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At least 1,297 records · Page 72Linked to original sources
PubMed1990

Provocation of convulsive activity in the EEG by promazine-HCl-induced sleep in children.

The authors report on the convulsive activity provoking effect of Promazine as shown on EEG during sleep. It has successfully been used in infants and children who do not tolerate sleep deprivation. Promazine had smaller effect on the EEG-pattern than other related compounds or barbiturates. The greatest efficacy could be reached in generalised epilepsy, but the method was also helpful in other epilepsies. It is emphasized that in cases of acute neurological symptoms of not epileptical origin the compound is helpful to exclude epilepsy since Promazine induced sleep was never associated with convulsive activity on EEG in these cases.

Adolescent↗
PubMedDate not supplied

Convulsive action of flunarizine in rabbits.

High doses of an anticonvulsant agent, flunarizine, given singly or repeatedly produce convulsions in rabbits. Albino rabbits were more vulnerable than mongrel ones. The flunarizine-induced convulsions are interrupted by diazepam.

Animals↗
PubMed1986

Anesthetic and convulsant barbiturates alter gamma-aminobutyric acid-stimulated chloride flux across brain membranes.

gamma-Aminobutyric acid (GABA), the major inhibitory neurotransmitter in the mammalian brain, increases membrane chloride conductance. Previously, the authors reported that GABA increases 36Cl- uptake by membrane vesicles (microsacs) prepared from mouse brain. In the present study, we examined the actions of barbiturates on basal and GABA-stimulated chloride influx by brain vesicles. The anesthetic barbiturates pentobarbital, phenobarbital, mephobarbital, amobarbital, hexobarbital and R-(-)-1-methyl-5-phenyl-5-propyl barbiturate enhanced GABA-dependent chloride flux. Barbiturate enhancement of GABA action was seen at concentrations that are subanesthetic in vivo (e.g., 10 microM pentobarbital was effective). Pentobarbital was about 10 times more potent than pentobarbital, suggesting that chloride flux is related to the sedative rather than anticonvulsant actions of barbiturates. Pentobarbital (1 mM) prevented the antagonism of GABA-stimulated 36Cl- produced by picrotoxinin. The barbiturates generally produced no change in GABA-independent flux, although large concentrations of pentobarbital or hexobarbital produced a slight enhancement of chloride flux in the absence of GABA. The convulsant barbiturate S-(+)-1-methyl-5-phenyl-5-propyl barbiturate inhibited GABA-stimulated chloride flux, an action opposite to that of its anesthetic enantiomer. These experiments provide evidence for a functional coupling among GABA and barbiturate receptors and the chloride ionophore and suggest that the GABA-activated chloride channel is a site of action for intoxicant-anesthetic and convulsant barbiturates.

Animals↗
PubMed1988

Convulsant-induced changes in perforant path-dentate gyrus excitability in urethane anesthetized rats.

The dentate gyrus of intact urethane-anesthetized rats was employed to evaluate the effects of different convulsive agents on granule cell excitability. One purpose of this study was to determine whether mechanisms of action suggested from in vitro studies of these compounds could be demonstrated over clinically relevant dose ranges in vivo. The data demonstrate that drugs capable of antagonizing gamma amino butyric acid (GABA)-mediated inhibition produced similar effects on the intact hippocampus. Bicuculline, picrotoxin, pentylenetetrazol and the insecticide lindane increased granule cell excitability to perforant path stimulation. The primary cause of this was an increase in the innate excitability of the granule cells. These compounds also modified field potentials in a manner consistent with a reduction in early GABA-mediated inhibition. They did not affect synaptically mediated facilitation. The magnitudes of the effects were dose dependent, and changes were clearly measurable at exposures that produce clinical effects in nonanesthetized rats. Other convulsants could be readily differentiated from those affecting GABA-mediated inhibition. Kainic acid depressed granule cell responses to perforant path stimulation and severely depressed both inhibition and facilitation. A decrease in granule cell responsiveness was also produced by exposure to beta carboline. Exposure to strychnine had little effect on granule cell excitability. These data indicate that for bicuculline, picrotoxin, pentylenetetrazol and lindane, an apparently selective antagonism of GABA-mediated inhibition is clearly demonstrable at exposures that also produce clinical intoxication.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[Effector modelling of the action of ligands of the GABA-receptor complex, cooperativity of the processes and the type of modification of the complex by convulsants and their reversible agonists].

The expression of cooperativity of pharmacological effects of convulsants--exogenic ligands of supramolecular GABA-receptor-channel ensemble (GABA-RC)--bicuculline, picrotoxin, pentylenetetrazole, bemegride at intravenous infusion to intact animals and against a background of administration of barbital-Na and phenazepam is determined. The supposed mechanism of bemegride effect is discussed. Analysis of principles of GABA-RC functioning in vivo on the base of pharmacological data (cooperativity coefficients and types of modulation of GABA-RC functions at the interaction of convulsants and their reverse agonists) suggests the formation of biosystem response at modification of structures adequate to one of four subunits of "quartet" (tetrameric) model of GABA-RC.

Animals↗
PubMed1983

[Demonstration and partial purification of a convulsant from Cnestis glabra (Connaracea): effect on cells in culture].

A dialysable and thermostable compound was partially purified from Cnestis glabra (Connaracea) seeds. It is insoluble in organic solvents. At a dose corresponding to 0.5 g of seeds it has a lethal effect on mice after convulsive attacks. Sodium dipropylacetate, an anticonvulsive agent prevents the convulsions but not the death of the animals. The toxic compound inhibits protein synthesis in a rabbit reticulocyte lysate and in hepatoma tissue culture; moreover in the cell culture, the incorporation of thymidine into DNA is inhibited.

Animals↗
PubMed1982

Convulsant action of pentetrazol in rats with selective lesions of the hippocampal pyramidal cells with intracerebroventricular kainic acid.

Rats were injected uni- or bilaterally with intracerebroventricular kainic acid (0.1 micrograms per one ventricle in a volume of 5 microliters) and the animals were subsequently challenged with penetetrazol (PTZ) on the 21st day after the administration of the neurotoxin. PTZ was given either subcutaneously in a single dose of 70 mg/kg or intraperitoneally, one injection every 48 hours for a total of 15 trials, in doses of 20 mg/kg to induce kindled seizures. It was found that kainic acid-lesioned animals (especially those injected bilaterally) were more sensitive to the convulsant action of PTZ both in acute and kindled convulsions. The disruption of the hippocampal pyramidal projection to the septum may be responsible for these effects.

Animals↗
PubMed1982

[Stimulatory effects of intraventricular administration of kynurenines, amino acids, and convulsants: differences between rats and mice].

Quinolinic acid appeared to be the only kynurenine metabolite among tested (L- and DL-kynurenine sulfate, kynurenic and nicotinic acids, nicotinamide) which induced locomotor excitation and clonic seizures in rats whereas all of them exerted convulsant action in mice. Excitatory 1-glutamic and 1-aspartic amino acids and inhibitory amino acids GABA, 1-glycine and taurine did not induce either excitation of seizures in rats but did so in mice. Moreover, GABA, 1-glycine and taurine induced obvious sedation, side position and discoordination in rats. Convulsants strychnine sulfate and pentylenetetrazol induced seizures both in rats and in mice. The differences between mice and rats seem to be due to better availability of hippocampus for the intraventricularly administered drugs in mice. Mice seem to be preferable for studies with intraventricularly administered excitatory amino acids including kynurenines, whereas rats are preferable for inhibitory amino acids.

Amino Acids↗
PubMed1982

Interactions of phenytoin with ouabain and other chemical convulsants.

Phenytoin potentiated the convulsive actions of bicuculline and picrotoxin in mice, whereas the action of bemegride was neither potentiated nor antagonized. Seizures induced by intracerebral injection of ouabain were antagonized by phenytoin, as well as by phenobarbital, chlordiazepoxide and valproic acid; trimethadione had a possible small effect, not quite significant at the 5% level; ethosuximide and muscimol did not show significant effects. Seizures induced by intracerebral injection of pentylenetetrazol were antagonized by phenobarbital but not by phenytoin. Tests of phenytoin against other chemical convulsants are reviewed, and it is suggested that phenytoin may be specific for seizures that arise from a derangement of mechanisms involving sodium ions. This strengthens the view that such a derangement is likely in many cases of human epilepsy.

Animals↗
PubMed1981

Muscimol as an antagonist of chemical convulsants.

Muscimol (MU) was tested on mice for anticonvulsive action against chemical convulsants. 3-Mercaptopropionic acid (3-MP) was more sensitive to inhibition by MU (1.5 mg/kg) than was either pentylenetretrazol (PTZ) or bicuculline (BIC); picrotoxin (PIC) and kainic acid were not measurably antagonized; aminophylline was potentiated. The profile of action of MU closely resembles that of aminooxyacetic acid (AOAA), except that the latter strongly antagonizes kainic acid. MU distinguished more clearly than did AOAA between the action of 3-MP and that of either PTZ or BIC, inasmuch as the differences between the respective potency ratios were larger with MU than with AOAA. The results are consistent with the view that MU acts as a GABA agonist, that GABA antagonism is not a sufficient basis on which to explain the convulsive action of BIC or PIC, and that the antagonism of AOAA toward seizures induced by kainic acid may not be due to an action on the GABA system.

Animals↗
PubMed1994

Pro and anticonvulsant effects of xylazine on convulsion models in rodents.

Pretreatment of mice with 30 mg xylazine/kg ip protected against convulsions induced by amphetamine, but it intensified pentylenetetrazole- and strychnine-induced seizures. Xylazine pretreatment also protected rats against electroshock-induced convulsions. These findings support a noradrenergic mechanism being involved in the proconvulsant and/or anticonvulsant effects of xylazine.

Amphetamine↗
PubMedDate not supplied

[The role of the muscarinic receptors in the pathogenesis of the convulsive state induced by korazol in rats].

It was established in experiments on albino rats that blockade of the muscarinic receptors by various M-cholinolytics reduces the dose of corazol necessary for the development of a convulsive state. Preliminary administration of some cholinopositive agents raises the corazol action threshold. It is suggested on the basis of pharmacological analysis that the role of the cholinergic system in the pathogenesis of corasol-induced convulsive state in rats is mediated by the function of cholinoreceptors related to subtype M4 or M1.

Animals↗
PubMedDate not supplied

Role of voltage dependent calcium channels and cholinergic receptors in the convulsant action of BAY k-8644.

The study was designed to investigate the effects of administration of cholinomimetic agents and nifedipine on seizures induced by BAY k-8644 in rats. Injection of pilocarpine (3 mg/kg) increased seizures induced by BAY k-8644 (2 mg/kg). Administration of nifedipine (10 mg/kg) did not affect the convulsions and mortality elicited by coadministration of BAY k-8644 and pilocarpine. However, the facilitating effect of pilocarpine on BAY k-8644-induced seizures was fully prevented by pretreatment of rats with a cholinergic antagonist atropine (5 mg/kg). No similar effects were observed after injection of another cholinomimetic agent physostigmine (0.3 mg/kg). This finding implies, that facilitation of convulsant action of BAY k-8644 by pilocarpine may be related to activity of cholinergic system, but not strictly to activity of voltage dependent calcium channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1994

Phenotypic expression of benign familial neonatal convulsions linked to chromosome 20.

OBJECTIVES: To determine whether the syndrome of benign familial neonatal convulsions in a large family was linked to markers on chromosome 20q and to study the seizure patterns in affected individuals. DESIGN: A clinical and molecular biologic study of a single large family in which the probands were identical twins with benign familial neonatal convulsions. PATIENTS: Thirteen living affected family members and 27 living unaffected family members were evaluated. RESULTS: Multipoint linkage analysis with use of the chromosome 20q markers CMM6 and RMR6 gave a maximum lod score of 3.13 at theta = 0.063, indicating linkage in this family. Of the 13 affected members, 10 had known neonatal seizures. Four subjects had febrile seizures, of whom only two had known neonatal seizures. Two members had afebrile seizures later, one of whom had not previously suffered neonatal or febrile seizures. CONCLUSION: The phenotypic heterogeneity in this family, with an epilepsy syndrome determined by a single gene, was striking. This suggests that molecular genetic approaches to the common forms of idiopathic epilepsy, involving patients with clinically similar phenotypes from unrelated families, may be inappropriate.

Chromosomes, Human, Pair 20↗
PubMed1980

Convulsions after carotid endarterectomy.

Convulsions have not been emphasized as a possible complication of carotid endarterectomy. We describe here three patients in whom seizures with a focal component developed postoperatively. We suspect that the convulsions were secondary to a cerebral embolus arising from the operative site. An unstable preoperative neurological status is not a prerequisite for this complication.

Aged↗
PubMed1984

Landmark article Sept 17, 1938: Sodium diphenyl hydantoinate in the treatment of convulsive disorders. By H. Houston Merritt and Tracy J. Putnam.

In a previous study it has been shown that sodium diphenyl hydantoinate is effective in preventing electrically induced convulsive seizures in cats. The drug is relatively nontoxic and well tolerated by the usual laboratory animals. A clinical trial of sodium diphenyl hydantoinate was made in 200 patients with frequent convulsive seizures which had not been relieved by the previous modes of therapy. In 142 such patients who have received the treatment for periods varying from two to eleven months, grand mal attacks were relieved in 58 per cent and greatly decreased in frequency in an additional 27 per cent; petit mal attacks were relieved in 35 per cent and greatly decreased in frequency in an additional 49 per cent, and psychic equivalent attacks were relieved in 67 per cent and greatly decreased in frequency in 33 per cent. There were no fatalities. A toxic dermatitis occurred in ten patients (5 per cent), nonthrombocytopenic purpura in one patient and minor (in many instances, transient) toxic reactions, tremors, ataxia, dizziness and the like in approximately 15 per cent.

Adolescent↗
PubMed2003

Novel mutations in the Na+, K+-ATPase pump gene ATP1A2 associated with familial hemiplegic migraine and benign familial infantile convulsions.

Familial hemiplegic migraine (FHM) is a rare, severe, autosomal dominant subtype of migraine with aura. Up to 75% of FHM families have a mutation in the P/Q-type calcium channel Ca(v)2.1 subunit CACNA1A gene on chromosome 19p13. Some CACNA1A mutations also may cause epilepsy. Here, we describe novel missense mutations in the ATP1A2 Na(+),K(+)-ATPase pump gene on chromosome 1q23 in two families with FHM. The M731T mutation was found in a family with pure FHM. The R689Q mutation was identified in a family in which FHM and benign familial infantile convulsions partially cosegregate. In this family, all available affected family members with FHM, benign familial infantile convulsions, or both, carry the ATP1A2 mutation. Like FHM linked to 19p13, FHM linked to 1q23 also involves dysfunction of ion transportation and epilepsy is part of its phenotypic spectrum.

Adolescent↗
PubMed1980

Heart rate changes in convulsive and nonconvulsive neonatal apnea.

One hundred twelve apneic spells of at least 4 seconds' duration were monitored in 15 neonates; 77 episodes were associated with convulsive discharges on the electroencephalogram and 35 were not. Convulsive apnea did not occur in conjunction with bradycardia. Nonconvulsive apnea of less than 20 seconds' duration occurred in the presence of variable heart rates, but nonconvulsive apnea of 20 seconds or longer was nearly always associated with bradycardia.

Apnea↗