Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Carbromal is metabolized extensively in humans. The major metabolites known to date are bromoethylbutyramide, ethylbutyrylurea and inorganic bromide. After ingestion of a therapeutic dose of 1.0 g carbromal (4.2 mmoles) by four healthy volunteers highest concentrations in serum were found to be for carbromal 30 mumoles/l, for bromoethylbutyramide up to 20 mumoles/l and for ethylbutyrylurea 2--3 mumoles/l. In patients acutely poisoned by carbromal-containing sedatives serum concentrations measured were in the range of 200 mumoles/l carbromal, 350 mumoles/l bromoethylbutyramide and 50 mumoles/l ethylbutyrylurea. These patients were comatose, apneic, had isoelectric encephalographic records and decreased body temperature. The degree of central nervous depression as judged by clinical signs was found to correlate with the serum concentrations of carbromal and of bromoethylbutyramide. Pharmacological activity and acute toxicity of carbromal and its two metabolites were examined in rats and compared with the activity of phenobarbitone. For intraperitoneal injection LD-50 values were found to be for carbromal 1.8 mmoles/kg, for bromoethylbutyramide 1.5 mmoles/kg, for ethylbutyrylurea 5.0 mmoles/kg and for phenobarbitone 0.9 mmoles/kg. Carbromal and bromoethylbutyramide severely decreased body temperature. The relative narcotic activity was estimated to be for carbromal = 100; bromoethylbutyramide = 66; ethylbutyrylurea = 33; phenobarbitone = 100. The anticonvulsive activity against pentetrazol-induced generalized seizures was nearly identical for carbromal, bromoethylbutyramide and phenobarbitone. Anticonvulsant activity of ethylbutyrylurea was two to three times less than that of carbromal. Inorganic bromide was found to increase the narcotic activity of carbromal and of bromoethylbutyramide. The findings show that the clinical signs of central nervous system depression seen in patients acutely poisoned with carbromal are caused mainly by unchanged carbromal and by its metabolite bromoethylbutyramide.
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PMID:[On the toxicology of carbromal. III. Role of active metabolites in humans acutely poisoned with carbromal-containing sedatives (author's transl)]. 2 10

A combined informant questionnaire and interview survey of self-injurious behavior (SIB) at a large state facility for the retarded was conducted independently three times over a 3-year period. Prevalence consistently was about 10% of the population. SIB cases tended to be younger and institutionalized longer than the rest of the population. Severe cases had a longer history of chronic SIB. SIB cases had more seizure disorders, severe language handicaps, visual impairments, and severe or profound retardation than the rest of the population. They appeared to fulfill most of the Rutter (1966) criteria for autism. But unlike the severely autistic, there was little relation of sex to incidence of SIB. Over 90% of SIB cases changed status over 3 years, suggesting that SIB was amenable to behavior modification in most cases (94%). Psychotropic behavior control medications helped in some intervention programs (32%). SIB remitted spontaneously in 21% of SIB cases where there had been no behavioral or drug intervention.
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PMID:Prevalence of self-injurious behaviors in a large state facility for the retarded: a three-year follow-up study. 2 30

Significant correlation in 11 different 1,4-benzodiazepinones has been established between log k2 (the second order rate constant for the reduction of the "azepinones" by sodium borohydride) and their ED50 against leptazol-induced seizures in mice. The results suggest a possible involvement of the carobnyl group at the receptor site.
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PMID:Structure activity relation for some 1,4-benzodiazepinones: correlation between rate constants for reduction by sodium borohydride and antileptazol ED50. 2 91

48 patients with several types of seizures (following the international classification of epileptic seizures), were studied. Dipotassium chlorazepate was administered as a secondary antiepileptic drug. The cases were selected due to the severity of their seizures. The therapeutic results were evaluated with a daily record of seizures and attempt was made to correlate the serum levels of nordiazepam with the clinical results.
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PMID:[Treatment of epileptic crisis with chlorazepate dipotassium. Clinical study of 48 patients with the determination of serum levels of nordiazepam]. 2 49

Rats with different levels of blood glucose concentration were exposed to 10 min of complete brain ischemia achieved by compression of neck vessels by a pneumatic cuff. All normoglycemic rats survived the ischemic period and made the best clinical recovery. Hyperglycemic rats died within 12 h. Seizure activity was observed in all animals in this group. Three of eight hypoglycemic rats died between 3 and 16 days. The clinical recovery was less complete than in the control group. Thus, recovery from cerebral ischemia depends upon preischemic blood glucose concentration. Hyper- and hypoglycemia hamper the clinical recovery after transient cerebral ischemia.
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PMID:Clinical restitution following cerebral ischemia in hypo-, normo- and hyperglycemic rats. 3 Feb 50

NADP+, NADPH and glucose 6-phosphate dehydrogenase were determined in the cerebral cortex of mice exposed to high O2 pressure for 0, 8 and 16 min. These time intervals corresponded to 0, 50 and 100% of the CT50 (the time taken for 50% of the mice to convulse). Cerebral NADP+, NADPH and glucose 6-phosphate dehydrogenase also were determined in O2-exposed mice exhibiting hyperactivity, convulsions, and in mice killed 10s after convulsions. Similar increases in cortical NADP+ and decreases in NADPH were found in mice exposed to 610kPa (6 atm.) of 100% O2 for 0, 50 and 100% of the CT50, during hyperactivity, onset of seizure and 10s after convulsions. The NADP+/NADPH ratio increased approx. 25% at 0% of the CT50, and remained at this increased value at all O2-exposure periods including the hyperactive state, onset of seizure and 10s after convulsions. Identical changes in cerebral NADP+ , NADPH and the NADP+/NADPH ratio were found in mice exposed for 16min to 100% O2 at 100, 350 or 610kPa. No change in cerebral glucose 6-phosphate dehydrogenase was found in mice exposed to 610kPa of 100% O2 during the various stages of O2 toxicity. Only in the 10s post-convulsive group was a statistically significant decrease in glucose 6-phosphate dehydrogenase observed. Disulfiram [bis(diethylthiocarbamoyl) disulphide], an effective O2-protective agent, did not prevent the O2-induced increase in cerebral NADP+ and the NADP+/NADPH ratio, or decrease in NADPH.
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PMID:Cerebral oxidized and reduced nicotinamide-adenine dinucleotide phosphate and glucose 6-phosphate dehydrogenase in mice during exposure to high oxygen pressure. 3 67

The authors examine the clinical problem of which antipsychotic drug to use when antipsychotics are indicated in patients with a seizuire disorder or who are susceptible to seizures. While definitive answers to this problem are still unknown, guidelines are offered for antipsychotic drug use in this situation, based on the author's understanding of psychotropics and epilepsy.
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PMID:Antipsychotic drugs and seizures. 3 57

A 5-year-old girl developed a progressive febrile neurological illness consisting of right focal seizures, right hemiparesis, and stupor evolving over a period of six weeks. During the month preceding the onset of her illness she had received two apparently unsuccessful smallpox vaccinations without a skin lesion. Elevation of cerebrospinal fluid gamma globulin and findings on brain biopsy were consistent with postinfectious encephalitis, and a simultaneous increase in serum vaccinia antibody titer suggested that the illness was postvaccinial encephalitis. Clinically, the child developed a severe extrapyramidal movement disorder during the acute phase followed by nine months of stuporous unresponsiveness, yet subsequently made a substantial recovery.
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PMID:Postvaccinal encephalomyelitis without cutaneous vaccination reaction. 3 58

Differential effects of neuropharmacological drugs upon susceptibility to flurothyl-induced myoclonic and clonic convulsions were assessed in two selectively bred lines of mice. Dopaminergic drugs (apomorphine and haloperidol) only affected myoclonus, whereas cholinergic (pilocarpine and scopolamine), gabaergic (AOAA and bicuculline), and serotonergic (PCPA) compounds principally influenced clonus. Noradrenergic drugs (clonidine, phentolamine and sotalol), however, altered the expression of both types of seizures. The apparent differential neurohumoral modulation of myoclonus and clonus is discussed in light of previous suggestions that these behaviors have separate neural substrates.
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PMID:Differential neurohumoral modulation of myoclonic and clonic seizures. 3 68

The anticonvulsant effects of four benzhydryl piperazines, SC-13504 (ropizine, an anticonvulsant), hydroxyzine (HDX, an anxiolytic), chlorcyclizine (CCZ, an antihistaminic) and buclizine (BUC, an antihistaminic), were investigated utilizing a modified maximal electroshock seizure test in rats. In addition to detecting the presence or absence of tonic hindlimb extension, the modified method quantified various phases of the seizure. All four benzhydryl piperazines exhibited anticonvulsant activity in maximal electroshock seizure, but SC-13504 was similar in efficacy to phenobarbital and phenytoin, and much more effective than HDX, CCZ or BUC. Additionally, SC-13504 possessed a therapeutic index much greater than any of the compounds tested. The duration of action of the benzhydryl piperazines, in hours was: SC-13504, 0.5 to 8; HDX, 0.5 to 2; CCZ, 0.5 to 16; and BUC, 2 to 8. Buc and CCZ are postulated to be converted to active anticonvulsant metabolites.
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PMID:Anticonvulsant effects of benzhydryl piperazines on maximal electroshock seizures in rats. 3 12


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