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PubMed2005

Expression of Hsp72 in lymphocytes in patients with febrile convulsion.

The pathophysiology of febrile convulsion, the most common childhood neurologic disease, remains unclear. In this study, we investigated what role a heat shock protein plays in this disease. We enrolled eight boys and two girls with febrile convulsion and 10 age-matched healthy controls. We did a biosynthetic evaluation of both groups by separating lymphocytes and measuring the expression of heat shock protein 72 before and after heat shock treatment. Before the treatment, both groups were found to have small amounts of constitutive heat shock protein 72. Afterwards, its expression increased in both groups, and no statistical difference was found between the increases in the two groups. In addition, there was no obvious difference in the susceptibility to produce heat shock proteins. However, the febrile convulsion group was found to have a significant decrease in phosphorylation of heat shock protein 72. These results suggest the possible involvement of post-translational modification of heat shock proteins, most likely phosphorylation, in the pathogenesis of febrile convulsion.

Case-Control Studies↗

PubMed1983

EEG abnormalities and convulsions in juvenile diabetes mellitus.

The clinical and EEG findings were reviewed for 270 juvenile children from the Montreal Children's Hospital Diabetic Clinic in an attempt to correlate the EEG findings at the onset of diabetes mellitus with the future risk of having a convulsion with a hypoglycemic reaction. Compared to a non-diabetic control population, the number of epileptiform EEG abnormalities was significantly increased in the initial EEG of diabetic patients who later had a hypoglycemic convulsion. The initial epileptiform EEG did not help to differentiate those diabetics with recurrent hypoglycemic induced convulsions from diabetics who would have only a single convulsion.

Age Factors↗

PubMed1983

Structure-activity relationships of convulsant and anticonvulsant barbiturates: a computer-graphic-based pattern-recognition analysis.

A computer-graphic-based pattern-recognition study of two series of 5-ethyl-5-substituted barbiturates has been undertaken in an attempt to find a correlation between molecular conformation and convulsant and anticonvulsant activity. Studies of a first (trial) set of barbiturates related to pentobarbital revealed a region of space in which at least one low-energy conformation of the hydrocarbon side chain of each of the anticonvulsant barbiturates resides. Another region was occupied by a low-energy conformation of each of the convulsant barbiturates. These regions of space are, thus, possible pharmacophores for convulsant and anticonvulsant activity. Analysis of a second (test) set of barbiturates related to phenobarbital has shown that the activities and structures of these molecules are consistent with the above model. These pharmacophores thus provide a basis for the design of rigid, new analogues with potent convulsant or anticonvulsant activities.

Anticonvulsants↗

PubMed1987

Prostaglandin D2 inhibits pentylenetetrazole-induced convulsions in rats by a serotonin-mediated mechanism.

Prostaglandins (PGs) of the E series are known to exert anticonvulsant action in experimental animals. Earlier studies from this laboratory have indicated that PGE1 inhibits pentylenetetrazole (PTZ)-induced convulsions in rats through a serotonin-mediated mechanism. PGD2, the major PG in the rodent brain, shares a number of central pharmacological actions of the PGEs, and like the latter it potentiates the anticonvulsant action of phenobarbitone and phenytoin in rats. The present study was undertaken to investigate the putative anticonvulsant action of PGD2 against PTZ-induced convulsions in rats and to evaluate the role of serotonin in the anticonvulsant action of PGD2. PGD2 (5, 10, and 20 micrograms, icv) produced a dose-related inhibition of PTZ-induced clonic convulsions in rats. The anticonvulsant action of PGD2 (20 micrograms, icv) was significantly attenuated following pretreatment of the rats with pharmacologic agents known to reduce central serotonergic activity, including 5,6-dihydroxytryptamine, a selective neurotoxin for serotonergic neurons, p-chlorophenylalanine, a specific inhibitor of serotonin biosynthesis, metergoline, a serotonin postsynaptic receptor antagonist, and quipazine, which is known to inhibit neuronal release of serotonin. These findings, in conjunction with an earlier study from this laboratory indicating that PGD2 augments rat brain serotonergic activity, suggest that the anticonvulsant activity of PGD2 against PTZ-induced convulsions in rats is mediated through a serotonergic mechanism.

Animals↗

PubMed1975

The effect of convulsions induced by flurothyl on ribonucleic acid synthesis in rat cerebral cortex during the recovery phase.

The effect of convulsions, induced by flurothyl, on RNA synthesis in purified unfractionated nuclei and the cytoplasm of rat cerebral cortex was studied by using a double-label technique involving injection of [3H]- and [14C]-orotate intracisternally. 2. Intact RNA was extracted in 80% yield by an enzymic method by using a proteinase in the presence of sodium dodecyl sulphate followed by deoxyribonuclease. Electrophoresis on 1.5% polyacrylamide-0.5% agarose gels revealed the presence of giant nuclear RNA of size up to approx. 300X 10(6) daltons and mRNA of maximal mol.wt. 9 X 10(6)-16 X 10(6). 3. Nuclear RNA synthesis was decreased to 27% in the first 15 min after convulsions but rapidly increased, so that at 1 1/2 h it was 124% of the control, and at 6 h 147%. 4. Labelling of cytoplasmic RNA was decreased to 15% at 15 min after convulsions but had not recovered to control values by 6 h. 5. Analysis of radioactive gel patterns and the 3H/14C ratio at six time-points (15 min-6h) showed that the major effect was inhibition of the processing of heterogeneous nuclear RNA resulting in a sharp decline in the export of newly synthesized RNA from the nucleus. 6. Cytoplasmic RNA patterns indicated that specific messengers were synthesized at different times during the recovery of the cell after convulsions.

Animals↗

PubMed2002

Convulsions following axillary brachial plexus blockade with levobupivacaine.

Neurotoxicity manifesting as convulsions is a recognised complication of the administration of local anaesthetic drugs as part of a regional anaesthetic technique. We describe a case of self-limiting convulsions following the institution of an axillary brachial plexus block with levobupivacaine. Although the occurrence of convulsions following the administration of racemic bupivacaine is a well-recognised complication, there have been no clinical case reports published describing convulsions following the use of levobupivacaine in regional anaesthesia.

Anesthetics, Local↗

PubMed2003

Pharmacokinetics and clinical effect of phenobarbital in children with severe falciparum malaria and convulsions.

AIMS: Phenobarbital is commonly used to treat status epilepticus in resource-poor countries. Although a dose of 20 mg kg(-1) is recommended, this dose, administered intramuscularly (i.m.) for prophylaxis, is associated with an increase in mortality in children with cerebral malaria. We evaluated a 15-mg kg(-1) intravenous (i.v.) dose of phenobarbital to determine its pharmacokinetics and clinical effects in children with severe falciparum malaria and status epilepticus. METHODS: Twelve children (M/F: 11/1), aged 7-62 months, received a loading dose of phenobarbital (15 mg kg(-1)) as an i.v. infusion over 20 min and maintenance dose of 5 mg kg(-1) at 24 and 48 h later. The duration of convulsions and their recurrence were recorded. Vital signs were monitored. Plasma and cerebrospinal fluid (CSF) phenobarbital concentrations were measured with an Abbott TDx FLx fluorescence polarisation immunoassay analyser (Abbott Laboratories, Diagnostic Division, Abbott Park, IL, USA). Simulations were performed to predict the optimum dosage regimen that would maintain plasma phenobarbital concentrations between 15 and 20 mg l(-1) for 72 h. RESULTS: All the children achieved plasma concentrations above 15 mg l(-1) by the end of the infusion. Mean (95% confidence interval or median and range for Cmax) pharmacokinetic parameters were: area under curve [AUC (0, infinity)]: 4259 (3169, 5448) mg l(-1).h, t(1/2): 82.9 (62, 103) h, CL: 5.8 (4.4, 7.3) ml kg(-1) h(-1), Vss: 0.8 (0.7, 0.9) l kg (-1), CSF: plasma phenobarbital concentration ratio: 0.7 (0.5, 0.8; n= 6) and Cmax: 19.9 (17.9-27.9) mg l(-1). Eight of the children had their convulsions controlled and none of them had recurrence of convulsions. Simulations suggested that a loading dose of 15 mg kg(-1) followed by two maintenance doses of 2.5 mg kg(-1) at 24 h and 48 h would maintain plasma phenobarbital concentrations between 16.4 and 20 mg l(-1) for 72 h. CONCLUSIONS: Phenobarbital, given as an i.v. loading dose, 15 mg kg(-1), achieves maximum plasma concentrations of greater than 15 mg l(-1) with good clinical effect and no significant adverse events in children with severe falciparum malaria. A maintenance dose of 2.5 mg kg(-1) at 24 h and 48 h was predicted to be sufficient to maintain concentrations of 15-20 mg l(-1) for 72 h, and may be a suitable regimen for treatment of convulsions in these children.

Anticonvulsants↗

PubMed2000

Ictal generalized rhythmic alpha activity during non-convulsive status epilepticus.

We investigated the repetitive manifestation of non-convulsive status epilepticus with an uncommon ictal electroencephalographic pattern observed in two patients suffering from epilepsy (aged 29 and 55 years). The patients had suffered from epilepsy since the age of 1 and 40 years, respectively. Interictal and ictal neurological, neuropsychological and electroencephalographic investigations were carried out. Non-convulsive status started and ended abruptly, clinically as well as electroencephalographically. The ictal electroencephalographic pattern was a monomorphic alpha activity with a generalized bilateral distribution. Altered responsiveness, sometimes eyelid myoclonia (in one patient) and amnesia were the most characteristic clinical findings during non-convulsive status. Intellectual development was delayed in the patient with early onset of epilepsy. However, this was not the case in the other patient, who developed memory impairment during the course of the disease. In both patients, lamotrigine added to valproate reduced the frequency of status epileptici significantly. Obviously, these patients suffer(ed) from a type of generalized non-convulsive status epilepticus with an uncommon electroencephalographic pattern.

Adult↗

PubMed2002

Idiopathic familial temporal lobe epilepsy with febrile convulsions.

Efforts to duplicate the genetic and molecular breakthroughs of autosomal dominant frontal lobe epilepsy have lead to increased interest in familial temporal lobe epilepsy. In this report we describe three kindreds. The epilepsy syndrome described manifests after the teenage years and was generally mild and treatment responsive. The predominant seizure types were simple and complex partial seizures, typical of mesial temporal onset. Some family members had febrile convulsions only and others had epilepsy without preceding febrile convulsions. Three patients had both febrile convulsions and temporal lobe epilepsy. High-resolution quantitative and qualitative MRI was normal. The syndrome in these three kindreds is distinct from temporal lobe epilepsy due to mesial temporal sclerosis and febrile convulsions and is probably a form of idiopathic localization related epilepsy. Its relation to other familial temporal lobe epilepsy phenotypes is discussed.

Adolescent↗

PubMed1970

Identification of L-methionine-S-sulfoximine as the convulsant isomer of methionine sulfoximine.

The convulsant agent methionine sulfoximine inhibits brain glutamine synthetase irreversibly and the inhibitor becomes bound to the active site of the enzyme as methionine sulfoximine phosphate. Only one of the four isomers of methionine sulfoximine, L-methionine-S-sulfoximine, inhibits glutamine synthetase. In the present work, D-methionine-SR-sulfoximine, and highly purified preparations of L-methionine-S-sulfoximine and L-methionine-R-sulfoximine were tested in mice for convulsant activity; only L-methionine-S-sulfoximine produced convulsions. The finding that only one of the four optical isomers of methionine sulfoximine induces convulsions, and that only this same isomer inhibits glutamine synthetase, lends support to the conclusion that these two effects of methionine sulfoximine are closely connected.

Animals↗

PubMed2004

Tolerance to pentylentetrazol-induced convulsions and protection of cerebrovascular integrity by chronic nicotine.

The authors' previous studies have shown that in nicotine-induced seizures sensitivity was decreased and blood-brain barrier (BBB) disruption was prevented as a consequence of nicotine pretreatment. This study aimed to investigate the possible protective actions of nicotine on cerebrovascular permeability and seizures induced by pentylentetrazol (PTZ) injection. Cerebrovascular effects of nicotine were evaluated by measuring the permeability changes of BBB using Evans-Blue (EB) dye and specific gravity (SG), which indicates brain water and protein content. The experiments were carried out on Wistar rats. Animals were randomly divided into two groups. Convulsions were induced by injection of PTZ (80 mg/kg i.v.) in rats either pretreated with nicotine daily with a low dose of 0.8 mg/kg day for 21 days or injected with a single dose of 6 mg/kg mecamylamine. The same procedures were followed in control rats with the exception that they were injected only with saline. PTZ injection caused tonic-clonic convulsions and increased the EB dye leakage and specific gravity values in saline-injected control rat brains. Daily injection of nicotine lessened the intensity of seizures. These were accompanied by marked decreases in both the leakage of EB and brain water content. Acute administration of a nAChR antagonist mecamylamine significantly increased seizure latency and decreased the duration of seizures. Thereby, mecamylamine reduced the EB leakage and water content in most brain regions. These results indicate that development of tolerance to PTZ convulsions can be produced by chronic nicotine administration in rats. The mechanism for this effect currently needs clarification. Moreover, the data also suggest that cholinergic activity may account for occurrence of PTZ-induced convulsions.

Analysis of Variance↗

PubMed1988

Rectal diazepam solution in the treatment of convulsions in the children's emergency room.

Rectal diazepam solution was administered to 55 convulsing children in the Children's Emergency Room. In 71%, the convulsion ceased within 5 min, and in 7%, between 5 and 10 min. In 16%, rectal diazepam was ineffective but there was a rapid response to intravenous diazepam. Convulsions that had lasted less than 15 min before treatment responded more often (81%) than those that had lasted more than 15 min (46%). Four children had transient respiratory depression. Though intravenous diazepam is superior, rectal diazepam solution is adequate for controlling most acute convulsions in children, and has the advantage that it can be administered by paramedical workers.

Administration, Rectal↗

PubMed1998

Convulsions due to increased permeability of the blood-brain barrier in experimental cerebral malaria can be prevented by splenectomy or anti-T cell treatment.

Experimental cerebral malaria (ECM) can be induced in C57B1 mice by infection with Plasmodium berghei K173 parasites. Behavioral changes shortly before they die of ECM may reflect disturbance of the integrity of the blood-brain barrier (BBB). Folic acid elicits strong convulsive activity if the permeability of the BBB is increased. Administration of folic acid to mice during development of ECM induced convulsions. Interventions known to prevent fatal outcome from ECM, such as splenectomy or treatment with anti-CD4 or anti-CD8 monoclonal antibodies, also prevented sensitivity to folic acid-induced convulsions. In addition, infected mice with ECM and sensitive to folic acid-induced convulsions, recovered from this sensitivity after treatment with anti-T cell antibodies within 4 h. These data suggest that disturbance of the permeability of the BBB can be reversed and depends on the involvement of T cells.

Animals↗

PubMed1977

gamma-Aminobutyric acid metabolism in subcellular particles of mouse brain and its relationship to convulsions.

The in vivo effects of convulsant drugs (hydrazine and penicillamine) on the metabolism of gamma-aminobutyric acid (GABA) in subcellular fractions of mouse brain were studied. Both substances inhibited the activity of glutamic acid decarboxylase [EC 4.1.1.15] (GAD) in the synaptosomal fraction (nerve ending particles) and reduced the concentration of GABA in the same fraction at the onset of convulsions, though changes in the total GABA concentration in the brain did not correlate with the onset of convulsions. Therefore, it is suggested that the concomitant decrease of GAD activity and GABA concentration in the nerve endings, independently of the total GABA concentration, is probably an important factor in the onset of some kinds of convulsions.

4-Aminobutyrate Transaminase↗

PubMed1995

Limbic and/or generalized convulsive seizures elicited by specific sites in the thalamus.

Convulsive seizures were elicited by a single unilateral microinjection of the cholinergic muscarinic agonist, carbachol, into the thalamus. Moreover, using systematic single microinjections of carbachol, we identified specific regions within the thalamus which were the origin of behavioural and electrocortical correlates associated with limbic and/or generalized convulsive seizures. Neither serotonin, noradrenaline nor glutamate had any convulsive effect when injected into the epileptogenic thalamic areas. The specific epileptogenic sites identified within the thalamus may provide a new experimental model which should prove useful for exploring the thalamic and thalamo-cortical mechanisms underlying limbic and generalized convulsive seizure disorders.

Animals↗

PubMed2002

The voltage-gated potassium channel KCNQ2 in Taiwanese children with febrile convulsions.

Mutations in the voltage-gated potassium channel genes KCNQ2 and KCNQ3 have been found to cause benign familial neonatal convulsions. Recent studies provided evidence that KCNQ2 and KCNQ3 contribute to the M-current, which regulates the subthreshold electrical excitability in the CNS. Febrile convulsions represent the majority of childhood seizures, and show a strong family history, suggesting a genetic predisposition. By performing an association study, we investigated whether KCNQ2 gene polymorphisms can be used as markers of susceptibility to febrile convulsions. These data suggest that the KCNQ2 gene might not be a useful marker for prediction of the susceptibility of febrile convulsions.

Child↗

PubMed1993

Convulsions and hypertension in children: differentiating cause from effect.

OBJECTIVE: To determine if the magnitude of blood pressure (BP) increase could differentiate convulsion caused by a hypertensive crisis from a primary convulsive disorder, which itself increases BP. DESIGN: Retrospective analysis. SETTING: Admission to a pediatric intensive care unit (ICU) within a tertiary care center. PATIENTS: All children with hypertensive crisis admitted to the pediatric ICU from 1976 to 1990 were studied. Thirty-eight episodes occurred in 36 patients. The charts of children admitted for status epilepticus from 1976 to 1986 were also reviewed. One hundred and fifty-three episodes occurred in 145 patients. MEASUREMENTS AND MAIN RESULTS: BP values at entry to the pediatric ICU in patients with hypertensive crisis were compared with the highest BP values obtained within an hour after cessation of convulsion in 120 patients admitted for status epilepticus. The Z scores for BP, adjusted for age and sex, were compared. The BP values for children in hypertensive crisis with or without convulsions were by far greater than the BP values observed in patients in status epilepticus (p < .0001). For a patient in the postictal phase, a BP > or = 4.0 SD above the mean for age and sex predicted with 78% probability the presence of a hypertensive crisis requiring emergency treatment. If the BP was < 4 SD below the mean, the possibility of a hypertensive crisis was excluded (negative-predictive value 100%). CONCLUSIONS: Children with hypertensive crisis, as well as children with status epilepticus, can present with a high BP. In a postictal patient, the magnitude of BP increase is a useful clinical parameter to exclude a hypertensive crisis that requires specific treatment of the BP.

Adolescent↗

PubMed1984

Adult respiratory distress syndrome and convulsions associated with administration of cyclosporine in liver transplant recipients.

A "capillary leak" syndrome resulting from cyclosporine-induced membrane toxicity has been postulated as the cause of convulsions and pulmonary edema in bone marrow transplant recipients. We describe here the occurrence of similar complications in a group of 21 adults receiving liver transplants since July 1982. Of 12 patients treated with i.v. cyclosporine (4 mg/kg/day), 2 developed an adult respiratory distress syndrome (ARDS) within five days of the operation, but it was not found in those given prednisolone (0.05-1.0 mg/kg/day) and azathioprine (1.0 mg/kg/day). ARDS only occurred when cyclosporine was administered through a central vein, and therefore might be related to high concentrations of cyclosporine reaching the pulmonary circulation and causing damage to vascular membranes. Convulsions occurred in one patient given i.v. cyclosporine, and in three when therapy was changed and cyclosporine and corticosteroids were used in combination. Convulsions did not occur inthe same patients as ARDS, were not part of a generalized "capillary leak" syndrome, and were not associated with hypertension or renal failure, as reported elsewhere in children. Fluid retention consequent on cyclosporine administration aggravated by the use of corticosteroids appears to be the most likely explanation of the convulsions.

Adult↗