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PubMed1993

Adrenal steroids mediate the increase of hippocampal nerve growth factor biosynthesis following bicuculline convulsions.

Northern blot analysis of nerve growth factor (NGF) messenger ribonucleic acid (mRNA), together with a two-site enzyme immunoassay for NGF protein, showed that a convulsive dose of bicuculline (0.4 mg/kg, IV) induced a rapid (within 1 hour) three-fold increase in hippocampal NGF mRNA. This increase was followed by a significant increase in NGF protein 5 hours later. No changes were detected in the cerebral cortex. The increase of rat hippocampal NGF mRNA and protein content was associated with an increase in plasma corticosterone content. Both responses were completely prevented by a pretreatment with diazepam (5 mg/kg, IP), which suggested that adrenal steroids might be a stimulus underlying the rapid increase in NGF biosynthesis following bicuculline convulsions. Therefore, we tested to determine whether a convulsive dose of bicuculline could increase NGF mRNA in adrenalectomized and sham-operated rats. Bicuculline increases hippocampal NGF mRNA in sham-operated rats, but not in adrenalectomized rats despite the presence of convulsions in both experimental groups. Moreover, in adrenalectomized rats, dexamethasone (0.5 mg/kg, SC) could partly restore the increase in hippocampal NGF mRNA content induced by bicuculline convulsions; thus, adrenal steroids might have an essential role in the induction of hippocampal NGF biosynthesis elicited by bicuculline convulsions.

Adrenal Cortex Hormones↗
PubMed1982

Protection from local anesthetic-induced convulsions by gamma-aminobutyric acid.

The effects of gamma-aminobutyric acid (GABA) on the induction of convulsions by local anesthetics were investigated in mice and rats. Intraventricular administration of 0.8-1.6 mg GABA protected rats against convulsions induced by procaine, lidocaine, cocaine, and tetracaine in a dose-related manner. Intraperitoneal gamma-acetylenic GABA was also effective against procaine-induced convulsions in mice, but the metabolites of GABA, gamma-hydroxybutyrate, and gamma-butyrolactone were without effect. Intraventricular GABA, 1.6 mg, delayed the onset of convulsions induced by hydrazine, but had no influence on the incidence of convulsions induced by nicotine, pentylenetetrazol, picrotoxin, or strychnine. These results suggest that the GABA system may be involved in the mechanisms of local anesthetic-induced convulsions.

Anesthetics, Local↗
PubMed1988

Characterization of seizure-induced cysteinyl-leukotriene formation in brain tissue of convulsion-prone gerbils.

Tonic-clonic seizures elicited in convulsion-prone gerbils resulted in a large increase in immunoreactive prostaglandin (PG) F2 alpha and in a smaller increase in immunoreactive leukotriene (LT) C4-like material in brain tissue. Brain tissue contents of both eicosanoids were found to reach a maximum at 6 min after the onset of seizures and were still elevated at 54 min after the beginning of convulsions. By reversed phase HPLC the immunoreactive LTC4-like material was identified as LTC4 and LTD4 at 6 min after the onset of convulsions, whereas at 54 min after the onset, transformation of LTD4 to LTE4 could be detected as well. In gerbils showing only weak seizure activity a small increase in PGF2 alpha but no increase in immunoreactive LTC4-like material could be detected at 6 min after the onset of convulsions. Pretreatment with indomethacin abolished the formation of PGF2 alpha but significantly enhanced the biosynthesis of immunoreactive LTC4-like material at 18 min after the beginning of seizures. The results demonstrate formation of cysteinyl-LT following tonic-clonic convulsions in spontaneously convulsing gerbils which could be enhanced by inhibition of the cyclooxygenase pathway of arachidonic acid metabolism. Since cysteinyl-LT have potent biological actions in various organs this finding warrants further investigations on the potential role of cysteinyl-LT in the CNS.

Animals↗
PubMed1979

Relative significance of isolated infantile convulsions as a primary cause of focal epilepsy.

Isolated infantile convulsions were noted in 206 patients (13%) of 1,572 patients who underwent cortical resection for medically refractory focal epilepsy at the Montreal Neurological Institute over the period 1928 through 1977. In 59 patients (29% of the 206), the isolated infantile convulsion was associated with an identifiable febrile systemic or neural illness. In 54 patients (26%), there was a definite history of cerebral birth injury in addition to the isolated infantile convulsions. Twenty patients (10%) had some other potential etiological factor for the later development of seizures, such as postnatal head injury, Sturge-Weber syndrome, etc., in addition to the isolated infantile convulsions. In 95 patients, 6% of the total 1,572 patient series and 41% of those with isolated infantile convulsions, the latter was the sole apparent cause for the later development of recurring seizures. Although this was the case in a small but significant percentage in this series of patients, more frequently, the isolated infantile convulsion represents a manifestation of invasion of the brain by an infectious agent of a systemic or brain disease, or is a harbinger of the later development of a seizure tendency due to some other preexisting etiological factor.

Birth Injuries↗
PubMed1980

Effects of kindling or brain stimulation on pentylenetetrazol-induced convulsion susceptibility.

The effects of either kindling or nonkindling brain stimulation on pentylenetetrazol (PTZ)-induced convulsion susceptibility was assessed, using rats. The results show that repeated brain stimulation alone is sufficient to reduce the threshold dose of PTZ required to evoke a generalized convulsion, and that kindled convulsions do not significantly reduce the threshold further. However, kindled convulsions do increase the PTZ-induced convulsion duration and severity relative to that seen in stimulated or unstimulated animals. These results suggest that the increased convulsion susceptibility has two components that depend on different aspects of brain stimulation kindling.

Animals↗
PubMed1980

Febrile convulsions in inbred strains of mice susceptible and resistant to audiogenic seizures.

The incidence of febrile convulsions was determined in six inbred strains of mice at four ages. Febrile convulsions were elicited by placing the mice in a cylinder with the air temperature raised to 51 +/- 2 degrees C; this elevated the mouse's body and brain temperature to between 40 and 46 degrees C. The strains used were DBA/2Bg, DBA/1Bg, DBA/1Bg-ras, C57BL/10Bg, C57BL/6Bg, and C57BL/6Bg-Gad-1 alpha; the ages were 21 +/- 1, 29 +/- 1, 59 +/- 1, and 119 +/- 1 days of age. DBA/2Bg, DBA/1Bg, and C57BL/6Bg-Gad 1 alpha are audiogenic seizure susceptible at 21 +/- 1 and 29 +/- 1 days of age, but not at 59 +/- 1 and 119 +/- 1 days of age; whereas C57BL/10Bg, C57BL/6Bg, and DBA/1Bg-ras are audiogenic seizure resistant at all ages. Mice of both sexes, all strains, and all ages had a febrile convulsion and died. Thus, in inbred mice, there does not appear to be either a genetic or developmental correlation between audiogenic seizures and febrile convulsions. This finding may be contrasted with that in other studies showing a correlation between susceptibility to audiogenic seizures and to either electroshock convulsions or chemoconvulsions. However, there are subtle strain and age variants in susceptibility to febrile convulsions of these mice.

Acoustic Stimulation↗
PubMed1982

Changes in the convulsive threshold in the developing rat following chronic administration of pentylenetetrazol.

The acute and chronic effects of pentylentetrazol (PTZ) on convulsive behavior in the developing rat pup were investigated. Acute treatment at 10 or 15 days of age with 50 or 80 mg/kg evoked clonic or tonic-clonic convulsions from all rats. However, daily administration of equivalent dose levels from 5 to 16 days of age was associated with a marked reduction in the incidence of these convulsions. Alternate day treatment from 5 to 16 days of age with 80 mg/kg or an ascending series of dose levels (10 mg/kg/day increments) was not accompanied by a reduction in convulsive behavior. The present results indicate that treatment of infant rats with PTZ is followed by a 24-48 h increase in convulsive threshold. This phenomenon may be associated with a developmental process since daily treatment past 15 days of age was characterized by a gradual reappearance of convulsive behavior.

Age Factors↗
PubMed1983

Long-term prognosis of convulsive disorders in the first year of life: mental and physical development and seizure persistence.

A follow-up study was made on 304 children (164 boys, 140 girls) with convulsive disorders, excluding occasional convulsions, in the first year of life. All patients except 45 who died were followed until 6 years of age or older. At the final follow-up, the subjects were divided into six groups according to the degree of mental and physical development (groups I-VI). Seizures were regarded as absent if the patient had been seizure free for more than 3 years. At the final follow-up, seizures had ceased in 57.7%, and 43.4% had normal mental and physical development (group I). As to the initial diagnosis, the percentage of group I at the final follow-up was 81.8% with febrile convulsions and 37.6% with epilepsy. In patients without seizures it was 69.7% with febrile convulsions and 55.8% with epilepsy. Some 80.6% of patients with unclassified generalized motor seizures, 11.5% of those with infantile spasms, 2.9% of those with secondary generalized epilepsy other than infantile spasms, 46.4% of those with partial seizures, and 25.0% of those with hemiconvulsive seizures were finally placed in group I. The percentage of patients without seizures was 81.4, 33.0, 34.4, 57.7, and 100%, respectively. As has been suggested, among the first-year epilepsies, a subgroup with a more favorable prognosis may exist. Further studies regarding the etiology, ictal EEGs, and effectiveness of treatment and long-term prognosis of these cryptogenic benign infantile convulsions are needed to provide a firm basis for understanding convulsive disorders in the first year of life.

Female↗
PubMed1984

Experimental febrile convulsions in the developing rat: effects on the cholinergic system.

The effects of hyperthermia-induced convulsions (HCs) on nicotinic and muscarinic receptor sites, choline acetyltransferase (ChAT), and acetylcholinesterase (AChE) in the rat were investigated. A series of 10 convulsions, evoked between 5 and 16 days of age, had marked effects on the development of the cholinergic system in the cerebellum and frontal cortex, but not in the hippocampus or hypothalamus. The concentration of muscarinic receptor sites in the cerebellum of the HC group was similar to that in controls at 2 days, greater than in controls at 8 days, but less than in controls at 55 days after the last convulsion. ChAT and AChE activities were increased at 2 days, similar at 8 days, and less than those in controls at 55 days. A decrease in muscarinic receptors and a decline in ChAT activity in the frontal cortex of the HC group were observed at 55 days after the last convulsion. The concentration of nicotinic receptor sites did not distinguish HC from control groups. A simple relationship between the experimental febrile convulsion and the cholinergic system was not found. The greatest effects were noted at 55 days after the last HC, which suggests that these may reflect secondary and possibly transsynaptic influences of the convulsion on cholinergic activity.

Acetylcholinesterase↗
PubMed2000

Evidence favoring genetic heterogeneity for febrile convulsions.

PURPOSE: Two large Canadian kindreds appearing to segregate febrile convulsions as an autosomal dominant trait were evaluated for linkage to three known FC loci, as well as other epilepsy loci. METHODS: Members of the two families were genotyped with microsatellite markers linked to the previously identified febrile convulsion loci, FEB1, FEB2, and GEFS+, and we performed two-point linkage analyses by assuming an autosomal dominant mode of inheritance. RESULTS: We report the exclusion of the FC trait in our families to FEB1 on 8q13-21 and to a second febrile convulsion locus on 19p13. Furthermore, we also excluded the GEFS+ locus on 19q13.1 as the cause of febrile convulsions in both kindreds. Microsatellite markers linked to juvenile myoclonic epilepsy (EJM1), benign neonatal familial convulsions EBN1 and EBN2, autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE), idiopathic generalized epilepsy (EGI), progressive myoclonic epilepsy of Unverricht-Lundborg (EPM1), and partial epilepsy with auditory features (EPT), were also excluded as potential loci linked to the FC trait in our families. CONCLUSIONS: These findings favor considerable genetic heterogeneity for febrile convulsions.

Age of Onset↗
PubMed2001

Concussive convulsions: emergency department assessment and management of a frequently misunderstood entity.

Immediate concussive convulsions are an unusual but dramatic sequela to head injuries. Previously believed to be an epileptic phenomenon, they are now thought to be a brief traumatic functional decerebration that results from loss of cortical inhibition. With concussive convulsions generally occurring within seconds of head impact and lasting up to several minutes, patients are initially in a tonic phase, followed by a clonic convulsion. A postictal phase is generally brief if it occurs at all with these episodes. Patients with isolated concussive convulsions have no evidence of structural brain injury as assessed with neuroimaging studies or physical examination. Neuropsychological testing often demonstrates transient cortical dysfunction consistent with the concussive episode. The long-term outcome for patients with isolated concussive convulsion is universally good, with no long-term neurologic sequelae and no increased incidence of early or late posttraumatic epilepsy. Emergency department management should focus on evaluation of the associated concussive injury. The concussive convulsion requires no specific therapy, and antiepileptic medication is not indicated.

Adult↗
PubMed1995

Estimation of the convulsive effect of cyanide in rats.

Convulsions are frequently observed in severe, acute cyanide intoxication. The mechanisms involved are not well known. In the present study, the convulsive effect of cyanide was examined in the rat by means of a dose threshold determination after infusion of cyanide. An optimal dose rate of 1.80 mg/min./kg was determined. By infusing this optimal dose rate it was possible to divide another cyanide-treated group of rats into two groups: one without and another with convulsions. After the experiment all animals were killed by exposure to high intensity microwave irradiation. Regional dopamine, noradrenaline and main dopamine metabolites were isolated and analyzed using high pressure liquid chromatography and electrochemical detection. Striatal noradrenaline was decreased but dopamine and its metabolites were increased in rats infused with cyanide at the optimal dose rate until the convulsions started. Animals infused with the threshold dose at the optimal dose rate did not show any significant changes in noradrenaline or in dopamine metabolites, but all animals showing convulsions also had increased striatal dopamine levels. Thus changes in dopamine appear to be dependent on convulsions.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1991

Parental reactions to a child's first febrile convulsion. A follow-up investigation.

The severe psychological reactions of most parents to the first febrile convulsions of their child contrast with the doctors' consideration of febrile convulsions as a simple and benign phenomenon. Fifty-two parents whose child had been admitted with febrile convulsions were interviewed about their immediate and long-term reactions. Most of the parents knew little about febrile convulsions before the fit. Parents with previous knowledge of febrile convulsions took more appropriate measures during the fit than parents without such knowledge. Sixty per cent of the parents slept restlessly for some time after the fit, 13% watched their child at night, and 29% had dyspeptic symptoms. Parents of young children should as a routine be offered general information by the family doctor about fever and febrile convulsions. Parents who have watched their child during a fit need specific information in order to avoid long-term reactions.

Behavior↗
PubMed1976

Failure of phenobarbitone to prevent febrile convulsions.

One-hundred-sixty-five children without known neurological disorder who presented with their first febrile convulsion between the ages of six months and three years were assigned to daily phenobarbitone treatment or to a control group and followed up at a special clinic for six months. One-hundred-and-sixty-one-one children completed the trial, and of the 88 children assigned to phenobarbitone treatment 10 had further convulsions during this period compared with 14 of the 73 control children. Only 49 of those assigned to phenobarbitone took the drug regularly throughout the trial, and four of these had further febrile convulsions, a proportion not significantly different from that in the controls. All four had mean plasma phenobarbitone concentrations over 69 mumol/l (16 mug/ml) during the trial and in three the plasma concentration was at or over this figure within eight hours over 69 mumol/l (16 mug/ml) during the trial and in three the plasma concentration was at or over this figure within eight hours of the repeat convulsion. Regular phenobarbitone does not seem to prevent febrile convulsions. Attention should instead be directed to organising emergency services to allow early termination of fevrile convulsions, whether first or subsequent, to prevent irreversible brain damage.

Child, Preschool↗
PubMed1977

Primary immunisation and febrile convulsions in Oxford 1972-5.

A three-year study of febrile convulsions in Oxford with comprehensive notification from general practice and hospitals showed a 3% risk for all children of suffering at least one febrile convulsion by the age of 5 years. Children were most at risk between 6 and 27 months, and febrile convulsions were most likely to be prolonged in children aged 9-15 months. The association between febrile convulsions and primary immunisations in the preceding 28 days was compared in case and control children, matched for age and sex. Results suggested that such association was a chance relationship with age. If association was direct, the febrile convulsion rates per 1000 immunisation doses were estimated as follows: diphtheria, pertussis, tetanus--0-09 per 1000; poliomyelitis--0-6 per 1000; and measles--0-9 per 1000. Hence if any of these vaccines had a secific causal relationship with febrile convulsions, these rates would probably have been much higher.

Child↗
PubMed1985

Febrile convulsions in a national cohort followed up from birth. I--Prevalence and recurrence in the first five years of life.

Of 13 135 children followed up from birth to the age of 5 years, 303 (2.3%) had febrile convulsions. Prior neurological abnormality had been noted in 13. Of the 290 remaining children, 57 (20%) presented with a complex convulsion, and 103 children (35%) went on to have further febrile convulsions. The risk of further febrile convulsions varied with the age at first convulsion and the presence of a history of convulsive disorders in relatives. There were no significant differences between the sexes.

Age Factors↗
PubMed1996

Evidence of a third locus for benign familial convulsions.

Two autosomal dominant forms of benign idiopathic epilepsy of early life have been described: benign neonatal familial convulsions and benign infantile familial convulsions. Herein we describe a pedigree with familial convulsions in which the age of onset is intermediate between that seen in these two disorders. Two genes responsible for benign neonatal familial convulsions have been mapped to chromosome 20q and to chromosome 8q. Previously, the chromosome 20q benign neonatal familial convulsions locus had been excluded in this pedigree. Further linkage analysis in our laboratory revealed that the chromosome 8 benign neonatal familial convulsions locus also is not responsible for seizures in this pedigree. These results indicate that there are at least three loci responsible for autosomal dominant benign epilepsies of early life.

Age of Onset↗
PubMed2001

Evidence for an involvement of the ammonia-decreasing action of L-arginine in suppressing picrotoxin-induced convulsions in rats and its additive action with diazepam.

The effects of pre- (30 min before challenge) and post-treatment (5 min after challenge) of L-arginine (840 mg kg(-1)) were tested on picrotoxin-induced increase in ammonia concentrations in brain regions (cerebral cortex, brain stem and cerebellum) and the accompanying convulsive responses in adult male rats. The effect of pre- and post-treatment of L-arginine was tested on the action of diazepam against picrotoxin-induced convulsions. Picrotoxin-induced increase in ammonia concentrations in the brain regions was reverted partially by L-arginine pre-treatment. However, L-arginine pre-treatment failed to inhibit convulsions independently and concurrently with diazepam. On the other hand, L-arginine post-treatment reverted ammonia to control level in all brain regions. A partial but significant inhibition of convulsions was found in these animals. The effect produced concurrently by L-arginine and diazepam post-treatment was much greater than that produced by these agents independently. These results suggest that brain ammonia has a partial but significant participation in the convulsant action of picrotoxin. L-arginine has produced a partial protection of picrotoxin-induced convulsions by reverting brain ammonia to control level. The data further suggest that the duration of action of L-arginine is considerably short and that L-arginine has an additive anticonvulsant action with diazepam.

Ammonia↗