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PubMed1981

Febrile convulsions and cot death.

Examination of the records of hospital admissions and all deaths among the 40,544 Sheffield children who were aged less than two years in the period 1975-79 revealed 475 children admitted with their first febrile convulsion and 50 children who presented as cot deaths. Rectal temperatures taken before refrigeration were traced for 24 of the latter. 10 of these 24 children had temperatures in excess of 38 degrees C and 5 were greater than 40 degrees C. There was a transition in age at presentation between the two groups, with most cot deaths occurring before six months of age and febrile convulsions after that age. No time-based clustering between the date of presentation with cot death or febrile convulsion was found to suggest a single aetiological agent. It is suggested that febrile convulsions and some inexplicable sudden infant deaths may be equivalent responses to a febrile stimulus, but with a different outcome because of the difference in age of occurrence. A common mechanism could be thermolabile syncope which, in the susceptible younger infant, leads to irreversible cerebral ischaemia. The rectal temperature should be taken as soon as possible in all cot deaths. An aberration of a vagally mediated reflex may be responsible for some cot deaths.

Age Factors↗
PubMed1990

The influence of stress on convulsive parameters in the mouse.

Mice exposed to the stress of conspecific aggression for 10 min showed shorter latencies to convulsions induced by pentylenetetrazol but not by pilocarpine. This effect was short lived and was not influenced by pretreatment with naltrexone (5 mg/kg, SC). The onset of pilocarpine-induced convulsions in stressed mice was reduced by the opioid antagonist. Aggression stress did not change the incidence, duration or severity of convulsions triggered by the chemoconvulsants or electroshock. The results differ widely from those obtained using other stressogenic models such as cold-restraint or swim stress. This suggests that alterations of convulsive parameters and the involvement of opioid mechanisms in their mediation are critically dependent on the characteristics of the stressogenic procedure employed.

Animals↗
PubMed2002

Synthesis, crystal structure, EPR properties, and anti-convulsant activities of binuclear and mononuclear 1,10-phenanthroline and salicylate ternary copper(II) complexes.

Two ternary Cu(II) complexes of 1,10-phenanthroline (phen) and singly (Hsal(-)) or dideprotonated (sal(2-)) salicylate ligands were synthesized, their X-ray crystal structure and electron paramagnetic resonance spectral characteristics determined, and evaluated for anti-convulsant activities in the maximal electroshock (MES) and Metrazol models of seizure and Rotorod toxicity. The X-ray crystal structure of [bis(1,10-phenanthroline)-mu-bis(salicylato-O,O')dicopper(II)] dihydrate, 1, ([Cu(II)(2)(phen)(2)(sal)(2)].2[H(2)O]), shows it to be binuclear. This dimer consists of two centrosymmetrically related pseudo-five coordinate Cu(II) atoms 3.242(2) A apart and bridged by two dideprotonated salicylate ligands. The X-ray crystal structure of [bis(1,10-phenanthroline)(salicylato)copper(II)][salicylate] monohydrate, 2, ([Cu(II)(phen)(2)(Hsal)](+)[Hsal](-)[H(2)O]), shows it to be mononuclear. This complex cation exhibits a highly irregular distorted square pyramidal geometry about the Cu(II) atom, (4+1+1*). Each salicylate is singly deprotonated and one of them is ligand bonded in an asymmetric chelating mode. EPR results for 2 indicate that in concentrated DMF solution phen remains bonded to copper but salicylate is likely monodentate in contrast to the situation for 1. However, in dilute DMF solution, both 1 and 2 form the same species, which accounts for the similarity in anti-convulsant activity of the two compounds. Both 1 and 2 were found to be effective in preventing MES-induced seizures and ineffective in preventing Metrazol-induced seizures. Rotorod toxicity, consistent with central nervous system depression, paralleled the observed anti-convulsant activity. It is suggested that the observed anti-convulsant activity is consistent with central nervous system depression as a physiological mechanism in overcoming MES-induced seizures due to MES-induced brain inflammatory disease.

Animals↗
PubMed2001

Do recurrent febrile convulsions decrease the threshold for pilocarpine-induced seizures? Effects of nitric oxide.

The aim of the study was to determine whether (1) number of febrile convulsions is a predictor of development of temporal lobe epilepsy, (2) the susceptibility of rats to pilocarpine-induced seizures is increased due to febrile convulsions and (3) nitric oxide is a mediator in the pathogenesis of febrile convulsions. Rat pups were exposed to single or multiple hyperthermic seizures. Subconvulsant doses of pilocarpine (100 mg/kg and 150 mg/kg) were injected intraperitoneally to these rats at 60--70 days of age. Also L-arginine was applied to some rats before a single hyperthermic seizure. We found that risk of future epilepsy increases parallel to the number of febrile convulsions and nitric oxide does not have a pathogenetic role at given doses.

Animals↗
PubMed2001

Lack of mu-opioid receptor leads to an increase in the NMDA receptor subunit mRNA expression and NMDA-induced convulsion.

The present study investigated in situ hybridization of N-methyl-D-aspartate (NMDA) receptor (NR) subunit mRNA and convulsion induced by intracerebroventricular injection of NMDA, in order to examine changes in NMDA receptor function in mu-opioid receptor gene knockout mice. Levels of NR1 and NR2A subunit mRNA were significantly increased in the parietal cortex (8.4 and 10.6%, respectively) and hypothalamus (8.7 and 15.2%, respectively) in mu-opioid receptor knockout mice. Levels of NR2B subunit mRNA were noted to be increased in the parietal cortex (9.1%), thalamus (7.7%), and hypothalamus (10.4%) in mu-opioid receptor knockout mice. The ED(50) for NMDA-induced convulsion in wild-type mice was 0.20 microg/10 microl/mouse. The ED(50) in mu-opioid receptor knockout mice was 0.14 microg/10 microl/mouse. There is a significant difference in the potency ratio of wild-type mice versus knockout mice (potency ratio: 1.44, P < 0.05). These results indicate that mu-opioid receptor knockout mice are more sensitive to NMDA-induced convulsion. Therefore, these results suggest that absence of mu-opioid receptor gene is accompanied by changes in the NMDA receptor system which can modulate the synaptic excitability in the process such as convulsion or epilepsy.

Animals↗
PubMed1999

Effects of diazepam or haloperidol on convulsion and behavioral responses induced by bilateral electrical stimulation in the medial prefrontal cortex.

1. Effects of diazepam (DZP) or haloperidol (HAL) on convulsions and behavioral responses (locomotion, circling, spying and head shaking) induced by bilateral electrical stimulation in the medial prefrontal cortex (mPFC) were examined. 2. Male Wistar rats were electrically stimulated (ten 30-sec trains, 60 Hz, 80-100 microA) bilaterally in the mPFC and their behavior was simultaneously observed in an open field in daily session. 3. DZP and HAL dose-response curves (0, 0.5, 1.25, 2.5 and 5 mg/kg, i.p., 30 min before electrical stimulation session) were determined after a baseline of behavioral responses was established. 4. DZP dose-dependently decreased head shaking and convulsions, had no effect in circling and spying behaviors, and increased locomotion except at the highest dose. HAL reduced locomotion, circling and spying behaviors in a dose-dependent manner, but did not affect convulsions or head shaking. 5. These results demonstrated that convulsion and behavioral responses induced by electrical activation of the mPFC were modified by DZP or HAL. Therefore, the mPFC is involved in the mediation of neural and/or behavioral activity that may be implicated in some central effects of psychoactive drugs.

Animals↗
PubMed1999

Cortical spreading depression reversibly disrupts convulsive motor seizure expression in amygdala-kindled rats.

To determine the role of the frontal cortex in the generalization of limbic seizures, we first produced unilateral cortical spreading depression to reversibly suppress neuronal activity in the motor cortex and then triggered an amygdala-kindled seizure. Three minutes following induction of unilateral spreading depression, stimulation of the ipsilateral kindled amygdala produced only a brief electrographic seizure, and completely failed to produce the bilateral electrographic and clonic convulsive seizures that were normally present during control trials. A very different outcome occurred when unilateral spreading depression was induced in the cortex contralateral to the kindled amygdala. In these cases, the electrographic amygdala seizures were normal and bilateral like control trials, yet the clonic convulsive seizures were lateralized and appeared to be controlled by the non-depressed, kindled hemisphere. These lateralized convulsions were identical to those observed following forebrain commissurotomy, when direct communication between the frontal cortices was permanently severed. The results of the present study further define the pathways of temporal lobe seizure propagation, and highlight the important contribution frontal cortical regions provide to both the electrographic and convulsive expression of amygdala-kindled seizures by amplifying local seizures and projecting them into downstream brainstem and spinal cord circuits.

Amygdala↗
PubMed1976

Simple febrile convulsions.

Simple febrile convulsions occur in otherwise normal children, aged six months to five years, with extracranial infection. Cerebrospinal fluid examination should be done on all children with their first febrile convulsion to rule out an underlying organic disease, especially purulent meningitis. Initial treatment includes antipyretics, tepid sponging and intramuscular phenobarbital. If a seizure recurs, the usual anticonvulsant measures should be carried out and, if prolonged, the patient should receive appropriated doses of diazepam or phenobarbital, intravenously. Patients with suspected epileptic convulsive disorders precipitated by fever, or those with seizures thought to be associated with underlying organic disease, should be hospitalized for further evaluation or treatment or both. Patients with simple febrile convulsions have a benign disorder and can be safely treated as outpatients.

Cerebrospinal Fluid↗
PubMed1997

Experimental study of the anticonvulsant plants used for treatment of infantile convulsion in Nigeria.

In Nigeria, convulsion, especially in children, is managed by traditional healers employing plant decoctions. A number of herbs are used for this purpose. We have carried out some preliminary studies on some of these traditional anticonvulsant plants. The experimental models were pentylenetetrazole- and electroshock-induced convulsions in mice. The acute toxicity (LD50) and the median effective (ED50) doses of the extracts of these plants were determined. Most of these plants exhibited potent anticonvulsant activity. The average onset of convulsion was delayed, while the average duration of convulsion was significantly reduced. Most of the animals showed signs of central nervous system depression. The results indicate that these plants possess anticonvulsant property, and this activity may be linked to their ability to depress the central nervous system.

Animals↗
PubMed2000

Co-segregation of benign infantile convulsions and paroxysmal kinesigenic choreoathetosis.

We report seven families and two sporadic cases in which benign infantile convulsions and paroxysmal kinesigenic choreoathetosis were co-segregated. Clinical investigations included physical and neurological examinations, blood electrolyte values, interictal and ictal electroencephalograms, and computed tomography or magnetic resonance imaging of the brain. The family pedigree was confirmed and the clinical history of the relatives was obtained. Seventeen individuals developed infantile convulsions followed by paroxysmal dyskinesias during childhood or adolescence. Six had only infantile convulsions, and two had only paroxysmal dyskinesias. The seizures never persisted into childhood or recurred in adulthood. The seizure type was a complex partial seizure, with or without secondary generalization, in nine of 14 patients. Paroxysmal dyskinesias, a subgroup of paroxysmal kinesigenic choreoathetosis, occurred for less than 5 min. The attacks of dyskinesias began at age 5-12 years in most patients, and tended to remit in adulthood. The mode of inheritance was apparently autosomal dominant in four of the families (17 affected individuals), who were diagnosed with ICCA syndrome (infantile convulsions and paroxysmal choreoathetosis). However, the condition occurred only among siblings in three families (six patients), and sporadically in two patients, suggesting genetic heterogeneity in this distinct co-segregation.

Adolescent↗
PubMed1981

Studies on homocarnosine in cerebrospinal fluid in infancy and childhood. Part II. Homocarnosine levels in cerebrospinal fluid from children with epilepsy, febrile convulsion or meningitis.

To clarify the pathophysiological role of homocarnosine in the cerebrospinal fluid (CSF) in children, homocarnosine levels in CSF were determined in patients with epilepsy (32 cases), febrile convulsion (5 cases) and meningitis (42 cases) with a high speed amino acid autoanalyzer (Hitachi Co.). Mean homocarnosine levels in CSF of controlled epileptic children, uncontrolled epileptic children and febrile convulsion cases were 0.61 +/- 0.25 mumol/dl, 1.03 +/- 0.37 mumol/dl and 1.09 +/- 0.04 mumol/dl, respectively. High homocarnosine levels in CSF of children with uncontrolled epilepsy or febrile convulsion may indicate the reduced turnover rate from homocarnosine to GABA. In patients with meningitis, the unconscious states were accompanied by significantly lower homocarnosine levels in CSF (0.39 +/- 0.20 mumol/dl) than those in the patients with clear conscious states (0.9 +/- 0.31 mumol/dl, however, in patients with clear conscious states homocarnosine in CSF were almost the same as those of normal children (0.89 +/- 0.23 mumol/dl). These data suggest that homocarnosine in CSF might be related to the convulsive tendency and consciousness.

Adolescent↗
PubMed1983

Prostaglandin F2 alpha concentrations in the cerebrospinal fluid of children with febrile convulsions, epilepsy and meningitis.

Cerebrospinal fluid prostaglandin F2 alpha (CSF PGF2 alpha) levels were measured by radioimmunoassay in children as follows: Febrile convulsions (31 cases), epilepsies (32 cases), meningitides (31 cases) and non-neurological diseases (20 cases), totaling 114 cases. A 4.5-fold increase in CSF PGF2 alpha levels was seen in simple febrile convulsion, and a 2.5-fold increase in those with complex febrile convulsion as compared to those with non-neurological diseases. On the other hand, no increase in CSF PGF2 alpha levels was seen in children with epilepsy. When the body temperature was normal, the mean CSF PGF2 alpha levels showed no relation with age. When the body temperature was between 37.5 degrees C and 40 degrees C, the CSF PGF2 alpha levels in infants were higher than those in older children. The CSF PGF2 alpha levels in children with meningitis were high. The mean CSF PGF2 alpha levels in bacterial meningitis were not statistically (p greater than 0.05) different from those in viral meningitis. The CSF PGF2 alpha levels in meningitis were high on admission and gradually decreased with therapy. The results of our studies indicate that PGF2 alpha of the central nervous system markedly increased in infants and children with febrile convulsions or meningitis but not in those with epilepsy.

Adolescent↗
PubMed1998

Effects of an educational program on parents with febrile convulsive children.

The purpose of this study was to characterize the effects of an educational program on knowledge, attitude, concern, and first-aid measures among parents with febrile convulsive children. All parents completed a pretest questionnaire 3 weeks before the meeting. The parents were assigned randomly into experimental (n = 65) and control (n = 64) groups on the day they attended the program. The control group completed the identical questionnaire (posttest) before the program, whereas the experimental group completed the same posttest after the program. In pretest, most parents considered electroencephalogram or computed tomography necessary in evaluating their children, suggested that immunization be postponed, and rated the risk of subsequent epilepsy as high for their children. Most of them favored frequent body temperature measurement, were very anxious about further febrile convulsion episodes during the night, and were fever phobic. After education, although only a slight change in fever anxiety was found, the experimental group showed significant improvement in knowledge, attitude, concerns, and anticipatory practice of febrile convulsion compared with the control group. In conclusion the parents' poor knowledge, negative attitudes, anxiety, and inadequate first-aid measures toward febrile convulsion can be effectively improved by an educational intervention program.

Analysis of Variance↗
PubMed1998

Induction of convulsive seizures by acoustic priming in a new genetically defined model of epilepsy (Noda epileptic rat: NER).

Noda epileptic rat (NER) is a mutant rat, found in a Crj: Wistar colony, which exhibits a tonic clonic convulsion spontaneously about once per 30 h from 14 weeks of age. We performed modified acoustic priming, that is, repeated weekly sound stimulations from 3 weeks of age. In addition, characteristics of audiogenic seizure (AGS), and ictal/interictal electroencephalograms (EEGs) were examined. We also studied the effect of repeated weekly stimulations from 14 weeks of age on AGS susceptibility in another NER. From 9 weeks of age, the NER primed from 3 weeks of age had a high incidence (100%) of AGS: a typical seizure was composed of sudden wild running and/or jumping (WRJ) followed by clonic or tonic-clonic convulsion. The severity and the duration of the AGS were intensified and prolonged with an increase in age, respectively. By contrast, the NER repeatedly stimulated from the age of 14 weeks, rarely showed AGS (20-40(%). The majority of the seizures in this NER were WRJ. The cortical and hippocampal EEG during the tonic convulsion showed a low-voltage spike-wave (5-7 Hz). This evolved into a high-amplitude spike- or polyspike-waves associated with the clonic convulsion. Immediately after cessation of the seizures, the EEG showed a flattening or diffuse slowing. In interictal EEG analysis, sporadic spikes predominantly in the hippocampus and spike-wave bursts in both the cortex and hippocampus occurred from 11 and 20 weeks of age, respectively. These results indicate that AGS susceptibility in NER can be induced consistently by modified acoustic priming and this rat strain is a new genetic model useful for experimental studies of human epilepsy.

Acoustic Stimulation↗
PubMed1998

Anoxia during kainate status epilepticus shortens behavioral convulsions but generates hippocampal neuron loss and supragranular mossy fiber sprouting.

In rats, this study determined the impact of systemic hypoxia during late kainate-induced status epilepticus on hippocampal neuron loss and mossy fiber sprouting. Non-fasted Sprague Dawley rats were prepared as follows: Naive controls (n=5); rats placed 2 min in a hypoxia chamber (hypoxia only; n=6); rats that seized for more than 6 h from kainic acid (KA-status; 12 mg/kg; i.p.; n=7); and another KA-status group placed into the hypoxia chamber 75 min after the convulsions started (KA-status/hypoxia; n=16). All rats, except for half of the KA-status/hypoxia animals, were perfused 2 weeks later (short-term). The other 8 KA-status/hypoxia rats were perfused after 2 months (long-term). Hippocampal sections were studied for neuron densities and aberrant mossy fiber sprouting at three ventral to dorsal levels. Fascia dentata (FD) mossy fiber sprouting was quantified as an increase in the inner minus outer molecular layer (IML-OML) gray value (GV) difference. Behaviorally, KA-status/hypoxia rats had a shorter duration of convulsive status epilepticus than KA-status animals without anoxia. Hippocampal sections showed that compared to controls: (1) hypoxia-only rats showed no differences in ventral neuron densities and neo-Timm's stained IML-OML GVs; (2) KA-status rats had decreased CA3 densities and a non-significant increase in ventral IML-OML GV differences; and (3) KA-status/hypoxia short-term animals showed decreased hilar, CA3 and CA1 densities and increased ventral IML-OML GV differences. Compared to KA-status/hypoxia short-term rats, long-term animals showed no differences in ventral hippocampal neuron densities, but middle and dorsal sections demonstrated increased IML-OML GV differences and animals were observed to have spontaneous limbic epilepsy. These results indicate that rats exposed to kainate-induced status epilepticus for over 1 h and then a hypoxic insult had a shorter duration of convulsive status, decreased hippocampal neuron densities and greater FD mossy fiber sprouting than controls and the amount of neuronal damage and sprouting was slightly more than animals subjected to 6 h of kainate-induced status. This supports the hypothesis that a physiologic insult during status can shorten the convulsive episode, but still produce hippocampal pathology with a number of clinical and pathologic similarities to human mesial temporal lobe epilepsy (MTLE).

Animals↗
PubMed1995

Psychiatric morbidity and psychodynamics of patients with convulsive pseudoseizures.

Forty-six female patients with pseudoseizures were compared with 50 female patients referred to a psychiatric outpatient clinic. Patients with convulsive pseudoseizures were more likely to be single and childless. An abnormal EEG was more frequently reported in patients with convulsive pseudoseizures, contributing to their earlier diagnosis of epilepsy. The defence mechanisms of patients with convulsive pseudoseizures using the Defense Mechanisms Inventory (DMI) were particularly characterized by higher scores on the 'reversal' scale and lower scores on the 'turning against self' scale. Mood disorders were more common in general psychiatric patients, while one-third of convulsive pseudoseizure patients did not complain of psychiatric symptoms.

Comorbidity↗
PubMed2003

GM1 ganglioside attenuates convulsions and thiobarbituric acid reactive substances production induced by the intrastriatal injection of methylmalonic acid.

The effects of the administration of monosialoganglioside (GM1) on methylmalonic acid (MMA)-induced convulsions, production of thiobarbituric acid reactive substances (TBARS) and on the striatal content of ascorbic acid and total non-protein thiol (SH) groups were evaluated in adult male rats. Animals received two intraperitoneal injections of GM1 (50 mg/kg) or saline (0.85% NaCl) spaced 24h apart. Thirty minutes after the second GM1 or saline injection, L-MMA (6 micromol) or NaCl (9 micromol) was injected into the right striatum and the animals were observed for the appearance of convulsions for 15 min. The animals were sacrificed and their striatal content of ascorbic acid, SH groups and TBARS was measured. The effect of GM1 on MMA-induced TBARS production in striatal homogenates was also evaluated in vitro.MMA injection caused convulsions (Sal-MMA: 9.8+/-1.4 episodes, which lasted 271+/-48 s) and increased the striatal content of TBARS (Sal-MMA: 149.0+/-11.5 nmol MDA/g tissue), but did not alter total striatal SH or ascorbic acid contents. GM1 pretreatment decreased MMA-induced convulsions (GM1-MMA: 6.3+/-2.0 episodes, which lasted 115.1+/-42.2s) and TBARS increase (GM1-MMA: 102.4+/-19.5 nmol MDA/g tissue). GM1 pretreatment increased ascorbic acid content of the striata (saline-pretreated: 1514+/-75.9; GM1-pretreated: 1878.6+/-102.8 microg ascorbic acid/mg tissue). MMA increased TBARS production in vitro, and GM1 had no effect on such MMA-induced effect. This study provides evidence that GM1 increases striatal ascorbic acid content and decreases MMA-induced neurotoxicity assessed by behavioral and neurochemical parameters.

Animals↗
PubMed2003

Convulsive ergotism: epidemics of the serotonin syndrome?

Between 1085 and 1927, epidemics of "convulsive ergotism" were widespread east of the Rhine in Europe due to consumption of grain contaminated with ergot, which is produced by the fungus Claviceps purpurea. West of the Rhine, consumption of ergot-contaminated food caused epidemics of gangrenous ergotism. The clinical features of convulsive ergotism--muscle twitching and spasms, changes in mental state, hallucinations, sweating, and fever lasting for several weeks--suggest serotonergic overstimulation of the CNS (ie, the serotonin syndrome). The ergot alkaloids are serotonin agonists. Dihydroergotamine binds to serotonin receptors in the dorsal horn of the spinal cord, which is the site of neuropathological changes in convulsive ergotism. Dihydroergotamine given to human beings can cause the serotonin syndrome. Ergots produced by different strains of Claviceps purpurea, and those growing in different soils, may have different ergot alkaloid compositions. An alkaloid, present in high concentrations in ergots from east of the Rhine, may have caused convulsive ergotism at a circulating concentration insufficient to produce peripheral ischaemia. The serotonin syndrome may, therefore, have been a public-health problem long before it was recognised as a complication of modern psychopharmacology.

Claviceps↗