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PubMed1989

Synergistic anticonvulsant action of diazepam & clonazepam with amino-oxyacetic acid against isoniazid-induced convulsions in rats.

The protective effect of two benzodiazepine compounds, diazepam and clonazepam was tested against isoniazid (INH)- induced convulsions in rats pretreated with the gamma-amino-butyric acid (GABA) transaminase inhibitor viz., aminooxyacetic acid (AOAA), and the result was compared with that produced by the two drugs independently. Rats treated 6 h and not 30 min previously with AOAA showed a dose-dependent inhibition of INH-induced convulsions. In these animals both diazepam and clonazepam showed a greater protective effect than that produced by them alone. It is suggested from these findings that, even if their anticonvulsant mechanisms are distinct, with or without the involvement of GABA, AOAA and the benzodiazepine compounds seem to act synergistically against INH-induced convulsions.

Acetates↗
PubMed1988

The clinical anti-convulsant effects of flumazenil, a benzodiazepine antagonist.

The clinical anti-convulsant effect of flumazenil in epilepsy has been demonstrated: (i) by acute i.v. administration under EEG control in an epileptic patient who had been previously heavily sedated with diazepam; (ii) in patients undergoing pharmaco-EEG studies whereby spike and wave counts were diminished following oral administration of 10 mg of flumazenil; and (iii) in a series of 27 epileptic patients treated chronically for periods of up to 42 months with flumazenil as monotherapy or as addition to basic therapy. The daily dose ranged from 10-90 mg. Before treatment all patients presented with frequent seizures and had an abnormal EEG. In these patients the anti-convulsant effect was good or very good in 70% of the previously untreated (naive) patients and in about half of the patients who had epilepsy of long duration and had been treated already with standard anti-convulsants. Side-effects with flumazenil were generally mild in nature and rarely led to discontinuation. About one-third of the patients expressed a feeling of well-being while under therapy with flumazenil. A possible mechanism of action is discussed.

Adolescent↗
PubMed1986

Neuropeptides: anticonvulsant and convulsant mechanisms in epileptic model systems and in humans.

Neuropeptides represent a new class of compounds with important implications for the understanding of the mechanisms and treatment of epileptic disorders. Several systems of peptide modulators--in particular the opioid-like peptides, vasopressin, somatostatin, thyrotropin-releasing hormone (TRH) and ACTH--have partially demonstrated endogenous roles in some forms of epilepsy. Seizures and stressful situations may release endogenous opioid peptides and mediate postictal depression and postictal seizure refractoriness. Vasopressin is believed to increase susceptibility to convulsions and may be involved in the pathogenesis of febrile convulsions. Derangements in TRH regulation may lower thresholds for seizure expression by regulating arousal systems; however, some TRH analogs have proven to be effective anticonvulsants. Long-term alterations in somatostatin regulation could be components of focal epilepsies. ACTH is particularly useful in the treatment of infantile spasms. Pharmacological effects of these and other peptides have potentials for defining new classes of anticonvulsants. Cholecystokinin (CCK) and its analogs, the opioid peptides beta-endorphin and FK33824, TRH analogs, and several dipeptides exhibit potent anticonvulsant properties in chemical, electroshock, and genetic model screens. Convulsant actions of CRF, somatostatin, TRH, vasopressin, and high doses of endorphin or enkephalins may provide new tools to study regulatory mechanisms of cerebral excitability. The enkephalin epileptogenic effect is being developed as a predictive tool for new anti-petit mal anticonvulsants. Advances in molecular biology have identified the genes of particular peptide families. A concept has developed that the large propeptide precursors, coded by these genes, whose processing leads to functional peptide formation and release, regulate peptidergic humoral responses to external stimuli. This idea may have particular application in the understanding of the genetic basis of some seizure states. Techniques for amplification of mRNA expression have identified specific neuronal proteins and peptides. Knowledge of protein and propeptide structural cleavage sites has suggested previously unknown candidates for modular systems in epileptic states. Technological advances in automated peptide sequencing and synthesis have allowed the development of metabolically resistant analogs and antagonist peptides. The anticonvulsant potencies of CCK, TRH, and opioid peptides have been defined more clearly with these methods.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenocorticotropic Hormone↗
PubMed1987

Clorazepate use may prevent alcohol withdrawal convulsions.

Clorazepate dipotassium was administered orally for the five-day prophylactic treatment of potential, incipient and overt withdrawal signs and symptoms in 226 patients on admission to an inpatient alcohol treatment unit. Conservative estimates based on these patients' histories and on literature reports predicted that between 7 and 40 (3% to 18%) of these persons would be expected to have a withdrawal convulsion. No patients experienced convulsions. This complete absence of seizures suggests that clorazepate is effective in counteracting convulsive and other manifestations of the alcohol withdrawal syndrome.

Administration, Oral↗
PubMed1987

[The influences of neurotransmitters on the traumatic unconsciousness, immediate convulsion and mortality in the experimental mice model].

In order to clearing the influence of neurotransmitters in concussive unconsciousness, immediate convulsion and mortality, the following experiments were performed. Awake male mice of dd-strain were restrained and subjected to head injury using a bakelite weight of 30 gm dropped from a height of 20 cm on to the skull. This injury resulted in immediate loss of consciousness in 100%, convulsive seizure in 66% and death in 30% of animals. The severity of consciousness disturbance was evaluated by two parameters; (1) time interval required for the recovery of righting reflex (RR) and (2) time interval for the recovery of spontaneous movement (SM). Agonist or antagonist of various neurotransmitters was given intraperitoneally 0.5 or 2 hours before injury. The following results were obtained although some of them were statistically not significant. Physostigmine shortened both RR (p less than 0.1) and SM (p less than 0.01), whereas scopolamine did not change these intervals. Atropine sulfate shortened both of them. Nevertheless, atropine methylbromide, which dose not pass through blood-brain-barrier, also had same effects. Methamphetamine shortened both RR (p less than 0.1) and SM (p less than 0.05), whereas haloperidol prolonged these intervals. 5-HTP shortened RR (p less than 0.05), but prolonged SM (p less than 0.1). Methysergide shortened both RR (p less than 0.05) and SM (p less than 0.01). Convulsive seizure was suppressed by physostigmine (p less than 0.01) or 5-HTP (p less than 0.20). These results suggested that suppression of dopaminergic and cholinergic systems, and/or activation of serotonergic system contribute to concussive unconsciousness.

Animals↗
PubMed1986

Interactions of angiotensin II and GABA-ergic agents at the threshold of convulsive reactions.

The effects of angiotensin II (AT II), GABA, muscimol (administered i.c.v.) and of amino-oxiacetic acid (AOAA) and baclofen (administered i.p.), as well as of the combinations of AT II with these substances and bicuculline, were studied with respect to the threshold of the convulsive seizures induced by timed intravenous infusion of pentylenetetrazol (PTZ) in mice. It was found in the experiments that the threshold-increasing effect of GABA, muscimol and AOAA was potentiated by AT II (applied in a dose which did not change essentially the convulsive threshold). The potentiated effect of GABA, muscimol and AOAA on the convulsive threshold, when applied in combination with AT II, was antagonized by bicuculline. The threshold-increasing effect of baclofen was not affected substantially by AT II; in this case bicuculline had no effect. On the basis of the results obtained it may be assumed that AT II performs the functions of an antocoid predominantly for the GABA-A receptors in the central nervous system.

Aminooxyacetic Acid↗
PubMed1986

[Effect of antidepressants on the convulsive action of thiosemicarbazide, strychnine and corasol].

Orally administered amitryptiline (25 and 50 mg/kg) protected animals against fatal convulsions induced by thiosemicarbazide, strychnine and metrazole. Vilaxazine had a protecting effect against death induced by strychnine. Impramine, maprotiline, mianserine and pirlindole (pyrazidol) only somewhat prolonged the latend period of convulsions and death, while incazane, caroxazone, nomifenzine and trazodone had practically no effect on the action of the three convulsants under study.

Animals↗
PubMed1986

[Autonomic disorders in children with hyperthermic and affective-respiratory convulsions].

The vegetative tone, vegetative reactivity in the Dagnini-Aschner parasympathic test, and vegetative provision of functions in the orthoclinostatic test as described by Vien et al. were determined on the basis of cardiovascular parameters (blood pressure, heart rate) in a group of 5-year-old children with hyperthermal (n = 44) or affective-respiratory (n = 21) convulsions. The children with hyperthermal convulsions showed an increase in the sympathic tone and hyperfunctional manifestations. Elevated vegetative reactivity was observed in these patients. In contrast, the children with affective-respiratory convulsions presented instability of both systolic and diastolic pressure and a higher pulse rate in head-down tilt test, as compared to normal subjects. This indicates insufficient development of the vegetative regulation mechanisms.

Autonomic Nervous System Diseases↗
PubMed1985

Recrystallization from ether causes unusual changes in the convulsant activity of pentylenetetrazol.

The convulsant activity of commercial pentylenetetrazol (PTZ) and that of pentylenetetrazol recrystallized from ether (PTZE) were compared in the waking rabbit by means of recording the electrical activity of the brain. In addition, the interaction between the two substances was studied. When given in slow intravenous infusion, PTZE proved only half as effective as PTZ (threshold doses: 23.18 +/- 1.8 mg/kg and 12.40 +/- 0.7 mg/kg, respectively). One single infusion of PTZE 5-10 days prior to the administration of PTZ decreased the latter's convulsant activity to half of the original, while PTZ pretreatment left the activity of PTZE unaltered. Previous physico-chemical investigations suggested that, after recrystallization from ether the molecule might be present in dimer form at the phase-boundaries. Such a process, if taking place also at the cell membrane surface might account for the diminished convulsant activity of the recrystallized molecule.

Animals↗
PubMedDate not supplied

[Electrolytic changes in febrile convulsions].

The authors valued some metabolic parameters (sodium, potassium, calcium, blood levels of glucose, proteins, nitrogen, creatinine) in 159 children with febrile convulsions and compared the results with those of a group of children with fever (50 subjects) and of a group of health, fever free children (50 subjects). In the patients with febrile convulsions serum levels of sodium, calcium and osmolarity resulted significantly lower than those obtained in both control groups. The electrolytic modification (overall hyponatremia, probably due to a SIADH) may have a role in short-term relapses of febrile convulsions. Hyponatremia is present also in some children with high fever, without seizures; it may be that hyponatremia, in predisposed subjects, lower the threshold of neuromuscular excitability.

Calcium↗
PubMed1979

Effect of helium/nitrogen/oxygen mixtures on HPNS convulsion threshold in euthermic rats.

This study compares the effects of various so-called trimix mixtures (10, 20, and 40% N2 in He-O2) on the convulsion threshold pressure (Pc) and EEG activity in 60 adult male Wistar rats with chronically implanted electrodes with those in 20 rats in He-O2 only. Restrained animals were individually compressed with trimix mixtures at 80 or 160 atm per hour to a simulated depth of 138 ATA; colonic temperature was maintained at normal levels. Pc was defined as the initial occurrence of overt sustained generalized tonic-clonic seizures, accompanied by typical "spike and wave" patterns in all EEG leads. As in man, in rats trimix increased the depth of the onset of HPNS tremors and myoclonic jerks in all six groups of rats. However, the Pc of the trimix groups was no different from the Pc of the helium-oxygen group (113 ATA), and at 40% N2, rats showed EEG seizures but no overt convulsions. These results are discussed in relation to those of other studies showing the extension of Pc in mice and monkeys attained by adding narcotics to heliox; the paper also considers the relevance of method of compression, addition of nitrogen, core temperature, and species differences, as well as the need for EEG measurements and direct observation of overt convulsions as indicators of an effective antagonism of HPNS.

Animals↗
PubMed1982

[Genetically determined predisposition to convulsive seizures as a result of a generalized defect in catecholamine metabolism in the central nervous system].

The author compared the functional properties of the strial system in KM rats sensitive to the convulsive effects of sound and in Wistar rats which are insensitive to those effects. It was shown that bulbocapnine (an antagonist of dopamine) administered to the Wistar rats in a dose of 40 mg/kg body weight caused catalepsy, depressed the motor cortex excitability and raised the threshold of the generalized Jacksonian-type convulsions. The KM rats showed neither catalepsy, nor the rise of the generalized convulsion threshold, and the depression of the motor cortex excitability in them was but slight. Examinations of the apomorphine-induced stereotypy (dose 1.0 to 10 mg/kg) showed that in the KM rats the sensitivity of the receptors to dopamine was changed. The hyperproduction of catecholamines in the striatum, the hypothalamus, and the adrenals in the KM rats suggests that the predisposition to epileptimorph states correlates with a generalized defect in the metabolism of catecholamines. It is supposed that the hypersensitivity of the KM rats to epileptogenic effects is due to a deficit (caused by the excess of dopamine) of striatum depressing function.

Acoustic Stimulation↗
PubMed1983

A comparison of flunitrazepam and diazepam in the prevention of local anesthetic-induced convulsions.

The anticonvulsive effects of equivalent strengths (ED50) of flunitrazepam and diazepam were compared in 60 Sabra mice injected i.p. with median convulsive (CD50) doses of lidocaine or bupivacaine. Convulsions occurred in 40% of those pretreated with diazepam but were completely prevented in those injected with flunitrazepam. Mortality was much higher in those mice pretreated with diazepam, three having died after the administration of lidocaine and four after bupivacaine. With flunitrazepam pretreatment, there were no deaths after lidocaine and only one after bupivacaine. Flunitrazepam protected these mice against local anesthetic-induced convulsions more effectively than did diazepam.

Animals↗
PubMedDate not supplied

[Effect of nicotinamide on generalized convulsions in mice].

It was shown in acute experiments on mice that nicotinamide in doses of 250-500 mg/kg given intraperitoneally increased the latent period of corasole clonico-tonic convulsions without affecting their expressiveness and mortality. When given in a dose of 1000 mg/kg nicotinamide prevented clonico-tonic convulsions and mortality, and considerably raised the latent period of convulsions and the lifespan of the animals intoxicated with thiosemicarbazide and strychnine. The expressiveness of the nicotinamide effects depended on the time of its administration.

Animals↗
PubMed1983

[Pharmacokinetic elements of sodium valproate. Use in febrile convulsions in children].

A pharmacokinetic study of sodium valproate (DPA) was undertaken in children treated with this drug after a febrile convulsion. In infants, after a single oral dose of 20 mg/kg body weight in the first morning meal, plasma kinetic data were as follows: T max 2.4 hr +/- 1.1; total DPA maximum plasma concentration: 94 micrograms/ml +/- 28; T 1/2: 12.4 hr +/- 4.9; the distribution volume was 0.25 l/kg +2- 0.07 and plasma clearance was 0.014 l/kg/hr +2- 0.004. Control of prolonged treatment showed that the measured plasma concentrations were not correlated with the daily dosage. Furthermore, when febrile convulsions are concerned, one should carefully weight the recently reported hepatic toxicity of DPA, against the usually good prognosis of febrile convulsions.

Child, Preschool↗
PubMed1981

[Effect of sodium dipropylacetate on experimental convulsions produced by pentetrazole and picrotoxin].

Sodium dipropylacetate, an anticonvulsant used in human therapy, gives a more efficient protection against convulsions elicited by pentetrazol than by picrotoxin. In the case of picrotoxin induced convulsive seizures where there is an alteration at the GABA receptor level, ther is a lack of efficiency after nDPA treatment which increases GABA at the synaptic level. DPA is more effective against pentetrazol convulsive seizures where no direct participation of GABAergic receptors seems to occur. The efficiency of potentialisation of GABAergic mediation is a function of the mechanism by which the seizure is triggered.

Animals↗
PubMed1984

[Potent convulsant effects of a benzodiazepine inverse agonist, methyl beta-carboline-3-carboxylate in cats].

The convulsant properties of methyl beta-carboline-3-carboxylate (beta-CCM), which is a homologue of a putative benzodiazepine receptor ligand in the mammalian central nervous system, were examined in cats. Subcutaneous injection of 0.5 mg/kg of the beta-CCM produced various degrees of myoclonic jerks always accompanied by cortical spike burst. Some autonomic symptoms such as tachypnea, hypersecretion of thick mucous saliva, vomiting and mydriasis were also presented. Subcutaneous injection of 1.0 mg/kg of the compound induced a generalized tonic-clonic convulsion. Injection of the same amount of the drug 1 hour later in the same cats failed to provoke a generalized seizure. Repeated injection of the same dose 3 hours later provoked a generalized seizure, but with a longer latency. However, repetition of the experiments 24 hours after or 10 days after the first injection consistently induced the same type of generalized seizure with the same latency as the first injections. These results support the suggestion that the pharmacological effect, especially the convulsive effect, of beta-CCM is dose-related, reversible and reproducible in the same cats and among different cats. Moreover, the postictal refractory period in this model of epilepsy may continue about for 3 hours.

Animals↗
PubMed1984

Convulsive status epilepsy: is there a role for thiopentone-induced narcosis?

Convulsive status epilepsy is a medical emergency with significant mortality and morbidity. This retrospective survey reports the use of non-anaesthetic doses of thiopentone, given either by intravenous or rectal infusion. The regime was effective in controlling convulsive status without significant complications. It is suggested that this regime can be used safely when standard doses of diazepam (or clonazepam), and/or phenytoin, fail to effect immediate control of convulsive status, and before anaesthetic agents are administered.

Adolescent↗