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PubMed1979

The time course of brain and blood catecholamines, catechol O-methyltransferase, and amino acids in rats convulsed by oxygen at high pressure.

The time course of changes in blood and brain catecholamines, catechol O-methyltransferase (COMT), ammonia, and amino acids leading to convulsion by high pressure oxygen breathing (OHP) in rats has been investigated. Brain catecholamines were suppressed by OHP. They changed in phase with brain COMT concentration and consequently were not due to the action of this degrading enzyme. Convulsive actions seem not to be influenced by brain catecholamine concentration. Blood adrenaline concentrations are, however, significantly elevated both prior to and during convulsions. In both brain and blood, ammonia concentration increases, glutamate decreases, and glutamine-aspargine increases. It is proposed that the efficacy of the glutamate-glutamine ammonia buffering system in blood and brain is important in the prevention of the onset of convulsions but that when brain gamma-aminobutyric acid is depressed to critical levels, convulsions result.

Amino Acids↗
PubMed1977

Time, rate, and temperature factors in the onset of high-pressure convulsions.

An interrupted compression profile technique was used to develop data to separate the effects of time and pressure factors governing increase of high-pressure neurological syndrome (HPNS) convulsion threshold pressures (the compression rate effect) during different compression profiles. A single differential equation fits all data available to date for compression rate effect on convulsion thresholds of CD-1 mice (three distinct types of compression profile; mean compression rates 12-1,000 atm/h). The process leading to increase in HPNS convulsion pressure is initiated at the very beginning of compression, proceeds at increasingly rapid rates as higher pressures are attained, and approaches a limiting upper convulsion pressure. The convulsion threshold pressure in any given experiment is independent of the compression rate prevailing during the time immediately preceding onset of the seizure. The magnitude of the compression rate effect in the CD-1 mouse is independent of chamber temperature over a range of 27-36 degrees C, and rectal temperatures of 29.2-37.5 degrees C. The bearing of these results on the design of optimal compression schedules and on the analysis of the neurological mechanisms underlying the HPNS is discussed.

Animals↗
PubMed2005

[Markers of poor prognosis in convulsive status epilepticus].

OBJECTIVE: To characterize the variables that might be associated with mortality and the development of neurological deficits in children with convulsive status epilepticus. PATIENTS AND METHODS: Children older than 1 month and younger than 15 years who were admitted to the pediatric intensive care unit of a university hospital between 2001 and 2004 were reviewed. Epidemiologic and clinical factors that might be related to neurological outcome at discharge from the unit were analyzed. RESULTS: Forty-one patients (median age 24 months) were included. A total of 48.3% developed refractory convulsive status epilepticus. Six patients died (mortality 14.6%) during their intensive care unit stay and neurologic worsening was observed in 8.6% of survivors (adverse outcome in 22%). Symptomatic epilepsy was present in all patients who died and in 88.9% of those who recovered with severe neurologic sequelae. Uni- and multivariate analysis showed that adverse outcome was related to symptomatic origin and refractory convulsive status epilepticus (p < 0.05). CONCLUSIONS: Mortality and morbidity is high in childhood convulsive status epilepticus. Refractory convulsive status and symptomatic origin were markers of poor outcome. Children who did not have symptomatic epilepsy had a favorable outcome.

Child↗
PubMed1979

A genetic study of febrile convulsions.

307 probands with febrile convulsions classed as the simple type (131 children) and the complicated type (176 children) were genetically analyzed. There was a tendency toward familial aggregation of febrile convulsions, and genetic involvement was suggested. The multifactorial mode of inheritance best agreed with the observations. (1) The ratio of incidence of febrile convulsions in siblings of probands in the present study (19.9%) to the incidence in the general population (2.9%), i.e., 6.85, was rather close to the expected ratio of 5.87 from the multifactorial inheritance system. (2) The incidence in siblings tended to be higher when either or both of their parents had a history of febrile convulsions. In 2-child families where the first child was affected, the incidence in the second child tended to increase in parallel with the increasing incidence in parents. (3) The incidence in siblings was higher if probands were males. (4) The heritability, when estimated by Falconer's procedure, was as high as 76%, showing that febrile convulsions are strongly genetically predisposed. These findings were more distinctly observed in the simple type than in the complicated type.

Adult↗
PubMed1983

Effect of phenoxybenzamine on the GABA system and on convulsive activity.

The effect of phenoxybenzamine on the concentration of GABA and the aminooxyacetic acid (AOAA) induced accumulation of GABA in four brain regions was compared with its effect on the occurrence and latency of picrotoxin-induced convulsions. Also the effect of phenoxybenzamine on post-decapitation convulsions was followed. Whereas 0.1 mg/kg of phenoxybenzamine decreased the levels and the AOAA-induced accumulation of GABA in the substantia nigra and cerebellar cortex, 1.0 mg/kg produced an increased GABA accumulation in the substantia nigra. Both doses of the drug decreased the AOAA-induced accumulation of GABA in the cingulate cortex. Administration of phenoxybenzamine decreased the latency and increased or decreased the occurrence of picrotoxin-induced convulsions depending on the intensity of picrotoxin effect. Phenoxybenzamine also prolonged the latency and shortened the duration of post-decapitation convulsions in rats. The results suggest that two different mechanisms mediate the effects of phenoxybenzamine on the latency and occurrence of picrotoxin-induced convulsions.

Aminooxyacetic Acid↗
PubMed2000

Febrile convulsions after 5 years of age: long-term follow-up.

In order to examine the natural history of febrile convulsions occurring after 5 years of age, we studied 44 children in whom febrile convulsions persisted after 5 years of age (group 1) and compared their development of unprovoked seizures with a group of 195 children in whom febrile convulsions occurred before 5 years of age (group 2). All subjects of group 1 were re-evaluated at the mean age of 13.4+/-1.7 years. The children in group 2 were followed up until they reached the same mean age as children in group 1 (13.1+/-2.3 years). In group 1, we found a higher percentage of unprovoked seizures than in children with febrile convulsions with onset before 5 years of age (18.1% vs 7.4%, P < .05). Our data suggest that children with febrile convulsions after 5 years of age probably must be considered as a group of patients at risk of developing unprovoked seizures.

Age of Onset↗
PubMed1999

Hydroxyl radicals detected via brain microdialysis in rats breathing air and during hyperbaric oxygen convulsions.

Microdialysis was done on 300-400 g, awake, male rats with microdialysis probes inserted through guide cannulas into the striatum (Bregma co-ordinates A 0.5, L 2.9, D -4.0 for guide cannulas implanted 5 days previously). Rats were exposed to hyperbaric oxygen (HBO; 6 atm absolute, 5 atm gauge pressure of oxygen with carbon dioxide absorbed by soda lime). Artificial cerebrospinal fluid (CSF) containing 5 mM sodium salicylate was perfused at 1 microl/min and collected over sequential 10 min intervals with rats breathing air, then HBO, and after decompression. Times to convulsions and duration and severity of convulsions were observed and recorded. CSF samples were analyzed for 2,3- and 2,5-dihydroxybenzoic acid (DHBA), reaction products of hydroxyl radicals with salicylate, by HPLC and compared to authentic standards. Recovery of DHBAs was 48% from fluid surrounding microdialysis probes, based on in vitro tests. The average time to the first convulsion was 21 min and rats convulsed an average of 4 times during 40 min in HBO. There were no significant differences in hydroxyl radical production by this protocol during any of the 10 min collection periods in air or HBO (average in pmoles for 10 microl of all samples: 2,3-DHBA = 7.0 +/- 2.5 and 2,5-DHBA = 11.3 +/- 4.1). The failure to detect an increase in hydroxyl radicals in HBO prior to or during convulsions appears valid since each rat served as its own control.

Air↗
PubMed2004

Benign afebrile cluster convulsions with gastroenteritis: an observational study.

BACKGROUND: The occurrence of afebrile seizures in association with viral gastroenteritis, without dehydration or electrolyte imbalance, is virtually unknown outside Asia. They are reported to have a benign prognosis and not to require specific investigations or therapy. METHODS: We report the occurrence of such afebrile convulsions in association with viral gastroenteritis without dehydration or electrolyte imbalance, over a 3-year period, in a cohort of 14 British children. RESULTS: The children (5 males and 9 females, 10 Caucasians and 4 Asians) were aged 9 to 60 months (median 14.5 months). All 14 had a normal neurological examination and normal serum biochemistry. Twelve children had generalised seizures and 2 had, in addition, absence seizures. The number of seizures per child ranged from 1 to 8. Most convulsions were short with 85.7% of children having the longest seizure not longer than 4 minutes. The longest duration for a seizure was 10 minutes and occurred in 2 children. Convulsions did not recur after the first day in 10 children, 3 children had recurrences the second day and one child on the fourth day. No convulsions recurred after 4 days. Cerebrospinal fluid studies, computed tomography and electroencephalogram (EEG) were performed on two children who had prolonged seizures and the results were normal. No pathogenic bacteria were grown in any of the stools. Enzyme immunoassay detection of Rotavirus in the stools was positive in 7 of the 10 children where it was tested. All 14 children recovered spontaneously within a few days. On long-term follow of up to 31 months (median 16 months), none had further convulsions and all had normal development milestones. CONCLUSIONS: Afebrile seizures in association with viral gastroenteritis do also occur outside Asia. Recognition of this entity should lead to reassurance of the parents. As in previously published series, investigations such as lumbar puncture, neuroimaging and EEG are usually normal and may not be necessary in most cases. Likewise, published data indicate that long-term anticonvulsant therapy is not usually warranted and the prognosis seems to be reassuring.

Acute Disease↗
PubMed2000

Paroxysmal kinesigenic dyskinesia and infantile convulsions: clinical and linkage studies.

OBJECTIVE: To clinically characterize affected individuals in families with paroxysmal kinesigenic dyskinesia (PKD), examine the association with infantile convulsions, and confirm linkage to a pericentromeric chromosome 16 locus. BACKGROUND: PKD is characterized by frequent, recurrent attacks of involuntary movement or posturing in response to sudden movement, stress, or excitement. Recently, an autosomal dominant PKD locus on chromosome 16 was identified. METHODS: The authors studied 11 previously unreported families of diverse ethnic background with PKD with or without infantile convulsions and performed linkage analysis with markers spanning the chromosome 16 locus. Detailed clinical questionnaires and interviews were conducted with affected and unaffected family members. RESULTS: Clinical characterization and sampling of 95 individuals in 11 families revealed 44 individuals with paroxysmal dyskinesia, infantile convulsions, or both. Infantile convulsions were surprisingly common, occurring in 9 of 11 families. In only two individuals did generalized seizures occur in later childhood or adulthood. The authors defined a 26-cM region using linkage data in 11 families (maximum lod score 6.63 at theta = 0). Affected individuals in one family showed no evidence for a shared haplotype in this region, implying locus heterogeneity. CONCLUSIONS: Identification and characterization of the PKD/infantile convulsions gene will provide new insight into the pathophysiology of this disorder, which spans the phenotypic spectrum between epilepsy and movement disorder.

Adolescent↗
PubMed1989

[Adverse drug interactions between pyridonecarboxylic acids and nonsteroidal antiinflammatory drugs: convulsion after oral or intracerebral administration in mice].

Comparing with other pyridonecarboxylic acids (PCAs), the neurotoxicity of (+/-)-7-(3-amino-1-pyrrolidinyl)-6-fluoro-1-(2,4-difluorophenyl)-1,4- dihydro-4-oxo-1,8-naphthyridine-3-carboxylic acid p-toluenesulfonate hydrate (T-3262), which is a new PCA, was investigated in mice in a combination with fenbufen (FBF). T-3262, ofloxacin (OFLX) and nalidixic acid (NA) did not produce convulsion, but enoxacin (ENX) and norfloxacin (NFLX) produced it after an oral administration with FBF. The intracerebral injection of drugs alone to mice revealed that both FBF and 4-biphenylacetic acid (BPAA), which is principally responsible for FBF's antiinflammatory action, scarcely had convulsant activity. While all the PCAs had convulsant activity and the order of potency was as follows; NFLX greater than ENX greater than OFLX greater than penicillin G potassium greater than the free base of T-3262 (T-3262 base) greater than or equal to NA. When orally pretreated with BPAA, the convulsive threshold was scarcely lowered for T-3262 base and OFLX, but for ENX and NFLX it was lowered to about 1/300 and 1/100 of the respective activity. As the result, convulsant activities of ENX and NFLX were greatly potentiated, and their potencies became almost equal. The adverse drug interactions between T-3262 and FBF were scarcely observed in mice.

4-Quinolones↗
PubMed1975

[Application of animal mass psychology to pharmacology (XI). The role of light in the induction of convulsions in E1-mice].

In preliminary experiments to investigate the influence of masking the eyes of E1-mice on the rate of non-convulsions (RNC), it was suggested that the quantity of light as well as visibility itself played a role in inducing convulsions. The following experiments were thus carried out: (a) Both TSC (the threshold of number of shakings required for induction of convulsions) and RNC increased remarkably on the 5th day after enucleation of bilateral eyeballs from E1-mice, but 15 days later recovery to control level was observed. Moreover, TSC and RNC at 2 p.m. increased considerably compared with the control, however, the increase was rarely observed at 10 a.m.. (b) 2 groups of E1-mice reared intact under radiation of light plus different time schedules were shaken at 10 a.m. and 2 p.m., respectively. Consequently, TSC after radiation for 5 hours was less than that after radiation for 1 hour. When observed 9 hr after radiation, TSC could not be differentiated from TSC at 5 hr after the radiation. (c) E1-mice were reared under continuous lighting, continuous darkness or a normal lighting situation, after which TSC and RNC were examined. From our observations, the intensity of light appears to play a role in inducing convulsions. (d) When mice were shaken immediately after lighting, RNC decreased in inverse proportion to increase in the quantity of light. TSC was not influenced by the luminosity itself. One hour after lighting, however, the influence of lighting had disappeared. The intensity, quantity or irradiation time would not, however, influence the induction of E1-mice convulsions so much as the cognizance of light by the individual animals. Such a conception is derived from the "cognitive theory" in psychology.

Animals↗
PubMed1982

Alteration of convulsive threshold and sensitivity to CNS acting drugs in sedative-hypnotics-experienced rat offspring.

The present study was made to investigate the developmental toxicity of ethanol and several sedative-hypnotics (barbital, diazepam, phenobarbital) administered to rat pups via dams for 18 days (day 3-21 after parturition) from the relatively early postnatal stage in terms of changes in the threshold for pentetrazol (PTZ)-induced convulsion, tolerance to, and physical dependence on barbital (B). In the pups of all dosed groups, the convulsive threshold for PTZ is reduced significantly compared with that in the naive group. The sleeping time with B in phenobarbital-exposed offspring was also reduced significantly compared with that in the naive pups. No difference was however, noted in the B concentration of the brain or plasma upon awaking between these groups of pups, which proved that the phenobarbital-exposed pups had obviously acquired a functional tolerance to B. B-dependence formation and the ensuring weight loss and appearance of withdrawal signs, especially clonic-tonic convulsion, were made intense in the phenobarbital-experienced pups. From these results, it may be concluded that exposure to sedative-hypnotics from the early CNS developing stage makes a lowered state of convulsive threshold for PTZ, and therefore, tends to enhance B-withdrawal convulsion. These phenomena were discussed from the viewpoint of monoamine metabolism in the brain.

Animals↗
PubMed1993

Involvement of brain serotonergic function in lidocaine-induced convulsions in mice.

Influences of drug-induced manipulations of central serotonergic function on lidocaine- and pentylenetetrazol (PTZ)-induced convulsions were examined in mice. Agents that suppressed serotonergic transmission increased, whereas drugs that facilitated serotonin (5-HT) function decreased the incidence of lidocaine-induced convulsions. These treatments had similar influences on the incidence of PTZ-induced convulsions. Lidocaine (10(-5)-10(-3) M) reduced the stimulation evoked [3H]5-HT release from cortical slices, followed with an increased spontaneous [3H] overflow at higher concentrations. These results may suggest that brain 5-HT neurons are causally involved as inhibitory neurons in lidocaine-induced convulsions as in the case of PTZ-induced convulsions.

5-Hydroxytryptophan↗
PubMed1998

Role of nitric oxide in the convulsions following the coadministration of enoxacin with fenbufen in mice.

Effects of nitric oxide (NO) synthase inhibitors on the enoxacin-induced convulsions were examined in mice pretreated with fenbufen. 7-nitroindazole markedly suppressed the incidence of convulsions, whereas L-arginine did not modify the convulsions at all. The suppression of the convulsions by 7-nitroindazole was not reversed by the pretreatment of L-arginine. Brain NO synthase activity was significantly raised at 30 min after enoxacin when combined with fenbufen. The increased NO synthase activity was found to be suppressed by the pretreatment of 7-nitroindazole. These findings suggest that endogenous NO may be involved as a proconvulsant substance in the development of enoxacin-induced convulsions in mice pretreated with fenbufen.

Animals↗
PubMed2004

Antiepileptic effects of single and repeated oral administrations of S-312-d, a novel calcium channel antagonist, on tonic convulsions in spontaneously epileptic rats.

We investigated the effects of single and repeated administrations of S-312-d (methyl-4,7-dihydro-3-isobutyl-6-methyl-4-(3-nitrophenyl)-thieno-[2,3-b]pyridine-5-carboxylate), a newly synthesized L-type Ca(2+)-channel blocker, on tonic convulsions and absence-like seizures in the spontaneously epileptic rat (SER: zi/zi, tm/tm), a genetically based animal model of human epilepsy. Single oral administrations of S-312-d dose-dependently inhibited tonic convulsions and the effects lasted for more than 2 h, although they did not attenuate the absence-like seizures. We also examined the effects of repeated administrations of S-312-d at 1 mg/kg once a day for 4 days on SER. A significant decrease in the number and total duration of tonic convulsions was observed 45 and 75 min after the first administration of the drug, respectively. The effects lasted for 24 h without changes in the background EEG or blood pressure. This inhibitory effect on the tonic convulsions was gradually strengthened by subsequent daily administrations of S-312-d and lasted for 3 days after the cessation of drug treatment. In contrast, the repeated treatment with S-312-d did not influence absence-like seizures of SER. These results suggest that S-312-d is a candidate drug that has antiepileptic effects against the convulsive seizures in human epilepsy.

Administration, Oral↗
PubMed1999

Parental perceptions of pre-adolescent children who have experienced a febrile convulsion: effects of social class and gender.

OBJECTIVES: To examine whether, in terms of parental reports, the behaviour of pre-adolescent children who have been hospitalized following a febrile convulsion in infancy--without intracranial infection--differ from a group hospitalized with a non-febrile illness. DESIGN: A between-groups comparison of febrile and non-febrile children and a within-group comparison by gender and social class design were used. METHOD: The study compared 57 children, aged 9-12 years, who had experienced febrile convulsions before the age of 4 with a group of 66 children of similar age who had been hospitalized for non-convulsive conditions. Behaviour was measured using the Rutter A Parent Scale, the Berg Self-Administered Dependency Questionnaire (SDAQ) and the Werry-Weiss-Peters Activity Rating Scale. RESULTS: The scores of the children who had experienced a febrile convulsion in early life did not differ significantly from those of unaffected controls on any of the three measuring instruments. There were, however, marked social class differences on all three, with working-class children tending to lean towards poorer social adjustment than their middle-class peers. There was also one significant gender difference: boys received higher Assistance scores than girls on the SDAQ. CONCLUSIONS: In terms of social behavioural sequelae, febrile convulsions do not appear to have long-term effects. Hence, reassurance of a favourable outcome at the time of the seizure may ameliorate parents' worries at this frightening event in their child's life.

Child↗
PubMedDate not supplied

[Concussive convulsions in the differential diagnosis of post-traumatic epilepsy].

INTRODUCTION: Concussive convulsions are motor manifestations in acute head injury. This clinical phenomenon should be distinguished from epileptic seizures. We present two young men with motor and convulsive manifestations in acute head injury. Patient 1. A 18-year old basketball player fell on the parquet during a game. Initially he was struck on the right shoulder which caused brief and vigorous twitch of the head towards the ground and additional temporal impact. At the moment of impact he lost consciousness and developed tonic leg and arm posturing with both clenched fists. His legs were extended during next 20 seconds. Thereafter he was still and his loss of consciousness lasted 3 minutes. Patient 2. A 26-year old man fell on the wooden ground from a 4 m high ferry. He got head impact and lost consciousness. In a few seconds he had tonic/clonic convulsions for the next 10-15 seconds. Ten minutes later he awaked. Results of subsequent neurological examination, electroencephalography and cerebral magnetic resonance imaging studies were normal in both patients. They returned to their occupations after four weeks without problems for a further one year. CONCLUSION: Described motor manifestations present concussive convulsions. These clinical features are due to transient functional decerebration and corticomedullary dissociation during cerebral concussion. Concussive convulsions are a non-epileptic phenomenon, they are not associated with structural brain injury and have good prognosis. Antiepileptic treatment is not indicated.

Adolescent↗
PubMed1999

[Convulsion associated with mild gastroenteritis: occurrence in identical twins on the same day].

We reported identical twin cases having convulsion associated with mild gastroenteritis almost simultaneously. The patients were 14-month-old boys. They suffered from vomiting from one day before the onset of convulsion. Convulsions occurred firstly in the first twin, and then in the second one immediately after the convulsion of the first one. The twins experienced 6 and 4 convulsions respectively, although they were treated with diazepam and phenobarbital. An ictal EEG of the second twin revealed a focal paroxysmal discharge in the right occipital area spreading rapidly to all areas. During the follow-up period, no recurrence of seizures was observed and psychomotor development was normal in both of them.

Diseases in Twins↗