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PubMed1984

Epidemiology of febrile and afebrile convulsions in children in Japan.

Prevalence rates in all 3-year-old children in Fuchu/Tokyo, for a 6-year survey from 1974 to 1980 (total number examined, 17,044), were 8.3% for febrile convulsion and 0.9% for afebrile convulsion. The figures in boys were higher than in girls for febrile convulsion (9.0%:7.5%), but for afebrile convulsion (0.9%:0.9%). Prevalence in a Miyake Island survey for 10 years, from 1973 to 1982 (total number examined, 543) was 9.9% for febrile and 0.4% for afebrile convulsion. Correlations among prevalence of febrile convulsion, epilepsy, and epileptic EEG abnormality in healthy children were inconsistent in geographically isolated villages identified in Miyake Island.

Child, Preschool↗
PubMed2004

Vasodilation increases the threshold for bupivacaine-induced convulsions in rats.

UNLABELLED: Bupivacaine affects the vascular resistance by peripheral and central nervous system (CNS) mechanisms. As vasoconstrictors increase the CNS toxicity of IV bupivacaine, vasodilators may decrease its CNS toxicity. We examined the hypothesis that vasodilators decrease the CNS toxicity of bupivacaine in awake, spontaneously breathing rats. Male Sprague-Dawley rats were randomly divided into control (C), nicardipine (N), and phentolamine (P) groups (n = 12 in each group). Racemic bupivacaine was administered IV at 1 mg/kg/min until tonic/clonic convulsions occurred. Saline, nicardipine (0.4 microg/min), and phentolamine (10 microg/min within 5 min, 50 microg/min thereafter) were simultaneously administered with bupivacaine in groups C, N, and P, respectively. Mean arterial blood pressure was significantly increased by infusion of bupivacaine in group C and was maintained at baseline levels before the onset of convulsions in groups N and P. The convulsive dose of bupivacaine in group C was 5.8 +/- 1.5 mg/kg, but was significantly larger in groups N and P (7.6 +/- 1.5 and 8.1 +/- 1.1 mg/kg, P = 0.02 and 0.001, respectively). However, there were no differences in total or protein-unbound plasma concentration of bupivacaine or in concentration of bupivacaine in the brain at the onset of convulsions among the 3 groups. We conclude that nicardipine and phentolamine increase the cumulative dose but do not affect the threshold plasma or brain concentrations required for bupivacaine-induced convulsions. IMPLICATIONS: Bupivacaine, a long-acting local anesthetic, induces central nervous system toxicity when its plasma concentration is increased. Nicardipine and phentolamine increased the cumulative dose but did not affect the threshold plasma concentrations, required for bupivacaine-induced convulsions, suggesting that both nicardipine and phentolamine inhibited the increase in the plasma concentration of bupivacaine by inducing peripheral vasodilation.

Adrenergic alpha-Antagonists↗
PubMed1991

Changes in convulsion susceptibility of lidocaine by alteration of brain catecholaminergic functions.

Influences of the manipulation of brain catecholaminergic neuronal activity on the incidence of lidocaine-induced convulsions in mice were studied and compared with those of pentylenetetrazol (PTZ)-induced convulsions. alpha-Methyl-p-tyrosine (alpha-MPT) decreased both brain noradrenaline (NA) and dopamine (DA) levels, and disulfiram decreased the NA level and increased the DA level. The incidence of lidocaine-induced convulsions was decreased by treatments with alpha-MPT and disulfiram, while that of PTZ was increased by either treatment. The incidence of lidocaine-induced convulsions was slightly, but not significantly increased by L-dihydroxyphenylalanine (L-DOPA), although the brain DA level was increased by L-DOPA. Methamphetamine and desipramine increased the incidences of lidocaine-induced convulsions. These results may suggest that brain catecholaminergic neurons, differing from their role in inhibiting control of PTZ-seizure, act to facilitate lidocaine-induced convulsions.

Animals↗
PubMed1992

Tolerance to the convulsions induced by daily nicotine treatment in rats.

Development of tolerance to the nicotine-induced convulsions in rats was examined. Acute intraperitoneal (i.p.) administration of nicotine (2.5, 3.75 and 5 mg/kg) produced convulsions in a dose-dependent manner. Mecamylamine (1 mg/kg, i.p.) antagonized the convulsions, but hexamethonium (5 mg/kg, i.p.) did not modify them. Daily nicotine administration (2.5, 3.75 and 5 mg/kg, i.p.) once a day for 6 days developed tolerance to the convulsions induced by nicotine. After the daily administrations of nicotine for 6 days, the effects of a challenge administration of nicotine (2 mg/kg) on the nicotine-induced convulsions were tested on the 7th-day. Further tolerances were also developed by the 7th-day challenge administration. After the 7th-day test, nicotine levels of the brain and blood 15 min after the challenge injection were measured. With nicotine (5 mg/kg once a day)-treatment, nicotine levels of all the brain regions were increased. In contrast, a similar challenge injection had no effect on blood nicotine level. These results indicate that the development of tolerance to the nicotine-induced convulsions is produced relatively earlier and day by day by daily administrations to rats, which is closely related with the increase in brain nicotine level.

Animals↗
PubMed1975

An unexpected incidence of convulsive attack in male mice after long-term isolated condition.

Unexpected convulsive attacks were observed in male dd-D mice which were reared for a long-term experiment. After three months from the onset of rearing, some of mice showed convulsive attacks when they were handled in such routine laboratory procedures as weighing, clearing of cage and feeding. The convulsive attack was observed only among the mice being reared individually in each of sections of cage and did not occur in the mice which had been reared as a colony. The incidence rate of convulsive attack increased as the rearing period was prolonged. Our finding was similar to King and coworkers' report (1955) in which convulsions were observed in the singly housed C3H mice. The one thing particular in our observation was the difference of incidence rate according to the extent of isolation, i.e., the higher rate was observed on the condition of mice without other mice in the neighbouring sections than those with neighbouring mate. The neighbouring mate acted some roles to change susceptibility to convulsive attack, even though separated by a sheet of wire-netting.

Animals↗
PubMed1978

Relationship between gamma-aminobutyric acid metabolism and antivitamin B6-induced convulsions.

The correlation between the gamma-aminobutyric acid (GABA) metabolism and convulsions by some vitamin B6 antagonists, DL-penicillamine (PeA), hydrazine (Hyd), thiosemicarbazide (TSC) were investigated. Glutamic acid decarboxylase (GAD) and gamma-aminobutyric acid transaminase (GABA-T) activities were inhibited during convulsions by three antagonists, and GABA content was not changed by PeA, increased by Hyd and decreased by TSC in mice whole brain. In subcellular fractions of brain, GAD activity was inhibited and GABA content decreased in synaptosomes during convulsions by the above three drugs. Aminooxyacetic acid (AOAA), a potent GABA-elevating agent, showed an anticonvulsant property against convulsions by TSC for several hours after the injection of AOAA, but lost this property 16hr after treatment. During the convulsions by TSC 16hr after the AOAA-pretreatment, the GABA content in synaptosomes was less than that from the group treated with AOAA alone, though its GABA level was higher than the normal level. From the above results, the GABA content and GAD activity in synaptosomes might be deeply associated with convulsions by B6 antagonists.

4-Aminobutyrate Transaminase↗
PubMed1995

Structural features resulting in convulsive activity of carbapenem compounds: effect of C-2 side chain.

The neurotoxicity of meropenem was much lower than that of both imipenem and panipenem after intraventricular administration to mice. To clarify the major structural features responsible for the induction of convulsions by carbapenem antibiotics, the structure-activity relationship on convulsant activity was investigated in N-acetyl-2-pyrroline and cyclopentene derivatives which correspond to the 5-membered ring containing the C-2 side chain of carbapenem antibiotics. Among these derivatives, compounds with strong basicity in the side chain showed convulsant activity similar to that of the parent carbapenem compounds. In addition to the strength of the basicity of the amino group, the distance from the carboxyl to the amino group and steric crowding around the amino group also appeared to play an important role in the induction of convulsions. The results of gamma aminobutyric acid (GABAA) receptor binding assays indicated that the induction of convulsions was caused predominantly by the inhibition of GABAA-mediated inhibitory transmission. However, the in vivo convulsant activity of some of these compounds did not correlate with their in vitro inhibitory effect on GABAA receptor binding.

Animals↗
PubMed1998

[Convulsions during prophylactic use of mefloquine].

In 1996 and 1997 the Dutch Pharmacovigilance Foundation LAREB received 6 reports of patients with convulsions that were attributed to prophylactic use of mefloquine. Five patients had no neurological history; one patient had a history of epilepsy but had not had any convulsion during the preceding 5-year period. The convulsions took place 1 to 23 days after start of the treatment with mefloquine. Because of the convulsions, the treatment was discontinued. The 4 patients with known follow-up showed full recovery with regard to the convulsions. The practising physician should be aware of the possible occurrence of rare neuropsychiatric adverse events like convulsions during the prophylactic use of mefloquine.

Adult↗
PubMed1994

Pertussis immunisation in children with a family or personal history of convulsions: a review of children referred for specialist advice.

Recent guidelines recommend that children with a family or personal history of convulsions should receive all vaccinations. To determine vaccination status and adverse events following vaccination, questionnaires were sent to the general practitioners of 83 children referred for specialist advice between January 1988 and June 1991 in Redbridge Health Authority. Details of consultations within seven days of vaccination, and of any subsequent neurological or developmental problems were collected. Follow-up data were obtained for 77 of the 83 children (93%); 66 of whom had a family history, and 11 a personal history, of convulsions. Of the 66 children with a family history of convulsions, 57 received pertussis-containing vaccines, of whom one child was reviewed for a possible neurological event. Of the nine remaining children who received diphtheria-tetanus (DT) only vaccine, two children were reviewed for possible neurological events. Of the 11 children with a personal history of convulsions, nine received pertussis-containing vaccines and two received DT vaccines; none had any further neurological event. At late follow-up, none of the 77 children vaccinated had developed recurrent convulsions or any other neurological or developmental problems. Children with a family or personal history of convulsions who are given pertussis-containing vaccines seem unlikely to suffer adverse events or long-term neurological sequelae, and should be considered for all routine vaccinations in line with current recommendations.

Child↗
PubMedDate not supplied

[Convulsions and epileptic syndromes of the newborn infant. Forms of presentation, study and treatment protocols].

OBJECTIVES: To review the different forms of presentation of convulsions and epilepsies in the newborn, and to establish a protocol for diagnosis and treatment. PATIENTS AND METHODS: To achieve this we reviewed the literature and our own series over the past 15 years of 179 newborn babies with convulsions. RESULTS AND CONCLUSIONS: We present the results of the etiological analysis of neonatal convulsions. Then we discuss a protocol for diagnosis and treatment of this condition, with particular emphasis on diagnostic methods according to their complexity. The different therapeutic options are considered using a protocol for treatment that starts with the use of phenobarbital, pyridoxine, biotin, folinic acid, intravenous sodium valproate, diphenylhydantoin, clonazepam, lidocaine + phenobarbital and if the convulsions persist thipentone. Finally, we analyze the duration of treatment and emphasise that after discharge from the unit, only convulsions persisting after the neonatal period or accompanied by severe electroencephalographic changes should be treated. Finally we evaluate the high morbi-mortality (48% and 20% respectively) of the neonatal convulsions seen in our series. This is mainly due to the fact that the population studied corresponded to a tertiary level hospital covering a large area with conditions of risk.

Diagnosis, Differential↗
PubMed1975

Antagonism of the convulsant effects of heroin, d-propoxyphene, meperidine, normeperidine and thebaine by naloxone in mice.

Naloxone antagonized convulsions produced by tail vein infusions of d-propoxyphene, heroin, meperidine, normeperidine and thebaine in mice in a dose-related manner. Pretreatment with naloxone (60 mg/kg i.p.) produced a 200 percent increase of the dose of d-propoxyphene or heroin needed to produce a seizure. A 40 percent increase in the convulsant dose of meperidine was observed after naloxone pretreatment (30 mg/kg i.p.). Naloxone (15 mg/kg i.p.) produced a 30 percent increase in the convulsant dose of normeperidine; however, larger doses of naloxone did not produce any further increase in the convulsant dose of either normeperidine or meperidine. Larger doses of naloxone were needed to antagonize convulsions produced by thebaine. Heroin, d-propoxyphene and meperidine produced nonlethal clonic seizures, whereas normeperidine and thebaine produced tonic-clonic seizures which were followed by death. These data suggest that there may be two mechanisms by which narcotic analgesics and their congeners produce convulsions.

Animals↗
PubMed2001

Recurrence risk after a first febrile convulsion.

OBJECTIVE: Fever is the most common cause of convulsions, in infancy and childhood. Parents usually are concerned by the risk of recurrence. Our aim is to determine this risk of subsequent convulsions within the first year of the first episode of convulsion. METHODS: This is a prospective study over one year, May 97 to April 98 in which all children with first febrile seizure were enrolled. RESULTS: There were two hundred and thirty six children who had their first febrile convulsion within the study period. Male-to-female ratio was 1.2:1; the mean age at onset was 19 months (standard deviation 14.4). Generalized seizure occurred in 95.6% of the patients with an average duration of 7 minutes (SD 6.4). Ten percent of patients needed anticonvulsant drugs to stop convulsion. Seizure clusters occurred in 13.6 %, and complex febrile seizure was noticed in 21%. Family history was positive for epilepsy in 6.6% and febrile convulsions in 22%. Recurrence within a year from onset occurred in 52 (21%) of the patients. Factors associated with recurrence were: male sex, as male to female ratio was 2.25:1 (P = 0.02) and history of seizure clusters, 23/52, 44% (P = 0.00001). CONCLUSION: Risk factors for recurrence noted were male sex, and complex febrile seizures.

Child↗
PubMed2001

[Convulsion following the combination of single preoperative oral administration of enoxacine and single postoperative intravenous administration of flurbiprofen axetil].

We experienced a case of convulsion following the combination of single oral administration of enoxacine before an emergency operation and single postoperative intravenous administration of flurbiprofen axetil. The patient was an 87-year-old female referred to our hospital for severe abdominal pain. She was diagnosed as having the strangulation ileus, then underwent the emergent operation of partial resection of the necrotic small intestine under general anesthesia. Unfortunately we did not know that she had temporarily received oral enoxacine 200 mg, a new quinolone, administered by the previous doctor on the day before the operation. After the operation, flurbiprofen axetil 50 mg, a nonsteroidal anti-inflammatory drug, was given intravenously in thirty seconds due to postoperative pain. One minute after administration of the drug, she immediately developed a convulsive fit, severe disturbance of consciousness and apnea. We then administered at once, a single dose of diazepam intravenously for convulsion treatment, kept her airway open and controlled her ventilation. Convulsion disappeared in a minute and her condition improved gradually. We suspect that convulsive seizure may have been induced by the drug interaction between single oral dose of enoxacine before the operation and single intravenous dose of flurbiprofen axetil after the operation. We also suspect that the serum concentration of enoxacine was kept high because of metabolic disturbance and renal dysfunction resulting from her old age and dehydration. This case suggests that medication before the emergency operation must be considered in anesthetic management because of the possible side effect such as convulsion induced by the drug interaction between neuquinolones and anti-inflammatory drugs.

Administration, Oral↗
PubMed2000

Human Herpesvirus 6 and Febrile Convulsions.

Human herpesvirus 6 (HHV-6) is a ubiquitous virus that causes the childhood febrile illness exanthem subitum. Primary infection usually occurs in the first few years of life and the virus is considered to be one of the most common causes of acute febrile illness in childhood. HHV-6 can infect the central nervous system, causing meningitis or encephalitis after an acute attack of exanthem subitum. Febrile convulsions are common in early childhood, affecting 2--3% of children between 6 months and 5 years of age. Primary HHV-6 infection has been reported to be complicated by febrile convulsions in 8--50% of cases. An association between HHV-6 and febrile convulsions was established on the basis of: the similarity between the age groups in which febrile convulsions and HHV-6 infection occur, the high incidence of febrile convulsions after HHV-6 infection and the neurotropic properties of the virus. The exact role of HHV-6 in the pathogenesis of febrile convulsions remains unclear.

Journal Article↗
PubMed2004

[Effect of acetazolamide on the latency of hyperbaric oxygen-induced convulsion].

The purpose of the present study was to explore the relation between the modulation of cerebral blood flow and the latency of hyperbaric oxygen-induced convulsion. There were two parts in this study. First, the effect of acetazolamide on the latency of hyperbaric oxygen-induced convulsion was observed. 32 Sprague-Dawley (SD) rats were randomly divided into four groups: the acetazolamide 200, 20, 2 mg/kg body weight and normal saline (NS) group. The animals were given intraperitoneally acetazolamide or NS, respectively, before being exposed to the pressure of 6 ATA (absolute atmosphere) of pure oxygen. The time from exposure to the onset of seizure (clonic-tonic convulsion) was recorded for each animal according to behavioral observation. Second, the changes in maleic dialdehyde (MDA) and the activity of glutathione peroxidase (GSH-PX) were measured after acetazolamide treatment. 40 SD rats were randomly divided into five groups: NS group, 6 min with NS group, 6 min with acetazolamide group, 16 min with NS group, and 16 min with acetazolamide group. The dose of acetazolamide was 20 mg/kg body weight. After injection of NS or acetazolamide, the animals were subjected to the pressure of 6 ATA of pure oxygen in respect to its time course group. The rats were decapitated and the cortex, hippocampus, and striatum of brains were dissected and homogenized. The content of MDA and the activity of GSH-PX in these tissues were determined. We found that (1) there was a significant difference in the latency of hyperbaric oxygen-induced convulsion between the acetazolamide 200 mg/kg group and the NS control group, as well as between the acetazolamide 20 mg/kg group and the NS control group (P<0.01), whereas there was no significant difference between the NS group and the acetazolamide 2 mg/kg weight group (P>0.05). The latency of these groups were listed as follows: 9.78+/-1.94 min for 200 mg/kg body weight group, 10.92+/-1.68 min for 20 mg/kg body weight group, 24.32+/-4.33 min for 2 mg/kg body weight group and 22.02+/-4.32 min for NS control group. (2) there was no significant difference between all groups in the activity of GSH-PX, though it varied with the oxidation levels. In the cortex and hippocampus, the activity of GSH-PX boosted up at first, but with the progress of the oxidation it was impaired. In the striatum, the activity of GSH-PX increased stepwise with the aggravation of the oxidation. The MDA content in the cortex increased significantly in the group of 6 min with acetazolamide (P<0.01), as well as the group of 16 min with acetazolamide group both in cortex and hippocampus (P<0.01, P<0.05). The MDA content of all groups is correlated with the dose of acetazolamide and the exposure time. These results suggest that acetazolamide which dilates the brain arteriolar obviously shortens the latency of hyperbaric oxygen-induced convulsion, and that acetazolamide dilates the vessels and increases the supply of the oxygen breaking into the brain tissues and aggravates the oxidation. The hyperbaric oxygen-induced convulsion correlates closely with the oxidation injury.

Acetazolamide↗
PubMed2005

[Low-dose therapy with carbamazepine for convulsions associated with mild gastroenteritis].

We investigated the effect of carbamazepine on convulsions associated with mild gastroenteritis. Sixteen infants and young children (aged 9 months to 3 years) who experienced repetitive convulsions associated with mild gastroenteritis were admitted to our hospital. We treated the sixteen affected patients with 5 mg/kg of carbamazepine once per day until the diarrhea had stopped. Thirteen of the sixteen patients were subjected to intravenous and/or suppository administration of diazepam (0.3-0.5 mg/kg/time), and one patient suppository administration of 0.5 mg/kg diazepam and 5.7 mg/kg phenobarbital before the administration of carbamazepine. In all patients who were given diazepam and/or phenobarbital, the convulsions recurred after the administration of these medicines. The convulsions occurred 2 to 8 times (mean, 4.1 times) before the administration of carbamazepine. Fifteen of the sixteen patients had no seizures after the administration of carbamazepine. One patient had one convulsion 15 min after the administration of carbamazepine. All patients were treated with 5 mg/kg of carbamazepine once per day until the diarrhea had stopped, i.e. for 2 to 9 days (mean, 6.4 days). Low dose therapy with carbamazepine once per day is thus effective for convulsions associated with mild gastroenteritis.

Anticonvulsants↗
PubMed1991

Prevention of hyperthermia-induced convulsions in immature rat by MR-2266, a kappa antagonist.

The opioid receptor subtypes involved in hyperthermia-induced convulsions were studied by testing different opioid receptor-selective antagonists in unrestrained 15-day-old rats. Saline-injected animals exposed to an ambient temperature of 40 degrees C showed a gradual increase in body temperature reaching a maximum of 40.4 +/- 0.2 degrees C at 60 min. At this time all rat pups had convulsions and died. Similar results were obtained when the animals were pretreated with beta-funaltrexamine or 1 mg/kg ICI-154129. However, the injection of 10 mg/kg ICI-154129 prevented hyperthermia-induced convulsions (only 20% of the rats showed generalized convulsions at 90 min). Rats treated with the kappa antagonist MR-2266 also showed an increase in rectal temperature. However, none of the animals had convulsions or died. These results suggest that the kappa-opioid receptors are involved in convulsions induced by hyperthermia.

Animals↗
PubMed1990

Selective blockade of N-methyl-D-aspartate (NMDA)-induced convulsions by NMDA antagonists and putative glycine antagonists: relationship with phencyclidine-like behavioral effects.

Antagonism of N-methyl-D-aspartate (NMDA)-induced convulsions by a variety of drugs was compared with their ability to produce phencyclidine (PCP)-like behavioral effects (locomotion and falling) in mice. Convulsions produced by i.c.v. administration of NMDA were antagonized, at doses that did not block kainate- and quisqualate-induced convulsions, by competitive NMDA antagonists (e.g., CPP and CGS 19755), noncompetitive antagonists (e.g., PCP and MK-801) and also by some putative glycine antagonists (7-chlorokynurenic acid and HA-966). Only the competitive and the noncompetitive NMDA antagonists produced locomotion and falling, and their potencies to do so correlated (r = 0.92) with their relative potencies to antagonize NMDA-induced convulsions. However, the PCP-like behavioral effects produced by the competitive antagonists were of a lesser magnitude than those of the noncompetitive antagonists, and occurred at doses higher than those needed to block NMDA-induced convulsions. The putative glycine antagonists 7-chlorokynurenic acid and HA-966 selectively blocked NMDA-induced convulsions, without producing PCP-like behavioral effects. The extent to which compounds produce PCP-like behavioral effects might depend in part on the specific component of the NMDA receptor complex with which they interact: i.e., the NMDA receptor, the NMDA receptor-associated ion channel or the glycine-sensitive modulatory site.

Animals↗