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PubMedDate not supplied

[Effect of phenytoin on neurotoxin homocysteine thiolactone-induced convulsions and epileptic status in rats with cobalt-induced epilepsy].

The administration of neurotoxin thiolactone homocysteine in rats with cobalt-induced epileptogenic focus in the sensomotor cortical region led to the development of secondary generalized convulsions and epileptic state. The pattern was analogous to the manifestation of convulsions in epileptic state in humans. Fenitoin (50 mg/kg) inhibited the development of convulsions, arrested the epileptic state, reduced the number and duration of the secondary generalized tonic--clonic attacks, decreased the behavioral manifestations (focal convulsions, lateral position etc.), normalized EEG, and prevented fatal outcome. An increase in the fenitoin dose to 100 mg/kg decreased the antiepileptic activity, enhanced side effects, and increased the lethality in test animals.

Animals↗
PubMedDate not supplied

Effects of convulsant ligands of the GABA-benzodiazepine receptor complex in conflict and learning tasks in mice.

A systematic study of the effects of convulsants acting at the GABA-benzodiazepine receptor complex was undertaken in mice to estimate their potential anxiogenic effects and/or performance enhancing effects in learning and memory tasks. Anxiogenic effects were assessed in a conflict task where lever presses delivered both a food pellet and a mild electric foot shock. Effects on learning were assessed through analysis of habituation to a new environment. The convulsant agents pentylenetetrazol (PTZ) and picrotoxin (PX), both acting through the GABA-benzodiazepine receptor complex, and strychnine, a convulsant acting through the glycine transmission were used. Our data show that non convulsive doses of PTZ (25 mg/kg) and PX (0.85 mg/kg), but not of strychnine (0.8 mg/kg), are anxiogenic in the conflict model. At lower doses PTZ (10 mg/kg) and PX (0.3 mg/kg), but not strychnine (0.1 to 0.6 mg/kg), enhance performance in the habituation model. Our results contribute to the validation of the idea that small decreases in GABAergic transmission are accompanied by improvement of learning whereas medium decreases induce anxiogenic effects.

Animals↗
PubMed1990

Convulsant and anticonvulsant cyclopentanones and cyclohexanones.

The convulsant and/or anticonvulsant activity of unsubstituted and mono-alkyl-substituted cyclopentanones and cyclohexanones were examined by testing the ability of these compounds to produce seizures or to inhibit seizures induced by pentylenetetrazol and maximal electroshock in CF-1 mice. In addition, these compounds were tested for their ability to bind to the picrotoxin receptor. The unsubstituted compounds, cyclopentanone and cyclohexanone, prevented both pentylnetetrazol- and maximal electroshock-induced seizures. Cyclopentanones and cyclohexanones with small (less than 3 carbon atoms) alkyl substituents in the 2-position were also anticonvulsant; all of these compounds, except 2-ethylcyclohexanone, blocked both pentylenetrazol- and maximal electroshock-induced seizures. 2-Ethylcyclohexanone was very effective against pentylenetetrazol seizures but did not prevent maximal electroshock seizures. Cyclohexanones with larger alkyl substituents in the 2-position, 2-propylcyclohexanone and 2-t-butylcyclohexanone, caused clonic seizures following injection into mice. Of the cyclopentanones and cyclohexanones with alkyl substitutions in the 3-position that were studied, one was an anticonvulsant (3-methylcyclopentanone), one was a mixed convulsant/anticonvulsant (3-ethylcyclohexanone), and the other two (3-ethylcyclopentanone and 3-t-butylcyclohexanone) were convulsants. Finally, two cyclohexanones with alkyl substituents in the 4-position were studied. Both 4-ethylcyclohexanone and 4-t-butylcyclohexanone produced convulsions when injected into mice. All the neuroactive cyclopentanones and cyclohexanones competitively displaced [35S]t-butylbicyclophosphorothionate, a ligand specific for the picrotoxin receptor, from rat brain membranes. The convulsant compounds were generally more potent than the anticonvulsants. The cyclohexanones were more potent than their corresponding cyclopentanones and the binding potency of both increased as the size of the alkyl substituent increased. These results suggest that cyclopentanone, cyclohexanone, and their alkyl-substituted derivatives act at the picrotoxin receptor to increase or decrease neuronal activity. Thus, they appear to have sites and mechanisms of action similar to those of the neuroactive gamma-butyrolactones and gamma-thiobutyrolactones.

Animals↗
PubMed1984

Multiple actions of convulsant barbiturates on mouse neurons in cell culture.

The convulsant barbiturate 5-(2-cyclohexylidene-ethyl)-5-ethyl barbituric acid (CHEB) depolarized most (greater than 90%) mouse spinal cord (SC) neurons in primary dissociated cell culture in a concentration-dependent fashion with threshold effects at 10 to 50 nM. Dorsal root ganglion (DRG) neurons were also depolarized by CHEB, but only about 50% of the neurons responded. The threshold concentration for depolarization of DRG neurons was several hundred-fold higher than for SC neurons. CHEB depolarizations may be mediated by an increase in a cation conductance which is calcium-dependent because CHEB depolarizations had an extrapolated reversal potential near 0 mV, were insensitive to intracellular anion (chloride ion) injection, were absent after removal of extracellular calcium ions and were reduced by cadmium ions. In contrast, the nonconvulsant barbiturates, pentobarbital and phenobarbital, did not produce membrane depolarization. However, at concentrations of CHEB somewhat higher than those which directly depolarized cells, CHEB resembled pentobarbital and phenobarbital because it reduced the spontaneous activity of SC neurons and shortened calcium-dependent action potentials of DRG neurons. Two other convulsant barbiturates, trans-5-ethyl-5-(3'-methyl-but-2'-enyl) barbituric acid and trans-5-ethyl-5-(1',3'-dimethyl-but-1'-enyl) barbituric acid, also produced membrane depolarization, reduced spontaneous activity and shortened calcium-dependent action potentials. Another convulsant barbiturate, S(+)-1-methyl-5-phenyl-5-propyl barbituric acid, did not alter membrane potential or conductance of SC neurons, suggesting that mechanistic subclasses of convulsant barbiturates exist.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1980

Effect of kynurenine and quinolinic acid on the action of convulsants in mice.

Intraventricular injection of DL-kynurenine and L-kynurenine sulfate (40 microgram) into conscious mice potentiated convulsions and lethality produced by strychnine (1 mg/kg) and not by thiosemicarbazide nor pentylenetetrazol. Another metabolite of tryptophan with convulsive effect, quinolinic acid, was ineffective. Intraperitoneal injection of DL-kynurenine sulfate and quinolinic acid (25-100 mg/kg) was associated with prolongation of the latency of strychnine and thiosemicarbazide (only the former drug) seizures. Nicotinic, picolinic, and anthranilic acids (100 and 250 mg/kg) did not modify the action of convulsants. Data and suggestions about probable involvement of brain glycine and gamma-aminobutyric acid receptors in the convulsive action of kynurenines is discussed.

Animals↗
PubMed1997

Pharmacokinetic-pharmacodynamic contributions to the convulsant activity of pefloxacin and norfloxacin in rats.

The purpose of this investigation was to compare the convulsant activity of two quinolones differing, respectively, by the presence (pefloxacin) or absence (norfloxacin) of a methyl group on the piperazine moiety at the position 7 of their parent nuclei and consequently by their lipophilicity. An in vivo model was used, which can distinguish between ease in reaching pharmacological receptors at the central nervous system level, and ability to interact with these receptors. Male Sprague-Dawley rats (approximately 230g-300g) received an i.v. infusion of pefloxacin or norfloxacin at one of four different rates: 480, 960, 1440 and 1920 micromol/hr, until the onset of maximal seizures. This occurred after an average of 12.7 to 69.4 min. We found enough evidence to suggest that in these conditions the contribution of pefloxacin metabolites, including norfloxacin, to its convulsant activity was negligible. Doses of pefloxacin and concentrations in cerebrospinal fluid and plasma (total and unbound) at the pharmacodynamic endpoint were all independent of infusion rate, whereas only cerebrospinal fluid concentrations of norfloxacin were independent of infusion rate. The overall cerebrospinal fluid concentration of norfloxacin (47.3 +/- 9.9 micromol/liter) was about 8-fold lower than that of pefloxacin (380 +/- 27 micromol/liter), indicating that on average the "intrinsic convulsant activity" of norfloxacin is 8-fold greater than that of pefloxacin. However, total doses of pefloxacin and norfloxacin at the onset of maximal seizures were in the same order of magnitude (1500-2000 micromol/kg), suggesting that the higher ability of the more lipophilic pefloxacin to reach central nervous system compensates for its lower intrinsic convulsant activity.

4-Quinolones↗
PubMed1999

Chronic ethanol differentially alters susceptibility to chemically induced convulsions in withdrawal seizure-prone and -resistant mice.

Withdrawal seizure-prone (WSP) and withdrawal seizure-resistant (WSR) mice were selectively bred to have severe (WSP) or mild (WSR) handling-induced convulsions after chronic ethanol inhalation. The purpose of the present experiments was to determine whether seizure susceptibility differences between WSP and WSR mice during ethanol withdrawal were specific to agents acting at gamma-aminobutyric acidA or excitatory amino acid (EAA) receptors. Male WSP and WSR mice were exposed to ethanol vapor or air for 24 or 72 h. During peak withdrawal (i.e., between 6.5 and 8 h after removal from the inhalation chambers), separate groups of animals were administered pentylenetetrazol, (+)bicuculline, N-methyl-D-aspartate, kainic acid, or strychnine via timed tail vein infusion. Withdrawal from ethanol significantly increased sensitivity to pentylenetetrazol and (+)bicuculline versus air-exposed WSP and WSR mice. In contrast, sensitivity to N-methyl-D-aspartate-induced convulsions was significantly decreased in the ethanol-exposed WSR and unchanged in the ethanol-exposed WSP mice. Sensitivity to kainic acid was significantly increased in both ethanol-exposed WSR and WSP mice, although the magnitude of change in sensitivity was greater in the ethanol-withdrawing WSP line. Interestingly, sensitivity to strychnine was decreased similarly in the ethanol-exposed WSP and WSR mice, compared with their respective air-exposed animals. These results suggest that chronic ethanol increased sensitivity to convulsants active at gamma-aminobutyric acidA receptors similarly in WSP and WSR mice, but differentially changed sensitivity to convulsants active at EAA receptors in the lines. This supports a role for EAA systems in determining genetic susceptibility to alcohol withdrawal.

Administration, Inhalation↗
PubMed2001

Convulsive-like movements in brainstem stroke.

BACKGROUND: Involuntary convulsive-like movements sometimes occur in patients with brainstem strokes. These movements vary in nature, frequency, and trigger, including fasciculation-like, shivering, jerky, tonic-clonic, and intermittent shaking movements. Some are interpreted as decerebrate postures or seizures. It is important to recognize this type of motor phenomenon since it may be a diagnostic clue for early diagnosis and treatment of brainstem strokes. DESIGN: Case report and review of the literature OBSERVATION: A 72-year-old-man presented with impaired consciousness and jerks of the upper limbs mimicking seizures. These episodes consisted of brief clonic contractions of the proximal and distal upper extremities. They were observed in paroxysms lasting for 3 to 5 seconds. Magnetic resonance imaging showed large midpontine infarction. Magnetic resonance angiography revealed the absence of basilar artery blood flow. No seizure discharges were observed in the electroencephalogram. Anticoagulation with intravenous heparin was started. Two days after admission, the patient had a cardiac arrest and died. We review the frequency and nature of convulsive-like movements in brainstem stroke in the literature. CONCLUSIONS: Movements associated with brainstem lesions are not easily differentiated from convulsions. Unexpected onset and inexperience of the observers limit the characterization of this phenomenon. Convulsive-like movements in brainstem stroke may occur more frequently than reported. Early detection of this motor phenomenon may have practical implications.

Aged↗
PubMed1978

Continuous phenobarbital treatment after a 'simple febril convulsion'.

In only a small proportion of young children with brief, generalized, febrile convulsions do afebrile seizures develop, but this fraction is several times the prevalence of epilepsy in an unselected population. The risk of another febrile convulsion is approximately 30%. Febrile status epilepticus during a subsequent infection is a potential source of serious morbidity and mortality. Intermittent phenobarbital administration during subsequent, febrile illnesses confers little protection against recurrent, febrile convulsions. Continuous phenobarbital administration during the preschool years is indicated for most children who have had a simple febrile convulsion.

Child↗
PubMed1983

Convulsions in shigellosis. Evaluation of possible risk factors.

We studied 158 children with culture-proven shigellosis, 37 (23.4%) of whom had convulsions. Historical, clinical, and laboratory data were compared between patients with and without convulsions to define risk factors for the development of seizures. Age was the most important predisposing factor. The highest incidence of shigellosis associated with convulsions was found in children between 6 months and 4 years of age. Peak body temperature and a family history of convulsions also independently affected the development of seizures. Sex and Shigella strain showed differences between the groups but failed to reach statistical significance.

Acid-Base Imbalance↗
PubMed1990

Recurrent seizures in children with Shigella-associated convulsions.

Fifty-five children with Shigella-associated convulsions were followed prospectively to investigate their risk of subsequent febrile or nonfebrile seizures. The duration of the follow-up period was between 6.9 and 14.1 years (9.7 +/- 3.1 years). No case of nonfebrile seizures and only 2 cases (3%) of subsequent febrile seizures were observed during this period. We conclude that although febrile and Shigella-associated convulsions share many clinical features, the natural history of these two conditions seems to be distinctly different. Shigella-related convulsions are not associated with an increased incidence of subsequent febrile or nonfebrile convulsions.

Child↗
PubMed1991

Benign familial neonatal convulsions: evidence for clinical and genetic heterogeneity.

The gene for autosomal dominant "benign" familial neonatal convulsions, a transient, primary epilepsy of infancy, has recently been assigned to chromosome 20q. To determine whether this disorder is genetically heterogeneous, we performed linkage analysis in two previously unreported pedigrees with benign familial neonatal convulsions in which clinical heterogeneity was evident. There were 14 affected persons in the first family, and none had seizures (febrile or afebrile) after the age of 2 months. The second family had 13 affected individuals and 2 obligate carriers; seizures frequently did not remit until 6 to 24 months, febrile convulsions occurred in at least 2 patients, apparent audiogenic seizures occurred in 4 patients, and 1 individual had refractory epilepsy until late adolescence. Linkage studies with the chromosome 20 markers D20S19 and D20S20 were performed in both families. The resulting data favored linkage of the disease and marker loci in Family 2 by a maximum odds ratio of 45:1 at 6% recombination. In Family 1, however, the odds were greater than 20,000:1 against linkage at 10% recombination or less. We conclude that the syndrome of benign familial neonatal convulsions is clinically and genetically heterogeneous. Further study will be necessary to clarify the relationship between phenotype and genotype in this disorder.

Chromosomes, Human, Pair 20↗
PubMed1993

Electroclinical signs of benign neonatal familial convulsions.

Benign neonatal familial convulsions comprise a distinct epileptic syndrome with an autosomal mode of transmission. The electroclinical signs of seizures in this syndrome are not yet well defined. In 3 children from two families presenting with benign neonatal familial convulsions, 14 seizures were recorded during electroencephalographic (EEG)-video sessions. All seizures occurred during sleep, after a short arousal reaction. Seizures started with bilateral, symmetrical flattening of the EEG for 5 to 19 seconds; simultaneously there was apnea and tonic motor activity. The EEG flattening was followed by a long (1-2-minute) bilateral discharge of spikes and sharp waves; simultaneously, there were vocalizations, chewing, and focal or generalized clonic activity. The prominence of EEG and motor abnormalities varied between the left and the right from one seizure to the next in any given child. The seizures stopped without EEG or clinical postictal depression. These electroclinical observations suggest that the convulsions of benign neonatal familial convulsions are a form of generalized tonic-clonic seizure whose expression may be asymmetrical, probably because of the immaturity of the corpus callosum or other structures ensuring seizure synchronization.

Adult↗
PubMedDate not supplied

Effect of acute pretreatment of lead on picrotoxin-induced convulsions in rats.

The effect of acute exposure to lead acetate (LA)/lead nitrate (LN) on onset and severity of convulsions induced by a low dose of picrotoxin was examined in rats. Both LA and LN reduced the time of onset and exacerbated the severity of convulsions, with a resultant high lethality. On comparison, it was noted that in the LA-pretreated group, convulsion scores and incidence of tonus and mortality were much higher; the appearance of tonus was more delayed than in the LN-pretreated group. In lead-pretreated animals, the potentiation of picrotoxin-induced convulsions was accompanied by higher lead levels in blood (p < 0.001). However, the whole-brain lead levels were not significantly different in these animals compared to the controls. The difference in the degree of potentiation by the two forms of lead could possibly be attributed either to the role of a combination of anions and cations or to the variable cerebral uptake and regional distribution of lead or due partly to the extent of competitive interaction involving d-aminolaevulinic acid--whose level is known to be elevated consequent to lead-induced disruption of haem biosynthesis--at GABA receptors.

Animals↗
PubMed1993

Metabolic and neuroanatomical correlates of barrel-rolling and oculoclonic convulsions induced by intraventricular endothelin-1: a novel peptidergic signaling mechanism in visuovestibular and oculomotor regulation?

The neuroactive peptide endothelin-1 has receptors distributed abundantly among subdivisions and nuclei of the visuovestibular and oculomotor systems. In previous work, we and others described the convulsive manifestations resulting from central injection of this neuropeptide, including nystagmus, oculoclonus, exophthalmos, tonic hindlimb extension, and a generalized repetitive motor disturbance called barrel-rolling. We applied the quantitative, autoradiographic [14C]deoxyglucose method to examine the hypothesis that visuovestibular and oculomotor structures would become metabolically stimulated when endothelin was introduced into the brain via the ventricular system in conscious rats. Since previous work had demonstrated that hypermetabolic responses to endothelin in other neural systems were inhibited by an antagonist of neuronal calcium L-type channels, nimodipine, we further tested whether the increased function of vestibulooculomotor nuclei whose metabolic activity was sensitive to endothelin could be altered following nimodipine pretreatment via the ventricle. A single unilateral injection of endothelin (9 pmol in 3 microliters saline) into a lateral ventricle provoked significantly increased rates of glucose metabolism in 22 of 39 individual anatomical structures of the visuovestibular and oculomotor systems. Among those affected were the superficial stratum of the caudal superior colliculus (+25%), the optic tract bilaterally (+35 to 43%), the oculomotor cranial nerve nuclei (III, IV, VI; range of +21 to 47%), and the medial terminal nucleus of the accessory optic tract which harbors dense fields of endothelin binding sites (bilateral increase of +70 to 96%). Several other nuclei involved in the proprioceptive and visuovestibular disturbance caused by endothelin displayed increased metabolic activity, including the cuneate, gracile, sensory trigeminal, and prepositus hypoglossal nuclei, the vestibular subnuclear system, and the cerebellar flocculus. Identification of hypermetabolic responsivity to endothelin in these structures provides further information on the anatomical substrates mediating the behavioral phenomenology of endothelin-induced motor convulsions which involve the paroxysmal participation of the extraocular muscles and motor control systems producing barrel-rolling convulsions. Nimodipine pretreatment inhibited both the convulsive activity and the cerebral hypermetabolic responses to intraventricular endothelin. The results indicate that the neural systems sensitive to intraventricular endothelin become functionally active via a calcium-mediated process that may involve the neuropeptide as an intrinsic signaling molecule.

Animals↗
PubMed1979

Involvement of central cholinoceptors in Metrazol-induced convulsions.

Atropine sulphate (10 mg/kg IP) afforded 90% protection against clonic convulsions induced by standard doses of metrazol (80 mg/kg SC) in mice, whereas atropine methonitrate (10 mg/kg IP) did not offer any protection. Furthermore, physostigmine (1 mg/kg IP) caused recurrence of convulsions in atropinzed metrazol-treated mice and converted the subconvulsive dose of metrazol (40 mg/kg SC) into a 100% convulsive dose. However, neostigmine (1 mg/kg IP) did not antagonize the protection afforded by atropine sulphate against metrazol. The results of the study suggest an involvement of central cholinergic mechanisms in metrazol-induced convulsions.

Animals↗
PubMed1981

Effects of drugs affecting the noradrenergic system on convulsions in the quaking mouse.

Handling-induced convulsions in the quaking mouse can be blocked by: phenobarbital, pentobarbital or phenytoin; postsynaptic alpha-adrenoceptor agonists (noradrenaline, phenylephrine, CRL 40028); presynaptic alpha-adrenoceptor blockers (yohimbine, mianserine); catecholamine liberating agent (amphetamine); noradrenaline reuptake inhibitors (cocaine, imipramine, desipramine). Moreover, the protective effect of yohimbine was antagonized by clonidine, prazosin or alpha-methylparatyrosine, and the protective effect of CRL 40028 was antagonized by prazosin but not by alpha-methyltyrosine. Drugs acting by other mechanisms (pilocarpine, atropine, trihexyphenidyl, (--)-5-HTP, methysergide, pimozide, clonidine, alpha-methyl DOPA, prazosin, isoprenaline, salbutamol) did not protect against convulsions. A slight protection was obtained with high doses of apomorphine and also with (+/-)-propranolol. This effect is probably not related to blockade of beta-adrenoceptors because the same effect was obtained with (+)propranolol. In young quaking mice, where susceptibility to convulsions is low, both postsynaptic alpha-adrenoceptor blockers and presynaptic alpha-adrenoceptor antagonist lowered the convulsive threshold. Thus, this seems to constitute an interesting model for the in vivo study of substances which affect the central alpha-adrenoceptors either pre- or postsynaptically.

Animals↗
PubMed1977

Genetic aspects of febrile convulsions.

A total of 6706 children 3 years of age (3491 boys, 3215 girls) in a particular geographical area in Fuchu (population approximately 182 000), Tokyo, was investigated. Some 654 children (9.8%; 10.5% for male, 9.0% for female) had had at least one convulsion, and the incidence of febrile convulsions was 6.7% (7.2% for male, 6.2% for female). The 450 FC children with febrile convulsions and 620 randomly selected control children were analyzed on the mode of inheritance. The incidence of the disease among siblings was 21.9% (29.7% after age correction), which rose greatly with increasing numbers of affected family members, and the segregation ratio among siblings was higher (36.5%) with one FC parent, and lower (18.5%) if neither parent had had a seizure. The more severe the illness in FC children, the larger the incidence among siblings. Population and family studies indicated that heredity plays an important role in febrile convulsions and that multifactorial inheritance is most likely.

Child, Preschool↗