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PubMedDate not supplied

[Experimental study of the toxic convulsant properties of commercial preparations of essences of sage and hyssop (author's transl)].

Commercial preparations of essences of sage and hyssop have caused poisoning of human beings and were found to possess a convulsant action of central origin in animals. The convulsant effect of hyssop essence appears to be more powerful than that of sage in non-anaesthetized rats. The dose limit, below which the cortical phenomena are subclinical, is 0.08 g/kg for hyssop, while above 0.13 g/kg convulsions appear and become lethal above 1.25 g/kg. The same doses for essence of sage are respectively 0.3, 0.5 and 3.2 g/kg. The neurotoxicity of hyssop appears to be related to the presence of two terpene ketones, pinocamphone and isopinocamphone, the former of which has powerful convulsant properties, and is lethal at doses above 0.05 ml/kg. The toxicity of essence of sage is due to the presence of camphor which is well-known to possess convulsant properties.

Animals↗
PubMed2000

Pharmacokinetic-pharmacodynamic modelling of the convulsant interaction between norfloxacin and biphenyl acetic acid in rats.

Fluoroquinolones (FQs) are associated with a low incidence of central nervous system (CNS) side effects, possibly leading to convulsions, especially when co-administered with nonsteroidal anti-inflammatory drugs (NSAIDS). Although the in vivo pro-convulsant activity of NSAIDS is essentially unknown, the convulsant potential of FQs is traditionally evaluated by in vitro gamma-aminobutyric acid (GABA) binding experiments in the presence of 4-biphenyl acetic acid (BPAA), the active metabolite of fenbufen. The aim of this study was therefore to investigate the BPAA-norfloxacin convulsant interaction in vivo. Male Sprague-Dawley rats (n = 27) were given BPAA orally, at various doses 1 h before norfloxacin infusion, which was maintained until the onset of maximal seizures, when cerebrospinal fluid (CSF) and plasma samples were collected for analysis. An inhibitory E(max) effect model with a baseline effect parameter was fitted to the norfloxacin versus BPAA concentrations in the CSF, previously shown to be part of the biophase. This model includes three parameters: the concentrations of norfloxacin in the absence of BPAA (C(CSF0, Nor)), and when BPAA concentration tends toward infinity (C(CSFbase, Nor)), and the BPAA concentration for which half of the maximal effect is observed (C(CSF50, BPAA)). The maximal proconvulsant effect of BPAA is given by the C(CSF0, Nor) / C(CSFbase, Nor) ratio, estimated to approximately 6 in this study. Derived models were developed in plasma to account for the non-linear CSF diffusion of norfloxacin and protein binding of BPAA. In conclusion this study has shown that the convulsant interaction between norfloxacin and BPAA in rats, can be adequately characterized by modelling of the CSF concentrations of the two drugs at the onset of activity, following their administration in various proportions.

Animals↗
PubMed1999

Nonimmobilizers and transitional compounds may produce convulsions by two mechanisms.

UNLABELLED: Some inhaled compounds cause convulsions. To better appreciate the physical basis for this property, we correlated the partial pressures that produced convulsions in rats with the lipophilicity (nonpolarity) and hydrophilicity (polarity) of 45 compounds: 3 n-alkanes, 18 n-haloalkanes, 3 halogenated aromatic compounds, 3 cycloalkanes and 3 halocycloalkanes, 13 halogenated ethers, and 2 noble gases (He and Ne). In most cases, convulsions were quantified by averaging the alveolar partial pressures just below the pressures that caused and slightly higher pressures that did cause clonic convulsions (ED50). The ED50 did not correlate with hydrophilicity (the saline/gas partition coefficient), nor was there an obvious correlation with molecular structure. For 80% of compounds (36 of 45), the ED50 correlated closely (r2 = 0.99) with lipophilicity (the olive oil/gas partition coefficient). Perhaps because they block the effect of GABA on GABA(A) receptors, five compounds were more potent than would be predicted from their lipophilicity. Conversely, four compounds may have been less potent than would be predicted because they (like conventional inhaled anesthetics) enhance the effect of GABA on GABA(A) receptors. IMPLICATIONS: Nonimmobilizers and transitional compounds may produce convulsions by two mechanisms. One correlates with lipophilicity (nonpolarity), and the other correlates with an action on GABA(A) receptors.

Alkanes↗
PubMed2001

The convulsant and anesthetic properties of cis-trans isomers of 1,2-dichlorohexafluorocyclobutane and 1,2-dichloroethylene.

UNLABELLED: The differences in potencies of optical isomers of anesthetics support the hypothesis that anesthetics act by specific receptor interactions. Diastereoisomerism and geometrical isomerism offer further tests of this hypothesis but have not been explored. They are the subject of this report. We quantified the nonimmobilizing and convulsant properties of the cis and trans diastereomers of the nonimmobilizer 2N (1,2-dichlorohexafluorocyclobutane). Although the lipophilicity of the diastereomers predicts complete anesthesia at the partial pressures applied, neither diastereomer had anesthetic activity alone, and the cis form may have a small (10%) capacity to antagonize anesthesia, as defined by additive effects on the MAC (the minimum alveolar concentration required to suppress movement to a noxious stimulus in 50% of rats) of desflurane. Both diastereomers produced convulsions, the cis form being nearly twice as potent as the trans form: convulsant 50% effective dose (mean +/- SD) was 0.039 +/- 0.009 atmospheres (atm) for the purified cis and 0.064 +/- 0.009 atm for the purified trans isomer. The MAC value for cis-1,2-dichloroethylene equaled 0.0071 +/- 0.0006 atm, and MAC for trans-1,2-dichloroethylene equaled 0.0183 +/- 0.0031 atm. In qualitative accord with the Meyer-Overton hypothesis, the greater cis potency was associated with a greater lipophilicity. However, the product of MAC x solubility differed between the cis and trans isomers by 40%-50%. We conclude that neither the cis nor trans isomers of 2N have anesthetic properties, but isomerism does influence 2N's convulsant properties and the anesthetic properties of dichloroethylene. These isomeric effects may be as useful in defining receptor-anesthetic interactions as those found with optical isomers. IMPLICATIONS: Cis-trans isomerism can influence the convulsant properties of the nonimmobilizer 2N (1,2-dichlorohexafluorocyclobutane) and the anesthetic properties of dichloroethylene. Such isomeric effects may be as useful as those found with optical isomers in defining receptor-anesthetic interactions.

Anesthetics, Inhalation↗
PubMed1982

Potencies of convulsant drugs in mice selectively bred for resistance and susceptibility to nitrous oxide anesthesia.

To test the possibility that mice selectively bred for resistance (HI mice) and susceptibility (LO mice) to nitrous oxide anesthesia have general differences in central nervous system excitability, we examined the effects of six convulsant agents in these two lines in mice. Using high-pressure helium, flurothyl, pentylenetetrazol, strychnine, (+)-bicuculline, and picrotoxin, we induced convulsions in HI and LO mice. For all of the agents tested, HI mice were significantly more susceptible to convulsions than LO mice. LO mice convulsed at a 13 to 25 per cent higher dose of convulsant agent than did HI mice. In contrast, nitrous oxide requirements (as measured by the partial pressure of nitrous oxide required to abolish the righting reflex), were 49 to 65 per cent higher in HI mice. Therefore, the higher nitrous oxide requirement in HI mice is probably due, at least in part to a generalized increase in central nervous system excitability.

Animals↗
PubMed1998

The effects of exogenous epinephrine on a convulsive dose of lidocaine: relationship with cerebral circulation.

In order to understand why exogenous epinephrine decreases the convulsive dose of lidocaine, the authors investigated cerebral circulation and plasma lidocaine concentrations in Wistar rats under general anesthesia. In the first experiment, baseline evaluations of each rat's electroencephalogram (EEG), mean arterial pressure (MAP), regional cerebral blood flow (r-CBF), cerebrospinal fluid (CSF) pressure, and cerebral perfusion pressure (CPP) were made. The rats were then assigned to one of three groups: Group L (n=6) received intravenous lidocaine (5 mg/kg/min); Group LE (n=6) received intravenous lidocaine (5 mg/kg/min) and epinephrine (2.5 kg/kg/min); and Group E (n=5) received intravenous epinephrine (2.5 microg/kg/min). Cumulative doses of lidocaine at the onset of EEG spike activity in Groups L and LE were compared. Blood-brain barrier (BBB) permeability was evaluated by observing extravasation of Evans blue (EB) dye. In the second experiment, additional rats were allocated to two treatment groups: Group L' (n=6) received intravenous lidocaine (5 mg/kg/min); Group LE' (n=6) received intravenous lidocaine (5 mg/kg/min) and epinephrine (2.5 microg/kg/min). Brain tissue oxygen partial pressure (PtO2) was monitored during infusion, and arterial and sagittal sinus blood samples were obtained immediately after the onset of EEG spike activity to determine plasma lidocaine concentration. The convulsive dose of lidocaine was significantly decreased when lidocaine was administered with epinephrine (Group L: 61.5+/-5.3 mg/kg (mean+/-SD); Group LE: 30.1+/-4.0 mg/kg) (p < 0.05), but there were no significant differences in plasma lidocaine concentration among these groups. R-CBF, CSF pressure, and CPP immediately before EEG spike activity were higher in Group LE than in Group L. Neither decreased PtO2 nor extravasation of EB was observed in rats treated with epinephrine and lidocaine, excluding cerebral ischemia and BBB breakdown from possible mechanisms by which epinephrine decreased the convulsive dose of lidocaine. None of the rats in Group E exhibited EEG findings suggestive of a preconvulsive state, ruling out a convulsive effect of epinephrine itself. The results suggest that an increase in lidocaine supply to the brain caused by increased CBF causes the low cumulative dose of lidocaine at the onset of convulsion in rats given lidocaine plus epinephrine.

Adrenergic Agonists↗
PubMed1990

Differential effects of petit mal anticonvulsants and convulsants on thalamic neurones: calcium current reduction.

1. Succinimide derivatives can be either convulsant (tetramethylsuccinimide (TMS)), or anticonvulsant (ethosuximide (ES); alpha-methyl-alpha-phenylsuccinimide (MPS)). ES, an anticonvulsant succinimide, has previously been shown to block calcium currents of thalamic neurones, while the convulsant succinimide TMS blocks gamma-aminobutyric acid (GABA) responses in a similar fashion to the convulsant pentylenetetrazol (PTZ). 2. Using voltage-clamp techniques, we analysed the effects of the anticonvulsant succinimides ES and MPS and the convulsants TMS and PTZ on calcium currents of acutely isolated thalamic relay neurones of the rat. 3. MPS and ES reduced low-threshold calcium current (LTCC) in a voltage-dependent manner, without affecting steady-state inactivation. MPS was less potent than ES (IC50 of 1100 vs 200 microM) but greater in efficacy (100% maximal reduction vs 40% for ES). 4. PTZ had no effect on calcium currents, and TMS only reduced LTCC at very high concentrations, and did not occlude MPS effects when applied concurrently. 5. These results, which demonstrate that anticonvulsant, but not convulsant, succinimides block LTCC, provide additional support for the hypothesis that LTCC reduction is a mechanism of action of the anticonvulsant succinimides related to their effects in petit mal epilepsy.

Animals↗
PubMed2002

Nitric oxide (NO) and convulsions induced by pentylenetetrazol.

Data about the role of nitric oxide (NO) in epileptogenesis are contradictory. It is found to exert both proconvulsant and anticonvulsant effects. In an attempt to elucidate the role of NO in seizures, male Wistar rats were treated intraperitoneally by pentylenetetrazol (PTZ) (60, 80, and 100 mg/kg) and by a nitric oxide synthase antagonist, N-omega-nitro-L-arginine-methyl-ester (L-NAME) (10, 40, and 70 mg/kg), applied before PTZ. The time to onset and incidence of forelimb dystonia (FLD), generalized clonic convulsions (GCC), clonic-tonic convulsions (CTC), and mortality were recorded. The most successful convulsive response and mortality prevention were found in PTZ (80 mg/kg)-treated groups, where L-NAME (70 mg/kg) decreased the incidence by 29, 50, 67 (p = 0.052), and 50%, respectively, and significantly prolonged the time to onset, except that for mortality. Unexpectedly, L-NAME (40 mg/kg) increased incidence of GCC and mortality by 16%, similar to L-NAME (10 mg/kg) in PTZ (60 mg/kg)-treated groups, where GCC, CTC, and mortality increased by 14, 14, and 28%, respectively. Convulsive latency was prolonged in some PTZ (100 mg/kg) + L-NAME (40 and 70 mg/kg)-treated groups. In the experimental model and protocol used, it is concluded that (1) the effects of NO are L-NAME- and PTZ-dose dependent; (2) clonic-tonic convulsions are more strongly influenced by NO than limbic, probably because of PTZ limbic structure overstimulation; (3) L-NAME decreases the incidence of CTC and prolongs FLD, GCC, and CTC times to onset, indicating that NO acts as a proconvulsant; and (3) increased GCC, CTC, and mortality that suggests an anticonvulsant effect of NO needs further investigation.

Animals↗
PubMed2006

Convulsant bicuculline modifies CNS muscarinic receptor affinity.

BACKGROUND: Previous work from this laboratory has shown that the administration of the convulsant drug 3-mercaptopropionic acid (MP), a GAD inhibitor, modifies not only GABA synthesis but also binding of the antagonist [3H]-quinuclidinyl benzilate ([3H]-QNB) to central muscarinic receptors, an effect due to an increase in affinity without modifications in binding site number. The cholinergic system has been implicated in several experimental epilepsy models and the ability of acetylcholine to regulate neuronal excitability in the neocortex is well known. To study the potential relationship between GABAergic and cholinergic systems with seizure activity, we analyzed the muscarinic receptor after inducing seizure by bicuculline (BIC), known to antagonize the GABA-A postsynaptic receptor subtype. RESULTS: We analyzed binding of muscarinic antagonist [3H]-QNB to rat CNS membranes after i.p. administration of BIC at subconvulsant (1.0 mg/kg) and convulsant (7.5 mg/kg) doses. Subconvulsant BIC dose failed to develop seizures but produced binding alteration in the cerebellum and hippocampus with roughly 40% increase and 10% decrease, respectively. After convulsant BIC dose, which invariably led to generalized tonic-clonic seizures, binding increased 36% and 15% to cerebellar and striatal membranes respectively, but decreased 12% to hippocampal membranes. Kd value was accordingly modified: with the subconvulsant dose it decreased 27% in cerebellum whereas it increased 61% in hippocampus; with the convulsant dose, Kd value decreased 33% in cerebellum but increased 85% in hippocampus. No change in receptor number site was found, and Hill number was invariably close to unity. CONCLUSION: Results indicate dissimilar central nervous system area susceptibility of muscarinic receptor to BIC. Ligand binding was modified not only by a convulsant BIC dose but also by a subconvulsant dose, indicating that changes are not attributable to the seizure process itself. Findings support the notion that the muscarinic receptors play a major role in experimental epilepsy and provide a new example of differential neuronal plasticity.

Animals↗
PubMed1996

Lack of potentiation with felbinac patch on the convulsive toxicity of enoxacin in rats.

We investigated the possible potentiation of the convulsive toxicity of enoxacin (ENX) by the concomitant topical application of a felbinac (FLB) patch in rats. A felbinac patch (Seltouch; 0.5%, 3 cm x 4 cm) was attached on the back of rats where their hair has been removed. ENX was infused from the left jugular vein at 8 h after the application of FLB patch under an unanesthetized and unstrained condition. Blood, CSF and brain samples were collected at the occurrence of convulsion, and ENX concentrations of each part were determined. As a result, no significant potentiation by FLB patch was found in the onset time of convulsion or in the ENX concentration of each part. Moreover, based on the assumption that there are no inter-species differences in ENX concentration in the brain at the occurrence of a convulsion (Cbr), the predicted plasma ENX concentration required to elicit convulsions in humans, which was estimated from the Cbr and Kp value of ENX in the brain of rats, was 20 times higher than the therapeutic plasma level.

Administration, Cutaneous↗
PubMedDate not supplied

Effect of adenosine A1 and A2 receptor stimulation on hypoxia-induced convulsions in adult mice.

Clinical observations indicate that seizures induced by hypoxia are common kind of convulsive activity in both infants and elderly patients. The occurrence of seizure episode during hypoxia is important risk factor of epilepsy development in the future. Experimental hypoxia was obtained by exposure of adult (20-23 g) Albino Swiss mice to spontaneous breathing in gas mixture composed of 5% oxygen and 95% nitrogen. The latency time to convulsive activity was determined. Single sublethal episode of seizures induced by hypoxia (HS) resulted in higher susceptibility to pentetrazol (PTZ), bicuculline (BCC), N-methyl-D-aspartic acid (NMDA) but not in electrically induced convulsions. Adenosine A1 receptor agonist, R(-)N6-(2-phenyl-isopropyl)adenosine (R-PIA) (0.01; 0.05; 0.1 mg/kg, i.p.) prolonged the latency to HS-induced convulsions. A1 receptor antagonist, 8-cyclopentyltheophylline (CPT), reversed the protective action of R-PIA. A2 receptor agonist, N(6)-[2-(3,5-dimethoxyphenyl)-2-(2-methylphenyl)]ethyladenosine (DPMA), only at the highest dose (5 mg/kg i.p.) prolonged the latency time to convulsive activity. This effect was only partially reversed by A2 antagonist 3,7-dimethyl-1-propargylxanthine (DMPX). Administered immediately after episode of HS R-PIA diminished the higher susceptibility to PTZ, BCC, NMDA at 3rd day after HS, while DPMA appeared to be ineffective. These results confirm the important role of adenosine A1 receptor agonist in protection against acute and chronic epileptogenic effect of hypoxia. The role of adenosine A2 receptors seems to be of minor importance.

Adenosine↗
PubMed1990

Binding interactions of convulsant and anticonvulsant gamma-butyrolactones and gamma-thiobutyrolactones with the picrotoxin receptor.

Alkyl-substituted gamma-butyrolactones (GBLs) and gamma-thiobutyrolactones (TBLs) are neuroactive chemicals. beta-Substituted compounds are convulsant, whereas alpha-alkyl substituted GBLs and TBLs are anticonvulsant. The structural similarities between beta-alkyl GBLs and the convulsant picrotoxinin suggested that alkyl substituted GBLs and TBLs act at the picrotoxin receptor. To test this hypothesis we examined the interactions of convulsant and anticonvulsant GBLs and TBLs with the picrotoxin, benzodiazepine and gamma-aminobutyric acid (GABA) binding sites of the GABA receptor complex. All of these convulsants and anticonvulsants studied competitively displaced 35S-t-butylbicyclophosphorothionate (35S-TBPS), a ligand that binds to the picrotoxin receptor. This inhibition of 35S-TBPS binding was not blocked by the GABA antagonist bicuculline methobromide. The convulsant GBLs and TBLs also partially inhibited [3H]muscimol binding to the GABA site and [3H]flunitrazepam binding to the benzodiazepine site, but they did so at concentrations substantially greater than those that inhibited 35S-TBPS binding. The anticonvulsant GBLs and TBLs had no effect on either [3H]muscimol or [3H]flunitrazepam binding. In contrast to the GBLs and TBLs, pentobarbital inhibited TBPS binding in a manner that was blocked by bicuculline methobromide, and it enhanced both [3H]flunitrazepam and [3H]muscimol binding. Both ethosuximide and tetramethylsuccinimide, neuroactive compounds structurally similar to GBLs, competitively displaced 35S-TBPS from the picrotoxin receptor and both compounds were weak inhibitors of [3H] muscimol binding. In addition, ethosuximide also partially diminished [3H]flunitrazepam binding. These data demonstrate that the site of action of alkyl-substituted GBLs and TBLs is different from that of GABA, barbiturates and benzodiazepines. We suggest that the GBLs and TBLs act at the picrotoxin receptor.

4-Butyrolactone↗
PubMed1985

Are "peripheral-type" binding sites for benzodiazepines in brain related to the convulsant actions of Ro 5-4864?

Previous studies have shown that Ro 5-4864 is a potent convulsant. Investigation of a series of compounds structurally related to Ro-4864 revealed a good correlation (r = .93, p less than 0.01) between their potencies as convulsants and their abilities to displace [35S]t-butylbicyclophosphorothionate from sites associated with the chloride ionophore. In contrast, there appears to be no direct relationship between the convulsant potencies of these compounds and their affinities for "peripheral-type" binding sites for benzodiazepines. These data suggest that "peripheral-type" binding sites for benzodiazepines are not directly involved in the convulsant actions of Ro 5-4864 and related compounds nonetheless, several lines of evidence suggest that "peripheral-type" binding sites for benzodiazepines may be indirectly involved in the convulsant properties of Ro 5-4864.

Animals↗
PubMed1979

Reduction of gamma-aminobutyric acid (GABA)-mediated transmission by a convulsant benzodiazepine.

In contrast to other benzodiazepine, Ro 5-3663 produces convulsions in mice. The CD50 of 7.0 mg/kg i.v. falls between that of picrotoxin and pentylenetetrazol. An electrophysiological study was made of the effects of this convulsant benzodiazepine on spinal reflexes and on ganglionic depolarization evoked by gamma-aminobutyric acid (GABA). In the unanesthetized spinal cat, Ro 5-3663 (15 mg/kg i.v.)depressed the dorsal root potentials and abolished the dorsal root reflexes evoked by muscle and cutaneous afferent inputs. The monosynaptic reflex was typically depressed, whereas polysynaptic potentials were enhanced. Diazepam reversed the depression of the dorsal root reflex and dorsal root potential produced by the convulsant benzodiazepine and reduced the enhancement of the polysynaptic potential. Presynaptic inhibition was attenuated by the convulsant, whereas strychnine-sensitive postsynaptic inhibition was slightly potentiated. Ro 5-3663 reduced the amplitude and duration of the GABA-evoked negative surface potential recorded from the superior cervical ganglion. The results indicate that the convulsant benzodiazepine acts in an opposite manner to the depressant benzodiazepines and support the hypothesis that these two types of compounds act through a modulation of GABAergic mechanisms.

Animals↗
PubMedDate not supplied

[Participation of GABA and other mediators in regulating the convulsive threshold].

The participation of GABA and some other transmitter systems in the regulation of the convulsive seizure threshold was studied using pharmacological tools. The convulsion were provoked by intravenous infusion of the GABAergic antagonists picrotoxin and bicuculline and, in some cases, of pentylenetetrazole and strychnine. The GABAergic transmitter mechanisms were established to play a major role in the regulation of the convulsive seizure threshold. Of some importance is also the participation of benzodiazepine receptors, cholinergic, dopaminergic, serotoninergic mechanisms, as well as of cyclic nucleotides. The interactions between the GABAergic and dopaminergic, cholinergic mechanisms, cyclic nucleotides, benzodiazepine receptors may also play a role in the convulsive threshold regulation. The changes in the threshold of convulsive reactions are closely related to the decrease or increase of both central inhibition (pre- or postsynaptic) and excitation.

Animals↗
PubMed1983

Tetanus toxin: convulsant action on mouse spinal cord neurons in culture.

The effects of direct application of tetanus toxin on fetal mouse spinal cord neurons in culture are described. Tetanus toxin produces increased excitation characterized by paroxysmal depolarizing events (PDE). In contrast to the abrupt onset of convulsant action produced by postsynaptic glycine antagonist strychnine, the convulsant action of tetanus occurs after a dose-dependent latent period. The onset of the convulsant action of tetanus toxin is paralleled by a reduction in observed spontaneous inhibitory synaptic potentials. Excitatory synaptic events can be identified as components of some tetanus-PDE. The toxin does not alter postsynaptic responses to the inhibitory amino acids glycine and gamma-aminobutyric acid. The latency and convulsant action of tetanus toxin are consistent with an irreversible presynaptic membrane interaction that reduces inhibitory transmission, a mechanism of action distinct from those of convulsants that antagonize inhibitory transmitters at the postsynaptic membrane.

Action Potentials↗
PubMed2002

Polymorphisms for interleukin 1 beta exon 5 and interleukin 1 receptor antagonist in Taiwanese children with febrile convulsions.

OBJECTIVE: To investigate whether interleukin 1 beta (IL-1 beta) exon 5 and IL-1 receptor antagonist (IL-1Ra) gene polymorphisms can be used as markers of susceptibility to febrile convulsions in children. METHODS: Children were divided into 2 groups: those with febrile convulsions (group 1; n = 51) and normal control subjects (group 2; n = 83). Polymorphisms for IL-1 beta exon 5 and IL-1Ra gene polymorphisms were detected by polymerase chain reaction. Genotypes and allelic frequencies for IL-1 beta exon 5 and IL-1Ra gene polymorphisms in both groups were compared. RESULTS: Genotype and allele frequencies for IL-1 beta exon 5 in both groups were not significantly different. Proportions of E1 homozygotes and E1/E2 heterozygotes for IL-1 beta exon 5 were 50 (98.1%) and 1 (1.9%), respectively, in group 1 and 82 (98.8%) and 1 (1.2%), respectively, in group 2. Frequencies of alleles E1 and E2 for IL-1 beta exon 5 were 101 (99.0%) and 1 (1.0%), respectively, in group 1 and 165 (99.4%) and 1 (0.6%), respectively, in group 2. Genotype proportions and allele frequencies for IL-1Ra between groups were significantly different. Proportions of genotypes I/I and I/II for IL-1Ra were 49 (96.1%) and 2 (3.9%) in group 1 and 69 (83.1%) and 14 (16.9%) in group 2. Frequencies of alleles I and II for IL-1Ra were 100 (98.0%) and 2 (2.0%) in group 1 and 152 (91.6%) and 14 (8.4%) in group 2. CONCLUSIONS: The IL-1Ra allele I is associated with a higher susceptibility to febrile convulsion, which may become a useful marker for predicting the development of febrile convulsions. The IL-1 beta exon 5 gene polymorphisms are not a useful marker for predicting the susceptibility to febrile convulsions.

Case-Control Studies↗
PubMed1983

Febrile convulsions and later development of epilepsy.

A group of 172 epileptic children who had had prior febrile convulsions was compared with a group of 674 who had not. Children with epilepsy and prior febrile convulsions were similar in some respects (sex ratio, positive family history for seizures) to children with pure febrile convulsions and in most respects (type of epilepsy, mental status, initial EEG, and two- and four-year remission rates in the long-term outcome) to epileptic children without prior febrile convulsions. Our data do not support the current view that febrile convulsions, per se, are the main cause of mesial temporal sclerosis, le, temporal lobe epilepsy. Thus, our clinical findings support previously expressed doubts on the role of febrile seizures in temporal lobe epilepsy that were based on pathohistologic findings.

Child, Preschool↗