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PubMed1962

Decarboxylase inhibitors affect convulsion thresholds to hexafluorodiethyl ether.

Alpha-methyl dihydroxyphenylalanine (alpha-MeDOPA) and alpha-methyl meta-tyrosine (alpha-MMT) do not lower significantly the convulsion thresholds to hexafluorodiethyl ether in the mouse, whereas reserpine and tetrabenazine produce marked lowering of these thresholds. Other workers have shown that alpha-MeDOPA and alpha-MMT decrease brain norepinephrine concentrations much more than brain 5-hydroxytryptamine concentrations, while reserpine and tetrabenazine decrease the brain level of these two amines in a parallel fashion. Thus, the fact that alpha-MeDOPA and alpha-MMT, even in very large doses, do not lower convulsion thresholds and in some cases raise them suggests that the decline in 5-hydroxytryptamine may be implicated in the lowering of convulsion thresholds produced by reserpine and other, similar agents.

Amines↗
PubMed1970

Unilateral inhibition of sound-induced convulsions in mice.

Loud sound repeatedly presented to one ear after an initial bilateral exposure produces a lateralized inhibition of convulsibility in SJL/J mice. Inhibition of the right side does not affect the convulsible state of the left side. Processes leading to inhibition and convulsibility may develop independently within the same animal.

Animals↗
PubMed1980

Picrotoxin convulsions involve synaptic and nonsynaptic mechanisms on cultured mouse spinal neurons.

The cellular mechanisms underlying picrotoxin-induced convulsive activity were studied by using mouse spinal neurons growing in tissue culture. Picrotoxin-induced convulsive activity in most but not all of the cells studied. The activity could be inverted by polarizing to positive potentials and eliminated either by decreasing the ratio of calcium to magnesium or by applying tetrodotoxin. When applied locally to individual cells, picrotoxin lowered spike threshold and induced spontaneous firing in some but not all cells tested. The results suggest that picrotoxin-induced convulsive activity involves rapidly summating synaptic activity which may be evoked by high-frequency repetitive firing.

Action Potentials↗
PubMed1999

Pharmacokinetic-pharmacodynamic contributions to the convulsant activity of fluoroquinolones in rats.

The in vivo convulsant activities in rats of five representative fluoroquinolones (FQs), norfloxacin, enoxacin, sparfloxacin, fleroxacin, and pefloxacin, were compared. The experimental approach allowed distinction between the drugs' ability to reach the pharmacological receptors at the level of the central nervous system (pharmacokinetic contribution) and their ability to interact with these receptors (pharmacodynamic contribution). The presence of a methyl group on the piperazine moiety decreased the pharmacodynamic contribution to the convulsant activity by severalfold, and the ratios of concentrations of the FQs in cerebrospinal fluid (CSF) to concentrations of unbound FQs in plasma varied from about 5 to 75% as a function of lipophilicity. Interestingly, FQs with the highest intrinsic convulsant activities had the lowest levels of diffusion in CSF and vice versa. This in vivo approach provides information complementary to that of in vitro experiments and should be recommended for early preclinical assessment of a new FQ's epileptogenic risk.

Animals↗
PubMed2002

Convulsant and subconvulsant doses of norfloxacin in the presence and absence of biphenylacetic acid alter extracellular hippocampal glutamate but not gamma-aminobutyric acid levels in conscious rats.

Fluoroquinolones are antibiotics with central excitatory side effects. These adverse effects presumably result from inhibition of gamma-aminobutyric acid (GABA) binding to GABA(A) receptors. This GABA antagonistic effect is greatly potentiated by the active metabolite of fenbufen, biphenylacetic acid (BPAA). Nevertheless, it remains questionable whether GABA receptor antagonism alone can explain the convulsant activity potentials of these antimicrobial agents. The present study was undertaken to investigate the possible effects of norfloxacin, both in the absence and in the presence of BPAA, on the extracellular hippocampal levels of GABA and glutamate, the main central inhibitory and excitatory amino acid neurotransmitters, respectively. This in vivo microdialysis approach with conscious rats allows monitoring of behavioral alterations and concomitant transmitter modulation in the hippocampus. Peroral administration of 100 mg of BPAA per kg of body weight had no effect on behavior and did not significantly alter extracellular GABA or glutamate concentrations. Intravenous perfusion of 300 mg of norfloxacin per kg did not change the rat's behavior or the concomitant neurotransmitter levels in about half of the experiments, while the remaining animals exhibited severe seizures. These norfloxacin-induced convulsions did not affect extracellular hippocampal GABA levels but were accompanied by enhanced glutamate concentrations. Half of the rats receiving both 100 mg of BPAA per kg and 50 mg of norfloxacin per kg displayed lethal seizures, while the remaining animals showed no seizure-related behavior. In the latter subgroup, again no significant alterations in extracellular GABA levels were observed, but glutamate overflow remained significantly elevated for at least 3 h. In conclusion, norfloxacin exerts convulsant activity in rats, accompanied by elevations of extracellular hippocampal glutamate levels but not GABA levels, even in the presence of BPAA.

Administration, Oral↗
PubMed2001

Whole-cell but not acellular pertussis vaccines induce convulsive activity in mice: evidence of a role for toxin-induced interleukin-1beta in a new murine model for analysis of neuronal side effects of vaccination.

Immunization with the whole-cell pertussis vaccine (Pw), while effective at preventing whooping cough in infants, has been associated with local, systemic, and neuronal reactions, including fevers and convulsions in children. In contrast, the new acellular pertussis vaccines (Pa) have a considerably improved safety profile. The lack of an appropriate animal model has restricted investigations into the mechanisms by which neurological reactions are induced by vaccination. Here we describe a novel murine model wherein seizure-like behavioral changes are induced following parenteral administration of Pw. The proinflammatory cytokine interleukin-beta (IL-1beta), production of which has been associated with many neurodegenerative conditions, was significantly increased in the hippocampus and hypothalamus of vaccinated animals. Accompanying this change was a decrease in release of the inhibitory neurotransmitters gamma-aminobutyric acid and adenosine in the hippocampus. Seizure-like behavioral changes were significantly reduced following inhibition of IL-1beta production by the administration of an inhibitor of IL-1beta-converting enzyme and were almost completely abrogated in IL-1 receptor type I knockout mice. These results suggest a causal relationship between IL-1beta induction and convulsive behavior following Pw vaccination. Significantly, Pa neither increased IL-1beta nor induced behavioral changes in mice, but did induce the anti-inflammatory cytokine IL-10. In contrast, administration of active pertussis toxin and lipopolysaccharide, residual in Pw but absent from Pa, also induced convulsive activity. Our findings provide the first direct evidence of an immunological basis for pertussis vaccine reactogenicity and suggest that active bacterial toxins are responsible for the neurologic disturbances observed in children immunized with Pw.

Animals↗
PubMed1977

Spontaneous fits after convulsions with fever.

112 of an original sample of 134 children with febrile convulsions were reviewed between 8 years and 9 years 10 months after their initial attack. 17% of those followed up had had at least one spontaneous fit. A significant correlation was found with perinatal abnormalities. 12% had continuing recurrent fits. Persisting grand mal occurred most commonly in lower social class children who had had perinatal abnormalities and continued to have long-term neurological disorders. Psychomotor epilepsy correlated significantly with a prolonged or repeated initial convulsion with unilateral features. It is suggested that the development of grand mal and temporal lobe epilepsies after convulsions with fever are determined by different mechanisms.

Child↗
PubMed1978

Hyponatraemia in children with febrile convulsions.

In a study of 23 children admitted to hospital with a febrile convulsion, mild hyponatraemia was found on 8 occasions. In 6 of these cases there was evidence of inappropriate secretion of antidiuretic hormone. The hyponatraemia is unlikely to be the cause of the convulsion, but probably predisposes the child to a subsequent convulsion during the same febrile illness.

Child, Preschool↗
PubMed1979

Role of viruses in febrile convulsions.

A disseminated viral illness was demonstrated by isolating a virus from the CSF, blood or urine in 27% of 73 children who were admitted to hospital after a first febrile convulsion. However, a viral aetiology could be implicated for 86% of the children after combining results of tissue culture, electron microscopy, mouse inoculation, complement fixation tests, and interferon assay. Parallel bacterial cultures showed a possible pathogen in 29% of children, but in only 4% was the pathogen isolated from the CSF, blood, or urine. No correlation was found between the nature of the pathogen (or evidence of its dissemination) and the severity of the convulsion, degree of fever, CSF protein, CSF white cells, or the WBC. The results suggest that a febrile convulsion could be a response to invasion of the blood stream or central nervous system by a micro-organism which is usually a virus. Invasion may be of such brief duration that successful isolation of the virus from the blood, CSF, or urine in not more commonly achieved.

Child↗
PubMed1980

Continuous sodium valproate or phenobarbitone in the prevention of 'simple' febrile convulsions. Comparison by a double-blind trial.

Of the 265 children aged between 6 and 18 months admitted to hospital in a 26-month period each with his first febrile convulsion, there were 64 who satisfied our criteria for a simple febrile convulsion. Of these, 43 (random) were entered into a double-blind trial of continuous sodium valproate versus phenobarbitone, and 21 were untreated. The dosage was phenobarbitone 3-6 mg/kg per day; sodium valproate 30-60 mg/kg per day. 39 completed treatment (21 phenobarbitone, 18 sodium valproate), 2 in each group being withdrawn because of unacceptable side effects. Close supervision and random serum drug estimations showed compliance to be good. After a mean treatment period of 12 months (mean age 25 months) there had been one recurrence in the sodium valproate group compared with 7 in the untreated group (P less than 0.05), and 4 recurrences in the phenobarbitone group. The difference between treatment and no treatment was significant (P less than 0.05). These results suggest that in simple febrile convulsions occurring between 6 and 18 months of age sodium valproate is as effective as phenobarbitone in preventing recurrence and that either treatment is better than none.

Clinical Trials as Topic↗
PubMed1985

Duration of admission for febrile convulsions?

Records of 199 children aged 5 to 71 months (mean 22.8) admitted after febrile convulsion were examined. Although 32 had recurrent convulsions (some before admission) none suffered a convulsion more than 24 hours after hospital admission.

Child, Preschool↗
PubMed1989

Effect of fever on recurrence rate of febrile convulsions.

We studied 154 children admitted consecutively with their first febrile convulsion to assess the influence of the temperature on the recurrence rate of convulsions. Those with temperatures of 40 degrees C or more were nine times less likely to have subsequent convulsions than those with temperatures of 38-38.9 degrees C.

Child, Preschool↗
PubMed1996

Long term outcome of prophylaxis for febrile convulsions.

A cohort of 289 children with febrile convulsions who had been randomised in early childhood to either intermittent prophylaxis (diazepam at fever) or no prophylaxis (diazepam at seizures) was followed up 12 years later. The study focused on the occurrence of epilepsy and on neurological, motor, intellectual, cognitive, and scholastic achievements in the cohort. At follow up the two groups were of almost identical age (14.0 v 14.1 years), body weight (58.2 v 57.2 kg), height (168.2 v 167.7 cm), and head circumference (55.9 v 56.2 cm). The occurrence of epilepsy (0.7% v 0.8%), neurological examination, fine and gross motor development on the Stott motor test, intellectual performance on the Wechsler intelligence scale for children verbal IQ (105 v 105), performance IQ (114 v 111), and full scale IQ (110 v 108), cognitive abilities on a neuropsychological test battery, including short and long term, auditory and visual memory, visuomotor tempo, computer reaction time, reading test, and scholastic achievement were also very similar. Children with simple and complex febrile convulsions had the same benign outcome. The long term prognosis in terms of subsequent epilepsy, neurological, motor, intellectual, cognitive, and scholastic ability was not influenced by the type of treatment applied in early childhood. Preventing new febrile convulsions appears no better in the long run than abbreviating them.

Adolescent↗
PubMed1997

Retinal haemorrhages and convulsions.

AIMS: To evaluate the incidence of retinal haemorrhages after convulsions in children. PATIENTS AND METHODS: All children who required hospital admission after an episode of convulsions were included in the study. Complete neurological and ocular examinations, including ophthalmoscopy, were undertaken within 48 hours of hospital admission. RESULTS: Thirty three children were examined according to the protocol and their seizures were classified by a paediatric neurologist. Despite the fact that some of the children also vomited or underwent cardiopulmonary resuscitation, none of the 33 children developed retinal haemorrhages. CONCLUSIONS: Convulsions rarely (if ever) give rise to retinal haemorrhages. The finding of retinal haemorrhages should stimulate a detailed assessment to exclude non-accidental injury, whatever the nature of the associated or antecedent events.

Adolescent↗
PubMed2002

Febrile convulsions and sudden infant death syndrome.

It has been suggested that sudden infant death syndrome (SIDS) and febrile convulsions are related aetiologically. We compared the risk of SIDS in 9877 siblings of children who had had febrile convulsions with that of 20 177 siblings of children who had never had febrile convulsions. We found no support for the shared susceptibility hypothesis.

Child, Preschool↗
PubMed2003

Pre-eclampsia and febrile convulsions.

An association between pre-eclampsia and febrile convulsions has been reported, but the association may not be causal. We compared the risk of febrile convulsions in 14 974 children who had been exposed to pre-eclampsia in fetal life with that of 39 210 unexposed children. Children exposed to pre-eclampsia had a slightly increased risk of febrile convulsions, but the association was apparently caused by a shorter gestation in pre-eclamptic women.

Child, Preschool↗
PubMed1980

Successful prophylaxis against febrile convulsions with valproic acid or phenobarbitone.

A total of 184 six-month periods were analysed during which feverish illnesses occurred in children aged 6-42 months with a history of a febrile convulsion. Fits occurred in 34 out of 100 such periods when no treatment was being given, in six out of 45 periods when the serum phenobarbitone concentration was 69.0 mumol/l (1.6 mg/100 ml) or more, and in five out of 39 periods when the plasma valproic acid concentration was 416.4 mumol/l (6.0 mg/100 ml) or more. Thus in adequate dosage both phenobarbitone and valproic acid were significantly better than no treatment in preventing febrile convulsions (p less than 0.02). The two drugs were of comparable efficacy. It is concluded that with improved compliance valproic acid, which is relatively free from side effects, might be an effective prophylactic agent against febrile convulsions.

Child, Preschool↗
PubMed1981

Electric convulsion therapy in depression: a double-blind controlled trial.

The therapeutic effect of simulated and real bilateral electric convulsion therapy was examined in a double-blind, randomised trial on 22 patients with a primary depressive illness. Each treatment was given twice weekly for three weeks and the results assessed by the psychiatrist using a visual analogue rating scale, nurses using a nine-point rating scale, and the patients themselves using the Beck Depression Inventory. With all three methods of assessment patients given the real treatment substantially improved (p less than 0.001), whereas those given simulated treatment showed little change. Three weeks after substituting real treatment for simulated, however, these patients were also significantly improved (psychiatrist's rating p less than 0.001; nurses' rating p less than 0.005; Beck inventory p less than 0.005). These findings confirm the value of electric convulsion therapy in severe depressive illness and strongly suggest that the convulsion is important for the therapeutic effect.

Clinical Trials as Topic↗