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PubMedDate not supplied

Generalized convulsions induced by pentylenetetrazol in the cat: participation of forebrain, brainstem, and spinal cord.

The respective capabilities of forebrain, brainstem, and spinal cord to generate seizures in response to intravenous pentylenetetrazol (PTZ) were determined in intact, precollicular, and spinal cord transected (C2-C3) cats. Threshold doses for the induction of generalized EEG seizures were similar, approximately 26 mg/kg, in all groups, but only in intact cats was this associated with generalized clonic convulsions. In cats with precollicular transection, in spite of an unchanged EEG seizure threshold, induction of convulsions required on average 63 mg/kg of PTZ. They consisted of generalized tonic contractions. In cats with spinal cord transection, convulsions began with a mean dose of 167 mg/kg of PTZ. They consisted of bilateral, frequently asynchronous jerks, although tonic contractions were also observed. These experiments show widespread central nervous system (CNS) sensitivity to PTZ, and demonstrate that (a) ictal EEG activity in the forebrain, normally associated with clonic convulsions, may occur independently from brainstem influence; (b) clonic convulsions in intact cats likely originate from the forebrain with little contribution from the brainstem; and (c) the brainstem and spinal cord can induce tonic and predominantly clonic seizures, respectively, at PTZ levels exceeding those required to induce seizures in intact cats.

Animals↗
PubMed1994

The prevalence and incidence of convulsive disorders in children.

Each year, about 150,000 children and adolescents in the United States will come to medical attention for evaluation of a newly occurring seizure disorder of some type. Between 2% and 4% of all children in Europe and the United States experience at least one convulsion associated with a febrile illness before the age of 5 years. The cumulative incidence of febrile convulsions among children ranges from about 1% in China to more than 8% in Japan and 14% in Guam. The peak incidence of a first febrile convulsion occurs in the second year of life. Between 0.5% and 1% of children and adolescents experience a seizure associated with other acute metabolic or neurologic insults; most of these occur in the neonatal period. The incidence of epilepsy (recurrent unprovoked seizures) in children and adolescents seems relatively consistent across all populations studied, ranging from 50 to 100/100,000. The highest incidence of epilepsy is in the first year of life. West syndrome accounts for about 2% of all childhood epilepsy. Lennox-Gastaut syndrome for 1-2%, childhood absence epilepsy (pyknolepsy) for 10-15%, juvenile myoclonic epilepsy for 5%, and idiopathic localization-related epilepsy for 10%. Between 0.5 and 1% of children experience a nonrecurrent, single, unprovoked convulsive episode. Following are the estimated numbers of children and adolescents with newly diagnosed convulsive disorders in the United States for the year 1990: febrile seizures, 100,000; neonatal seizures, 4,000; other provoked seizures, 6,000; single unprovoked seizures, 10,000; and epilepsy, 30,000.

Adolescent↗
PubMed1999

Ictal video-EEG recording of three partial seizures in a patient with the benign infantile convulsions associated with mild gastroenteritis.

PURPOSE: In infants, benign convulsions can be triggered by febrile illness or mild diarrhea such as Rotavirus gastroenteritis. The triggering mechanism of these convulsions is still unknown. In spite of several reports concerning clinical features, the ictal EEG recordings were rarely analyzed by a video-EEG monitoring system. To reveal a clue for the triggering mechanism of these convulsions, we analyzed the correlation of clinical manifestations and the EEG discharges during the ictal events and compared with previous reports. METHODS: The ictal EEG of a cluster of three afebrile convulsions associated with mild gastroenteritis was recorded by an EEG closed-circuit TV (EEG-CCTV) monitoring system in a 6-month-old healthy female infant. RESULTS: All seizures began as complex partial seizures (CPSs), which exhibited a motionless stare with or without leftward deviation of both eyes, and evolved to secondarily generalized tonic-clonic seizures (SGTCSs) for approximately 90 s. Each of three ictal discharges began from the right occipital, right centroparietotemporal, and left occipital regions, respectively. CONCLUSIONS: Although initiating sites of ictal discharges of benign infantile convulsions associated with mild gastroenteritis (BICE) were previously reported to be variable among patients, these results indicated that those differ among seizures even in a same infant.

Cerebral Cortex↗
PubMed1994

Prenatal ethanol exposure: susceptibility to convulsions and ethanol's anticonvulsant effect in amygdala-kindled rats.

The present experiments assessed the effects of prenatal ethanol exposure on the susceptibility to convulsions and on the anticonvulsant effect of ethanol using the electrical kindling model of epilepsy in rats. Adult male Sprague-Dawley rats from prenatal ethanol (E), pair-fed (PF), and ad libitum-fed control (C) treatment groups were tested following the implantation of a stimulation electrode in the left amygdala complex. The same rats were tested in four consecutive experiments. Both E and PF rats showed a slightly slower rate of kindling than C rats, as measured by convulsion class but not as measured by forelimb clonus duration (experiment 1). However, the groups did not differ significantly in the electrical stimulation threshold for kindled convulsions (experiment 2). Furthermore, prenatal ethanol exposure had no significant effect on the dose-response curve for ethanol's (0, 0.9, 1.1, 1.3, and 1.5 g/kg, ip) anticonvulsant effect (experiment 3), or on the rate of tolerance development to ethanol's (1.5 g/kg, ip) anticonvulsant effect (experiment 4) on kindled convulsions. Thus, prenatal exposure to ethanol does not appear to have long-term effects on the susceptibility to convulsions or on the anticonvulsant effect of ethanol in adult male rats in the kindling model as used in the present experiments.

Amygdala↗
PubMed1990

Epilepsy and other convulsive disorders in Saudi Arabia: a prospective study of 1,000 consecutive cases.

The pattern of epilepsy and other convulsive disorders in 1,000 consecutive Saudi nationals is described. These disorders were common with a hospital frequency rate of 8 per 1,000. Men were more frequently affected than women and 60% of the patients were under 10 years old at the onset of their illness. The epilepsies were the commonest type (74%). Febrile convulsions (20%) presented mainly between the ages of one and five years. Isolated seizures (3%) and acute symptomatic convulsions (3%) were uncommon. In the epileptic group, generalised seizures (71%) were more frequent than partial (29%) and complex partial seizures occurred mainly in those above 21 years old. Absences (4%), infantile spasms (3%) and atonic seizures (3%) were uncommon. No specific etiology of the epilepsy was determined in the majority of the cases (63%). The identified major etiologic factors of the epilepsies were perinatal encephalopathy (21%), cerebral trauma (11%), sequelae of meningitis or encephalitis (2%), brain tumors (0.5%), and vascular lesions such as stroke and arteriovenous malformation. Perinatal encephalopathy accounted for 40% of the epilepsies in children less than 5 years old, and trauma for 20% of those above 20 years old. A family history of epilepsy in close relations was obtained in 23% of the cases, and the consanguinity rate among the parents was 53%. The high incidence of associated perinatal encephalopathy found in this study suggests that perinatal factors play a major role in the pathogenesis of epilepsy in Saudi Arabia. The high frequency of cerebral trauma was also striking. Although consanguinity of the parents appeared not to be a major factor in the genetics of convulsive disorders in this environment, it might have potentiated the tendency of familial aggregation of convulsive disorders in this community. Consanguinity may be an important factor in the production of some of these disorders but its precise role has not been determined.

Adolescent↗
PubMed2005

Convulsive episodes in patients with group A xeroderma pigmentosum.

OBJECTIVES: To clarify the incidence of convulsive episodes in patients with group A xeroderma pigmentosum (XPA). MATERIALS AND METHODS: By investigating the history of convulsive episodes of our 33 XPA patients through either their medical charts or direct interviews with their caretakers. RESULTS: Five patients had several episodes of afebrile convulsion at ages older than 12. With the exception of one patient who began to show convulsive episodes at 13, no other XPA patients exhibited febrile seizures. As far as our 33 XPA patients were concerned, 15% exhibited epilepsy, and 3% experienced febrile seizures. CONCLUSIONS: Japanese XPA patients showed a lower incidence of febrile seizures, while exhibiting a higher incidence of epilepsy. It is assumed that the brain of young patients with XPA is difficult to develop convulsions.

Adolescent↗
PubMed1993

BRL 38227--a potassium channel opener, antagonizes digoxin-induced convulsions.

Experimental evidence suggests that potassium channel openers play an important role in convulsions. In this study, the anticonvulsant activity of BRL 38227, a new potassium channel opener against digoxin-induced convulsions, is reported. Intraventricular administration of digoxin (7.5 micrograms), included "popcorn-type" convulsions in rats. BRL 38227, injected centrally increased the onset time of convulsions and decreased the mortality rate in a dose-dependent manner. Pretreatment with 4-aminopyridine, a potassium channel blocker antagonized the protective effect of BRL 38227. These findings show the involvement of potassium channels in digoxin-induced convulsions. Further these results indicate that in the future potassium channels might be a target for new anticonvulsant drugs.

4-Aminopyridine↗
PubMedDate not supplied

Alterations of lidocaine and pentylenetetrazol-induced convulsions by manipulation of brain monoamines.

The thresholds for pentylenetetrazol and lidocaine-induced clonic convulsions were significantly influenced by manipulation of brain biogenic amines. Pretreatment with inhibitors of monoamine synthesis, alpha-methyl-p-tyrosine and p-chlorophenylalanine, caused significant decreases in brain monoamine contents and pentylenetetrazol seizure threshold, while the threshold for lidocaine-induced convulsions was significantly increased by either treatment. Moreover, the inhibitor of dopamine-beta-hydroxylase, disulfiram, caused significant decrease in brain noradrenaline (NA) and significant increase in brain dopamine (DA) contents. The threshold for pentylenetetrazol-induced convulsions was decreased by treatment with disulfiram, while that of lidocaine was increased by the same treatment. Furthermore, treatment with L-dihydroxyphenylalanine (L-DOPA) caused significant increase in brain DA contents, while 5-hydroxytryptophan (5-HTP) treatment caused significant increase in brain 5-hydroxytryptamine (5-HT) contents, but the thresholds for lidocaine and pentylenetetrazol-induced convulsions were not influenced by either treatment. These results may suggest that the brain monoaminergic systems, different from their ability to inhibit control of pentylenetetrazol seizures, act to potentiate lidocaine-induced convulsions.

Animals↗
PubMed1998

Excitatory amino acid antagonists alleviate convulsive and toxic properties of lindane in mice.

Pesticides acting at GABAA receptors may induce convulsions in man and animals, but the mechanisms responsible for their convulsant activity are not fully explained. The following excitatory amino acid antagonists were studied for their protective action in mice intoxicated with chlorinated hydrocarbon insecticide lindane (gamma-hexachlorocyclohexane): the competitive NMDA antagonist: 3-(2-carboxypiperazine-4-yl)propenyl-1- phosphonic acid (D-CPPene, 20 mg/kg), the non-competitive NMDA antagonist: dizocilpine (MK-801, 0.4 mg/kg), the glycine site antagonist of NMDA receptor: 2-phenyl-1,3-propane-diol dicarbamate (felbamate, 400 mg/kg) and the competitive AMPA antagonist: 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline (NBQX, 100 mg/kg). Systemic administration of an antagonist prior to lindane resulted in a strong anticonvulsant effect. D-CPPene, MK-801 and NBQX produced a marked increase of CD50 values of lindane for clonic convulsions. All the antagonists protected animals against tonic convulsions. Toxicity of lindane was potently reduced, as assessed 2, 24 and 120 hr after administration of the pesticide. Our results demonstrate that excitatory amino acid antagonists reduce convulsant properties and toxicity of lindane, suggesting that excitatory amino acid neurotransmission may be involved in its central action.

Animals↗
PubMedDate not supplied

Increased interleukin-1 (IL-1) production from LPS-stimulated peripheral blood monocytes in children with febrile convulsions.

Peripheral blood mononuclear cells (MNC) from 27 children with a febrile convulsion were tested for production of interleukin-1 (IL-1) in culture. MNC stimulated with lipopolysaccharide (LPS) showed a significantly increased production of IL-1 when compared to MNC from children without convulsions but with bacterial infections (p less than 0.001), viral infections (p less than 0.005) or no infection (p less than 0.005). Children who had experienced a febrile convulsion were retested several months later; this time the IL-1 production from LPS-stimulated MNC was not different from controls. These results demonstrate that MNC at the time of febrile convulsions have increased sensitivity to LPS and possibly to other IL-1 inducers; the resulting enhanced IL-1 response from sensitized MNC may have a role in the pathogenesis of febrile convulsions.

Bacterial Infections↗
PubMed2005

Early post-convulsive prolongation of QT time in children.

AIM: An important differential diagnosis of seizures in childhood is the long QT syndrome. Childhood epilepsy occurs about 400 times more often than long QT syndrome. We had observed children with slight post-convulsive prolongation of QT time more often than the reported incidence of long QT syndrome. We therefore conducted a prospective study to define the characteristics of post-convulsive prolongation of QT time in children. METHODS: We investigated 30 consecutive infants and children (3 mo to 14 y) within 2 h after seizures. A follow-up ECG was obtained 1-9 d later. We also obtained ECGs from 30 healthy age- and gender-matched controls. We calculated the QT interval corrected for heart rate (QTc) by Bazett's formula in leads II, V5, V6, QT dispersion and the number of notched T waves. RESULTS: We found a QTc interval of more than 440 ms in one or more leads in the first ECG in seven of 30 infants and children compared to 1 of 30 in the follow-up ECG (p=0.0003) and two of 30 in the healthy controls (p=0.14). Average QTc was higher for all leads in the first ECG. This was statistically significant in leads II (414 vs 402 ms, p=0.008), V5 (416 vs 404 ms, p=0.002) and V6 (415 vs 399 ms, p=0.001). Compared to healthy controls, QT dispersion was slightly larger in the early post-convulsive ECG (36 vs 31 ms, p=0.03). Notched T waves occurred more frequently in the early compared to the late post-convulsive ECGs (p=0.009). CONCLUSION: Slight to moderate post-convulsive prolongation of the QT interval is not rare but transient in paediatric patients.

Adolescent↗
PubMed1989

Systemically administered glycine protects against strychnine convulsions, but not the behavioural effects of high pressure, in mice.

1. The effects of intraperitoneal administration of glycine were studied on the behavioural effects of raised ambient pressure in mice, compared with the effects of such administration on the actions of chemical convulsants. 2. Glycine did not alter the onset pressures for the occurrence of tremor, myoclonic jerks or clonic convulsions, when the ambient pressure was raised using helium. 3. Glycine showed a protective action against the convulsant effects of strychnine. 4. No protective action of glycine was found against the convulsant actions of pentylenetetrazol or bicuculline. 5. It is suggested that the results provide evidence that the high pressure neurological syndrome and strychnine convulsions have different neurophysiological origins.

Animals↗
PubMed1977

Cerebrospinal fluid acid-base status and lactate and pyruvate concentrations after convulsions of varied duration and aetiology in children.

Twenty-two infants and children were studied after convulsions of varied cause and duration. Arterial and CSF acid-base variables, lactate and pyruvate concentrations, and lactate/pyruvate ratios were measured between 3 and 18 hours after convulsive episodes. Biochemical signs of cerebral hypoxia were found in 7 patients with prolonged (greater than 30 minutes) or recurrent short convulsions. These signs were absent in patients with single short convulsions. These findings indicate that cerebral hypoxia and possible brain damage is a hazard of prolonged or rapidly recurring short convulsions.

Acid-Base Equilibrium↗
PubMed1977

Viruses and febrile convulsions.

In 276 children admitted to hospital with febrile convulsions a wide range of virus types was identified by means of nasopharyngeal secretions and cough/nasal swabs. The overall virus identification rate was 49%. Analysis of age, sex, family history, and past history showed no marked differences between the virus-positive and the virus-negative children. More than 80% had symptoms of respiratory infection in association with their convulsions, whether or not a virus was identified. Convulsions were not apparently more severe in the virus-positive group. Rapid virus diagnosis was found helpful in the management of children with febrile convulsions. The virus aetiology of many febrile convulsions has implications both for hospital cross-infection and for research into methods of prevention.

Child, Preschool↗
PubMed1995

Cerebrospinal fluid zinc concentrations in febrile convulsions.

Zinc modulates the activity of glutamic acid decarboxylase, the rate limiting enzyme in the synthesis of gamma-aminobutyric acid (GABA), which is a major inhibitory neurotransmitter. Low cerebrospinal fluid GABA values have been reported in association with several seizure disorders, including febrile convulsions. It is also known that fever and/or infections may cause a reduction in serum zinc concentrations. In this study the hypothesis that febrile convulsions are related to low cerebrospinal fluid zinc was tested. Cerebrospinal fluid zinc concentrations were measured in 66 febrile children: 32 with febrile convulsions, 18 with fever but without convulsions, and 16 with aseptic (viral) meningitis. There was no statistically significant difference in the cerebrospinal fluid zinc between the three groups of children, and the mean concentration was 26.2 micrograms/l. No significant relationship was found between either age, gender, maximal temperature, type of infection, or time of performance of the lumbar puncture and cerebrospinal fluid zinc concentration. These results do not support the hypothesis that febrile convulsions are related to reduced cerebrospinal fluid zinc concentrations.

Age Factors↗
PubMed2002

Convulsions and retinal haemorrhage: should we look further?

BACKGROUND AND AIMS: The prevalence of retinal haemorrhages after convulsions is not well established. As these haemorrhages are considered characteristic of child abuse, we investigated their occurrence after convulsive episodes to see whether the finding of haemorrhage should prompt further investigation. METHODS: Prospective study of 153 children (aged 2 months to 2 years), seen in the emergency department after a convulsive episode. After a thorough history and physical examination, a retinal examination was performed by an ophthalmologist. If findings were positive, further investigation was undertaken to rule out systemic disorder or child abuse. RESULTS: One child was found with unilateral retinal haemorrhages following an episode of a simple febrile convulsion. A thorough investigation uncovered no other reason for this finding. CONCLUSION: Retinal haemorrhages following a convulsive episode are rare. Such a finding should trigger an extensive search for other reasons, including child abuse.

Child Abuse↗
PubMed1996

Suggestion of a major gene for familial febrile convulsions mapping to 8q13-21.

Febrile convulsions affect 2 to 5% of all children under the age of 5 years. These convulsions probably have a variety of causes, but a genetic component has long been recognised. A large and remarkable family is described in which febrile convulsions appear to result from autosomal dominant inheritance at a single major locus. A gene for febrile convulsions was excluded from regions of previously mapped epilepsy genes and extension of exclusion mapping, using microsatellite markers, to the entire genome implied that a locus on chromosome 8q13-21 may be involved. Linkage analysis of markers on chromosome 8 gave a multipoint lod score of 3.40, maximised over different values of penetrance and phenocopy rate, for linkage between the gene for febrile convulsions and the region flanked by markers D8S553 and D8S279. This lod score was calculated assuming the disease has a penetrance of 60% and a phenocopy rate of 3%. Although there was no indication of linkage other than to markers on chromosome 8, linkage remains suggestive rather than significant because of the maximisation procedure applied. The support for linkage involving a major gene, as opposed to an alternative hypothesis of a complex inheritance pattern, relied upon the assumption of low penetrance.

Adolescent↗
PubMed1987

Nocturnal convulsions and insulin-induced hypoglycaemia in diabetic patients.

Convulsions may occur as a consequence of insulin-induced hypoglycaemia. We report three patients with insulin-dependent diabetes, who presented with generalized tonic-clonic seizures associated with nocturnal hypoglycaemia. None of the patients had experienced hypoglycaemia during waking hours and the convulsions were mistakenly diagnosed as idiopathic epilepsy. Recognition of the possible hypoglycaemia aetiology of these convulsions permitted appropriate alteration of the insulin regimens with no recurrence of convulsions. In one case, the seizure was associated with bilateral fractures of the neck of the humerus. Unrecognized hypoglycaemia should be considered as a possible cause of convulsions in insulin-dependent diabetic patients.

Adult↗