Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CONVULSIONS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 793 records · Page 44Linked to original sources

Convulsive effect of theophylline in conscious and anaesthetized guinea-pigs.

In urethane-anaesthetized guinea-pigs, the effect of theophylline (theo) on heart rate, arterial blood pressure, respiration rate and limb movements were recorded. Continuous intravenous infusion of theo initially increased the respiratory and heart rates and lowered the arterial blood pressure. After infusion of about 50 mg/kg of theo, the cardiovascular effects reached a maximum and were then only slightly changed until the terminal stage. A tonic stretching of the limbs (at 155 +/- 15 mg/kg) preceded generalized seizures of clonic tonic convulsions which were recorded after infusion of 367 +/- 25 mg/kg of theo. At this stage, respiration was highly irregular. PaO2 started to fall and PaCO2 to rise, while a plasma acidosis developed rapidly. The convulsions progressed in frequency and intensity and were terminally associated with respiratory and cardiovascular collapse. The convulsive effects of theophylline were similar to those observed in conscious guinea-pigs after 250 mg/kg of theo orally. The present findings agree with the view that the convulsive effect is a primary life-threatening action of theophylline. The method described may be of use in the search for new, less toxic xanthine drugs.

Administration, Oral↗

Binding of beta-carbolines and caffeine on benzodiazepine receptors: correlations to convulsions and tremor.

Compounds from both the beta-carboline (BC) and xanthine groups have been suggested to be the natural ligands for benzodiazepine (BZ) receptors. In this study we examined the effects of several BC's and caffeine, 1,3,7-trimethylxanthine, on the binding of 3H-flunitrazepam (3H-FZ) and beta-3H-carboline-3-carboxylic acid ethyl ester (3H-BCCE) to the BZ receptors of rat and mouse brain. In mice, convulsion-producing doses of caffeine (120 mg/kg intravenously) and harmane (30 mg/kg intravenously) lowered the specific binding of 3H-FZ in vivo by 12-31%. A tremorogenic dose of harmaline (30 mg/kg intravenously) increased binding by 31%. Caffeine and harmane also slightly decreased the in vivo binding of 3H-BCCE, a compound that binds preferentially to the cerebellar type of BZ receptors. Harmaline stimulated the binding of 3H-BCCE only in the forebrain. Both harmaline and harmane increased by 41-111% the amount of 3H-BCCE that was distributed to the brain. In vitro BC's and caffeine displaced 3H-FZ from receptors in the rat brain with various Ki values (4.7 to 206.9 microM). The antagonism for BZ binding was competitive and in Scatchard analysis produced linear plots. Exceptions were harmaline and caffeine in the forebrain: both exhibited curvilinear plots for 3H-FZ binding. Harmaline increased the binding, and caffeine decreased it by altering the affinity of a subgroup of BZ receptors. In the hindbrain both harmaline and caffeine inhibited binding and produced linear plots. BC-induced tremor and convulsions unveil a large number of spare receptors in the brain, and these seem to be of the cerebellar type of BZ receptors. In addition, our results show that tremorogenic and convulsive BC's act differently on BZ receptors: during harmaline-induced tremor the affinity of some BZ receptors is increased, while harmane-induced convulsions are connected to direct occupation of BZ receptors.

Animals↗

Cerebrospinal fluid acid-base status and lactate and pyruvate concentrations after short (less than 30 minutes) first febrile convulsions in children.

Twenty-nine infants and children with short (less than 30 minutes) first febrile convulsions were studied between 3 and 22 hours after convulsive episodes. Arterial and CSF acid-base variables, lactate and pyruvate concentrations, and lactate/pyruvate ratios were measured. Biochemical signs of cerebral hypoxia were found in only 2 patients, one of whom had short, repeated convulsions. Our findings indicate that hypoxic damage is unlikely to result from a short-duration febrile convulsion.

Acid-Base Equilibrium↗

Prophylactic diazepam or phenobarbitone in febrile convulsions: a prospective, controlled study.

After their first episode of febrile convulsions, 195 previously healthy children, aged 6--30 months, were given either diazepam or phenobarbitone for a year. Each child was assigned at random to one of the two medications: children admitted on even days were given a suppository containing 5 mg diazepam every 8 hours when the rectal temperature was greater than or equal to 38.5 degree C. Children admitted on odd days were given treatment with phenobarbitone, 3.5 +/- 1 mg/kg per day. 156 children completed treatment and outpatient control for a year, 83 in the diazepam and 73 in the phenobarbitone group. The rate of recurrence was independent of the prophylactic and 15--16 % of the children in both groups had new febrile convulsions within a year. The recurrence rate after 6 months was also similar, 11% in the diazepam group and 9% in the phenobarbitone group. New convulsions were of similar duration and severity in both groups. In both groups 6% of all febrile episodes led to new convulsions. Long-term treatment with phenobarbitone thus offered no advantage over intermittent diazepam.

Child, Preschool↗

Neonatal convulsions--a 10 year review.

The incidence and aetiologies of neonatal convulsions within a hospital population were reviewed over 10 years (1971-80 inclusive). Three periods, 1971-4 (12 904) live births). 1975-7 (13 304 live births), and 1978-80 (14 849 live births) during this decade are compared. The overall incidence of neonatal convulsions rose from 2-6/1000 and then to 8.6/1000 live births. Most convulsions were associated with cerebral hypoxia and 'fifth day fits'. Increasingly thorough investigations reduced the number of infants in whom no cause was identified to 11%. Although there was an appreciable overall reduction in mortality associated with convulsions, mortality among babies whose fits were caused by cerebral hypoxia remained over 50%.

Australia↗

Febrile convulsions--what do parents do?

To find out about the medical and parental management of children having their first febrile convulsion a hospital-based questionnaire study was carried out in which parents were asked what they did at the time. Fifty-four out of 89 parents brought their child directly to hospital while the remainder attempted to contact their general practitioner, usually successfully, and were then referred to hospital. Whichever course of action the parents chose the outcome was satisfactory. Eighty-seven per cent of convulsions lasted for less than 15 minutes and in only two instances did they last longer than 30 minutes. One child who had convulsions for an hour was given intramuscular phenobarbitone at home without success, and the fit was finally terminated with intravenous diazepam. Parental management of the fit was often widly inappropriate. Only a few parents laid the child on his side and waited for the fit to stop. The parents were bewildered and frightened--30% thought their child was dying or dead. Education of patents of young children is needed. Simply written instructions on how to reduce the temperature of a febrile child and manage a convulsion might help.

Attitude↗

Occult pneumococcal bacteraemia and febrile convulsions.

Over two years 29 children had bacteraemia due to Streptococcus pneumoniae at this hospital. In 15 previously healthy children the site of infection could not be identified, and in most of them, bacteraemia was not suspected clinically. All 15 had high total white cell (greater than or equal to 17 x 10(9)/1) and neutrophil (greater than or equal to 11 x 10(9)/1) counts. Twelve children were under 4 years of age, and of these, 10 had been admitted because of a simple febrile convulsion and one had a prolonged febrile convulsion. Occult pneumococcal bacteraemia has been reported in the USA for more than 10 years, but no series has been reported from the United Kingdom. Occult pneumococcal bacteraemia may be an important cause of febrile convulsions. Persisting bacteraemia and the development of focal infections, including pneumococcal meningitis, have been reported. Meningitis did not occur after occult bacteraemia in our patients. Studies to date have been retrospective, and thus the true incidence of the complications and the best treatment are not clear. A prospective study of children with febrile convulsions could provide answers.

Age Factors↗

Febrile convulsions in a national cohort followed up from birth. II--Medical history and intellectual ability at 5 years of age.

Three hundred and three children with febrile convulsions were identified in a national birth cohort of 13 135 children followed up from birth to the age of 5 years. Breech delivery (p less than 0.05) was the only significantly associated prenatal or perinatal factor. There were no associations with socioeconomic factors. Excluding the 13 known to be neurologically abnormal before their first febrile convulsion, children who had had a febrile convulsion did not differ at age 5 from their peers who had not had febrile convulsions in their behaviour, height, head circumference, or performance in simple intellectual tests.

Analysis of Variance↗

Outcome of childhood status epilepticus and lengthy febrile convulsions: findings of national cohort study.

OBJECTIVE: To study outcome after lengthy febrile convulsions and status epilepticus in children. DESIGN: Population based birth cohort study. SETTING: The child health and education study (16,004 neonatal survivors born in one week in April 1970). SUBJECTS: Information available for 14,676 children. OUTCOME MEASURES: Clinical information and tests of intellectual performance at five and 10 years after birth. RESULTS: 19 children had lengthy febrile convulsions and 18 had status epilepticus. Two children with status epilepticus died (one at 5 years old); neither death was directly due to the status epilepticus. Four of the 19 (21%) developed afebrile seizures after lengthy febrile convulsions compared with 14 of the 17 (82%) survivors after status epilepticus. Measures of intellectual performance were available for 33 of the 35 survivors: 23 were normal and 10 were not normal but eight of them had preceding developmental delay or neurological abnormality. CONCLUSION: The outcome in children after lengthy febrile convulsions and status epilepticus is better than reported from studies of selected groups and seems determined more by the underlying cause than by the seizures themselves.

Child↗

A magnetic resonance study of complicated early childhood convulsion.

OBJECTIVES: The relation between complicated early childhood convulsion (ECC) and adult epilepsy is unclear, although a history of complicated ECC is obtainable in half of adults with epilepsy associated with hippocampal sclerosis. It is not known if the ECC is a marker of pre-existing brain damage or is itself harmful to the developing brain. The objective of the study was to assess the extent of structural brain abnormality present soon after a first complicated early childhood convulsion with a view to obtaining data which might contribute to an understanding of whether such abnormalities were likely to be pre-existing or caused by the convulsion. METHODS: Children under the age of 5 years were recruited into the study after their first complicated febrile or non-febrile ECC. None had previously experienced an epileptic seizure. All underwent MRI of the brain within 14 days. Hippocampal volumes and T2 relaxation times were measured. The results were compared with a neurological control group of children without gross structural abnormalities of the neocortex undergoing MRI of the brain for reasons other than epilepsy. RESULTS: Eighteen patients and 10 control subjects were recruited into the study. One patient was subsequently excluded because of EEG and clinical evidence of benign childhood epilepsy. Nine patients had volumetric evidence of significant hippocampal volume asymmetry (3 SD from the mean of the control group), although in only three of these was the asymmetry apparent on visual inspection of the MRI. Three patients had extrahippocampal neuropathology. None of the control subjects had significant hippocampal volume asymmetry (p<0.001). T2 relaxometry showed no evidence that postictal hippocampal oedema contributed to the asymmetry. CONCLUSIONS: There is a high prevalence of structural brain abnormalities in children within 2 weeks of the first complicated early childhood convulsion, including significant hippocampal asymmetry unrelated to oedema. This does not exclude a damaging effect of complicated ECC on the brain, but suggests that in at least some patients the complicated ECC is the result of pre-existing brain abnormalities.

Brain↗

Hypocalcaemia and convulsions.

Hypocalcaemia may manifest with tetany, convulsions and even status eqilepticus. Recognition of underlying hypocalcaemia in convulsions is mandatory because the fits may not be adequately controlled by anti-convulsant drugs which may also aggravate hypocalcaemia. Vitamin D, by relieving hypocalcaemia, reduces the frequency of convulsions and may even eliminate them.

Adult↗

Predictors of posttraumatic convulsions in head-injured children.

The purpose of this study was to determine predictors of posttraumatic convulsions in children. Study subjects included children under 12 years of age, who were admitted to the Safdarjang Hospital, New Delhi, during the year 1997 (January to December) after suffering head trauma. The occurrence of first convulsion after head injury was taken as the outcome variable in the study. Medical records were reviewed for data about clinical, radiological and epidemiological features of such children. The study revealed that children younger than 2 years of age (odds ratio, OR 2.96; 95% confidence interval, CI 1.42-6.21), those suffering severe head injuries, i.e. with low Glasgow Coma Score (OR 3.07; 95% CI 1.40-6.77), and those with longer period of unconsciousness after head trauma, especially longer than 12 h (OR 1.71; 95% CI 0.69-4.19) have higher likelihood of suffering convulsions after head injury. However, none of the radiological findings were found to be significantly associated with posttraumatic convulsions.

Age Factors↗

Excitatory amino acid-elicited tonic convulsions in mice and N-methyl-D-aspartate receptor activation: role of Ca(2+) influx and involvement of intracellular Ca(2+)-dependent biochemical processes.

Intravenously administered nimodipine (an L-type Ca(2+) antagonist) as well as dizocilpine (an N-methyl-D-aspartate--NMDA--antagonist) showed a wide spectrum of anticonvulsant activity in intracerebroventricular mouse models for excessive activation of excitatory amino acid receptors. The duration of Bay k-8644 (L-type Ca(2+) agonist; intracerebroventricular administration) caused seizures was significantly reduced by intravenously administered nimodipine. Intracisternal administration of Bay k-8644 lowered the convulsion threshold of an intracerebroventricular injection of NMDA. Intracisternal administration of omega-conotoxin GVIA (N-type Ca(2+) antagonist) only tended to inhibit the NMDA-induced tonic convulsions. Intracisternal administration of staurosporine (a protein kinase C inhibitor) or calmidazolium (a calmodulin antagonist) was effective in inhibiting the NMDA-induced tonic convulsions. Calmidazolium, unlike staurosporine, produced side effects at a dose showing its anticonvulsant activity. From these results, it is suggested that excessive activation of excitatory amino acid receptors results in tonic convulsions by virtue of a massive increase of Ca(2+) influx mainly through NMDA receptor channels, and at least in part through L-type Ca(2+) channels, and in subsequent activation of protein kinase C and possibly calmodulin.

Animals↗

Sodium valproate in the prophylaxis of simple febrile convulsions.

Thirty children with simple febrile convulsions were treated with sodium valproate following their second convulsion. Twenty-two of the 30 (73%) had no further convulsions during the one-year period of observation compared with 17 of 28 in the control group (61%). This was not a statistically significant difference. Side effects attributed to sodium valproate treatment were noted in 7 patients (23%), although 4 of these showed only mild transient gastrointestinal symptoms at high dosage. The study did not confirm any advantage in the use of sodium valproate as a prophylaxis for febrile convulsions, although compliance was good and significant side effects infrequent.

Chemical and Drug Induced Liver Injury↗

A controlled trial of pyridoxine supplementation in children with febrile convulsions.

A total of 107 children who had been hospitalized following a febrile convulsion were enrolled into the trial. By random allocation, 55 children were treated with pyridoxine hydrochloride (20 mgs twice daily) and the remaining 52 children were treated with a placebo until there had been either a further convulsion or a year had passed without recurrence. Eighty children were adequately followed up and of these, 17 had a recurrent febrile convulsion while receiving medication. Recurrences occurrences occurred in 7 of the 38 children receiving pyridoxine and in 10 of the 42 children receiving placebo (X2 = .346, p greater than 0.5). Initial tryptophan load tests had been abnormal in 34 children, and of these, recurrences occurred in 3 of the 17 who received pyridoxine and in 3 of the 17 who received placebo. It has yet to be shown that pyridoxine supplementation protects children from recurrent febrile convulsions.

3-Hydroxyanthranilic Acid↗

Benign familial infantile convulsions: phenotypic variability in a family.

Benign familial infantile convulsion is an autosomal dominant epilepsy syndrome characterized by seizures starting from 3 to 12 months and a favorable outcome. We present a Turkish family with benign familial infantile convulsions and report the clinical variability associated with this syndrome in three generations. All 11 affected members had benign infantile seizures, which were primarily generalized in all but one patient, who had partial seizures with secondary generalization. The seizures started within the first year and were accompanied by normal neurologic development and a good response to treatment with phenobarbital. In this family, the phenotype extended beyond infancy. The index patient had unilateral occipital spike and waves on electroencephalography (EEG), although he had no clinical seizures at 4 years of age. Follow-up EEG of this patient 1 year later showed that the discharges shifted to the occipital lobe of the other hemisphere. The grandmother of this patient had temporal lobe seizures as an adult, years after the remission of infantile convulsions. One of the patients experienced paroxysmal choreoathetosis during adolesence. Our findings highlight the intrafamilial phenotypic variability of benign familial infantile convulsions in a large pedigree with long-term follow-up.

Adolescent↗

Secondarily generalized convulsive seizures induced by daily amygdaloid stimulation in rhesus monkeys.

Amygdaloid kindling in rhesus monkeys resulted in development of secondarily generalized convulsive seizures in an average of 196 days. Prior pharmacologic (bemegride) kindling accelerated this seizure development in one animal. None of the animals reached the stage 5 primary generalized seizure of baboons (Papio papio), even after 400 daily amygdaloid stimulations. Seizure stage instability, with frequent regression to an earlier stage, and the difficulty of establishing a generalized seizure triggering threshold in most of the rhesus monkeys, contrasts with our experiences in Papio papio. Thus, differences in the speed of kindling and in the quality of kindled convulsion between rhesus monkeys and epileptic baboons probably reflect the presence or absence of an epileptogenic predisposition in these two species. The difficulty of developing convulsive seizure in rhesus monkeys suggests that this species is particularly suited for the study of partial complex seizure. These studies indicate that the abrupt onset of human epilepsy with a fully developed convulsive seizure must represent and overwhelming central pathophysiologic event resulting from an endogenous, exogenous or a combined insult interacting with a genetically predisposed seizure susceptibility.

Amygdala↗

[Anti-convulsion effects of choto-san and chotoko (Uncariae Uncis cam Ramlus) in mice, and identification of the active principles].

The crude drug, Chotoko (Uncariae Uncis cam Ramlus), the hooks of Uncaria spp. (Rubiaceae), has been claimed to possess sedative and anti-spasmodic actions, and is contained in a Chinese traditional preparation, Choto-san, as a main crude drug. Examinations were made on the anti-convulsion effects of Choto-san and Chotoko against some animal models of epilepsy conducted by the stimulation of drugs or electricity. Oral administration of the Choto-san extract to mice at the doses of 1.0 g/kg and 3.0 g/kg tended to inhibit the glutamate-induced convulsion in a dose-dependent manner, and the effect of the Chotoko extract at a 3.0 g/kg dose was significant, while both the extracts showed no activity against the picrotoxine-induced, strychinine-induced, and electroshock convulsions. The Choto-san preparation without Chotoko was inactive, and the activity of the Chotoko extract was more potent than that of the every crude drug comprising Choto-san, suggesting that Chotoko plays the most important role in the Choto-san prescription and contains some active compounds. Bioassay-guided fractionation of the Chotoko extract led to the location of the active components in the less polar alkaloids-containing fraction, from which three indole alkaloids, geissoschizine methylether (1), hirsuteine (2) and hirsutine (3), and an oxyindole alkaloid, isocorynoxeine (4) were isolated and identified. Oral administration of 1 and 2 to mice at the doses of 50, 100, and 200 mg/kg inhibited the glutamate-induced convulsion in a dose-dependent manner. The effect of 3, the dihydro derivative of 2, was less potent than those of 1 and 2. Compound 4 showed no activity at a 100 mg/kg dose compared with control. The above results support the Chinese herbal description of the anti-spasmodic action of Chotoko, and show that 1 and 2 contained in Chotoko must be mainly contributed to the activity. It is also suggested that Choto-san may be clinically available for treatment of epilepsy.

Alkaloids↗