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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was made of the interrelationship between the minimal effective doses of pseudoclonic and clonico-tonic convulsions, and also tonic extension caused by the intravenous injection of corazol to mice and the effect of anticonvulsive action of sulazepam and its metabolites (diazepam, desmethyldiazepam and oxadiazepam) on this process. It was shown that all the compounds under study increased the values of the minimal effective doses by the recorded indices of the convulsive seizure, whereas the maximum of the anticonvulsive activity was reached 15 minutes after the sulazepam and oxazepam, and 5 to 30 min after diazepam administration. There proved to be a distinct correlation between the minimal effective doses values of the recorded indices of the confulsive seizure in the control animals which also persisted after the administration of the agents under study. It is supposed that sulazepam and its metabolites increased the minimal effective doses of corazol for the recorded effects, but failed to alter the general picture of the convulsive attack and did not influence the dispersion corazol dose-effect dependence.
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PMID:[Analysis of the structure of the components of the convulsive action of corazole following administration of sulazepam and its metabolites to mice]. 1 Oct 12

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

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

Veratridine causes deplorization of excitable cells and produces marked elevation of adenosine 3',5'-monophosphate (cyclic AMP) and guanosine 3',5'-monophosphate (cyclic GMP) levels in incubated slices of mouse cerebral cortex. Phenytoin, carbamazepine, phenobarbital, primidone, phensuximide, methsuximide, alpha-methyl-alpha-phenylsuccinimide, and high concentrations of clonazepam are anticonvulsant drugs that preferentially prevent maximal electroshock seizures (MES) and generalized tonic-clonic convulsions; all these agents inhibit veratridine-induced accumulation of both cyclic AMP and cyclic GMP. In contrast, ethosuximide, trimethadione, valproic acid, and low concentrations of clonazepam are anticonvulsant drugs that act predominantly against Metrazol and absence seizures; these agents are ineffective or inhibit accumulation of only cyclic GMP. The results suggest that inhibition of cyclic AMP and cyclic GMP accumulation in depolarized brain tissue is a molecular neuropharmacological action characteristic of anticonvulsant drugs that have direct effects on cellular membrane function and prevent MES. Anticonvulsant drugs that do not inhibit accumulation of both cyclic AMP and cyclic GMP in depolarized brain tissue preferentially prevent Metrazol and absence seizures and probably exert their effects by altering neurotransmission mechanisms.
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PMID:Inhibitory effects of anticonvulsant drugs on cyclic nucleotide accumulation in brain. 3 36

The antagonism of various seizure and time-related components of the convulsions resulting after IV injection of D,L-allylglycine into male Wistar rats were assessed in a standard test procedure. Trimethadione and ethosuximide did not antagonize the seizure components, whereas clonazepam, phenobarbital, diphenylhydantoin, primidone, valproate sodium, aminoxyacetic acid, etomidate, acetazolamide, flunarizine, pipamperone and baclofen did. The allylglycine test may thus represent a relatively specific method of differentiating between drugs effective against partial or generalized convulsive seizures from those effective against absence seizures. The neuroleptics haloperidol and pimozide were completely inactive in contrast to their reported antagonism of bicuculine seizures. The spectra of the active substances are discussed with respect to Principal Component and Cluster Analysis. Noteworthy are the similarities between baclofen and etomidate; between aminoxyacetic acid, phenobarbital and valproate sodium; and between diphenylhydantoin and flunarizine.
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PMID:Effects of some anti-epileptic, neuroleptic and gabaminergic drugs on convulsions induced by D,L-allylglycine. 4 Dec 64

The unilateral and bilateral therapy differ in psycho-organic effects but have the same antidepressive efficiency. This is due to the facts that the organic effects are mainly caused by the electrical current whereas the antidepressive effect is dependent on the seizure activity. Compared to the bilateral treatment, unilateral gives reduced confusion, anterograde and retrograde amnesia as well as reduced experience of memory impairment. The difference is explained by a lower density of current in the brain. The unilateral treatment should be the treatment to be chosen. The antidepressive action of ECT fits the amine hypothesis, ECT causes a sustained increase of the synthesis of norepinephrine and of the sensitivity of amine receptors and creates conditions for alleviating both "low-output" and "low-sensitivity" depression. The antidepressive action is probably mediated by release of hypothalamic neurohormones.
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PMID:[Unilateral and bilateral shock therapy: mechanism of action (author's transl)]. 4 67

Procaine HCl and diphenylhydantoin (DPH) increased the duration and propagation of epileptiform afterdischarges (ADs) produced by electrical stimulation of the amygdala in rats. Procaine and DPH also increased the rate of seizure development (kindling) produced by repeated stimulation of the amygdala. Procaine and to a limited extentDPH would themselves act as convulsants in well kindled subjects. Diazepam, on the other hand, retarded or blocked amygdaloid kindling. Diazepam trigered a high frequency (20-30 c/sec) rhtthm in the amygdala, hippocampus and preoptic area. None of these drugs had any significant effect on potentials evoked in secondary limbic sites by single electrical pulses applied to the amygdala. Also, none of these drugs had any effect on recruiting or post-tetanic potentiation (PTP) in secondary sites produced by amygdala stimulation and none of the drugs had any effect on amygdaloid AD thresholds. The effects of these drugs on the responses evoked by anterior neocortex stimulation were quite different. Diazepam had no effect on any of the characteristics of the discharge or convulsion even at twice the dose levels used for the amygdala group. Procaine and DPH, however, blocked not only the eonvulsion but the AD as well. Eighty percent of the procaine- and DPH-treated rats failed to respond with neocortical AD even at current levels as high as 2000 muA. The few cortically stimulated subjects that did respond with an AD showed a subcortical rather than a neocortical seizure response. DPH had no effect on recruiting or PTP of the transcallosal response. Both procaine and DPH produced a weak but significant increase in the amplitude of the transcallosal evoked potential, while diazepam produce a weak decrement in that response.
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PMID:Effects of procaine hydrochloride, diazepam, and diphenylhydantoin on seizure development in cortical and subcortical structures in rats. 4 16

Temporal-lobe epilepsy commonly has its origins in childhood, particularly when the lesion involved is mesial temporal (Ammon's horn) Sclerosis. Evidence suggests that this lesion is probably a common cause of chronic epilepsy in adults and that often it is probably the result of a severe febrile convulsion in infancy. 40 children, fifteen years of age and younger, who had an anterior temporal lobectomy were followed up for one to twenty-four years. The findings confirm those already established in adults, that the best results of surgery, not only in seizure relief but also in behaviour, are obtained when mesial temporal sclerosis is the lesion found at operation, and also indicate that a severe febrile convulsion in infancy is often the chief provocative factor in the development of epilepsy.
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PMID:Outcome of surgery in 40 children with temporal-lobe epilepsy. 4 95

The diagnosis of brain tumour could not be made in 91 cases at the first investigation in a group of 1155 brain tumours. Slowly growing gliomas causing only epileptic fits and no other symptoms are especially difficult to diagnose. Of 21 personal observations of tumour seizures, in which the diagnosis of the neoplasm was missed at the first investigation in hospital, 9 were oligodendrogliomas, 5 astrocytomas, 3 glioblastomas, 2 spongioblastomas, 1 gangliocytoma and 1 a metastasis. They were all located in the frontal or centroparietal region. In most cases the seizures appeared during the third or fourth decade. The average interval between the first epileptic fit and the tumour diagnosis was 8.2 years in cases of oligodendrogliomas and 2.2 years in astrocytomas. 5 patients had major seizures, 2 had psychomotor attacks and all the others suffered from partial epilepsy. Anticonvulsive therapy was often successfull; either the frequency of the fits diminished or, in 2 cases, the character of the seizures changed. 18 patients had a normal neurostatus at time of the first investigation. Only 3 patients had a slight difference of physiological reflexes, but no other pathological signs. In none of the patients did investigation of the CSF, skull X-rays, brain scanning, pneumencephalography or cerebral angiography first lead to the diagnosis of a brain tumour. The EEG alone showed focal signs corresponding to the location of the tumour in about 50% of the cases.
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PMID:[The problem of early diagnosis of brain tumours causing seizures only (author's transl)]. 5 Oct 77

The effect of chlormadinone acetate (24 mg/day) upon the plasma levels of pituitary gonadotropins and gonadal hormones on the number of generalized convulsions and spike EEG density was studied in a group of epileptic children with intractable seizures and with clinical signs suggestive of hyperandrogenism. In each case, the effect of chlormadino ne was evaluated in relation to hormone levels and seizures observed during a control period and under the effect of placebo, as follows: Control (PC); Chlormadinone acetate (PCL1); Placebo (PP); Chlormadinone acetate (PCL2). In a male child, the number of convulsive attacks observed in the control period (26/month) was reduced during PCL1 (2/month), increased during PP (12/month) and reduced again during PCL2 (0/month). Spike EEG density showed a parallel course to the clinical attacks. In this case, control testosterone levels were markedly high (40 ng/ml) and decreased during PCL1 to 4.0, increased again during PP to 34.0 and decreased again during PCL2 to 1.2 ng/ml. Plasma levels of pituitary gonadotropins were unchanged during the entire period of study. In other cases, neither the number of epileptic attacks nor spik e EEG density were apparently affected by this treatment and plasma levels of pituitary gonadotropins and gonadal hormones were also unchanged. These findings suggest that a latent state of hyperandrogenism may be detected in some epileptic patients with intractable seizures and that chlormadinone may reduce convulsive attacks in these patients, probably by decreasing plasma testosterone levels.
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PMID:[Effect of chlormandinone acetate upon seizures in epileptic children with latent signs of hyperandrogenism]. 5 36


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