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PubMed1987

Hippocampal neuron loss in temporal lobe epilepsy: correlation with early childhood convulsions.

Hippocampal neuron densities in three areas (H1 zone, end folium, and dentate gyrus) were counted in each of 32 temporal lobectomy excision specimens using the technique of Mouritzen Dam. The association between severe neuronal loss in all three areas and early childhood convulsions that were prolonged and/or lateralized was highly significant. Lesser degrees of neuron loss in H1 and/or end folium were common and were not associated with early childhood convulsions, but were most often found in older patients with a particularly long history of epilepsy.

Adolescent↗
PubMed1976

Antivitamin B6 induced ultrastructural changes in the hippocampus of the convulsant rabbit and its biochemical correlates.

In rabbits epileptiform seizures were induced by systemic application of methoxypyridoxine, an antimetabolite of vitamin B6. The regional distribution of GABA was measured in 11 brain structures, before the onset of the seizure and during the generalized convulsions. In brain regions with a high GABA level the GABA content drops already preictally, in contrast to the GABA poor structures where no preictal decrease takes place. From this it is concluded that there exist two GABA pools, a functional one containing the GABA for chemical transmission, which is exhausted already preictally giving rise to the seizure discharges, and a metabolic one, which is utilized as an additional energy-source during the convulsions. Due to the decrease of the hippocampal GABA the endings of the dentate gyrus granule cells, the giant boutons contacting the apical dendrites of the pyramidal cells of CA3 and CA4, can discharge unrestrained. An ultrastructural correlate of the increased excitation is demonstrated. The dense-core vesicles of the giant boutons fuse in an omega-shaped form with the presynaptic membrane of the spines. This fusion-phenomenon is observed in ultrathin sections as well as in freeze-fractured replicas of this region.

Animals↗
PubMed1992

Confirmation of linkage of benign familial neonatal convulsions to D20S19 and D20S20.

Benign familial neonatal convulsions (BFNC) is an idiopathic form of epilepsy beginning within the first six months of life. Its genetic origin and autosomal dominant mode of inheritance have been suspected since its first description. Recently, the BFNC gene has been localised within chromosome 20q in one large pedigree. For the first time, we confirm here (with D20S19 and D20S20) the close linkage of BFNC to chromosome 20q in six French pedigrees. In addition, the existence in these families of several cases of febrile convulsions (FC), another epileptic syndrome with an autosomal dominant genetic component, led us to study the possibility of a genetic background identical to BFNC. Our results suggest the existence of different susceptibility genes for BFNC and FC.

Blotting, Southern↗
PubMed1991

Convulsions and wet-dog shakes produced by systemic or intrahippocampal administration of ruthenium red in the rat.

In this work we have studied in the rat the behavioral effects of the intraperitoneal (i.p.) and intrahippocampal (i.h.) administration of ruthenium red (RuR), an inorganic dye which has been shown to inhibit neurotransmitter release in synaptosomes. The i.p. injection induced initially flaccid paralysis and subsequently generalized tonic-clonic convulsions. It contrast, unilateral RuR microinjection into the CA1 area of the hippocampus produced complex seizure behavior and wet-dog shakes (WDS). The i.p. administration of the serotonin receptor antagonist ketanserin markedly inhibited the WDS induced by i.h. RuR. In contrast, the i.h. injection of ketanserin and of the gamma-aminobutyric acid (GABA) agonists 4,5,6,7-tetrahydroisoxazol[5,4-c]pyridin-3-ol(THIP) and baclofen together with RuR did not affect the frequency of WDS nor the seizure behavior. However, the i.h. injection of the GABA uptake blocker nipecotic acid, simultaneously with RuR, increased the frequency of WDS. The release of [3H]GABA, measured in synaptosomes of different cerebral structures of the rats injected i.p. with RuR, and in slices of the CA1 area after i.h. injection of the dye, was not affected. Histological observations of the injected area showed a specific and intense staining of the somas of the CA1 pyramidal neurons. It is concluded that the convulsant action induced by i.h. RuR microinjection is probably the result of an increased excitability of these CA1 neurons, which is independent of any action on GABA release.

Animals↗
PubMed1996

A study of childhood febrile convulsions with particular reference to HHV-6 infection: pathogenic considerations.

Most febrile convulsions (FC) in infants occur during a viral infection, particularly in children of less than 3 years of age; human herpesvirus 6 (HHV-6) has an important pathogenic role. To evaluate the link between this and other viruses and FC, a group of 65 children (mean age 18.46 months, SD +/- 9.19) with a first episode of simple FC (G1) was compared with 24 children (mean age 19.29 months, SD +/- 13.17) with a febrile syndrome but without FC (G2). Virological study showed the following infections: HHV-6 in 23/65 of G1 and in 12/24 of G2, adenoviruses (ADV) in 9/65 of G1 and in 0/24 of G2, syncytial respiratory virus (SRV) in 3/28 of G1 and in 0/2 of G2, HSV-1 in 6/65 of G1 and in 1/24 of G2, cytomegalovirus (CMV) in 2/65 of G1 and in 0/24 of G2 and HHV-7 in 1/42 of G1 and in 1/13 of G2. Children in G1, statistically compared with G2, were significantly more likely to have a family history of FC and circulating granulocytes, while IgM and alpha 2-globulin were less probable. Some cytokines (IL 1 beta, TNF beta and GM-CSF) were found in 24 children in G1 and 12 in G2; no differences were found between the two groups. In the light of our data and of the recent literature, the possibility that the cytokines may act on the nervous system cannot be excluded. Among the HHV-6-infected children, those suffering from convulsions were statistically more likely to have a family history of FC and IgM, while IgA were less likely. In G1, 57 cases were followed up over 2 years: 9 of them had a second episode of FC. Virological diagnosis at the first episode of FC revealed HHV-6 infection in 3 cases, 2 of these being due to viral reactivation. We underline the important role of HHV-6 infection in FC and postulate a relationship between family history and the immunity of the patient; this is confirmed by the loss of statistical significance in the reduction of IgM in G1 compared with G2 with no family history of FC. The reactivation of FC by HHV-6 is a possibility to be borne in mind; an increased number of cases would be needed to confirm this hypothesis.

Adenovirus Infections, Human↗
PubMed1993

Febrile and afebrile convulsions: a clinical follow-up.

A joint study was performed on 204 children who suffered separate febrile (FS) and afebrile seizures (aFS) within a short space of time to evaluate the risk of subsequent convulsive crises. The data obtained revealed frequent recurrence of seizures and high risk of subsequent convulsive afebrile crises in these children.

Atrophy↗
PubMed1987

Genetic analysis of febrile convulsions: twin and family studies.

Thirty-two twin pairs and 673 sibship-cases with febrile convulsions (FC) were studied. Twin study: The pairwise concordance rate for FC was 56% (10/18 pairs) in monozygotic and 14% (2/14 pairs) in dizygotic twins (P less than 0.05). Intra-pair similarity of clinical symptoms in concordant twin pairs was greater than that in sibship-cases. Sibship-pair study (population): In sibship-pair study a large positive correlation of some clinical symptoms - in particular, age at onset of FC, exogenous factors, and degree of fever (P less than 0.001 for each) - was indicated. Compared with FC children with no family history, those with such family history had a higher frequency of age at onset between 8 and 19 months, exogenous factors, low degree of fever before onset of convulsions, many recurrences, and recurrence after age 3 (P less than 0.01-0.001 for each). Morbidity risk among near relatives was highest in first-degree relatives (16%) than in second (4.0%) or third-degree relatives (4.1%). The following differences were found: siblings (24%) greater than parents (12%), uncles (4.5%) greater than aunts (3.5%), male cousins (4.4%) greater than female cousins (3.8%). Segregation ratio, influence by affection of father or mother, and maternal preponderance were analysed. Similar findings were also observed in the clinic study. A multifactorial mode of inheritance for FC receives some support from this study, and the heritability was estimated to be 75% in the population study. The results may be useful for genetic counselling for FC.

Child, Preschool↗
PubMed1983

Low CSF GABA concentration in children with febrile convulsions, untreated epilepsy, and meningitis.

In 14 children with epilepsy, 51 with febrile convulsions and 22 with meningitis gamma-aminobutyric acid (GABA) concentrations in lumbar CSF were determined. While the mean for CSF GABA concentrations for all epileptic children was unchanged [144 (range: 73-285) pmol/ml; controls: 148 (range: 90-243) pmol/ml] extraordinarily high GABA levels were found in the CSF of two children on valproate (525 and 557 pmol/ml) and remarkably low GABA concentrations in hitherto untreated epileptic children [109 (range: 67-176) pmol/ml]. Children with febrile convulsions [103 (range: 63-170) pmol/ml] and acute meningitis [105 (range: 65-171) pmol/ml] had significantly decreased CSF GABA concentrations (P less than 0.001 and P less than 0.02 compared with controls). The data indicate that valproate intake increases dramatically the GABA concentrations in the CSF of epileptic children. Furthermore, the study supports the concept that low GABAergic activity within the CNS may be one cause for an increased seizure frequency.

Adolescent↗
PubMed1977

Spastic constriction of cerebral vessels after electric convulsive treatment.

The brains of nine cats were subjected to bitemporal electric convulsive treatment. The current (AC, 220 V, 50 Hz, ca. 500 mA, 500 ms) was applied two to five times. Pial vessels were observed through a skull window. Immediately after current application, some pial arteries exhibited segmental spastic constriction which usually did not disappear until the animals were killed. Before sacrificing the animals, 20 min after convulsive treatment they were perfused with a carbon suspension. In some cortical areas blackening was impaired indicating that perfusion was not complete. Electron-microscopic investigation revealed that spasm also occurred in arterioles of the brain parenchyma. Many arterial vessels, some of them possessing only one muscular cell sheat, had collapsed so that the lumen was merely a small cleft. The spasms were irregularly distributed and confined to small segments of the vessel. Small arteriolar vessels were more affected than large pial arteries. Arterial spasms continued for 20 min. In a total of 39 control animals spastic constriction was observed only once; this animal had been subjected to prolonged hypocapnia.

Animals↗
PubMed1983

Facilitation of diazepam action by anticonvulsant agents against picrotoxin induced convulsions.

A subeffective dose (2 mg/kg) of diazepam produced only 50% protection against picrotoxin-induced (PTX) convulsions in rats. Simultaneous administration of GABA and other GABA-ergic substances such as piracetam and sidium valproate, which did not have any effect by themselves, potentiated diazepam action. The onset of convulsions and mortality due to PTX were significantly delayed. The other conventional anticonvulsants phenobarbitone, phenytoin and ethosuximide also enhanced the protective effect of diazepam. Inosine, a putative benzodiazepine ligand, also enhanced diazepam action. These observations are explained on the basis of data from in vitro studies indicating that GABA-ergic agents and barbiturates enhance both the number of benzodiazepine binding sites and benzodiazepine binding. The protective effect of clonidine, however, may be mediated by a different mechanism unrelated to the GABA-ergic system.

Animals↗
PubMed1978

The effects of atropine on the tolerance and the convulsions seen after withdrawal from forced barbital drinking in the rat.

Male rats were forced to drink a barbital solution as their only drinking fluid for 33 weeks. During the last part of the treatment the average dose of barbital was around 200 mg/kg/day. In the abstinence period after barbital treatment, tolerance was recorded with a hexobarbital anaesthesia threshold utilizing an EEG criterium. Convulsions were recorded in jiggle cages. On days 3 and 28 of the abstinence period, i.p. pretreatment with atropine (2, 4, and 8 mg/kg) was given 1.5 h before threshold determinations. The barbital treatment induced a clear tolerance to the hexobarbital, which still could be detected on day 28 of abstinence. Atropine (8 mg/kg) reduced the hexobarbital threshold in tolerant and in control animals at both the time of maximum tolerance (day 3) and later during abstinence (day 28). The magnitude of the response was greater in tolerant animals, but no parallel shift in the dose-response curve was seen. The convulsions during abstinence were reduced for at least 8 h after atropine treatment (8mg/kg) on day 3. These results support the hypothesis that cholinergic mechanisms are involved in the changes induced by chronic barbiturate treatments.

Animals↗
PubMed1978

Inhibition of pentylenetetrazol-induced convulsions in rats by prostaglandin E1: role of brain monoamines.

Prostaglandin E1-(PGE1-) induced inhibition of pentylenetetrazol (PTZ) convulsions in rats were significantly antagonized after pretreatment with drugs known to reduce brain serotonin activity, but not by pharmacological agents that decrease brain catecholamine activity. PGF2alpha also significantly inhibited PGE1 action. The results suggest that PGE1-induced inhibition of PTZ convulsions is not a direct effect, but an indirect one mediated through increase in brain serotonin activity.

Animals↗
PubMed1981

Sodium valproate versus phenobarbital in the prophylactic treatment of febrile convulsions in childhood.

Phenobarbital has been shown to offer effective prophylaxis against childhood febrile convulsions. However, a high percentage of children do not tolerate phenobarbital, mainly due to behavioral changes. Valproate, due to its low toxicity, appears to be an attractive alternative to phenobarbital treatment. Ninety children admitted with their first febrile convulsion were offered prophylactic treatment with either phenobarbital 3-5 mg/kg/day or valproate 20-30 mt/kg/day. Twenty-five children whose parents refused prophylactic treatment make up an untreated control group. Serum levels of the appropriate drug were measured at each follow-up visit. The three groups appear to be comparable. Twenty-one per cent of the phenobarbital treated children required discontinuation of the drug due to side effects. All the children tolerated valproate therapy. Twelve out of 25 untreated children suffered recurrences. Eight out of 33 children treated with phenobarbital suffered recurrences. Four out of 32 children on valproate therapy had recurrences. The difference between valproate treatment and no therapy at all is highly significant (p less than 0.001). Phenobarbital did not reduce the risk of recurrence. We now recommend prophylactic treatment with valproate to children with febrile seizures.

Child Behavior Disorders↗
PubMed1989

Further confirmation of serotonin reduction in the neostriatum during hyperthermia-induced convulsions: a quantitative immunohistochemical study.

Changes occurring in serotonin neurons during hyperthermia and hyperthermia-induced convulsions were examined by quantitative immunohistochemistry. A marked increase in serotonin immunoreactivity was observed at the rostral and intermediate levels of the neostriatum of mice kept at high temperatures with no convulsions, and a significant reduction in serotonin immunoreactivity was verified throughout the neostriatum of mice which had hyperthermia-induced seizures. These results suggest that serotonin neurons change significantly during thermal stress and seizures, and that regional analysis is essential for an understanding of the role of serotonin neurons.

Animals↗
PubMed1988

Decreased susceptibility to local anesthetics-induced convulsions after paradoxical sleep deprivation.

The effect of 50% convulsant (CD50) and 50% lethal (LD50) doses of lidocaine, bupivacaine and pentylenetetrazol were determined in mice stressed by paradoxical sleep deprivation (PSD). The results showed a reduced mortality after high doses of local anesthetics and decreased seizure susceptibility induced by bupivacaine after 48 h and 72 h of PSD. On the other hand this stressful manipulation increased the susceptibility to pentylenetetrazol-induced convulsions. These data may suggest a different mechanism of action for these drugs. Possible alterations in drug metabolism or on aminergic transmission after PSD may be involved in the protection to the toxic effect of the local anesthetics.

Anesthetics, Local↗
PubMed1981

Reduced and oxidized glutathione in brain and convulsions.

Concentration changes of reduced glutathione (GSH) and oxidized glutathione (GSSG) were studied by fluorometric assay with omicron-phthalaldehyde to clarify the relationship between seizure mechanism and the glutathione redox state. In cerebellum the GSH/GSSG ratio was significantly decreased in the interictal stage of E1 mice (stimulated group), but in ddY mice this ratio was decreased before convulsions induced by pentylenetetrazol and during submaximal ECS. No change was found in the GSH/GSSG ratio of the cerebellum during and after convulsions induced by pentylenetetrazol and maximal ECS. GSH levels in cerebrum in the interictal stage of E1 mice (stimulated group) were lower compared to control E1 mice. In ddY mice submaximal ECS increased GSSG levels in cerebrum so that the GSH/GSSG ratio was decreased.

Animals↗
PubMed1979

The convulsant drugs 3-mercaptopropionate and methionine sulfoximine inhibit L-glutamate and L-aspartate binding to a hydrophobic protein fraction from rat cerebral cortex.

The action of the convulsant drugs, methionine sulfoximine (MSO), 3-mercaptopropionate (3-MP), megimide (MG), and allylglycine on the binding of L-[14C]aspartate, L-[14C]glutamate and [14C]GABA to a hydrophobic protein fraction isolated from rat cerebral cortex was studied. Using the convulsant at 10(-4) M concentration and the radioactive ligands as 10(-6) M the binding of L-[14C]glutamate was inhibited 60% by 3-MP and 40% by MSO, while MG and allylglycine had no effect. The binding of L-[14C]aspartate was inhibited 55%, and 10--20% by 3-MP and MSO, respectively, while MG and allylglycine had not effect. None of the drugs mentioned, except for a minimal inhibition by MG, altered the binding of [14C]GABA. Neither MSO nor 3-MP affected the high-affinity sites for L-[14C]glutamate of L-[14C]aspartate, but they had a strong inhibitory action on the medium affinity site. These results are discussed in relation to the possible mechanism of action of these drugs on L-glutamate and L-aspartate receptors.

3-Mercaptopropionic Acid↗
PubMed1985

Effects of piperine on convulsions and on brain serotonin and catecholamine levels in E1 mice.

Convulsions of E1 mice were completely suppressed by 60 mg/kg of piperine injected intraperitoneally. The ED50 was 21.1 mg/kg. The brain 5-HT, dopamine and norepinephrine levels were estimated 1 hour after the intraperitoneal injection of piperine. The 5-HT level was significantly higher in the cerebral cortex of piperine treated mice than in control mice. This increase may be related directly to the mechanism of inhibition of convulsions by piperine. On the other hand, lower levels of 5-HT were observed in the hippocampus, midbrain and cerebellum. The dopamine level in the piperine treated mice was markedly higher only in the hypothalamus, while the norepinephrine levels were lower in every part of the brain.

Alkaloids↗