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PubMedDate not supplied

Peptidergic mechanisms of hyperthermia-evoked convulsions in rats in early postnatal ontogenesis.

This report addresses the verification of the hypothesis that arginine-vasopressin affects the formation of hyperthermia-evoked convulsions in early ontogenesis in rats on days 3, 5, 7, and 9 of postnatal life. The modification of experimental febrile convulsions by PACAP (pituitary adenylate cyclase-activating peptide) was investigated; PACAP is a physiological regulator of the neurosecretion of arginine-vasopressin. Arginine-vasopressin (10 microg/rat) and PACAP (0.01 microg/rat) decreased the latency of generalized tonic-clonic convulsions and the time of truncal generalization of convulsive activity on days 3 and 5 of rat development. Animals given arginine-vasopressin (0.1-10 microg/rat) sowed significant increases in the duration of generalized convulsions to the level of status epilepticus on day 9 of life. Conversely, administration of higher doses of PACAP (0.1 microg/rat) increased the threshold of tonic-clonic convulsions on days 3 and 5 and decreased it on days 7 and 9 of postnatal development. The indirect involvement of PACAP in the mechanisms of experimental febrile convulsions is suggested to act via changes in arginine-vasopressin neurosecretion.

Animals↗
PubMed2004

Studies of the roles of NMDA and AMPA glutamate receptors in the mechanism of corasole convulsions in mice.

Experiments on mice were performed to study the ability of monocationic and dicationic adamantane and phenylcyclohexyl derivatives to prevent convulsive syndrome induced by i.p. corasole (pentylenetetrazole; 80 mg/kg). Monocationic phenylcyclohexyl derivatives, which are selective blockers of NMDA glutamate receptor channels, along with memantine and MK-801, effectively prevented the appearance of the clonic and tonic components of convulsions at micromolar concentrations. Their dicationic analogs, which block both NMDA and AMPA receptor channels, were ineffective against clonic convulsions, but prevented corasole-induced tonic convulsions at much lower concentrations. The convulsive action of corasole, whose primary target is weakening of the inhibitory action of GABA, appears to be mediated by glutamatergic synaptic transmission. NMDA receptors have a much greater involvement than AMPA receptors in the genesis of clonic convulsions, while AMPA receptor activation appears to be an important component of tonic convulsions.

Animals↗
PubMed1999

Effects of information on parental knowledge of febrile convulsions.

The purpose of this study was to study the effects of giving information to parents with febrile convulsive children. All parents of children with febrile convulsions who are seen at Worcester Royal Infirmary are given information. Fifty parents of children who had had a first febrile convulsion during May 1996 to December 1996 were interviewed by telephone from July to September 1997. The same questions were asked of 50 parents of children who came to a community health clinic and who had not had febrile convulsions. The design used open questions and covered medical history, general child health knowledge and knowledge of febrile convulsion. The answers were compared using a chi-squared test (significance level P < 0.05). Possible confounding factors were tested by a correlation test. No difference was found between the two groups in family structure, housing, and general child health knowledge. Information about febrile convulsions was retained by informed parents. Both groups thought the given information was useful and should be written in the child health record book. Information about febrile convulsions was remembered by parents.

Child, Preschool↗
PubMed1987

Factors prognostic of unprovoked seizures after febrile convulsions.

We evaluated the risk of unprovoked seizures after febrile convulsions and the factors prognostic of them in a cohort of 687 children who had an initial febrile seizure while residing in Rochester, Minnesota. Overall, children with febrile convulsions had a fivefold excess of unprovoked seizures, and the risk until the age of 25 was 7 percent. The risk ranged from 2.4 percent among children with simple febrile convulsions to 6 to 8 percent among children with a single complex feature--i.e., focal or prolonged seizures or repeated episodes of febrile convulsions with the same illness. For children with any two of the complex features, the risk was 17 to 22 percent, and for those with all three features, 49 percent. The occurrence of subsequent partial unprovoked seizures was strongly associated with all three of the complex features, whereas the occurrence of subsequent unprovoked seizures of generalized onset was associated with the number of febrile convulsions and a family history of unprovoked seizures. These results are consistent with the view that the increased risk of generalized-onset unprovoked seizures reflects a predisposition to both simple febrile convulsions and generalized-onset unprovoked seizures. The association between complex febrile convulsions and partial seizures, on the other hand, may reflect either a causal association or the presence of preexisting brain disease that is responsible for both the complex febrile seizures and later partial seizures.

Adolescent↗
PubMed1998

A comparison of four treatments for generalized convulsive status epilepticus. Veterans Affairs Status Epilepticus Cooperative Study Group.

BACKGROUND AND METHODS: Although generalized convulsive status epilepticus is a life-threatening emergency, the best initial drug treatment is uncertain. We conducted a five-year randomized, double-blind, multicenter trial of four intravenous regimens: diazepam (0.15 mg per kilogram of body weight) followed by phenytoin (18 mg per kilogram), lorazepam (0.1 mg per kilogram), phenobarbital (15 mg per kilogram), and phenytoin (18 mg per kilogram). Patients were classified as having either overt generalized status epilepticus (defined as easily visible generalized convulsions) or subtle status epilepticus (indicated by coma and ictal discharges on the electroencephalogram, with or without subtle convulsive movements such as rhythmic muscle twitches or tonic eye deviation). Treatment was considered successful when all motor and electroencephalographic seizure activity ceased within 20 minutes after the beginning of the drug infusion and there was no return of seizure activity during the next 40 minutes. Analyses were performed with data on only the 518 patients with verified generalized convulsive status epilepticus as well as with data on all 570 patients who were enrolled. RESULTS: Three hundred eighty-four patients had a verified diagnosis of overt generalized convulsive status epilepticus. In this group, lorazepam was successful in 64.9 percent of those assigned to receive it, phenobarbital in 58.2 percent, diazepam plus phenytoin in 55.8 percent, and phenytoin in 43.6 percent (P=0.02 for the overall comparison among the four groups). Lorazepam was significantly superior to phenytoin in a pairwise comparison (P=0.002). Among the 134 patients with a verified diagnosis of subtle generalized convulsive status epilepticus, no significant differences among the treatments were detected (range of success rates, 7.7 to 24.2 percent). In an intention-to-treat analysis, the differences among treatment groups were not significant, either among the patients with overt status epilepticus (P=0.12) or among those with subtle status epilepticus (P=0.91). There were no differences among the treatments with respect to recurrence during the 12-hour study period, the incidence of adverse reactions, or the outcome at 30 days. CONCLUSIONS: As initial intravenous treatment for overt generalized convulsive status epilepticus, lorazepam is more effective than phenytoin. Although lorazepam is no more efficacious than phenobarbital or diazepam plus phenytoin, it is easier to use.

Aged↗
PubMed1994

Seizure recurrence after a first febrile convulsion.

In this study, 140 children aged from 6 months to 6 years who presented with a first febrile convulsion at the King Fahad Hofuf Hospital, Al-Hassa, Saudi Arabia were retrospectively identified. Information about these children was obtained from their medical records covering a follow-up period of 3 years from July 1989 to June 1992. Recurrent febrile convulsions occurred in 60 of them (43%). Relevant risk factors that were observed to be significantly associated with seizure recurrence included an age of less than 18 months (odds ratio [OR] = 3.82; 95% confidence interval [CI] = 9.26, 1.58), an initial febrile convulsion that was complex (OR = 4.41; CI = 9.50, 2.05) and a positive family history of febrile convulsions (OR = 4.12; CI = 10.74; 1.58), while a decreased risk of recurrence occurred with a temperature of over 39 degrees C (OR = 4.60; CI = 9.44; 2.24). There was no association between seizure recurrence and the duration of the initial febrile convulsion (OR = 0.93; CI = 2.33; -2.04) or family history of epilepsy (OR = 0.88; CI = 4.22, -3.27). An important observation in the present study is the close association (ORM-H = 2.36; X2M-H = 9.65) between the development of an afebrile convulsion and seizure recurrence among the group of children with CFC. Anticonvulsant prophylaxis should therefore be considered for children whose initial febrile convulsions are complex in nature.

Child↗
PubMed1988

Lack of correlation between the anaesthetic and anti-convulsant potencies of althesin, ketamine and methohexitone.

Using Sprague-Dawley rats, the anti-convulsant potencies of Althesin, ketamine and methohexitone were determined for bicuculline-and strychnine-induced seizures and compared with their effects on hyperbaric seizures. All three anaesthetics protected against both types of chemical convulsants; the degree of protection varied from 34 to 151%, with Althesin being the most effective. However, there was no correlation between their anti-convulsant and anaesthetic potencies, and no relationship between the effects on chemical convulsions and the interactions of the same agents with hyperbaric convulsions. These data suggest that the order of anti-convulsant potencies at equivalent anaesthetic concentration is Althesin much greater than ketamine = methohexitone, and that neither bicuculline-nor strychnine-induced seizures are a good model for hyperbaric convulsions.

Alfaxalone Alfadolone Mixture↗
PubMed1994

Quantitation of GABAA receptor inhibition required for quinolone-induced convulsions in mice.

We quantified the amount of inhibition of gamma-aminobutyric acid (GABA)A receptor binding required for the onset of convulsions induced by ciprofloxacin in combination with biphenylacetic acid (BPAA) in mice. In fasting mice iv ciprofloxacin given 30 min after oral BPAA (50 mg/kg) induced convulsions at doses of 40 mg/kg or above. In contrast, ofloxacin caused no convulsions even at 100 mg/kg, the highest dose tested. When mice received 40 mg/kg of ciprofloxacin or ofloxacin, maximal brain concentrations of each quinolone at 30 min were 0.37 or 1.97 micrograms/g, respectively. These brain concentrations of ciprofloxacin and ofloxacin were not affected by combination with BPAA. In the presence of ciprofloxacin and BPAA (at brain tissue concentrations which induced convulsions), the binding of 3H-muscimol to GABAA receptor sites was inhibited by approximately 30%. Using results from a similar binding study, an impracticable iv dose of ofloxacin (500 mg/kg) was estimated to be required to inhibit GABAA receptor binding by 30%, and therefore to induce similar convulsions to those seen with ciprofloxacin at a dose of 40 mg/kg. These results may indicate that epileptic convulsions occur when ciprofloxacin and BPAA interact with each other to antagonize at least 30% of GABAA receptor binding in mice, and provide evidence for a significant role of GABAA receptor inhibition in the occurrence of quinolone-induced convulsions.

Animals↗
PubMed1993

Convulsions with malaria: febrile or indicative of cerebral involvement?

Evaluation of 446 infants and young children (6 months to 5 years olds) with malaria parasitaemia showed a significant relationship (P < 0.05- < 0.001) (a) between coma and age, pattern of convulsions, haematocrit, and blood glucose, and (b) between the severity of parasitaemia and risk of convulsions, prevalence of hepatosplenomegaly, and severe anaemia. No significant relationship was observed between convulsions and temperature or haematocrit. Comatose children were older and had a higher prevalence of repeated convulsions, severe anaemia, and hypoglycaemia than non-comatose children. Convulsions, hepatosplenomegaly, and severe anaemia were more prevalent in children with moderate-severe parasitaemia. It is concluded that convulsions with malaria are more often a manifestation of cerebral dysfunction rather than being simply febrile in nature. All forms of cerebral dysfunction in malaria, including repeated convulsions, should be managed as being clinical manifestations of cerebral malaria.

Anemia↗
PubMed1998

Rat strain minimally influences anesthetic and convulsant requirements of inhaled compounds in rats.

UNLABELLED: We assessed the effect of rat strain on susceptibility to anesthesia and convulsions produced by inhaled compounds. We determined the minimum alveolar anesthetic concentration (MAC) of desflurane and nitrous oxide, and the convulsive 50% effective dose (ED50) of 1,2-dichlorohexafluorocyclobutane, flurothyl, and difluoromethyl-1-chlorotetrafluoroethyl ether in five strains (three inbred [Long Evans, Sprague-Dawley, and Wistar] and two outbred [Fischer and Brown Norway]). Strain had slight effects on anesthetic potency, the strains with the highest MAC values (Long Evans and Brown Norway) having values < or =28% greater than the strains with the lowest values (Sprague Dawley and Wistar). MAC for nitrous oxide correlated directly with MAC for desflurane as a function of strain. MAC for either desflurane or nitrous oxide correlated inversely with the convulsive ED50 of 1,2-dichlorohexafluorocyclobutane, but correlated poorly (and directly) with the convulsive ED50 of the remaining compounds. Convulsivity varied little as a function of strain (greatest difference 21%) and did not vary consistently as a function of strain. No consistent difference was seen between inbred versus outbred strains. IMPLICATIONS: Rat strain has a minimal effect on the potency of inhaled anesthetics or the convulsant activity of inhaled compounds. It seems that the sites acted on by inhaled compounds to produce anesthesia and convulsions are conserved across common rat strains.

Anesthesia↗
PubMed2002

Acetylcholine receptors and thresholds for convulsions from flurothyl and 1,2-dichlorohexafluorocyclobutane.

UNLABELLED: There are acetylcholine receptors throughout the central nervous system, and they may mediate some forms and aspects of convulsive activity. Most high-affinity binding sites on nicotinic acetylcholine receptors for nicotine, cytisine, and epibatidine in the brain contain the beta2 subunit of the receptor. Transitional inhaled compounds (compounds less potent than predicted from their lipophilicity and the Meyer-Overton hypothesis) and nonimmobilizers (compounds that do not produce immobility despite a lipophilicity that suggests anesthetic qualities as predicted from the Meyer-Overton hypothesis) can produce convulsions. The nonimmobilizer flurothyl [di-(2,2,2,-trifluoroethyl)ether] blocks the action of gamma-aminobutyric acid on gamma-aminobutyric acid(A) receptors, whereas the nonimmobilizer 1,2-dichlorohexafluorocyclobutane (2N, also called F6) does not. 2N can block the action of acetylcholine on nicotinic acetylcholine receptors. We examined the relative capacities of these compounds to cause convulsions in mice having and lacking the beta2 subunit of the acetylcholine receptor. The partial pressure causing convulsions in half the mice (the 50% effective concentration [EC(50)]) was the same as in control mice. For the knockout mice, the EC(50) for flurothyl was 0.00170 +/- 0.00030 atm (mean +/- SD), and for 2N, it was 0.0345 +/- 0.0041 atm. For the control mice, the respective values were 0.00172 +/- 0.00057 atm and 0.0341 +/- 0.0048 atm. The ratio of the 2N to flurothyl EC(50) values was 20.8 +/- 3.5 for the knockout mice and 21.7 +/- 7.0 for the control mice. These results do not support the notion that acetylcholine receptors are important mediators of the capacity of 2N or flurothyl to cause convulsions. However, we also found that both nonimmobilizers inhibit rat alpha4beta2 neuronal nicotinic acetylcholine receptors at EC(50) partial pressures (0.00091 atm and 0.062 atm for flurothyl and 2N, respectively) that approximate those that produce convulsions (0.0015 atm and 0.04 atm). IMPLICATIONS: The results from the present study provide conflicting data concerning the notion that acetylcholine receptors mediate the capacity of nonimmobilizers to produce convulsions.

Animals↗
PubMed2004

Febrile convulsion during the acute phase of Kawasaki disease.

BACKGROUND: Although seizures occur in association with meningitis or encephalitis in Kawasaki disease, febrile convulsions in Kawasaki disease are considered to be extremely rare. The aim of the present study is to elucidate the incidence of febrile convulsion in the acute phase of Kawasaki disease, in Niigata City General Hospital, Niigata, Japan. METHODS: The study included 177 patients with Kawasaki disease. Patients ranged in age from 2 months to 10 years (mean age 26.89 +/- 22.44 months). The study included 105 males and 72 females. The clinical records of Kawasaki disease patients were examined retrospectively. RESULTS: Febrile convulsions were not recognized in these 177 patients throughout the course of the disease, despite the presence of a high grade fever and their young age. However, eight of the 177 patients had experienced simple febrile convulsions during other febrile illness except for those with Kawasaki disease. In the acute phase of Kawasaki disease, only two patients showed generalized convulsion associated with prolonged consciousness disturbance and pleocytosis in the cerebrospinal fluid. CONCLUSION: The incidence of febrile convulsions in the acute phase of Kawasaki disease might be extremely low, confirming the results of previous reports. Kawasaki disease is characterized by systemic vasculitis and is sometimes complicated by intracranial vasculitis. The incidence of electroencephalographic abnormalities and pleocytosis in the cerebrospinal fluid is higher in patients with Kawasaki disease. However, the reason why febrile convulsions did not occur in the acute phase of Kawasaki disease remains unknown, despite the presence of central nervous system involvement.

Acute Disease↗
PubMed1998

Is the long-term outcome of children following febrile convulsions favorable?

The study comprised 80 children aged 6 to 9 years with a history of febrile convulsions. A neurological examination, an interview to assess psychiatric anomalies, and a series of neuropsychological tests were performed on patients with previous febrile convulsions and on matched healthy controls. Children with non-febrile seizures or CNS infections were excluded. Recurrence of febrile seizures in the study group was 41% (N=33), 18 children (22%) had prolonged febrile convulsions, six (7.5%) patients and two controls showed discrete neurological abnormalities. Behavioral anomalies were exhibited by 22% of the patients and 6% of the healthy children. The neuropsychological test results did not demonstrate significant differences between the children with febrile convulsions and the healthy controls. However, in children with prolonged febrile convulsions, non-verbal intelligence was found to be significantly lower as compared with children with simple febrile seizures and with controls. None of the other parameters tested yielded any differences between patients and controls. Children with multiple recurrences of febrile convulsions performed poorer in all tests when compared with children with only one febrile seizure or with controls. Other factors such as a positive family history of epilepsy, age at onset of febrile convulsions, or duration of the seizure were not found to be of prognostic significance.

Child↗
PubMedDate not supplied

Pentylenetetrazol-induced convulsion and effect of anticonvulsants in mutant inbred strain El mice.

The El mouse is an inbred strain developed from ddY mice and is very susceptible to seizure. In El mice, convulsions could be induced by 18 mg/kg of pentylenetetrazol, which is an inert dose in ddY mice. The features of the convulsions were the same as those induced by the tossing-up procedure, a common method to evoke convulsions in El mice. Phenytoin, phenobarbital, valproate sodium, and ethosuximide clearly inhibited pentylenetetrazol-induced convulsions in El mice. These findings suggest that induction of convulsions by pentylenetetrazol in the El mouse is a simple method as compared with induction of convulsions by the tossing-up procedure, and convulsions evoked by this method are a precise experimental model for the study of hereditary epilepsy and for the evaluation of anticonvulsant drugs.

Animals↗
PubMedDate not supplied

Temporal lobe epilepsy after prolonged febrile convulsions: excellent outcome after surgical treatment.

We studied 47 consecutive patients who underwent temporal resection for seizure control. Nineteen (40%) had febrile convulsions preceding onset of their habitual seizures. In 17 of 18 patients whose disease duration was known, the febrile convulsions were prolonged (mean 4 h). As compared with patients without preceding febrile convulsions, patients with antecedent febrile convulsions had a significantly higher prevalence of positive family history of febrile convulsions, an increased incidence of retrospectively identified gestational or perinatal complications, and no foreign tissue lesions. Pathologic studies showed gliosis and cell loss in mesiotemporal structures, usually moderate, in addition to usually mild gliosis in lateral temporal cortex. These patients had an excellent outcome after temporal resection: 84% were seizure-free, had residual auras only, or occasional convulsions with medication discontinuation. One patient (5%) had > 90% improvement. Two patients (11%) in whom the hippocampus was totally spared continued to have complex partial seizures: in both, seizures stopped after reoperation and hippocampal resection. Thus, 95% of these patients had an excellent result. Only 16% required invasive preoperative studies to confirm lateralization. These results were significantly better than those of the group without preceding febrile convulsions (p = 0.0013).

Adolescent↗
PubMedDate not supplied

5-Hydroxyindoleacetic acid and homovanillic acid in cerebrospinal fluid of children with febrile convulsions.

5-Hydroxyindoleacetic acid (5-HIAA) and homovanillic acid (HVA) were measured by high-performance liquid chromatography (HPLC) in lumbar cerebrospinal fluid (CSF) obtained from febrile children subdivided according to the presence or absence of convulsions. Lumbar puncture was made either early (mean time 2 h) or late (3-6 days) after the febrile convulsion. The level of 5-HIAA was significantly decreased in children early and late after the febrile convulsion as compared with the convulsion-free group, but the HVA level was reduced only early after the febrile convulsion. These results support the hypothesis that a decrease in CSF 5-HIAA may be a biologic marker of susceptibility to convulsions and indicate that the transient decrease in HVA is a secondary phenomenon related to occurrence of convulsions.

Child, Preschool↗
PubMed1991

Lithium modifies convulsions and brain phosphoinositide turnover induced by organophosphates.

Inositol-1-phosphate (Ins1P), an index of phosphoinositide (PI) turnover, was measured in frontal and piriform cortices, caudate, thalamus, hippocampus and cerebellum in saline or LiCl (5 m Eq./kg) pretreated rats 60 min. after graded doses of DFP, paraoxon, or soman. DFP only produced bursts of convulsive activity whereas both paraoxon and soman produced prolonged tonic-clonic convulsions. All three organophosphates (OP) produced convulsions at a lower dose in LiCl than in saline pretreated rats. Regional Ins1P correlated better with the presence or absence of convulsions than with the dose of paraoxon or soman. This was true both in saline and LiCl pretreated rats. In saline pretreated non-convulsing rats, there was a cholinergic increase (1.5-2.0 X) in Ins1P in all brain regions except cerebellum after OP injection. In saline pretreated convulsing rats, there was a marked seizurogenic further increase in Ins1P; highest in caudate (8 X) and cortex (6 X). In LiCl pretreated nonconvulsing rats, the OP-induced cholinergic increase in Ins1P was significant only in caudate, thalamus and hippocampus. In LiCl pretreated convulsing rats, the further seizurogenic increase in Ins1P was less than in saline pretreated rats except in thalamus and hippocampus. Thus, OP produce both a cholinergic and a seizurogenic increase in PI turnover. These data suggest that increased PI turnover in the hippocampus may indicate a lithium-induced lowering of the seizure threshold for OP in limbic regions.

Animals↗
PubMed1995

The role of fever on cerebrospinal fluid glucose concentration of children with and without convulsions.

In febrile convulsions glucose concentrations are known to increase both in the blood and cerebrospinal fluid (CSF). The reason behind this increase is, however, incompletely understood. We have studied the effects of convulsion and fever on the CSF and blood glucose concentrations in four different groups of children: febrile and non-febrile children, with and without convulsions. The concentration of glucose in the CSF was significantly higher in febrile children with (4.4 +/- 0.1 mmol/l, mean +/- SEM n = 35, p < 0.01. ANOVA, Duncan's test) and without convulsions (3.9 +/- 0.2 mmol/l, n = 22, p < 0.05) than in non-febrile, non-convulsive children (3.3 +/- 0.1 mmol/l, n = 21). In non-febrile convulsive children, the CSF glucose concentration was 3.7 +/- 0.2 mmol/l (n = 10). Both fever and seizures increased the CSF glucose levels (p < 0.0001) and p = 0.028, respectively, analysis of covariance). There was a linear correlation between the body temperature and concentration of glucose in the CSF (r = 0.454, p < 0.0001, n = 88, Pearson's correlation analysis). The changes in blood glucose concentrations between the groups paralleled those found in the CSF. Our results show that hyperglycaemia and an increase in the CSF glucose concentration in febrile convulsions is not explained just by a stress reaction, evoked by the seizure, as has been hypothesized earlier, but by the influence of increased body temperature as well.

Blood Glucose↗