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PubMed1979

Effects of focal vs generalized kindled convulsions from anterior neocortex or amygdala on CER acquisition in rats.

Kindling of the anterior neocortex (AC) was shown to produce a brief focal motor seizure, characterized by a clonic-tonic-clonic response of the forelimbs with the animal in a prone posture. These same brief seizures, as previously reported, did not produce retrograde amnesia in a CER paradigm. With repeated evocations, over several days, the AC convulsions exhibited a dramatic increase of the second clonic phase (generalized) and came to appear similar to amygdala kindled convulsions. These generalized AC convulsions, like briefly kindled amygdala convulsions, produced good retrograde amnesia for a CER. With extensive amygdala kindling prior to CER training, a severe CER acquisition deficit was observed. These latter as well as other data suggest that protracted amygdala kindling produces a subsequent reduced ability to acquire fear motivated responses.

Amygdala↗

PubMedDate not supplied

Convulsions in childhood malaria.

A retrospective survey was conducted of all 2911 children admitted with malaria to 4 provincial hospitals in eastern Thailand between 1977 and 1987. 96 (3.3%) had cerebral malaria of whom 21 (22%) died, 225 (7.7%) had convulsions but were not comatose (4 died), and 2590 were conscious and had no fits (5 died). Thus the relative risk of a fatal outcome associated with convulsions, in the absence of cerebral malaria, was 9.2 (95% confidence interval [CI] = 2.5-34.1), P = 0.004. Overall, Plasmodium falciparum caused 81% of infections, P. vivax 16%, and 3% were mixed. Convulsions without cerebral malaria were more common in children under 3 years old (16%) compared with older children (3%): relative risk 5.6 (95% CI = 4.2-7.5), and were significantly associated with falciparum malaria (8.3%) compared with vivax malaria (4.7%): relative risk 1.7 (95% CI = 1.1-2.7). Convulsions are an important complication of malaria in young children, and are associated specifically with P. falciparum infection, even in otherwise uncomplicated malaria.

Age Factors↗

PubMed1983

Increased susceptibility of audiogenic rats to barbital withdrawal convulsions.

Non-responsive progeny from Sprague-Dawley derived rats genetically susceptible to sound-induced (audiogenic) convulsions (AGS-negative) and non-responsive progeny from Sprague-Dawley derived rats not gentically susceptible to audiogenic convulsions (SD-negative) were subjected to a seven-day treatment regimen of sodium barbital. 125 mg/kg, every 12 hours. This represents a lower dose and shorter treatment period than that normally used in this laboratory to induce barbiturate dependence in rats. Animals were subjected to a 115 dB sound stimulus 38 hours following the last dose of sodium barbital. SD-negative rats did not become susceptible to sound-induced convulsions, but AGS-negative rats did experience convulsions when exposed to the sound stimulus during withdrawal. These results are consistent with the hypothesis that rats generally referred to as "audiogenic" may actually suffer from differences which result in an increase of susceptibility to seizures induced by any of several means.

Acoustic Stimulation↗

PubMed1988

Effects of isofloxythepin enantiomers on prolactin secretion and postdecapitation convulsions in rats.

Racemic isofloxythepin and its enantiomers (0.05-1.0 mg/kg) administered subcutaneously increased serum prolactin levels in a dose-dependent manner in rats. The potencies of the drugs were equal for this variable. They (0.05-1.0 mg/kg, SC) also decreased dose-dependently the incidence and duration of postdecapitation convulsions, the convulsions being abolished at 1.0 mg/kg in all groups. Although (-)-enantiomer had slightly stronger effects than those of raceme and (+)-enantiomer, there were no great differences in their inhibitory effects on postdecapitation convulsions. The results indicate that isofloxythepin enantiomers in addition to raceme increase serum prolactin levels and inhibit postdecapitation convulsions and that they seem to have similar potency in blocking of dopamine receptors and alpha 1-adrenoceptors.

Animals↗

PubMed1993

Strain differences in convulsions induced by alarm substance.

Rats exhibit considerable immobility in the forced swim test when tested in fresh water but almost no immobility when tested in soiled water, that is, water previously swum in by another rat. In this study, we examined the response of different strains of rats to soiled water after treatment with imipramine, which precipitates convulsions in rats tested in soiled water. Male Long-Evans, Sprague-Dawley, Wistar, or Fischer rats were injected with imipramine (20 or 30 mg/kg, IP) and subsequently tested in water soiled by either a Sprague-Dawley or Wistar rat. Significantly more animals convulsed when the soiled water was produced by a Sprague-Dawley rat than a Wistar. More rats also convulsed after receiving the 30-mg/kg dose. Different strains did not react differently to soiled water. This study corroborates and extends previous findings that alarm substances can induce convulsions in imipramine-treated rats and indicates that some strains produce a more potent alarm substance than others.

Animals↗

PubMed1981

The involvement of brain amines in pinealectomy-induced convulsions in the gerbil: I. Serotonin.

Pharmacological induction of changes in the serotonergic system was used to study the involvement of telencephalic serotonin (5-HT) in pinealectomy (PX) induced convulsions in the gerbil (Meriones unguiculatus). The reactions of the catecholamines norepinephrine (NE) and dopamine (DA) to both PX and drug treatment were also studied. Serotonin is apparently of little importance in the PX-induced convulsion since the artificial elevation by administration of tryptophan and 5-hydroxytryptophan, or depression by treatment with p-chloramphetamine, of telencephalic 5-HT had little effect on the convulsions. In other models for the study of epilepsy, lowered 5-HT results in an increase in seizure intensity. In this study, as in previous ones, telencephalic NE was repeatedly and significantly lowered after PX. None of the serotonergic drugs resulted in changes in NE. Data such as presented here are supportive of previous reports which indicate that a depression of NE facilitates convulsions.

5-Hydroxytryptophan↗

PubMed1994

Ontogenetic differences in convulsive action and cerebral uptake of uremic guanidino compounds in juvenile mice.

Guanidinosuccinate (GSA) and methylguanidine (MG) are endogenous, convulsant guanidino compounds which have been shown to be greatly increased in uremic patients. In the present study, we have investigated the age-related differences in convulsive action and cerebral uptake of these compounds in juvenile mice of 7, 14 and 21 days old. An age-dependent decrease was apparent in the severity of the GSA- and MG-induced convulsions and toxicity. Mean latency for the appearance of clonic convulsions increased with increasing age. Two hours following the i.p. injection of GSA or MG in a dose of 250 mg/kg, the resulting brain concentration decreased with increasing age of the animals. This effect was more pronounced in the case of MG. Neither for GSA, nor for MG was this age-dependent effect apparent after 30 min. GSA and MG serum as well as brain concentrations were lower in 21-day-old mice than in 7-day-old ones. However, the brain/serum concentration ratios of GSA and of MG were significantly lower in 21-day-old mice than in 7-day-old ones, indicating that at least part of the difference in brain level can be explained by higher permeability of the immature blood-brain barrier to these uremic guanidino compounds. In addition, brain/serum ratios of GSA in mice of 7 days old and in mice of 21 days old were significantly lower than the ratios of MG in these age groups, indicative of lower overall blood-brain barrier permeability to GSA than to MG.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed1988

Anti-convulsant effects by reduced glutathione and related aminoacids in rats treated with isoniazid.

Rats were treated with different doses of isoniazid (INH) causing convulsions. Lethal dose (DL50) and effective convulsant dose (ED50) were calculated. Reduced glutathione (GSH) and related aminoacids were administered to rats receiving INH: the latency and duration of convulsions were recorded; cerebral gamma-aminobutyric acid (GABA) concentrations were determined in rats receiving INH and an association of GSH and INH. GSH and its related aminoacids as cysteine and glycine greatly decreased the duration of INH-induced seizures, while glutamic acid did not protect against convulsions caused by INH. Furthermore, INH causes a decrease in cerebral GABA levels to about half and GSH repeated pretreatment did, however, not prevent the INH induced decline of GABA content: hence, the anticonvulsant effect of GSH can not be ascribed to the restoration of normal levels of anti-epilectically acting GABA, but can be attributed to cysteine and glycine, aminoacids linked to GSH.

Animals↗

PubMed1986

Convulsant effect of Ro 5-4864, a peripheral type benzodiazepine, on the baboon (Papio papio).

The effects of Ro 5-4864, a 1,4-benzodiazepine with a high affinity for the peripheral-type benzodiazepine (Bz) binding site, were investigated in the baboon (Papio papio), which is genetically predisposed to epilepsy. A proconvulsant effect of low doses (1-3 mg/kg, i.v.) of Ro 5-4864 was observed by studying its effect on the photic responses induced by intermittent light stimulation in non-photosensitive baboons. Higher doses of Ro 5-4864 (10 mg/kg, i.v.) were overtly convulsant. The Bzs clonazepam and diazepam blocked these convulsant actions of Ro 5-4864 whereas neither Ro 15-1788, an antagonist of central Bz binding sites, nor PK 11 195, an antagonist of peripheral Bz binding sites, had any effect. It thus appeared that the convulsant effect of Ro 5-4864 was not mediated by Bz binding sites of either the central or the peripheral type. It is possible that Ro 5-4864 exerts its convulsant action at the picrotoxin site of the central Bz receptor - gamma-aminobutyric acid receptor-chloride ionophore complex.

Animals↗

PubMed1988

Depolarizing actions of convulsant barbiturates on isolated rat dorsal root ganglion cells.

The actions of convulsant barbiturates were studied on dorsal root ganglion (DRG) cells in vitro using intracellular recording techniques. Only the convulsant barbiturates (+)-DMBB and CHEB produced a concentration-dependent depression in the responses to gamma-aminobutyric acid (GABA). All convulsant barbiturates were found to produce a direct depolarization of the DRG cell membrane which was accompanied by a decrease in the input resistance of the cell and a reduction in the orthodromic action potential. A sub-population of DRG cells were found to be refractory to these actions but there was no relationship between the cell type (A beta, A delta and C) and ability to respond to the convulsant barbiturates.

Animals↗

PubMed1993

Effect of one hyperbaric oxygen-induced convulsion on cortical polyamine content in two strains of mice.

In rat striatum, after one hyperbaric oxygen (HBO)-induced convulsion, polyamine changes are found that could promote N-methyl-D-aspartate (NMDA) activation. In the HBO-sensitive CD1 mouse, unlike in the common C57 strain, there is some support for NMDA activation after the HBO seizure. We measured PA cortical content before and after the first HBO-induced convulsion (about 608 kPa O2) in CD1 and C57 strains. Putrescine, spermidine and spermine were dansyl derived and analysed by HPLC. Exposure to HBO significantly increased putrescine content only in CD1 though a similar trend was observed in C57. No further increase was observed after convulsion whatever the strain. There were no significant changes in spermidine or spermine to support NMDA activation. Therefore, putrescine increase in CD1 cortex could reflect the free radical formation that is known to be greater in CD1 than in C57 mouse. Attempts to increase putrescine levels before HBO exposure hastened HBO-induced convulsion, less than spermidine or spermine. Because of physiological polyamine interconversion, additional experiments with indirect manipulation of putrescine levels and study of their time-course would precise these preliminary reports on putrescine and HBO.

Animals↗

PubMed1986

Cerebellar cyclic nucleotides and the development of convulsion, with reference to the anticonvulsant activity of diazepam.

Dibutyryl cyclic GMP (DbcGMP) or dibutyryl cyclic AMP (DbcAMP) given to rats intracerebellarly in a dose of 200 nmol/head produced electroencephalographic convulsive changes. Intracerebellar (i.c.) administration of lower doses (100 nmol/head) of DbcGMP and DbcAMP and 200 nmol/head of norepinephrine (NE) and glutamate (Glu) facilitated the pentylenetetrazol (PTZ)-induced convulsions. Diazepam (100 nmol/head, i.c.) suppressed the PTZ-induced convulsions. GABA (400 nmol/head, i.c.) did not affect the PTZ-induced convulsions. These results suggest that DbcGMP, DbcAMP and Glu inhibit seizure control mechanisms in the cerebellum, and that one of the sites of the anticonvulsant action of diazepam is located in the cerebellum.

Animals↗

PubMed1990

Involvement of the nigral output pathways in the inhibitory control of the substantia nigra over generalized non-convulsive seizures in the rat.

Activation of GABAergic transmission within the substantia nigra has been shown to suppress several forms of generalized seizures in experimental models of epilepsy. More especially, such pharmacological manipulations suppress spontaneous and chemically-induced generalized non-convulsive seizures in the rat. The aim of the present study was to examine the role of the dopaminergic and GABAergic thalamic and collicular nigral outputs in this antiepileptic effect. For this purpose, we examined the effects of output destruction on the antiepileptic effect of intranigral injections of a GABA agonist or pharmacological blockade of the neurotransmission at the nerve terminal level in rats with spontaneous absence seizures. After selective destruction of dopaminergic neurons within the substantia nigra with 6-hydroxydopamine (5 micrograms/side) or hemisection of the ascending nigral output, bilateral intranigral injection of muscimol (2 ng/side) still significantly suppressed generalized non-convulsive seizures. Bilateral lesioning of the ventromedial nucleus of the thalamus did not abolish the antiepileptic effects of intranigral muscimol (2 ng/side) and the GABA antagonist, picrotoxin, when given into this thalamic nucleus (10 ng/side) also failed to induce suppression of spike and wave discharges. The antiepileptic effects of intranigral injection of muscimol (2 ng/side) was reversed by bilateral electrolytic lesions of the superior colliculus. Blockade of the GABAergic transmission at this level with picrotoxin (40 ng/side) significantly suppressed generalized non-convulsive seizures. Finally, excitation of collicular cell bodies with low doses of kainic acid (4 and 8 ng/side) also resulted in a suppression of spike and wave discharges. These results demonstrate that the GABAergic nigrocollicular pathway is critical for the inhibitory control of the substantia nigra over generalized non-convulsive seizures. The data further suggest that antiepileptic effects observed following potentiation of GABAergic transmission in the substantia nigra result from a disinhibition of collicular cell bodies.

Animals↗

PubMed1992

Cerebral blood flow and metabolism in soman-induced convulsions.

Regional cerebral blood flow (CBF) and regional cerebral glucose utilization (CGU) were studied by quantitative autoradiographic techniques in rats. Animals were treated either with a toxic dose of soman, an irreversible organophosphorus cholinesterase inhibitor, that produced convulsions or with saline as controls. An increased arterial blood pressure (mean increase = 41% of control) always preceded onset of convulsions. Convulsive activity was associated with an increase of plasma glucose concentration and marked increases over controls of CGU [average of all regions: control = 75 +/- 5 mumol.100 g-1.min-1, n = regions/animals (304/8); seizures = 451 +/- 20 mumol.100 g-1.min-1, n = 190/5] and CBF [average of all regions: control = 135 +/- 6 ml.100 g-1.min-1, n = 190/5; seizures = 619 +/- 29 ml.100 g-1.min-1, n = 190/5). Regional distribution of these effects revealed a greater proportional increase of CBF over CGU in cingulate, motor, and occipital cortex and caudate-putamen. In contrast, a lower proportional increase of CBF over CGU in CA3 region of hippocampus, dentate gyrus, medial thalamus, and substantia nigra was observed, implying the existence of a relative ischemia in these brain areas. These findings may be relevant to the pathogenesis of brain lesions associated with soman-induced convulsions.

Animals↗

PubMedDate not supplied

Benign convulsions with mild gastroenteritis: a report of 10 recent cases detailing clinical varieties.

To better define the characteristic clinical features of benign convulsions with mild gastroenteritis, recently recognized as a new entity in Japan, we reviewed all the 10 patients we have seen from 1992 to 1994. The clinical features have been previously reported in the literature to be afebrile generalized tonic-clonic seizures occurring between the first and the fifth sick day of mild gastroenteritis. In our series, four of 10 patients had convulsions before the onset of gastroenteritis. Overall, seizures were mostly brief and often repetitive occurring in cluster (19 seizures/10 episodes). Among these, a prolonged or partial seizure was frequently observed. In six of the 10 patients, the seizure type changed during an episode: from generalized to partial seizures (n = 2), from partial to generalized seizures (n = 2), or from partial to another type of partial seizures (n = 2). None in our series experienced a recurrence episode of afebrile convulsion during follow-up. These findings suggest that benign convulsions with mild gastroenteritis exhibit some variations in their clinical manifestation.

Child, Preschool↗

PubMed1992

Free radical generation in the brain precedes hyperbaric oxygen-induced convulsions.

We tested the hypothesis that hyperbaric oxygenation (HBO) generates free radicals in the brain before the onset of neurological manifestations of central nervous system (CNS) oxygen poisoning. Chronically cannulated, conscious rats were individually placed in a transparent pressure chamber and exposed to (1) 5 atmospheres absolute (ATA) oxygen for 15 min (n = 4); (2) 5 ATA oxygen for 30 min (n = 5), during which no visible convulsions occurred; (3) 5 ATA oxygen for 30 min with recurrent convulsions (n = 6); (4) 5 ATA oxygen until the appearance of the first visible convulsions (n = 5); (5) 4 ATA oxygen for 60 min during which no convulsions occurred (n = 5); and (6) 5 ATA air for 30 min (n = 5, controls). Immediately before compression, 1 mL of 0.1 M of alpha-phenyl-N-tert-butyl nitrone (PBN) was administered intravenously (iv) for spin trapping. At the termination of each experiment, rats were euthanized by pentobarbital iv and decompressed within 1 min. Brains were rapidly removed for preparation of lipid extracts (Folch). The presence of PBN spin adducts in the lipid extracts was examined by electron spin resonance (ESR) spectroscopy. ESR spectra from unconvulsed rats exposed to 5 ATA oxygen for 30 min revealed both oxygen-centered and carbon-centered PBN spin adducts in three of the five brains. One of the five rats in this group showed an ascorbyl signal in the ESR spectrum.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Suppression of spontaneous generalized non-convulsive seizures in the rat by microinjection of GABA antagonists into the superior colliculus.

Intranigral injections of GABA agonists suppress spontaneous and chemically induced generalized non-convulsive seizures in the rat. In order to examine whether the GABAergic nigrotectal pathway could be involved in this suppression, bilateral injections of GABA antagonists were performed in the superior colliculus of rats with spontaneous generalized non-convulsive seizures. Bilateral microinjections into this structure of the GABA antagonists picrotoxin (20 and 40 ng/side) and bicuculline methiodide (5 ng/side) suppressed spike-and-wave discharges for 40 min and 20 min post injection, respectively. Unilateral injections of picrotoxin (40 ng) into the superior colliculus as well as bilateral injections of a GABA agonist (muscimol; 80 ng) did not induce significant modifications. These results show that blockade of the GABAergic transmission at the level of the superior colliculus results in a suppression of generalized non-convulsive seizures. These data support the hypothesis that the suppressive effect of intranigral injections of GABA agonists over generalized non-convulsive seizures involves, at least in part, the nigrotectal GABAergic pathway.

Animals↗

PubMed2005

Low-dose carbamazepine therapy for benign infantile convulsions.

Benign infantile convulsions (BIC) are characterized by: (1) onset at up to 2 years of age, (2) normal development, (3) mostly brief, often clustered convulsions, and (4) normal electroencephalography during the interictal stage. BIC follow a favorable course and disappear before 2-3 years of age, although convulsions for which diazepam is ineffective frequently develop. We treated 15 children (3-16 months of age) diagnosed as having BIC, excluding convulsions associated with mild gastroenteritis, with a once-daily dose of 5mg/kg of carbamazepine until up to 2 or 3 years of age. The serum concentration of carbamazepine was as low as below the effective range in six patients, but the treatment was dramatically effective in all the BIC children. Seizures did not recur in any patients during oral administration of carbamazepine. The treatment was finished in 12 patients at age 2 years, two at age 3 years, and one at 16 months-old. Therefore, we recommend the administration of a once-daily dose of 5mg/kg of carbamazepine until up to 2 or 3 years of age as a treatment for BIC.

Acute Disease↗