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PubMed1990

Adverse effects on EEG and clinical condition after immunizing children with convulsive disorders.

116 immunizations were given to 61 children with febrile convulsion or epilepsy who had not had a seizure for 1 year since the last attack. In 92 of the 116 immunizations the electroencephalogram (EEG) was examined before and after immunization. No adverse effects on the EEG were observed in 19 immunizations with Japanese encephalitis, measles, mumps or rubella vaccines. Epileptic spikes reappeared after 10 immunizations and epileptic spikes increased after 10 immunizations among 73 given for diphtheria, acellular pertussis and tetanus (DPT), diphtheria and tetanus (DT), or Bacillus Calmette-Guerin (BCG). A convulsion was observed once in one child 7 days after immunization with BCG. A follow-up EEG examination is necessary after children with convulsive disorders are immunized.

Adolescent↗
PubMed1980

Long-term outcome in children with temporal lobe seizures. IV: Genetic factors, febrile convulsions and the remission of seizures.

Three groups of children are considered: 100 children with temporal lobe epilepsy, 59 of whom had also had febrile convulsions; their 214 sibs; and an unselected coeval sample of 438 children with febrile convulsions. When the family history is positive for seizures, the adverse factors described in previous papers in this series do not discriminate between those who remit their epilepsy and those who do not. Interactions between age of onset, family history and outcome are displayed. In the absence of an affected relative, none of 26 children with an onset below four years remitted. Six had their first seizure at a later age, of whom three remitted. In the presence of a first-degree affected relative, 10 out of 19 remitted: age of onset was cut off at 2 years 9 months. Eight children had second-degree affected relatives; there were four remissions, all with onset after three years. The authors compared the proportion of simple benign febrile convulsions in 438 unselected children who had fits with fever, with the same ration in the probands' affected siblings. The two ratios were the same. They conclude that one gene promoting febrile seizures was common to both groups. The siblings of those probands who remitted their seizures had a 38 per cent risk of seizures: the siblings of non-remitters had an 11 per cent risk. A new genetic theory is proposed to account for these data. Practical considerations include genetic advice, the necessity of weaning some patients from anticonvulsants, and early discrimination of those likely to need neurosurgical relief of their epilepsy.

Adolescent↗
PubMed1989

Polychlorinated convulsant insecticides potentiate the protective effect of NaCl against heat inactivation of [3H]flunitrazepam binding sites.

Six polychlorinated convulsant insecticides that potently inhibit t-[35S]butylbicyclophosphorothionate ([35S]TBPS) binding to rat brain membranes also potentiate the protective effect of NaCl (200 mM) against heat inactivation of [3H]flunitrazepam binding sites on the same membranes. Similar effects were obtained with all "cage" convulsants tested. The rank order of potencies as heat protection potentiators was similar to the rank order of potencies as inhibitors of [35S]TBPS binding (alpha-endosulfan greater than endrin greater than dieldrin greater than toxaphene greater than lindane). alpha-Endosulfan and endrin are more potent in both respects than any previously reported picrotoxin-like (cage) convulsant, but are much less toxic to mammals. The greatly reduced toxicities of alpha-endosulfan and endrin in mammals may reflect partial gamma-aminobutyric acid (GABA)-neutral properties of these compounds. Time courses of heat inactivation of [3H]flunitrazepam binding sites in the presence of 200 mM NaCl plus saturating concentrations of endrin or picrotoxin revealed monophasic components constituting about 88% of the binding sites, suggesting that virtually all [3H]flunitrazepam binding sites are coupled to picrotoxin binding sites in the GABA/benzodiazepine/picrotoxin receptor complex. Protection against heat inactivation constitutes a useful tool for characterizing the various allosterically linked binding sites in neurotransmitter receptor complexes.

Animals↗
PubMed2006

Involvement of the somatostatin-2 receptor in the anti-convulsant effect of angiotensin IV against pilocarpine-induced limbic seizures in rats.

The anti-convulsant properties of angiotensin IV (Ang IV), an inhibitor of insulin-regulated aminopeptidase (IRAP) and somatostatin-14, a substrate of IRAP, were evaluated in the acute pilocarpine rat seizure model. Simultaneously, the neurochemical changes in the hippocampus were monitored using in vivo microdialysis. Intracerebroventricularly (i.c.v.) administered Ang IV or somatostatin-14 caused a significant increase in the hippocampal extracellular dopamine and serotonin levels and protected rats against pilocarpine-induced seizures. These effects of Ang IV were both blocked by concomitant i.c.v. administration of the somatostatin receptor-2 antagonist cyanamid 154806. These results reveal a possible role for dopamine and serotonin in the anti-convulsant effect of Ang IV and somatostatin-14. Our study suggests that the ability of Ang IV to inhibit pilocarpine-induced convulsions is dependent on somatostatin receptor-2 activation, and is possibly mediated via the inhibition of IRAP resulting in an elevated concentration of somatostatin-14 in the brain.

Angiotensin II↗
PubMed1969

Effects of ganglion blocking agents on nicotine extensor convulsions and lethality in mice.

1. The ganglion blocking agents, chlorisondamine, pentamethonium, mecamylamine, decamethonium and hexamethonium all block nicotine extensor convulsions when administered intraventricularly in mice. Tetraethylammonium was inactive.2. For the intraventricular route, there is a relationship between ganglionic blocking potency and blocking of nicotine extensor convulsions. Indirect evidence suggests that the site(s) of action of nicotine extensor convulsions and lethality is central in origin and associated with brain areas near the ventricles.3. When ganglion blocking agents are given orally, subcutaneously or intravenously varying degrees of protection can be observed probably depending on factors such as whether or not the drugs cross the blood-brain barrier, absorption, etc., and the effectiveness in protecting mice from nicotine is not related to ganglionic blocking potency.4. Atropine and morphine given intraventricularly or subcutaneously did not protect mice from the LD95 of nicotine. Chlorpromazine gave very erratic results and phenobarbitone was effective subcutaneously and to a lesser extent intraventricularly.

Animals↗
PubMed1980

Brain and serum calcium concentrations following electroconvulsive shock or bicuculline-induced convulsions in rats.

1 A single electroconvulsive shock (ECS; 125 V, 1 s, 50 Hz) given to rats anaesthetized with halothane produced little change in either serum or regional brain calcium concentrations, compared to rats anaesthetized with halothane, either 5 min or 24 h after the convulsion. Both anaesthetic and ECS-treated rats showed an elevated serum concentration 5 min after the ECS. 2 When 5 ECS were given spread out over 10 days there were no significant calcium concentration changes in either serum or brain except for an increase in the pons/medulla. 3 A single convulsion produced by bicuculline (0.375 mg/kg i.v.) resulted in a marked increase in the calcium concentration in serum, but not brain, 5 min later. Diazepam pretreatment (10 mg/kg i.v.) prevented both the convulsion and the serum calcium change. 4 Results are discussed in relation to clinical data on calcium changes following electroconvulsive therapy (ECT) and the enhanced monoamine-mediated behaviours which follow ECS administration to rats.

Animals↗
PubMed1989

Convulsions induced by centrally administered NMDA in mice: effects of NMDA antagonists, benzodiazepines, minor tranquilizers and anticonvulsants.

1. Convulsions were induced reproducibly by intracerebroventricular injection of N-methyl-D-aspartic acid (NMDA) to conscious mice. 2. Competitive (carboxypiperazine-propylphosphonic acid, CPP; 2-amino-7-phosphonoheptanoic acid, AP7) and non-competitive (MK801; phencyclidine, PCP; thienylcyclohexylpiperidine, TCP; dextrorphan; dextromethorphan) NMDA antagonists prevented NMDA-induced convulsions. 3. Benzodiazepine receptor agonists and partial agonists (triazolam, diazepam, clonazepam, Ro 16-6028), classical anticonvulsants (diphenylhydantoin, phenobarbitone, sodium valproate) and meprobamate were also found to prevent NMDA-induced convulsions. 4. Flumazenil (a benzodiazepine receptor antagonist) and the GABA agonists THIP and muscimol (up to subtoxic doses) were without effect. 5. Flumazenil reversed the anticonvulsant action of diazepam, but not that of MK801. 6. Results obtained in this model differ somewhat from those described in a seizure model with systemic administration of NMDA. An explanation for this discrepancy is offered. 7. This model is a simple test for assessing the in vivo activity of NMDA antagonists and also expands the battery of chemically-induced seizure models for characterizing anticonvulsants not acting at NMDA receptors.

Animals↗
PubMed1975

Prevention of febrile convulsions with dipropylacetate (Depakine).

In 47 children followed for 1 year after the first "simple" febrile convulsion, dipropylacetate (Depakine, 20 mg/kg) was as effective in preventing new febrile convulsions (a single recurrence in 4% of 47 children) as was phenobarbital (5 mg/kg) or primidone (25 mg/kg) (a single recurrence in 4% of 47 children), and there were no side effects. Of 47 untreated children followed for 1 year, 55% had 1 to 4 new febrile convulsions. All medications were given in divided doses morning and evening.

Anticonvulsants↗
PubMedDate not supplied

Anticonvulsant properties of calcium channel blockers in mice: N-methyl-D-,L-aspartate- and Bay K 8644-induced convulsions are potently blocked by the dihydropyridines.

Ten calcium channel blockers were evaluated in mice after intraperitoneal (i.p.) administration for prevention of seizures induced by various convulsants. The dihydropyridines (class II calcium antagonists, i.e., nisoldipine, nitrendipine, nicardipine, nifedipine, and nimodipine) selectively prevented seizures elicited by administration of pentylenetetrazol (PTZ), N-methyl-D,L-aspartate (NMDLA) and the dihydropyridine calcium channel agonist BAY K 8644. With regard to prevention of NMDLA-induced seizures and the subsequent mortality, these compounds were similar in potency to the noncompetitive NMDA receptor antagonist MK801. Unlike MK801 (IC50 = 0.014 microM), the dihydropyridines did not inhibit in vitro binding of MK801 to synaptic membrane fractions prepared from rat cerebrohippocampal tissue. The dihydropyridines did not influence seizures elicited by maximal electroshock (MES). Flunarizine (diphenyl-alkylamine, class IV) was selectively active in the MES test, considerably less potent against NMDLA-induced convulsions/mortality, exhibited weak noncompetitive NMDA antagonism in vitro (IC50 = 28 microM), and was inactive in the PTZ and BAY K 8644 testing paradigms. Diltiazem, a class III benzothiazepine, possessed relatively weak broad spectra of activity against MES, PTZ, NMDLA, and BAY K 8644 test situations. It was inactive in vitro as a noncompetitive NMDA antagonist. The class I compound verapamil (phenylalkylamine) displayed only moderate inhibition of NMDLA-evoked seizures/mortality. Prenylamine (class V) was moderately active against convulsions produced by MES and NMDLA while retaining a degree (IC50 = 16 microM) of noncompetitive NMDA antagonism. Lidoflazine (class VI) was inactive in all tests. The Ca2+ channel blockers and MK801 were inconsistent in their ability to prevent bicuculline (BIC)-elicited convulsions.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1997

Intravenous carbamazepine: comparison of different parenteral formulations in a mouse model of convulsive status epilepticus.

PURPOSE: A drawback of carbamazepine (CBZ), a major antiepileptic drug (AED) with clinical efficacy against partial and generalized convulsive seizures, is its isolubility in aqueous vehicles, which is generally considered a contraindication to parenteral administration in epileptic patients. However, CBZ can be dissolved in glycofurol, a solvent used clinically as a vehicle for parenteral preparations of drugs such as diazepam (DZP) and phenytoin (PHT). Furthermore, aqueous CBZ solutions can be prepared by complexing CBZ with 2-hydroxypropyl-beta-cyclodextrin (HP beta CD), an inert beta-cyclodextrin derivative believed to have acceptable tolerability for human use. Such solutions of CBZ have been proposed to be suitable for intravenous administration in treatment of convulsive (grand mal) status epilepticus (CSE). METHODS: A series of five generalized tonic-clonic seizures (GTCS) in 30 min was induced by repeated transauricular electrical stimulation in mice. In this model of convulsive (grand mal) SE, the anticonvulsant potency of intravenous CBZ dissolved in aqueous dilutions of either HP beta CD or glycofurol was evaluated. RESULTS: In both solutions, CBZ rapidly suppressed seizures after intravenous bolus injection. Potent anticonvulsant activity was obtained as early as 30 s after injection, and peak effects were observed at approximately 3 min. ED50 for blockade of GTCS throughout the 30-min period of repeated electrical stimulation was approximately 7 mg/kg, similar to the potency of DZP in this model. Whereas the HP beta CD/CBZ solutions were tolerated by the animals, with no pronounced behavioral or motor adverse effects, the glycofurol/CBZ solutions induced marked sedation and motor impairment, indicating interactions between drug and solvent. Determination of CBZ in plasma and brain demonstrated that the rapid onset of anticonvulsant action after intravenous bolus injection was related to rapid drug penetration into brain tissue. CONCLUSIONS: An intravenous formulation of CBZ achieved through complexing with HP beta CD might be suitable for parenteral use in acute clinical conditions such as SE, particularly because CBZ has the advantage of being almost free of respiratory or cardiovascular adverse effects.

2-Hydroxypropyl-beta-cyclodextrin↗
PubMed1999

Prospective population-based study of intermittent and continuous convulsive status epilepticus in Richmond, Virginia.

PURPOSE: Previous work suggested that there is a lower mortality for convulsive status epilepticus (SE) with intermittent seizures (intermittent SE) as opposed to SE with continuous seizure activity (continuous SE). A plausible hypothesis to explain this difference is that the shorter ictal time in intermittent SE is responsible for the lower mortality in this group. This study investigates the relative contributions of total ictal time and SE duration to the differing mortalities of intermittent and continuous SE. METHODS: Six hundred forty-five cases of prospectively identified convulsive SE were examined. Nonparametric statistical methods were used to compare continuous SE and intermittent SE variables. Multivariate logistic regression analyses were used to determine which factors were most highly associated with mortality. Intermittent SE cases were analyzed to evaluate the relative contributions of ictal time versus SE duration to mortality. RESULTS: Intermittent SE had a significantly lower mortality than continuous SE (19.6 vs. 31.4%; p < 0.001) in adults but not in children. Intermittent and continuous SE durations did not significantly differ in adult cases but did differ in pediatric cases. Ictal time was significantly shorter than SE duration for intermittent SE in both adults and children. After adjusting for age, etiology, and SE duration, SE type (continuous SE vs. intermittent SE) was shown to have an independent effect on mortality in adults. The relative risk of mortality for continuous SE was 1.79 times that of intermittent SE (p = 0.04). After controlling for SE duration, ictal time did not significantly affect mortality in adults. CONCLUSIONS: Intermittent and continuous convulsive SE were common in both pediatric and adult populations. Intermittent SE had a significantly lower mortality than did continuous SE. This difference in mortality was not completely explained by differences in SE duration, total ictal time, etiology, or age. Further research is needed to identify the factor(s) contributing to the significant difference in mortality between intermittent SE and continuous SE.

Adolescent↗
PubMedDate not supplied

Effects of thiopental, ketamine, diazepam, xylazine, and nitrous oxide on EEG spike activity and convulsive behavior during enflurane anesthesia in atropinized cats. Effect of increasing inhalant concentrations.

The effects of thiopental, ketamine, diazepam, xylazine, and nitrous oxide, and the combinations of thiopental-nitrous oxide and ketamine-nitrous oxide, on both enflurane-induced electroencephalographic (EEG) spike activity and convulsive behavior were measured quantitatively in atropinized cats receiving enflurane with controlled ventilation. Pretreatments with thiopental, ketamine, and diazepam reduced both EEG spike frequency and amplitude at 2.5% to 4.5% inspired enflurane but did not abolish spike activity. Nitrous oxide (66% of inspired gas) did not significantly alter spike frequency or amplitude during 2.5% to 4.5% inspired enflurane, but the combination of thiopental-nitrous oxide or ketamine-nitrous oxide reduced EEG spike activity during 2.5% inspired enflurane. Enflurane-induced convulsive score was markedly suppressed by thiopental and ketamine and was significantly reduced by diazepam, xylazine and nitrous oxide. The combinations of thiopental-nitrous oxide and ketamine-nitrous oxide greatly reduced behavioral-convulsive responses induced by 2.5% to 4.5% inspired enflurane.

Anesthesia, Inhalation↗
PubMedDate not supplied

Effects of thiopental, ketamine, diazepam, xylazine, and nitrous oxide on EEG spike activity and convulsive behavior during enflurane anesthesia in spontaneously breathing atropinized cats. Effect at surgical depth.

The effects of thiopental, ketamine, diazepam, xylazine and nitrous oxide, and combinations of thiopental-nitrous oxide and ketamine-nitrous oxide on electroencephalographic (EEG) spike activity and convulsive behaviors in atropinized cats at surgical depth of enflurane anesthesia were assessed quantitatively for 60 minutes during spontaneous ventilation. Mean inspired enflurane concentrations (MIEC) were reduced 16% to 29% by pretreatment with thiopental, ketamine, diazepam, and xylazine, and were reduced 19% by 66% nitrous oxide. The MIEC of cats anesthetized with thiopental-nitrous oxide-enflurane and ketamine-nitrous oxide-enflurane were 35% to 38% lower than that with nitrous oxide-enflurane. Pretreatment with thiopental, ketamine, diazepam, and xylazine did not reduce the EEG spike frequency during anesthesia but did markedly reduce the spike amplitude. The addition of 66% nitrous oxide did not alter the spike frequency during anesthesia but tended to reduce the spike amplitude. Combinations of thiopental-nitrous oxide and ketamine-nitrous oxide almost abolished the spike activity. The addition of 66% nitrous oxide prevented convulsive responses elicited by photic and auditory stimulation during enflurane anesthesia. Treatment with thiopental, ketamine, diazepam and xylazine, and combinations of thiopental-nitrous oxide and ketamine-nitrous oxide, completely prevented convulsive responses during enflurane anesthesia.

Anesthesia, Inhalation↗
PubMed1984

Seasonal variation of febrile convulsion in Japan.

The 6-year incidence rates of febrile convulsions in all 3-year-old children in Fuchu (covering 95% of children, number examined 17,044) was 8.2%. The incidence was higher in boys than in girls (9.0%: 7.5%, P less than 0.001). The incidence rates varied with the month and year of birth, but the variations observed were slight. Two peak appearances of seasonal variation of the first febrile convulsion were found in November-January and in June-August. The former could be interpreted as a tendency to winter virus infection of the upper respiratory tract in children. The other peak in summer could be explained as a tendency to gastrointestinal infection. Liability to febrile convulsion was influenced by the age of children and by the seasonal variations of febrile illness, but not by the season of birth.

Age Factors↗
PubMed1994

Effects of febrile and epileptic convulsions on daily variations in plasma melatonin concentration in children.

Plasma melatonin was measured in 118 infants and children (39 controls, 28 with epileptic convulsions, and 51 with febrile convulsions). The control group displayed a typical circadian rhythm, with melatonin peaking between 0200 and 0400. This normal daily variation significantly changed in the epileptic group, which showed a characteristic phase-advance, with the nocturnal melatonin peak appearing between 2400 and 0200. Febrile convulsions were associated with the disappearance of the normal circadian rhythm of melatonin, which was replaced by melatonin bursts throughout the light:dark cycle. In both febrile and epileptic children, melatonin levels were significantly increased in comparison with normal children.

Child↗
PubMed1981

Prophylaxis against febrile convulsions with phenobarbital. A 3-year prospective investigation.

An unselected patient material of 182 children admitted consecutively with febrile convulsions during a period of two years was classified into five risk-groups. Continuous phenobarbital therapy for two years was recommended for 113 children (Groups I--IV). These children were followed-up as out-patients for at least one year after admission. In children receiving phenobarbital therapy, serum concentrations were controlled every third month. A total of 59 children completed the treatment according to the directives given and seven of these (12%) developed renewed febrile convulsions despite serum phenobarbital concentrations within the therapeutic range (70--120 mumol/l). No particular characteristics for these children could be established on the basis of the parameters registered. The therapeutic model established was found to be suitable for distinguishing between children with massive risk for renewed convulsions (Group I--IV) compared with children for whom treatment was not recommended (Group V).

Child↗
PubMed1986

Prophylactic treatment with valproic acid or diazepam in children with febrile convulsions.

The purpose of this study was to limit prophylactic treatment of children with febrile convulsions to patients who have the highest risk of recurrence. Two hundred and thirty-one children with a first febrile seizure were divided into high- and low-risk groups according to estimated risk of recurrence. All high-risk children were offered treatment with valproic acid. If this was declined they were offered treatment with diazepam instead. Low-risk children were untreated. Valproic acid and diazepam were found to be equally effective in reducing the risk of recurrence of febrile convulsions. By selecting for prophylactic treatment according to estimated risk of recurrence it is possible to reduce the rate of recurrence of febrile seizures in children at high-risk (60%) to the same level as that of untreated low-risk children (23%). Only about half of all children with febrile convulsions need treatment and follow-up according to these criteria.

Child↗
PubMed1988

Hypocalcemia and hyperphosphatemia in severely dehydrated children with and without convulsions.

Tetanic convulsions are not uncommon among severely dehydrated children in the developing countries. This raises the question whether these children have disturbances in the homeostasis of divalent ions. Serum values are reported of calcium, magnesium, phosphorus, sodium and potassium, as well as blood pH in children below 3 years of age with acute watery diarrhoea and with an estimated weight loss of about 10%. The study was performed on dehydrated children with (DC) or without (D) convulsions. Values were obtained on admission and following rehydration therapy (RT). On admission serum calcium was low in both D and DC children. Serum phosphorus was likewise elevated in both D and DC children. Serum magnesium was slightly elevated in the DC but not in the D group. No patient had hypernatremia. During RT, serum calcium increased significantly and serum phosphorus decreased significantly in D and DC children. Serum calcium showed a significant inverse correlation with serum phosphorus and a significant direct correlation with blood pH. Treatment of DC children with i.v. calcium and i.m. magnesium had no immediate effect on the convulsions. Our conclusion is that severely dehydrated children will develop hypocalcemia. The cause may be a redistribution of calcium into the cells, parallelled by a redistribution of phosphorus from the intra- to the extracellular space.

Child, Preschool↗