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PubMed2003

Increased frequency of interleukin-1beta-511T allele in patients with temporal lobe epilepsy, hippocampal sclerosis, and prolonged febrile convulsion.

PURPOSE: To confirm the high frequency of interleukin (IL)-1beta-511T allele occurrence in patients with temporal lobe epilepsy (TLE) and hippocampal sclerosis (HS), with special attention given to the impact of prolonged febrile convulsions (PFCs) on IL-1beta genotype distribution. METHODS: Patients with evidence of unilateral HS on magnetic resonance (MR) images were chosen as study subjects (TLE+HS; n = 66). Other patients with essentially normal MRI findings or only foreign tissue (TLE without HS; TLE-HS; n = 64), and those with symptomatic localization-related epilepsy but without TLE (SLE; n = 89) were selected as disease controls. A single base pair polymorphism at position 2511 in the promoter region of the IL-1beta gene was analyzed. RESULTS: The distribution of IL-1beta-511 genotypes as well as allele frequency was significantly different between TLE+HS patients and controls. In contrast, no difference was found between TLE-HS patients and controls or between SLE patients and controls. Further, in the group of patients with TLE+HS, the frequency of the IL-1beta-511T allele tended to increase as a function of febrile convulsions [0.531 without either PFC or simple febrile convulsion (SFC); 0.633 with SFC; 0.686 with PFC]. Although no statistically significant difference was noted between patients without PFC and the controls, a chi2 analysis of allele distribution revealed a significant difference between those with PFC and the controls. CONCLUSIONS: PFC proved to be a potent determinant of IL-1beta-511T allele frequency; thus a discrepancy of PFC incidence should be considered an explanation of recent conflicting results regarding the association between the gene polymorphisms of IL-1beta-511 and TLE+HS.

Adult↗
PubMed2000

Provocation of non-convulsive status epilepticus by tiagabine in three adolescent patients.

Three girls, two aged 12 years and one aged 17 years with refractory localization-related epilepsy were treated on an add-on basis with tiagabine. At dosages 22.5-30 mg/day (0.45-0.57 mg/kg/day) longstanding non-convulsive status epilepticus was noted in all three patients. The events of non-convulsive status epilepticus subsided following reduction in tiagabine dosages. In two cases, tiagabine was withdrawn, whereas it was continued at a lower dosage in one case. This is the first report of non-convulsive status epilepticus provoked by tiagabine in adolescent patients.

Adolescent↗
PubMed1991

Misuse of zopiclone and convulsions during withdrawal.

It has been documented that benzodiazepines have the potential to cause dependence and withdrawal reactions, including convulsions. However, the available data concerning zopiclone, a nonbenzodiazepine hypnotic, are insufficient. The present study describes the case of a 36-year-old man who repeatedly misused zopiclone, in daily doses of 60-90 mg. Furthermore, the patient suffered from convulsion on two occasions following abrupt withdrawal of zopiclone. The concomitant use of alcohol, trimipramine, and promazine may have contributed to the development of convulsions. It is concluded that zopiclone may cause problems associated with misuse and withdrawal reactions similar to those of benzodiazepines.

Adult↗
PubMed1984

Prevention of recurrent febrile convulsions--a randomized therapeutic assay: sodium valproate, phenobarbital and placebo.

The purpose of this study was to compare three different modes of treatment in the prevention of relapses of febrile convulsions (Phenobarbital = PH, Sodium Valproate = SV, Placebo = PO) in a randomized therapeutic trial. The patients included in the study had shown their first generalized convulsive seizure during a bout of fever (greater than or equal to 38.5 degrees C) and were aged between 6 months and 4 years. They were subsequently followed up as outpatients, and Phenobarbital and sodium valproate levels were measured regularly to ascertain compliance with the treatment and to adjust the dosage accordingly. The patients' families were questioned with respect to the occurrence of feverish bouts and convulsive seizures during the interval between visits, as well as possible adverse reactions. An EEG was carried out yearly. Results were as follows: - 69 patients - 35 boys and 34 girls - with an average age of 24 months were divided into 3 groups according to treatment: 21 cases on PH, 22 cases on SV, and 26 cases on PO. - they were followed up for an average duration of 21 months. - the average number of feverish bouts per child and per year was evaluated at 2.5, no statistically significant difference being noticeable between the various modes of prophylaxis. - 15 relapses of febrile seizures were noted in 14 children, over an average duration of 23 months; on average, relapses occurred after 9 months; among the 14 children who had relapsed, one had been treated with SV, 4 with PH and 9 with PO, leading to estimated relapse rates of 4%, 19%, and 35% respectively. There is a statistically significant difference in the relapse rates between the treated groups (SV and PH) and the Placebo group, and a particularly significant difference between Sodium Valproate and Placebo.(ABSTRACT TRUNCATED AT 250 WORDS)

Child, Preschool↗
PubMed1981

Increased nucleotide catabolism after cerebral convulsions.

Cardiazol induced seizures in rabbits showed that the highest oxypurine concentrations can be detected in the CSF 1 hour after the convulsions. There is a sharp decline continuing until the third hour. After that the CSF values remain nearly constant until the 24th hour being about ten times higher than in the controls. There is a good correlation of these results obtained through the densitometric thin-layer, enzymatic-oxymetric, and HPLC-methods. Creatinine and potassium were raised only during the first two hours postconvulsively. Uracil appeared in the CSF slightly higher at the 1 hour and at the 12 and 24 hour values. A parallel increase of the oxypurine and creatinine concentrations was found in the serum between 30 to 120 minutes postconvulsively. After that the raised serum values decreased slowly to the initial values. CSF samples were examined in 31 children postconvulsively: Hypoxanthine was found to be raised in 8 of 12 patients with severe grand mal seizures, 1 of 6 patients with hypsarrhythmia, 1 of 8 patients with short seizures (less than 2 min) and in all 5 patients with petit mal status. In contrast to these groups the hypoxanthine concentrations was raised only in 2 of 20 children with aseptic meningitis. The difference between the group of children with convulsions and the group of children with aseptic meningitis is significant (p less than 0.005). Also, the frequency of raised uric acid concentration is higher in the group of children with convulsions (70%) than in the group of children with aseptic meningitis (40%); (p less than 0.05).

Animals↗
PubMed1993

Molybdenum-cofactor deficiency: an easily missed cause of neonatal convulsions.

Intractable seizures in the neonatal period may be caused by molybdenum-cofactor deficiency, an inborn error which combines the deficiencies of sulphite oxidase and xanthine dehydrogenase. The neurological symptoms of molybdenum cofactor and isolated sulphite oxidase deficiencies are identical. Two new cases are reported, and the literature on neonatal convulsions due to molybdenum-cofactor and sulphite deficiencies is reviewed. Because of the high incidence of neonatal convulsions a search for this deficiency is advocated in each case of unexplained refractory neonatal convulsions. Diagnosis may be missed or delayed on standard metabolic screening for several reasons discussed. By simply using a sulphite strip test in a fresh urine sample an indication for the defect can be obtained. Antenatal diagnosis can be performed by assay of sulphite oxidase activity in a chorionic villus sample.

Amino Acids↗
PubMed1970

Retrograde amnesia gradients by subconvulsive and high convulsive transcranial currents in chicks.

Either a subconvulsive or a high convulsive current was delivered transcranially at various intervals after a learning trial to independent groups of newly hatched chicks. The one-trial learning involves suppression of the chicks' predilection to peck at a small shiny bead. The effect of current on retention was measured one day later. Results indicate a current-sensitive memory consolidation period of about 30 seconds that cannot be appreciably prolonged by a tenfold increase in current intensity and a simultaneous twofold increase in current duration. On the other hand, at comparable trial-to-current intervals within this brief consolidation period, more retention deficit was caused by the higher current. Beyond this critical period, both currents still effected some retention deficit, but it did not seem to vary with the trial-to-current interval from one minute to 24 hours. Overt muscular convulsion was unnecessary for the retrograde amnesia effect. The subconvulsive current may be a more pure agent for consolidation studies because the high, convulsive current may affect test performance in ways other than disrupting the consolidation processes.

Amnesia↗
PubMed2003

Hydrocortisone-induced convulsions.

Glucocorticoids may indirectly cause convulsions by the induction of electrolytes abnormalities, severe hypertension, or severe hyperglycemia. These agents may rarely cause convulsions by a direct toxicity to the central nervous system (CNS). We describe a 23-yr-old patient with Crohn's disease in whom generalized convulsions developed on two occasions while receiving intravenous hydrocortisone.

Adult↗
PubMed1997

Familial infantile convulsions and paroxysmal choreoathetosis: a new neurological syndrome linked to the pericentromeric region of human chromosome 16.

Benign infantile familial convulsions is an autosomal dominant disorder characterized by nonfebrile seizures, with the first attack occurring at age 3-12 mo. It is one of the rare forms of epilepsy that are inherited as monogenic Mendelian traits, thus providing a powerful tool for mapping genes involved in epileptic syndromes. Paroxysmal choreoathetosis is an involuntary-movement disorder characterized by attacks that occur spontaneously or are induced by a variety of stimuli. Classification is still elusive, and the epileptic nature of this movement disorder has long been discussed and remains controversial. We have studied four families from northwestern France in which benign infantile convulsions was inherited as an autosomal dominant trait together with variably expressed paroxysmal choreoathetosis. The human genome was screened with microsatellite markers regularly spaced, and strong evidence of linkage for the disease gene was obtained in the pericentromeric region of chromosome 16, with a maximum two-point LOD score, for D16S3133, of 6.76 at a recombination fraction of 0. Critical recombinants narrowed the region of interest to a 10-cM interval around the centromere. Our study provides the first genetic evidence for a common basis of convulsive and choreoathetotic disorders and will help in the understanding and classification of paroxysmal neurological syndromes.

Adult↗
PubMed1984

The biphasic pattern of the convulsive property of enflurane in cats.

The nature of the epileptoid state produced by enflurane was examined in the concentration range 2-5% in cats. A biphasic pattern in the convulsant property was revealed. The ease of induction of seizure by repetitive peripheral stimulation, the duration of seizures, and the activation of reticular neuronal firing during seizure activity showed peak values between 3 and 4%, whereas the values were significantly lower both above and below this range. The amplitudes of the somato-sensory evoked potential also showed a biphasic pattern which correlated well with the severity of the epileptoid state as judged by the aforementioned indices. These findings, when compared with evidence on the actions of other convulsant drugs, and with the known depressant actions of enflurane, suggest a combination of depressant and convulsant properties, the balance of which varies depending on the depth of anaesthesia.

Animals↗
PubMed2003

Hippocampal abnormalities after prolonged febrile convulsion: a longitudinal MRI study.

Mesial temporal sclerosis (MTS) is the most common lesion in patients who require epilepsy surgery, and approximately 50% of patients with MTS have a history of prolonged febrile convulsion (PFC) in childhood. The latter led to the hypothesis that convulsive status epilepticus, including PFC, can cause MTS. Our recently published data on children investigated within 5 days of a PFC showed that children investigated by MRI within 48 h of a PFC had large hippocampal volumes and prolongation of T2 relaxation time. Patients investigated >48 h from a PFC had large hippocampal volumes and normal T2 relaxation time. These data are strongly suggestive of hippocampal oedema that is resolving within 5 days of a PFC, but do not exclude the possibility of a pre-existing hippocampal lesion. Fourteen children from the original study had follow-up investigations carried out 4-8 months after the acute investigations. Of the 14 patients, four have had further seizures. Two had short febrile convulsions, one had PFC and one had non-febrile seizures. There was a significant reduction in hippocampal volume and T2 relaxation time between the first and second investigations, and there is now no difference in hippocampal volume or T2 relaxation time in patients compared with a control population. Moreover, there is a significant increase in hippocampal volume asymmetry in patients at follow-up when compared with initial data. Five out of 14 patients had asymmetry outside the 95th percentile for control subjects and, of these, three had one hippocampal volume outside the lower 95% prediction limit for control subjects. A reduction in hippocampal volume or T2 relaxation time, into or below the normal range between the first and second scans, indicates that the earlier findings are temporary and are strongly suggestive of hippocampal oedema as the abnormality in the initial investigations. The change in hippocampal symmetry in the patient group is consistent with injury and neuronal loss associated with a PFC, especially in the three individuals who now have a single small hippocampus. However, as there is no T2 relaxation time abnormality, the hippocampi do not meet the criteria for MTS. There may be a lag period of several years between a PFC and the onset of epilepsy, and therefore some of these patients may be developing MTS. Alternatively, the asymmetry could represent return (post-acute oedema) to a pre-existing hippocampal abnormality similar to that identified in family members of patients with MTS and a history of PFC.

Brain Edema↗
PubMed2002

Convulsive syncope associated with acupuncture.

Syncope is a rare but known reaction to acupuncture; however, convulsive syncope has never been previously documented as a reaction to acupuncture. This case report describes an episode of convulsive syncope, characterized by irregular clonic-tonic movements while the patient was unconscious. The episode occurred immediately after the insertion of acupuncture needles into the bilateral ST-36 acupuncture point. Here we discuss the presentation, possible causes, and prevention of convulsive syncope.

Acupuncture↗
PubMed2000

Evidence for GABA(A) receptor agonistic properties of ketamine: convulsive and anesthetic behavioral models in mice.

UNLABELLED: We examined the potentiation by ketamine of the gamma-aminobutyric acid(A) (GABA(A)) receptor function using convulsive and anesthetic behavioral models in adult male ddY mice. General anesthetic potencies were evaluated by a rating scale, which provided the data for anesthetic scores, loss of righting reflex, duration, and recovery time. All drugs were administered intraperitoneally. Small subanesthetic doses of ketamine did inhibit tonic seizures induced by a large dose of the GABA(A) receptor antagonist bicuculline (8 mg/kg). The 50% effective dose value was 15 (95% confidence limits 10-22) mg/kg. Even large anesthetic doses (100-150 mg/kg) did not suppress clonic seizures in 50% of the animals. The GABA(A) receptor agonist, muscimol (0.32-1.12 mg/kg), potentiated ketamine-induced anesthesia in a dose-dependent fashion (P < 0.05). Similarly, the benzodiazepine receptor agonist, diazepam (1-3 mg/kg), augmented ketamine anesthesia in a dose-dependent manner (P < 0.05). Bicuculline (2-5 mg/kg) dose-dependently antagonized ketamine-induced anesthesia (P < 0.05). Neither the benzodiazepine receptor antagonist, flumazenil (2-20 mg/kg), nor the GABA synthesis inhibitor, L-allylglycine (200 mg/kg), affected the anesthetic action of ketamine. These results suggest that ketamine has GABA(A) receptor agonistic properties and that ketamine-induced anesthesia is mediated, at least in part, by GABA(A) receptors. IMPLICATIONS: We examined the potentiation by ketamine of the gamma-aminobutyric acid(A) receptor function using convulsive and anesthetic behavioral models in mice. Subanesthetic doses of ketamine-inhibited tonic convulsions induced by the gamma-aminobutyric acid(A) receptor antagonist bicuculline. The gamma-aminobutyric acid(A) receptor agonist, muscimol, potentiated ketamine-induced anesthesia. Bicuculline antagonized ketamine anesthesia, but the benzodiazepine receptor antagonist, flumazenil, and the gamma-aminobutyric acid synthesis inhibitor, L-allyglycine, did not. The effects of ketamine on the gamma-aminobutyric acid(A) receptors appear to correlate with its anesthetic actions.

Allylglycine↗
PubMed1985

Effect of anesthetics and a convulsant on normal and mutant Caenorhabditis elegans.

The authors have developed a method for studying the action of volatile anesthetics in Caenorhabditis elegans (C.e.), a free living nematode. C.e. appears to be a useful model for the study of the influence of genetics on susceptibility to anesthetics. This worm has a small, completely defined nervous system, easily manipulated genetics, and a large number of nervous system mutants. Under normal conditions C.e. moves almost constantly. When exposed to anesthetics there is an initial phase of increased locomotion, followed by uncoordinated motion that progresses to immobility. Motion returns quickly when the nematodes are removed from the anesthetic. The authors called loss of locomotion "anesthesia." The ED50S of various anesthetics with C.e. are as follows: methoxyflurane 0.45%, chloroform 1.25%, halothane 2.7%, enflurane 4.2%, isoflurane 5.6%, fluroxene 9.9%. The authors also studied the action of a convulsant, flurothyl, on C.e. Flurothyl has anesthetizing properties in these animals with an ED50 of 8.1%. No convulsant activity was noted. However, mixtures of halothane and flurothyl were antagonistic in their effects, while halothane and enflurane were additive. Furthermore, the authors isolated a mutant strain (HS1) of C.e. that shows altered responses to several anesthetics and a convulsant. HS1 is uncoordinated when not exposed to anesthetics. Like the normal strain (N2) HS1 loses mobility when exposed to anesthetics. The ED50S for various anesthetics in HS1 were as follows: methoxyflurane 0.04%, chloroform 0.52%, halothane 0.85%, isoflurane 4.9%, enflurane 6.0%, fluroxene 10.9%.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics↗
PubMed1999

Febrile convulsions and mesial temporal sclerosis.

Patients with intractable temporal lobe epilepsy and mesial temporal sclerosis often have histories of severe febrile convulsions as infants. Diagnostic advances made possible by magnetic resonance imaging have shown that very prolonged febrile convulsions may produce hippocampal injury and that focal cortical dysgenesis may play a role in the etiology of febrile convulsions, mesial temporal sclerosis, and temporal lobe epilepsy.

Brain Damage, Chronic↗
PubMed2004

Lipopolysaccharide-induced febrile convulsions in the rat: short-term sequelae.

PURPOSE: Febrile convulsions (FCs) occur in children as a result of fever. The mechanisms involved in the genesis of FCs and their long-term consequences on brain development remain unclear. We have developed a model of FC, by using fever as a parameter, to test the hypothesis that fever can lower seizure threshold and to examine the neurologic sequelae of FCs. METHODS: Fourteen-day-old rat pups equipped with body-temperature telemetry devices exhibited approximately 1.5 degrees C fevers after lipopolysaccharide (Escherichia coli, 200 microg/kg). During such fevers, concurrently administered doses of kainic acid that are normally subconvulsant were used to induce convulsions with fever. Animals were then killed at varying times for pathological and immunohistochemical studies. RESULTS: The pairing of lipopolysaccharide and subconvulsant kainic acid resulted in convulsions in approximately 50% of febrile animals, with very low mortality. To study the neural correlates of these FCs, we used fos immunohistochemistry and found that animals with FCs had fos-positive immunoreactivity in brain regions involved in seizures. After a period of 72 h, we also examined brains for pathologic changes and found no differences among our groups. CONCLUSIONS: Our data indicate that a neuroimmune challenge and its accompanying fever reduce the seizure threshold. Furthermore, the FCs induced by fever in this model do not have short-term adverse effects on the brain. In addition, this model, by incorporating physiologic fever, may be useful for examining the role of fever and its constituent mediators in the genesis of FCs.

Animals↗
PubMed1983

Antidepressant drugs, convulsions and epilepsy.

1 Evidence concerning the convulsant effects of non-monoamine oxidase inhibitor antidepressant drugs has been reviewed. 2 Mianserin is convulsant in therapeutic doses but seizures have not been reported following overdose. 3 The convulsant effects of mianserin are probably no greater than for other non-monoamine oxidase inhibitor antidepressant drugs. 4 Enzyme-inducing anti-epileptic drugs can reduce the peak plasma concentration of mianserin and shorten its elimination half-life, probably by inducing its metabolism.

Antidepressive Agents↗
PubMedDate not supplied

Modification by GABA-ergic agents and clonidine of morphine-induced convulsions and toxicity in rats.

Intracerebroventricular (i.c.v.) administration of morphine produced dose-dependent behavioural changes in rats, the highest dose producing violent tonic convulsions. Naloxone (up to 10 mg/kg i.p., or 100 micrograms i.c.v.) failed to reverse morphine-induced toxicity. The conventional anticonvulsant drugs also failed to offer protection to morphine-induced seizures. GABA-ergic substances, GABA, piracetam and diazepam, on the other hand, protected the animals against morphine-induced convulsions and toxicity. Similarly, clonidine pretreatment also had a protective action against morphine-induced convulsions.

Animals↗