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PubMed1999

Risk factors for a first febrile convulsion in children: a population study in southern Taiwan.

PURPOSE: To identify risk factors for a first febrile convulsion among 3-year-old children by a matched case-control population study. METHODS: All 11,714 neonatal survivors born in Tainan City between October 1989 and September 1991 were enrolled. At age 3, 10,460 children were available for telephone survey for febrile convulsions, and were confirmed by home visit interviews. Those without history of seizure were randomly matched to each febrile convulsion case by age, gender, and residence district. RESULTS: Two hundred fifty six children had febrile convulsions, and 218 of them and their matched controls were available for analysis. The febrile convulsion cases had significantly more febrile episodes (four or more) per year (33.0 vs. 22.5%; p = 0.021), and cases had a higher percentage of developmental delay (3.7 vs. 0.4%; p = 0.046) and a higher percentage of febrile convulsions in their siblings (12 vs. 0.4%; p = 0.011) than controls. The other sociodemographic, environmental, and biologic variables showed no differences between cases and controls. Step-wise logistic regression showed a highly significant independent association between febrile convulsions and history of febrile convulsions in the siblings, and a moderate one between febrile convulsions and the number of febrile episodes per year. CONCLUSIONS: The presence of febrile convulsions in the siblings and the number of fever episodes per year were the independent and significant predictors of febrile convulsion for an individual case in our population-based sample.

Case-Control Studies↗
PubMed1986

Neuropharmacological modification of central catecholamines: effects on pinealectomy-induced convulsions.

Removal of the pineal gland produces stereotyped tonic convulsions in parathyroidectomized rats. Inasmuch as central levels of norepinephrine (NE) are decreased in these animals, the purpose of this study was to investigate the effects of alterations in central catecholamine function on convulsions produced by pinealectomy in parathyroidectomized rats. The treatment of rats with alpha-methyl-p-tyrosine or FLA-63 produced large reductions in forebrain levels of both NE and dopamine or NE alone, respectively, which were not associated with facilitation of convulsions. However, the incidence of convulsions was increased by FLA-63 in rats pretreated with the catecholamine precursor L-dihydroxyphenylalanine. Reserpine, a monoamine depleter, had no effect on either the incidence or severity of convulsions. An acute injection of desipramine, an inhibitor of the reuptake of NE, however, significantly lowered the incidence of convulsions. Timolol, a beta-adrenergic receptor antagonist, reduced, in a dose-dependent manner, the average latency to onset of convulsions and increased the average number of convulsions each rat experienced. Clonidine, an alpha 2-adrenergic agonist, did not significantly alter convulsions. Thus presynaptic mechanisms such as synthesis and storage of both NE and DA appear to have little, if any, effect on pinealectomy-induced convulsions, whereas enhancing synaptic levels of NE by blocking its reuptake into adrenergic axons had an anticonvulsant effect. Further evidence suggesting a role for NE in modulating these convulsions is provided by the proconvulsant effect of blocking central beta-adrenergic receptors.

Animals↗
PubMed1991

Risk of epilepsy after febrile convulsions: a national cohort study.

OBJECTIVE: To identify children with febrile convulsions, classify their febrile convulsions into simple and complex, and determine the number and type of subsequent afebrile seizures in those children. DESIGN: National population based study. SETTING: United Kingdom. SUBJECTS: 16,004 neonatal survivors born during one week in April 1970. MAIN OUTCOME MEASURES: Information about febrile and afebrile seizures obtained from questionnaires at 5 and 10 years of age and from hospital records. RESULTS: Information was available for 14,676 of the cohort children. 398 (2.7%) of them had had at least one febrile convulsion. 16 children were known to be neurologically or developmentally abnormal before the first attack. Of the remaining 382 children, 305 had had a simple first febrile convulsion and 77 a complex first febrile convulsion. Thirteen of the 382 had had one or more afebrile seizures, nine of whom had developed epilepsy (recurrent afebrile seizures). A higher proportion of children with complex febrile convulsions (6/95) rather than simple febrile convulsions (3/287) developed epilepsy, the risk being highest for those who had had focal febrile convulsions (5/17; chi 2 = 39.9, p less than 0.001). Three of the 32 children who had prolonged febrile convulsions developed afebrile complex partial seizures. CONCLUSIONS: The risk of epilepsy after febrile convulsions is much less than reported in many hospital studies, and if febrile convulsions cause brain damage that leads to later epilepsy this is a rare occurrence.

Age Factors↗
PubMed1978

Effect of 6-hydroxydopamine on brain and blood catecholamine, ammonia, and amino acid metabolism in rats subjected to high pressure oxygen induced convulsions.

Effects of 6-hydroxydopamine (6-OHDA) on rat brain and blood adrenaline (A), noradrenaline (NA), ammonia (NH3), gamma-aminobutyric acid (GABA), and amino acid metabolism prior to and after high pressure oxygen (OHP) induced convulsions have been studied. 6-OHDA reduces GABA and glutamate (Glu) rior to OHP exposure in rat brain so that the concentration is even equal to that seen in nondrugged animals after convulsion. Concomitantly, 6-OHDA reduces the latency of OHP-induced convulsion significantly, and increases brain NH3, glutamine, and asparagine significantly. Although 6-OHDA, in increasing dosage, elevates blood A concentration, convulsion produces a significant further increase in A. Blood NA was not significantly changed in drugged, convulsed animals and was much less than blood NA concentrations in nondrugged convulsed animals. Increasing doses of 6-OHDA also increase NH3 in the blood significantly and convulsion increases its concentration further. Latency of convulsion seems to be related to certain monoamine levels since in some drugged animals where A and total catecholamines are still reduced 96 h after the first of two doses of 6-OHDA, NA concentrations are recovered to relatively normal and the convulsion latency time is also increased although it remains significantly abbreviated from undrugged animals' convulsion time. Low brain GABA levels seem to be a prime effector of convulsive activity.

Amino Acids↗
PubMed1978

Anti-convulsant effect of phthalazino-2,3b-phthalazine-5(14H),12(7h)-dione (L-5418). I. Behavioral effect.

Since it had been demonstrated that L5418 has an anti-convulsant effect with no relation to its anti-inflammatory properties, comparative studies were carried out with the use of currently available anti-convulsant agents as controls. L-5418 inhibited tonic convulsions induced by maximal electroshock and strychinine in mice and prevented animals from the death sequence. L-5418 had an inhibitory effect on tonic convulsions induced by pentetrazol and N-sulfamoyl-hexahydroazepine (SaH 41-178), but not on clonic convulsions by those compounds at even a high dosage or on clonic convulsions induced by picrotoxin and bemegride. Trimethadione produced an inhibitory effect on both tonic and clonic convulsions. The hypnotic agents, phenobarbital and glutethimide inhibited both convulsions, but a higher dose was required in the case of clonic convulsions. Anti-convulsant agents are classified into three different groups according to their mode of action. L-5418 had the same mode of action as seen with diphenylhydantoin and carbamazepine. As L-5418 did not inhibit tremor induced by tremorine, an anti-Parkinson effect was ruled out. When L-5418 was administered alone, the animals did not lose the righting reflex nor show muscle relaxation observed in inclined screen and rotarod tests. Moreover, the compound had no influence on the aggressive behavior induced by electrical stimulation or olfactory bulb ablation. L-5418 possesses a selective anti-convulsant effect, yet has no sedative, tranquilizing or disturbing effects on movement such as equilibrium disturbance or muscle relaxation. L-5418 may prove useful for grand mal epilepsy as it is less toxic than diphenylhydantoin and carbamazepine.

Aggression↗
PubMed2000

[Convulsions in the early neonatal period].

Convulsions are relatively frequent in neonatal population. They are also the most dramatic sign of a disorder of the central nervous system. Clinical signs of convulsive seizures in neonatal period differ greatly from those occurring in a later stage. Our study involves a five year period, in the course of which we analysed all newborns with convulsions occurring in the early neonatal period. The objective of the study was to determine the incidence, aetiology and time of occurrence of convulsions, to determine the mortality rate in this group of newborns and to assess risk factors for the development of convulsions. In 29.423 newborns tested in the course of the study at our Clinic, convulsions were found in 38 (0.13%) of them. Regarding the gestation age, 68.4% of the cases of convulsion occurred in at term newborns. The most frequent aetiology factor was a perinatal damage, in 60.4%, and the majority of convulsive seizures occurred in the period between the 2nd and 7th day (84.3%). Five of the tested newborns died (13.5%), three of them having suffered from convulsions in the first 24 hours. The authors came to the conclusion that many factors influence the development of convulsions, and that the occurrence of convulsions in the first 24 hours and heavy perinatal brain damage give bad prognostics for survival.

Epilepsy, Benign Neonatal↗
PubMed1991

Altered response to GABAergic agents following electro and chemo convulsions in mice.

Effects of GABAergic agents and that of electroconvulsive shock (ECS) treatment were studied on bicuculline and picrotoxin (PTX)-induced convulsions in mice. Neither acute nor chronic ECS had any significant effect on bicuculline-induced convulsions, whereas the latency for PTX-induced convulsions was delayed by both acute and chronic ECS. Baclofen treatment delayed significantly the latency for PTX-induced convulsions in animals which were subjected to both acute and chronic ECS, whereas in bicuculline-induced convulsions, it shortened the latency of convulsions 24 hr after acute ECS. Progabide delayed the bicuculline-induced convulsions except in the case of 24 hr after acute ECS and PTX-induced convulsions except in the case of animals treated chronically with ECS. Fengabine showed no significant effect on bicuculline-induced convulsions. However, on PTX-induced convulsions, the latency was delayed in animals not subjected to ECS and in those subjected to chronic ECS. The possible explanations for the alterations in the effect of GABAergic agents following electro and chemo convulsions are (i) differences in the nature of antagonism by bicuculline and PTX, (ii) alterations in receptor sensitivity or number, and (iii) alterations in the levels of endogenous neurotransmitters, the latter two resulting as a result of acute or chronic ECS.

Animals↗
PubMed1988

Evidence that changes in levels of cyclic nucleotides in the CNS are not related to soman-induced convulsions.

Others have suggested that organophosphate-induced convulsions are related to changes in levels of cyclic nucleotides, especially in cerebella. We have examined this question by subcutaneously injecting male Sprague-Dawley rats (approx 250-300 gm) with three different doses of soman: a subconvulsive dose of 40 micrograms/kg, a convulsive dose of 120 micrograms/kg (which is approx 90% of the ED50 for convulsions) and a higher convulsive dose of 150 micrograms/kg. The incidence and severity of convulsions were monitored until the rats were sacrificed by focused microwave irradiation of the head at the following times after injections: 4 min, 10 min, 1 hr and 6 hr, which represent times prior to onset of convulsions, at onset of convulsions, at peak convulsive activity and during recovery from convulsions, respectively. Results showed that in rat striata, cerebella and thoracic spinal cord, neither changes in levels of cyclic AMP and cyclic GMP nor changes in ratios of cyclic AMP to cyclic GMP were correlated with soman-induced convulsions, i.e., none of the changes in cyclic AMP and cyclic GMP and/or in the ratios of cyclic AMP to cyclic GMP were related to the initiation of, maintenance of, or recovery from soman-induced convulsions.

Animals↗
PubMed2002

Convulsant activity of a non-peptidic delta-opioid receptor agonist is not required for its antidepressant-like effects in Sprague-Dawley rats.

RATIONALE: Non-peptidic delta-opioid receptor agonists possess antidepressant-like activity in the forced swim assay in the rat. These compounds have also previously been shown to possess convulsant properties in mice. OBJECTIVE: The aim of the present study was to examine whether such convulsions occurred in rats and to investigate if delta-mediated convulsant activity was necessary for the mediation of delta-opioid agonist-induced antidepressant-like activity. METHODS: The peripheral administration of delta-opioid receptor agonists to male Sprague-Dawley rats was followed by a period of observation for convulsant activity. Following this period and 60 min after delta-opioid agonist administration, rats were tested in the forced swim assay. RESULTS: The non-peptidic delta-opioid receptor agonists (+)-4-[(R)-[(2S,5R)-2,5-dimethyl-4-(2-propenyl)-1-piperazinyl]-(3-methoxyphenyl)methyl]-N,N-diethylbenzamide (SNC80) and (+)-4-[(R)-[(2S,5R)-2,5-dimethyl-4-(2-propenyl)-1-piperazinyl]-(3-hydroxyphenyl)methyl]-N,N-diethylbenzamide dihydrochloride [(+)BW373U86] both produced dose-dependent convulsant activity in rats and decreased immobility in the forced swim assay. The delta-opioid receptor antagonist naltrindole prevented the convulsant activity of (+)BW373U86 and its effects in the forced swim assay. This suggested a delta-opioid mechanism for both effects. Midazolam prevented convulsions but did not prevent activity in the forced swim assay. Rats tolerant to the convulsive effects of (+)BW373U86 still displayed antidepressant-like effects. CONCLUSION: delta-Mediated convulsions do occur in rats and can be prevented without affecting the delta-mediated effects in the forced swim assay. Therefore the convulsant activity of (+)BW373U86 and possibly other non-peptidic delta-agonists is not required for activity in the forced swim assay.

Animals↗
PubMed2006

Absence of convulsive liability of doripenem, a new carbapenem antibiotic, in comparison with beta-lactam antibiotics.

beta-Lactam antibiotics have been suggested to have some degree of convulsive activity and neurotoxicity in experimental animals as well as in clinical situations. We examined the convulsive activities of a new carbapenem antibiotic, (+)-(4R,5S,6S)-6-[(1R)-1-hydroxyethyl]-4-methyl-7-oxo-3-[[(3S,5S)-5-[(sulfamoylamino)methyl]-3-pyrrolidinyl]thio]-1-azabicyclo[3.2.0]hept-2-ene-2-carboxic acid monohydrate (doripenem) using several animals and compared them with beta-lactam antibiotics. In intravenous (IV) injection studies, imipenem/cilastatin, at 400/400mg/kg produced seizure discharges on electroencephalogram (EEG) accompanied with clonic convulsions in rats. Meropenem showed only wet dog shaking behavior at 200 and 400mg/kg. Doripenem caused no changes in the EEG and behavior in rats at 400mg/kg. Imipenem/cilastatin IV potentiated the pentylenetetrazol (PTZ)-induced convulsions in mice at 250/250 mg/kg, while meropenem, panipenem/betamipron, cefazolin or doripenem did not cause any marked effects at up to 500 mg/kg. In mouse intracerebroventricular (ICV) injection studies, imipenem, panipenem and cefazolin induced clonic convulsions in a dose-dependent manner in mice. Doripenem and meropenem did not induce convulsions at up to 100 microg/mouse. In dog ICV injection studies, imipenem produced generalized seizure discharge with clonic convulsions at 100 microg/dog. Meropenem also produced spikes or seizure discharges at 100, 300 and 1,000 microg/dog. However, doripenem had no effects on the EEG and behavior in dogs at any doses. In in vitro binding studies, imipenem, panipenem, cefazolin and meropenem inhibited [(3)H]muscimol binding to the GABA(A) receptor in mouse brain homogenates while doripenem did not cause any inhibition at up to 10mM. In addition, doripenem had no influence on the anti-convulsant actions of valproic acid in the PTZ- or bicuculine-induced convulsive model. These results clearly indicate that doripenem has no convulsive activity, suggesting that its neurotoxicity may be negligible in clinical use.

Alanine↗
PubMed1984

Central nervous effects of the convulsant protein canatoxin.

Some pharmacological-toxicological effects of canatoxin, a toxic protein purified from the seeds of Canavalia ensiformis have been studied in mice and rats. The most obvious effect, a lethal tonic convulsion, was generally produced 10-15 min. after intravenous injection of 2-3 mg/kg of the highly purified protein (mol. wt. 88,000). After intraperitoneal, intramuscular or subcutaneous administration the convulsion produced by the same toxin dosis occurred within 24 hours. A spinal transection at the midthoracic level did not abolish the convulsions of the hindlimbs while destruction of the medulla below this level completely blocked the convulsions of the hindlimbs. The convulsions of the head and forelimbs were unaffected by these surgical pretreatments. The toxic protein did neither affect the isolated skeletal muscle nor did it potentiate nerve impulse induced contractions. The convulsive effect of canatoxin was potentiated by reserpine and attenuated by phenobarbital, diazepam, methenesine and also by haloperidol and spiroperidol. The total concentration of brain and spinal cord neurotransmitters seemed to remain unchanged after subconvulsive and convulsive doses of canatoxin. In the conscious rat the toxic protein did not change the blood pressure except for a shortlasting hypertensive response observed immediately before the onset of the convulsions. The heart frequency was lowered at subconvulsive and convulsive doses but no effect was seen on the frequency of the rat isolated right atria exposed to high doses of canatoxin. The body temperature was lowered by a convulsive doses of the toxic protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

Convulsive syncope in blood donors.

Syncope with and without convulsion was studied in unselected blood donors in a community blood center. Convulsive syncope occurred in 0.03% of all blood donors and was more commonly observed when nursing personnel were alerted to its possible occurrence. It was more common in men. Although tonic extensor spasm was the most common convwithout convulsion was studied in unselected blood donors in a community blood center. Convulsive syncope occurred in 0.03% of all blood donors and was more commonly observed when nursing personnel were alerted to its possible occurrence. It was more common in men. Although tonic extensor spasm was the most common convwithout convulsion was studied in unselected blood donors in a community blood center. Convulsive syncope occurred in 0.03% of all blood donors and was more commonly observed when nursing personnel were alerted to its possible occurrence. It was more common in men. Although tonic extensor spasm was the most common convulsive movement, other complex convulsive phenomena occurred, some simulating epileptic seizure. No statistical difference in changes of pulse or blood pressure was found between subjects with convulsive versus nonconvulsive syncope. Similarly, no difference was found between subjects with tonic spasm and those with other convulsive phenomena, nor between those with "early" and those with "delayed" reactions. Marked individual variation may exist in the susceptibility of the central nervous system to ischemia. Some individuals appear to be predisposed to development of seizures in situations of global cerebral ischemia such as occur in hypotension and bradycardia.

Blood Donors↗
PubMed1980

Production of convulsions in mice by the combination of methionine and homocysteine.

Behavioral effects of methionine have been attributed to either increased availability of methyl groups for the production of methylated amines or accumulation of convulsive metabolites. If the second hypothesis is correct, methionine would be expected to have convulsive properties either by itself or in combination with subconvulsive dosages of other known convulsants. Methionine alone did not induce convulsions when administered by various routes in dosages of 250--13,000 mg/kg, although larger doses of methionine (500--4,000 mg/kg) decreased behavioral activity. However, methionine pretreatment (125--1,000 mg/kg) markedly enhanced convulsions in animals challenaed with subconvulsine dosages of homocysteine. Pentylenetetrazol was less effective than homocysteine in promoting convulsions in methionine-pretreated animals. Although the convulsive effects of methionine were not shared by other natural amino acids (glutamate, asparate, cysteine, tryptophan, and others), ethionine enhanced homocysteine-induced convulsions almost as effectively as did methionine. Methionine thus promotes convulsions under certain conditions, plerhaps due to an accumulation of homocysteine or of other metabolites with convulsive properties.U

Animals↗
PubMed1981

Facilitation of kindling by convulsions induced by cocaine or lidocaine but not pentylenetetrazol.

The effect of drug-induced convulsions on kindling was studied in male Long-Evans rats. In Experiment 1 rats experienced a single convulsion induced by the intravenous infusion of cocaine, lidocaine, or pentylenetetrazol (PTZ), or received a control infusion of saline. Beginning eight days later all animals were kindled by daily stimulation of the olfactory bulb. Animals which had been convulsed by cocaine or lidocaine kindled significantly faster than either saline controls or PTZ-convulsed animals, which did not differ significantly. Experiment 2 was conducted to determine if an effect of PTZ on kindling could be obtained with repeated convulsions. Rats experienced three convulsions induced by cocaine or PTZ at 72 hr intervals, or control infusions of saline. Kindling began on the eighth day after the last infusion. Cocaine-convulsed animals again kindled significantly faster than saline or PTZ-convulsed animals, which did not differ significantly. The cocaine animals also had significantly longer afterdischarges than the saline group at the end of kindling and when stimulated again 21 days after kindling was completed. These results suggest that the facilitating effect of cocaine-induced convulsions is not a general property of all convulsants but is a more specific effect which is apparently shared by other local anesthetics.

Animals↗
PubMedDate not supplied

alpha-Tocopherol protects against pentylenetetrazol- and methylmalonate-induced convulsions.

Increased excitatory amino acid transmission and decreased GABAergic inhibitory responses seem to be important mechanisms in the genesis of convulsions, where reactive oxygen species (ROS) have recently been suggested to play a critical role. Therefore, administration of antioxidants may be potentially beneficial for the treatment of convulsive states. In the current study we investigated the effect of the systemic Vitamin E administration, an antioxidant, on the convulsions and oxidative damage induced by two convulsant agents with different mechanisms of action: methylmalonic acid (MMA), which induces convulsions through energy depletion and secondary activation of glutamatergic mechanisms and ROS production and pentylenetetrazol (PTZ), which is a chemical convulsant that causes convulsions by blocking the GABAA receptor-coupled chloride ionophore. Adult male Wistar rats (270-300 g) were injected with vehicle (5% Tween 80 in 0.9% NaCl; 1 ml/kg, i.p.) or alpha-tocopherol (25, 75 or 225 mg/kg, i.p.), once a day for 7 days. On the seventh day of antioxidant treatment, the animals were injected with the antioxidant (or vehicle) and, 30 min later, they were intrastriatally injected with NaCl (9 micromol/2 microl) or with MMA (6 micromol/2 microl) or PTZ (3.26 mmicromol/2 microl). The animals were observed for the appearance of convulsive behavior and the striatal content of thiobarbituric acid-reactive substances (TBARS) and total protein carbonylation were determined. Intrastriatal injection of increasing amounts of PTZ and of MMA caused the appearance of convulsive behavior. PTZ- and MMA-induced convulsions, TBARS production and total protein carbonylation were attenuated by alpha-tocopherol in a dose-dependent manner.

Analysis of Variance↗
PubMed2000

Molecular serotonergic mechanisms appear to mediate genetic sensitivity to cocaine-induced convulsions.

Cocaine-induced convulsions appear to be mediated by serotonin (5-HT) neurotransmission, acting primarily at 5-HT(2) receptors. However, this effect of cocaine is attenuated by cocaine binding at sigma and muscarinic M(1) and M(2) sites. This study examined whether the aforementioned neural sites mediate the nearly two-fold difference in sensitivity to cocaine-induced convulsions across C57BL/6J (6J) and C57BL/6ByJ (6ByJ) mice. Experiment 1 compared 5-HT transporter densities across several brain regions of 6J and 6ByJ mice and cocaine-induced convulsions following pretreatment with the 5-HT reuptake inhibitor fluoxetine. Experiment 2 compared 5-HT(2) receptor densities across these mice and cocaine-induced convulsions following pretreatment with the 5-HT(2) antagonist cinanserin. There were no differences in 5-HT transporter densities, however, fluoxetine produced a greater facilitation of cocaine-induced convulsions in 6ByJ relative to 6J mice, suggesting that sensitivity to convulsions is mediated postsynaptically. Indeed, 5-HT(2) density was higher in 6ByJ relative to 6J mice in the amygdaloid ridge, hypothalamus, and midbrain. In addition, cinanserin attenuated convulsions more potently in 6J relative to 6ByJ mice. There were no differences in the densities or affinities of 5-HT(1), muscarinic, or sigma receptors across these strains, suggesting that density of these latter sites does not mediate genetic sensitivity to cocaine-induced convulsions. Since 6ByJ mice are less sensitive to convulsions despite the fact that they have more 5-HT(2) receptors, we hypothesized that these mice may exhibit a weaker linkage of 5-HT(2) sites to their second-messenger system relative to 6J mice. However, in experiment 3 we demonstrated that 5-HT(2)-receptor mediated phosphoinositide hydrolysis was higher in 6ByJ relative to 6J mice in the same regions also displaying higher 5-HT(2) densities. This study suggests that 5-HT(2) receptors mediate genetic sensitivity to cocaine-induced convulsions, further supporting the role of these sites in mediating this toxic effect of cocaine.

Animals↗
PubMed1995

Mortality related to convulsive disorders in a developing country in Asia: trends over 20 years.

The cause of death as recorded in 37125 death certificates (DC) issued in the Kandy District over 20 years at five-year intervals beginning 1967 was analysed to determine the trends in mortality caused by convulsive disorders in the community. Convulsions accounted for 881 (23.7/1000) deaths, the highest number being in infancy (35.8%). A slight male preponderance of 51.5% was observed. Most of the deaths occurred in the periphery (51.6%) and in the tea estates (36.3%) as opposed to town area (12.0%). "Febrile convulsions' was the most common diagnosis in 396 (44.9%) deaths. "Convulsions' which included neonatal and infantile convulsions accounted for 186 (21.1%) deaths. Other causes included chest complications (60, 6.8%), drowning (28, 3.2%), asphyxia (20, 2.3%), status epilepticus (19, 2.2%), burns (7, 0.8%), and poisoning (2, 0.2%). The proportion of deaths due to convulsive disorders showed a decrease from 37.28/1000 in 1967 to 9.55/1000 in 1987, which was most evident in the periphery, from 60.49/1000 to 13.19/1000. This parallelled a drop in the proportion of deaths attributed to "febrile convulsions' and "convulsions'. The study shows the need to educate the public about first-aid and the subsequent management of convulsions, especially in childhood. Health personnel in developing countries should consider it mandatory to make a specific diagnosis in children who present as febrile convulsions. Appropriate antiepileptic medication and compliance can prevent death due to status epilepticus and injuries associated with seizures.

Adolescent↗
PubMed1995

Febrile convulsions. Is seizure duration the most important predictor of temporal lobe epilepsy?

The association between febrile convulsions and temporal lobe epilepsy is recognized, but is controversial. We attempted to clarify this and to determine which attributes of febrile convulsions were associated with temporal lobe epilepsy. During a study of genetic linkage in febrile convulsions, families with at least four affected members were identified. Clinical features of febrile seizures and EEG findings were compared in those who did and did not develop later afebrile seizures. In six selected families, 59 family members had febrile convulsions. Temporal lobe epilepsy developed in eight of these, whereas only one of 213 family members with no febrile convulsions had temporal lobe epilepsy (P < 0.0001). The mean durations of febrile convulsions in those with and without progression to temporal lobe epilepsy were 100 and 9 min, respectively (P = 0.02). Five patients had temporal lobectomies, which revealed mesial temporal sclerosis in all cases. Four patients who developed other types of epilepsy had a mean duration of febrile convulsions of 90 min. The total number, the maximum number in any one day, and the age at onset of febrile convulsions did not differ significantly between groups. Only two patients had neurological deficits, both of whom subsequently had nonlocalizable partial epilepsy. In these families, selected to reduce genetic and phenotypic heterogeneity, a strong association was evident between febrile convulsions and temporal lobe epilepsy with mesial temporal sclerosis. A prolonged febrile convulsion was the most important determinant of this association.

Adult↗