HPNS. The major effect of pressure on the EEG was to increase alpha and theta wave amplitude in a linear manner. Alpha wave amplitude was reduced by sodium valproate.
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PMID:Sodium valproate interactions with the HPNS: EEG and behavioral observations. 249 71

We reported a girl with mitochondrial encephalomyopathy, who had various neuromuscular symptoms including dilated cardiomyopathy, generalized convulsions, myoclonus, muscular weakness and growth retardation. Lactate levels in the serum and CSF were elevated. Muscle biopsy showed scattered ragged-red fibers, and complex I (NADH-CoQ reductase) and complex IV (cytochrome c oxidase) were markedly reduced. Although she was treated with coenzyme Q, DL-carnitine and sodium succinate, she died of progressive congestive heart failure at 9 10/12 years of age.
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PMID:[A case of mitochondrial encephalomyopathy with cardiomyopathy due to decreased complex I and IV activities]. 255 57

A 44-year-old man suffered from repeated impairment of consciousness associated with flapping tremor, myoclonus and generalized convulsions, and died in coma 6 months after admission. He had had a psychosomatically underdeveloped childhood, with a propensity for legumes without a family history of the same or a record of consanguinity. On admission, he had disturbed consciousness and emaciation without other physical abnormalities. The EEG revealed diffuse slow waves with occasional appearance of triphasic waves. A high level of serum citrulline (534.7 nmol/ml) was recognized and the assay of urea cycle enzymes in the liver demonstrated decreased argininosuccinate synthetase (ASS) activity (0.062 U/g liver, 7.4% of that in normal liver), although no kinetic abnormality was found. Accordingly he was diagnosed as having type II citrullinemia. In addition, this case could be classified as cluster type of localization of the ASS in the liver by immunohistochemical study. There were characteristic findings concerning his clinical picture and laboratory data, such as a significant correlation between the grade of disturbed consciousness and arterial blood gas pH (r = 0.61, p less than 0.01). However, the blood ammonia level did not always correlate with the severity of disturbed consciousness. Oral treatment with sodium citrate and sodium benzoate was very effective, though transiently, for disturbed consciousness in this case. Pathological findings of the autopsied liver were fatty change and fibrosis. Neuropathologically, characteristic findings were brain edema with cerebellar tonsilar herniation, laminar necrosis with spongy formation in cerebral cortex, and Alzheimer type II glia. The relationship between citrullinemia and other hepatic encephalopathy was also discussed.
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PMID:[An autopsied case of type II citrullinemia--transient effectiveness with either citrate or benzoate to the consciousness disturbance]. 269 30

A case of tuberculous pleurisy associated with myoclonus and Quincke's edema due to isoniazid (INH) and isoniazid sodium methanesulfonate (IHMS) was reported. A 75-year-old man was admitted to our division because of chest discomfort and the left chest pain of one month's duration. A conventional chest roentgenogram revealed pleural effusion in the left thoracic cavity. The pleural specimen obtained from the left parietal pleura revealed caseating granuloma. Myoclonus suddenly appeared two months after the administration of antituberculous drugs for tuberculous pleurisy. Therefore, INH was discontinued. Three days later the patient's myoclonus disappeared and nine days later IHMS was newly administered. The patient abruptly developed myoclonus and Quincke's edema. IHMS was discontinued and 30 mg of prednisolone was simultaneously given. Two days later myoclonus disappeared and two days more later Quincke's edema was improved. The lymphocyte stimulation test using IHMS was positive. At that time, levels of serum vitamin B6 were within normal levels. These results suggest that myoclonus may result from epileptogenic action caused by INH or IHMS, and Quincke's edema may result from hypersensitive reaction associated with IHMS.
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PMID:[A case of tuberculous pleurisy associated with myoclonus and Quincke's edema due to isoniazid and isoniazid sodium methanesulfonate]. 279 12

CM 40907 [3-(4-hydroxypiperidyl)-6-(2'-chlorophenyl)-pyridazine] is a chemically original compound which possesses the pharmacological properties of a potent, p.o. active anticonvulsant. The anticonvulsant activity of CM 40907 was examined in mice, rats and photosensitive Papio-papio baboons and compared to that of phenobarbital, diphenylhydantoin, carbamazepine, sodium valproate and ethosuximide. In mice, CM 40907 antagonized electroconvulsive shock and chemically induced seizures with an overall potency comparable to that of carbamazepine and a therapeutic ratio (ED50 rotorod/ED50 electroshock) superior to that of ethosuximide, sodium valproate, phenobarbital and carbamazepine. In the rat CM 40907 suppressed completed kindled amygdaloid seizures and was approximately as active as phenobarbital. In naturally photosensitive Senegalese Papio-papio baboons CM 40907 antagonized myoclonus and cortical paroxysmal discharges. In this model CM 40907 was approximately one-fourth as potent as phenobarbital, twice as potent as carbamazepine and 6 times more potent than sodium valproate. In mice CM 40907, at anticonvulsant doses, increased the affinity of [3H]flunitrazepam for its central receptor site. Based on these results it is postulated that CM 40907 is a potent and relatively nonsedative anticonvulsant and may be of therapeutic benefit in epileptic disorders.
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PMID:CM 40907: a structurally novel anticonvulsant in mice, rats and baboons. 298 99


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