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PubMed1993

[Intracerebral-ventricular injection of 4-aminopyridine induced convulsion in rabbits].

Intracerebral-ventricular (icv) injection of 4-aminopyridine (4-AP) 8 micrograms to rabbits generated convulsions and epileptic discharges in electrocorticogram (ECoG). With 40 rabbits, the occurrence of convulsion at this dose level was 100%. The results from five rabbits showed that seizures may break out repeatedly at intervals of 1-5 min and such state may last about 1.5 h. Antiepileptic drugs, such as phenytoin sodium, phenobarbital sodium and diazepam, were found to effectively control the seizures provoked by icv 4-AP. Sodium valproate was less effective than the foregoing drugs. The icv 4-AP-induced convulsion appeared to have some merits as compared with the old epilepsy models, such as those induced by electric stimulation, cardiazol, or icv ferrous sulfate. We feel that it may be recommended as a model for the preliminary screening of antiepileptic drugs. The seizures provoked by icv 4-AP were shown to be antagonized by scopolamine, haloperidol, phentolamine, or propranolol, but potentiated by l-dopa. It is now recognized that 4-AP can enhance the release of ACh, DA, and NE in the central nervous system. The present results suggest that the convulsion elicited by 4-AP seems to be related to the disturbance of synaptic transmission in the brain.

4-Aminopyridine↗
PubMed1993

Pregnancy decreases the threshold for cocaine-induced convulsions in the rat.

The objective of this study was to test our hypothesis that pregnancy modifies the central nervous and cardiovascular toxicity of cocaine. Ten chronically catheterized term pregnant rats and 13 chronically catheterized nonpregnant female rats were infused with cocaine (2 mg/kg/min) intravenously to observe the sequential toxic manifestation of cocaine from mild central nervous stimulation (hyper-locomotor activities) to fatal cardiovascular collapse. Arterial blood samples were withdrawn at the onset of major toxic signs or symptoms--namely convulsion, hypotension, and circulatory collapse--for determination of cocaine concentrations and plasma cholinesterase activity. The dosage and plasma concentrations of cocaine associated with the onset of convulsions and cardiovascular depression were significantly lower in pregnant rats when compared with the nonpregnant animals. The mean time required to develop convulsions in the pregnant rat was significantly shorter (21 minutes) than that in the nonpregnant animal (33 minutes). However, once convulsive activity had developed, the time interval to achieve circulatory collapse was similar in both groups. Although the baseline plasma cholinesterase activity was higher in the pregnant rats than in the nonpregnant ones, the values in the samples obtained from the pregnant group at the onset of circulatory collapse were similar to the baseline values for the nonpregnant group. These findings suggest that a higher enzyme activity does not protect the development of toxic manifestations in the pregnant rat as compared to the nonpregnant animal when cocaine was administered at the same infusion rate.

Animals↗
PubMed1993

MK-801 and dopaminergic system in electrically-induced convulsions in mice.

In this study, the effects of MK-801 and selective dopaminergic agents on electrically-induced convulsions in mice were examined. MK-801 (0.004-0.1 mg/kg, ip) showed significant and dose-dependent anticonvulsive effects, and the anticonvulsive effects of MK-801 (0.02 mg/kg, ip) were not antagonized by dopamine selective antagonists, SCH-23390 (D1, 0.1 mg/kg, sc), sulpiride (D2, 100 mg/kg, sc) and pimozide (D2, 0.5 mg/kg, sc). Apomorphine (0.02-0.5 mg/kg, sc), a D1/D2 agonist, showed proconvulsant effect on electrically-induced convulsions. Dopamine selective antagonists, SCH-23390 (0.02-0.5 mg/kg, sc), sulpiride (5-100 mg/kg, sc) and pimozide (0.1-2.5 mg/kg, ip), also showed proconvulsant effect. However, these effects of dopamine agonist and antagonists were not dose-dependent. These findings suggest that the dopaminergic system neither plays an inhibitory role, at least on electrically-induced convulsions in mice, nor contributes to the anticonvulsant effect of MK-801 in electrically-induced convulsions.

Animals↗
PubMed1993

[Complicated febrile convulsion vs herpes-encephalitis].

Since Acyclovir is available a sufficient treatment of herpes simplex virus (HSV) encephalitis exists. Febrile convulsions may occur as the initial manifestation of an encephalitis, particularly of an HSV encephalitis. Within 25 months out of 151 children with febrile convulsions five children with complicated febrile convulsions were admitted at the pediatric department of Graz. In all children HSV antibodies in serum and cerebrospinal fluid (CSF) were negative and the diagnosis of an HSV encephalitis was made by positive CSF HSV polymerase chain reaction (PCR). Therefore, in any suspected case, i.e. in any case of a complicated febrile convulsion, CSF should be investigated including a HSV PCR to rapidly confirm or exclude HSV encephalitis.

Acyclovir↗
PubMedDate not supplied

The convulsive action of pentylenetetrazol and electroshock in irradiated rats.

Convulsive activity of pentylenetetrazol and electroshock was measured in rats irradiated 24 hr earlier with 800 R of X rays. At this time the content of "free" acetylcholine (ACh) was increased in the cerebral cortex, and the content of "bound" ACh was depressed in the brain stem. Irradiation facilitated the action of convulsogenic agents. Atropine did not prevent convulsions but facilitated them. An increase in the endogenous pool of ACh by eserine similarly to atropine facilitated the action of convulsogenic agents in control rats. In irradiated rats eserine shortened the duration of electrogenic convulsions, but it did not change significantly the latency of pentylenetetrazol convulsions. A causal relationship between the effects observed and post-irradiation modification of the content of "free" and "bound" ACh in the cerebral cortex and brain stem is discussed.

Acetylcholine↗
PubMed1996

[Neonatal convulsions in health care. I. Incidence, etiology and clinical aspects].

OBJECTIVE: To determine the incidence, etiology and course of neonatal convulsions in the Albacete Health District between 1991 and 1993. DESIGN: A descriptive study of retrospective cohorts. SCOPE: 12,427 new born babies in the province of Albacete. The Hospital General de Albacete looks after a population of 376,071 inhabitants, attends 82% of the births in this area and its Neonatology Department is the only one in the province. METHOD: Incidence: we found 25 new born babies (RN) with neonatal convulsions: absolute incidence (IA) in live RN0/00.; IA in live full-term RN (RNI) 1.4(0/00); IA in preterm RN (RNPT) 13.4(0/00) and in immature RN (with a gestational age of < 29 weeks) 27.8(0/00). ETIOLOGY: hypoxic-ischaemic encephalopathy 32%, malformations or cerebral dysgenesis 24%, intracranial hemorrhage 16%, with less frequency: infections, metabolic and pharmacological changes 8%, epileptogenic diagnosis 4%. COURSE: 10 of the RN (40%) died, 8 (32%) had sequelae, although in 3 cases these were transient, and 7 had developed normally (28%). Other relevant aspects are described: neurological findings between crises, type of crisis, EEG and neuroimaging techniques. DISCUSSION: We attribute the poor prognosis of our series, as compared to other published series, to an increase in the incidence of convulsions associated with a worse prognosis (RN with antepartum fetal distress, cerebral malformations and metabolic encephalopathies), and a decrease in acute intercurrent conditions; hypoglucemia, hipocalcemia and hypothermia, which do not leave sequelae after treatment. Also when methods of clinical inclusion/EEG are used, evaluating only the epileptic phenomena, convulsive crises with minimal clinical signs are observed.

Electroencephalography↗
PubMed1997

Febrile convulsions in selected large families: a single-major-locus mode of inheritance?

As part of a genetic linkage study of febrile convulsions, families with at least four members with the disorder were identified. By applying known principles of human inheritance, possible modes of transmission of febrile convulsions and factors which might impede progress in understanding their inheritance were analyzed. In eight families, 75 of 333 members had febrile convulsions. Inheritance of the disorder occurred in 43, 51, and 46% of children, siblings and all first-degree relatives of probands respectively. Vertical transmission occurred through three to four generations, including from male to male. In these families with multiple affected members, the findings support an autosomal dominant mode of inheritance of febrile convulsions.

Electroencephalography↗
PubMed1996

[Neonatal convulsions in health care. II. Prognostic factors].

OBJECTIVE: To determine whether neonatal convulsions make up a homogeneous pathological group when it comes to establishing indices of prognosis. DESIGN: Descriptive study of retrospective cohorts. SCOPE: Twenty five cases of neonatal convulsions out of the 12,427 new born babies in the province of Albacete in the period 1991-1993 and the follow-up of their development up to December 1994. MATERIAL AND METHODS: Univariant analysis (variable dependent evolution; variable independent: type of crisis identified, interictal clinical features, EEG pattern and cerebral Eco-CT/MR) and multivariant analysis using a maximal logistic regression model. RESULTS: I. Univariant analysis. Type of crisis: we found differences between the types of crises presented (clonic, focal tonic, myoclonic, subtile with apnea, with no obvious crisis) and the prognosis, but no significant result. Neurological findings between crises: the RN who showed no change in consciousness following the convulsion had a better prognosis than those with changes in the level of consciousness between crises. The difference was significant (P = 0.03). Post-critic EEG pattern. The RN with a normal or a focal EEG were grouped together as opposed to those who showed alterations which were multifocal, had changes in the basic rhythm, were paroxysmal or of low voltage; the first type of EEG indicated the best prognosis (OR = 12.0; IC 95%; 1.1-159.5; p = 0.2). Radiodiagnosis: the RN with no changes on Eco or CT-RM had better prognoses (p > 0.001) than those with pathological ones. None had pathological sequelae (OR = 0.0). II. Multivariant analysis. The final method only retained the variable Rx (Radiodiagnosis) which implied that the other variables lost significance when corrected for association with Rx (p < 0.001) OR = 0.0. DISCUSSION: Although the clinical and EEG findings are indicators of prognosis, they lose their significance when correction is made for the underlying cerebral damage. The cause of the convulsions and the associated underlying cerebral lesion is the most important factor in determining the final outcome.

Electroencephalography↗
PubMed1997

[The clinical study of the first febrile convulsion in children with brain-damage].

Forty-nine patients with cerebral palsy, mental retardation, or other congenital neurological disorders who had experienced febrile convulsions and had no previous nonfebrile seizures were presented. They were followed for 1.6 years to 15 years (mean: 6.8 years) after the initial febrile convulsion. The incidence of subsequent epilepsy (two or more afebrile seizures) was 39%, and 80% of them developed epilepsy within 2 years after the first febrile convulsion. The paroxysmal discharges on EEG recorded prior to or after the first febrile convulsion did not predict the occurrence of later epilepsy. Also under 3 years of age, EEG findings led to the same result. There was no definite evidence that administration of anticonvulsive drugs prevented later epilepsy. Pre-existing neurological abnormality was identified as a risk factor for epilepsy, and was an indication of persistent medication. There is no clear prophylactic procedure against long-lasting attacks. Accordingly, medical therapy can be started when epilepsy has developed. Patients with very severe brain damage who could not move except lying comprised only 6% of all cases, and 69% of the epilepsy patients were well controlled. They showed a good prognosis as compared with children with brain-damage in general with epilepsy.

Adolescent↗
PubMed1998

Two cases of glufosinate poisoning with late onset convulsions.

Glufosinate ammonium (GLA), the active ingredient in the non-selective herbicide BASTA (18.5% GLA), is a phosphinic acid analogue of glutamic acid. We report 2 cases of GLA poisoning with late onset convulsions and increased serum CK in spite of low blood concentrations of GLA after hemodialysis. A 69-y-old female was admitted to the emergency department after taking 500 ml of BASTA. On arrival she was conscious, and gut decontamination, hemodialysis and hemoperfusion were performed. However, 8 1/2 hours after ingestion, general convulsions occurred. Her serum OK increased to a peak of 24,900 IU/L on the third day of admission. An 87-y-old male was admitted to the emergency department 3 1/2 hours after taking 200 ml of BASTA and receiving gastric lavage at a local emergency room. On arrival he was conscious, and serial activated charcoal and hemodialysis was performed. Blood concentration of GLA after hemodialysis decreased from 1.56 micrograms/ml to 0.68 micrograms/ml. Thirty hours after admission he had general convulsions. GLA was not detected in the cerebrospinal fluid 6 h after the convulsions. His serum CK increased to a peak of 17,870 IU/L on the fifth day of admission.

Aged↗
PubMed1996

Intracerebroventricular pertussis toxin enhances sensitivity to chemical convulsants and decreases the protective efficacy of carbamazepine in mice.

The effects of pretreatment with pertussis toxin on pentylenetetrazole-, bicuculline-, aminophylline- and pilocarpine-induced seizures were investigated in mice. In animals treated intracerebroventricularly with pertussis toxin (0.5 microgram animal-1 120 h prior to testing), the CD50 (convulsive dose in 50%) values were considerably decreased in comparison with the CD50 in sham-treated animals. CD50 values of pentylenetetrazole, bicuculline, pilocarpine and aminophylline were calculated to be 39.9, 2.0, 262 and 141 mg kg-1, whereas they were calculated to be 57.7, 2.7, 324 and 230 mg kg-1 in sham-treated animals. The observations suggest that the enhanced sensitivity to a number of chemical convulsants irrespective of their mode of action possibly results from a functional suppression of inhibitory transmission at receptors coupled to pertussis toxin sensitive G proteins, rather than a direct action on G protein linked excitatory neurotransmission. Pertussis toxin significantly decreased the protective action of carbamazepine, increasing its ED50 (effective dose in 50%) from 14.8 to 20.1 mg kg-1 in a maximal electroshock convulsive test. It influenced the ED50 of neither diphenylhydantoin nor diazepam. The diminution of carbamazepine's efficacy might result from a summation effect of adenosine receptor antagonist properties of the drug and a suppression of transmission at adenosine receptors coupled to G proteins sensitive to pertussis toxin. Pertussis toxin pretreatment remained without any significant influence on the total plasma levels of carbamazepine, diphenylhydantoin and diazepam. This may lead to the conclusion that the interaction between pertussis toxin and carbamazepine does not seem to be of a pharmacokinetic nature and occurs probably at neuronal level.

Animals↗
PubMed1982

Excitatory effects of kynurenine and its metabolites, amino acids and convulsants administered into brain ventricles: differences between rats and mice.

When introduced intracerebroventricularly, quinolinic acid appeared to be the only kynurenine metabolite among those tested (L- and DL-kynurenine sulfate, kynurenic and nicotinic acids, nicotinamide) which induced locomotor excitement and clonic seizures in rats; in high dosage all exhibited convulsant action in mice. L-Kynurenine sulfate (500 micrograms) induced continuous rotation in rats around a longitudinal axis in one or other direction. It also potentiated the convulsant effect of strychnine sulfate and caffeine. Neither the excitatory amino acids, L-glutamic and L-aspartic acids nor the inhibitory amino acids, GABA, glycine and taurine induced excitement or seizures in rats but did in mice. In rats, GABA, glycine and taurine induced sedation, side position and discoordination. The convulsants, strychnine sulfate and pentylenetetrazole, induced seizures both in rats and mice. Differences between species may derive from the better access of intracerebroventricularly administered drugs to mouse hippocampus. Thus mice may be preferable for studies of this type on excitatory amino acids (including kynurenine pathway metabolites) and rats for those on inhibitory amino acids.

Amino Acids↗
PubMed1990

Convulsants induce interleukin-1 beta messenger RNA in rat brain.

The effects of systemic administration of kainic acid and pentylenetetrazol on interleukin-1 beta gene expression in the rat brain was studied. After the administration of kainic acid in a convulsive dose (10 mg/kg i.p.), Interleukin-1 beta mRNA was induced intensely in the cerebral cortex, thalamus and hypothalamus, moderately in the hippocampus and weakly in the striatum, but not in the midbrain, pons-medulla and cerebellum. Pentylenetetrazol induced Interleukin-1 beta mRNA in the cerebral cortex, hypothalamus, and hippocampus with a faster time-course than kainic acid. Diazepam suppressed both the convulsion and the induction of Interleukin-1 beta mRNA produced by kainic acid. Dexamethasone suppressed the induction of Interleukin-1 beta mRNA, but did neither the convulsion nor the induction of c-fos mRNA following the injection of kainic acid. These results provide the first evidence that intensive neuronal excitation induces Interleukin-1 beta mRNA in particular regions of the brain.

Animals↗
PubMed1984

Effect of spinal cord lesions on convulsive activity induced by intrathecal morphine.

Non-specific convulsive behavior induced by intrathecal (IT) morphine microinjection appears to be tonically modulated by centrifugal pathways originating within the brain since the frequency of IT morphine-induced hindlimb seizures and myoclonic twitches are both increased following spinal transection. These effects on convulsant activity are dissociable by selective neural lesions. Bilateral dorsolateral funiculus lesions potentiate seizure activity whereas ventral funiculus lesions and, to a lesser extent, interruption of cerebral cortical influences enhance myoclonic twitch activity. These initial studies indicate that distinct supraspinal centers differentially modulate myoclonic and seizure activity and suggest that an understanding of these systems may have clinical implications for the control of convulsant activity.

Animals↗
PubMed1988

Intrahippocampal injections of a specific mu-receptor ligand PL017 produce generalized convulsions in rats.

The effects of a selective mu-agonist, [NMe-Phe3-D-Pro4]morphiceptin (PL017), and a selective mu-antagonist, beta-funaltrexamine (beta-FNA), on convulsions and wet dog shakes (WDS) were studied. Electroencephalogram demonstrated that a single injection of PL017 into the ventral hippocampus evoked epileptiform spiking which appeared initially in the ventral hippocampus and spread to the cortical area when the animal developed generalized convulsion. Behavioral studies showed that PL017-induced convulsions and WDS were dose-dependent, and these behavioral changes were blocked by beta-FNA pretreatment. The results indicate that mu-receptors in the hippocampus may play an important role in seizure activities evoked by opioids.

Animals↗
PubMed1989

Homocysteic acid: convulsant action of stereoisomers in mice.

An effect of excitatory amino acid antagonists, 2-amino-7-phosphonoheptanoate (AP7), a selective N-methyl-D-aspartate (NMDA) antagonist, and gamma-D-glutamylaminomethylsulphonate (gamma-D-GAMS), a preferential kainate/quisqualate antagonist, on convulsions induced by intracerebroventricular administration of stereoisomers of homocysteic acid (HCA) was tested in mice. AP7, 0.025 mumol, blocked myoclonic seizures induced by L-HCA and D,L-HCA, and had no anticonvulsant action against D-HCA, gamma-D-GAMS, 0.5 mumol, was preferentially active against myoclonic seizures induced by D-HCA, had moderate anticonvulsant action against D,L-HCA, and no effect against seizures induced by L-HCA. These results indicate that activation of NMDA receptors contributes substantially to the convulsant action of L-HCA, while the convulsant action of D-HCA may be mediated mainly by non-NMDA related mechanisms.

Animals↗
PubMed1982

Effects of tetrazole derivatives on [3H]diazepam binding in vitro: correlation with convulsant potency.

A series of 8 tetrazole derivatives which differ more than one hundred-fold in their potencies as convulsants were tested for their abilities to inhibit [3H]diazepam binding to benzodiazepine receptors in vitro. The concentrations of drug necessary to inhibit 50% of specifically bound [3H]diazepam ranges from 18 micro M for undecamethylenetetrazole to 20 mM for trimethylenetetrazole. A comparison of the minimum convulsive doses for the 8 tetrazole derivatives tested with their relative potencies in displacing [3H]diazepam binding in vitro revealed a highly significant correlation (r = 0.98, P less than 0.001). In contrast, several representative tetrazole derivatives were found to have no inhibitory effects on beta-adrenergic, alpha-adrenergic or muscarinic cholinergic receptors in the same membrane preparation. These results suggest that pentamethylenetetrazole and related tetrazole derivatives may elicit their convulsant effects by interaction with the benzodiazepine receptor.

Animals↗
PubMed1984

Electrophysiological and pharmacological actions of the convulsant benzodiazepine Ro 5-4864.

Ro 5-4864 (4'-chlorodiazepam) elicited convulsions in mice with a CD50 of 23.5 mg/kg (i.p.) and increased the firing rate of substantia nigra zona reticulata neurons in a dose dependent fashion (0.5-4 mg/kg i.v.). Diazepam and clonazepam, but not Ro 15-1788, were potent inhibitors of Ro 5-4864 induced convulsions. Ro 15-1788 was also ineffective in reversing Ro 5-4864 induced increases in cell firing of zone reticulata neurons. Muscimol potently inhibited the seizures and reversed increases in cell firing elicited by Ro 5-4864. Phenobarbital and pentobarbital inhibited Ro 5-4864 induced convulsions with moderate potencies, while phenytoin and carbamazepine were ineffective at doses of up to 100 mg/kg. These observations suggest that Ro 5-4864 does not elicit its pharmacologic actions through a direct action at a 'brain-type' benzodiazepine receptor. However, both the profile and potency of compounds effective in inhibiting the electrophysiological and pharmacological effects of Ro 5-4864 suggest that this compound may act by perturbation of a component of the GABA-benzodiazepine receptor chloride ionophore complex. These findings do not, however, rule out a direct involvement of the high affinity 'peripheral-type' benzodiazepine receptors found in brain.

Animals↗