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PubMed1989

[Convulsions observed during administration of antidepressants].

We investigated the incidence of convulsions observed during treatment with antidepressants. Among the patients observed in this department, 582 cases received the antidepressants for more than 2 months were selected. 8 cases (1. 4%) of these patients showed convulsions. Detailed evaluation revealed a high incidence of convulsions occurred in patients who were administered more than two kinds of antidepressants. Among tetracyclic antidepressants, viz. maprotiline and clomipamine, and tricyclic antidepressants, viz. amitriptyline indicated a high incidence rate of convulsions. On the contrary, mianserin and imipramine tended to show a lower incidence. In 4 cases, acute toxic symptoms were seen before the convulsion, and the serum concentration of antidepressants in these patients was high. If toxic symptoms and elevated level of serum concentration are useful indicator for prediction of convulsion by treatment with antidepressants, these might be a noteworthy clinical findings. At present, if doctors are required to administer more than moderate amounts of more than two antidepressants, careful administration is desirable. With the accumulation of such cases, it is necessary to obtain further evaluation of the relationship between toxic symptoms and serum concentration of antidepressants.

Adult↗
PubMed1986

Effects of thioglucoses on sensitivity to insulin hypoglycemic convulsions.

Based on the effects of gold thioglucose (GTG), we have previously proposed a regulatory center in brain which adjusts the convulsive response to insulin hypoglycemia. The sensitivity to insulin hypoglycemic convulsions is decreased 24 hr and increased 1 week after a single i.p. injection of GTG. The differences are in the brain's convulsive response to equal hypoglycemia, as the blood glucose response to insulin is unchanged. The generalized convulsive threshold, reflected in the sensitivity to nonmetabolic pentylenetetrazol (Metrazol) convulsions, is not altered. Despite its systemic administration, GTG causes lesions focused in the ventromedial hypothalamus. In the present study, this regulatory center was explored further by the ability of two thioglucoses to substitute for GTG. beta-D-Thioglucose had no effect. 5-Thioglucose simulated the early (24 hr) action of GTG but had no effect at 1 week. However, unlike GTG, 5-thioglucose did not cause the ventromedial hypothalamus lesion. The early (24 hr) and late (1 week) components are thus dissociated. The early effect on insulin hypoglycemic convulsions does not require a ventromedial hypothalamus lesion. Structure-activity relationships and relationships to glucoregulatory systems are discussed.

Animals↗
PubMed1987

Neuronal expression of mutations affecting primarily glia in the mouse: studies in the dysmyelinated and convulsive mutant quaking.

1. Various aspects of the noradrenergic system in the brain of the dysmyelinating convulsive mutant mice quaking have been examined. 2. Determination of the endogenous contents of noradrenaline and its metabolite 3-methoxy 4-hydroxyphenyl-ethyleneglycol (MOPEG), as well as measurement of the electrically-evoked release of (3H)-noradrenaline shows an increased noradrenergic activity in the brain of the mutants, when compared to non convulsive controls of the same strain. 3. Ontogenic development of alpha adrenergic receptors indicate that an increased density of alpha-2 sites precedes the appearance of the first convulsions by approximately one week. 4. Anatomical determination of the number of noradrenergic neuronal cell bodies in the locus coeruleus shows a hyperplasia of this nucleus in the mutants. 5. Electrolytic coagulation of the locus coeruleus inhibits the convulsions of the quaking mice. 6. These results suggest that an alteration of the embryonic differentiation of the locus coeruleus, which gives rise to the majority of brain noradrenergic neurons, provokes a hyperactivity of this neuronal system, thereby triggering the convulsions of the quaking mutant mice. 7. The possible involvement of other neurotransmitter systems in the convulsions of these mutants, together with the nature of the relationship between neuronal abnormalities and dysmyelination phenomenon, are discussed.

Animals↗
PubMed1986

Amphetamine as a protective agent against oxygen-induced convulsions in mice.

Male mice exposed to hyperbaric oxygen (HBO) at 4.5 ATA O2 exhibit a number of toxic symptoms including convulsions, diminished respiration and an acoustic reaction controlled by the central nervous system. To study whether stimulation of the nervous system could offer protection against the convulsions, mice were injected i.p. with various doses of d-amphetamine before HBO. At a dose of 1.0 mg X kg-1 of d-amphetamine the mice could stay at 5 ATA O2 without convulsions about three times as long as those injected with saline only. At high doses, 4 and 8 mg X kg-1, there was a weak protective effect or the time to convulsions was shortened. Amphetamine increases the release of dopamine in the brain and it is possible that the mechanisms of protection against HBO induced convulsions are involved in that process. The degree of protection, however, depends on the dose; therefore, it also is supposed that amphetamine in low doses acts on the autoreceptors with a presynaptic effect, which in this case is protective against the convulsions without affecting the respiration.

Animals↗
PubMed1986

[Clinical analysis of immediate postoperative convulsion].

For the prevention and treatment of immediate postoperative convulsion which develops within 24 hours after neurosurgical operation, clinical analysis of consecutive 1293 cases in Kyoto University Hospital was done. Overall incidence was 3.1% and the incidence was highest in supratentorial craniotomy (5.7%). Previous history of convulsion was not contributory. In 77.5% of all cases, the convulsion was developed within 6 hours after operation and focal convulsion was more often than the generalized one. Status epilepticus was often developed. The incidence of convulsion was well correlated to the level of consciousness. Prognosis was not always poor if appropriate treatment was done without delay. CT showed mild degree of hemorrhage or mass effect. Our study suggests the contribution of focal brain damage at the operation to the development of immediate postoperative convulsion. Further study is necessary to elucidate the pathogenesis and to make appropriate plan to treatment.

Brain Neoplasms↗
PubMed1980

Deaths from local anesthetic-induced convulsions in mice.

Median convulsant (CD50) and median lethal (LD50) doses of three representative local anesthetics were determined in adult mice to evaluate the threat to life of local anesthetic-induced convulsions. The CD50 and LD50, respectively, were 57.7 and 58.7 mg/kg for bupivacaine, 111.0 and 133.1 mg/kg for lidocaine, and 243.4 and 266.5 mg/kg for chloroprocaine. When given intraperitoneally, bupivacaine thus was only about twice as toxic as lidocaine and four times as toxic as chloroprocaine. Convulsions always preceded death, except after precipitous cardiopulmonary arrest from extreme doses. A CD50 dose of local anesthetic (causing convulsions in 50% of mice) was fatal in 90% of bupivacaine-induced seizures, in 57% of the chloroprocaine group, and in 6% of the lidocaine group. The narrow gap between convulsant and lethal doses of local anesthetics indicates that untreated convulsions present much more of a threat to life than heretofore appreciated.

Anesthetics, Local↗
PubMed1981

Benzodiazepines protect mice from local anesthetic convulsions and deaths.

Median convulsant (CD50) and median lethal (LD50) doses of intraperitoneal lidocaine, bupivacaine, and etidocaine were determined in 149 mice. Another 496 mice were pretreated with intramuscular diazepam, lorazepam, or midazolam, 1 mg/kg. Fifteen minutes later, lidocaine, bupivacaine, or etidocaine was given intraperitoneally and the incidence of convulsions and deaths recorded. Benzodiazepines significantly reduced the incidence or convulsions. For instance, etidocaine, 54.9 mg/kg, produced 50% convulsions in untreated mice compared to 6.9%, 3.4%, and 3.4% after diazepam, lorazepam, or midazolam, respectively. Benzodiazepines also enhanced survival, as shown by significant increases in the LD50s. The bupivacaine LD50, for example, increased from 58.7 mg/kg in untreated mice to 75.2, 79.1, and 83.6 mg/kg after diazepam, lorazepam, or midazolam, respectively. Similarly, bupivacaine, 58.7 mg/kg, killed 50% of untreated mice, but only 1.2%, 9.7%, and 4.5% of mice treated with diazepam, lorazepam, or midazolam, respectively. It is concluded that premedication with a benzodiazepine significantly reduces the incidence of convulsions in mice and lowers the mortality rate as well. In equal intramuscular doses, midazolam proved to be the most effective anticonvulsant and diazepam the least. Etidocaine and bupivacaine convulsions were more difficult to suppress than those induced by lidocaine. On the other hand, the lethality of lidocaine was least reduced by these benzodiazepines.

Anesthetics↗
PubMed1993

[Long-term neurological outcome in children with convulsions during exanthema subitum].

We examined long-term neurological outcome of 12 patients, whose first febrile seizures had occurred during exanthema subitum (ES) and who had been treated with continuous daily administration of anticonvulsant drugs. Six of 12 children had a family history of febrile or afebrile convulsions and in a sister of one patient, athetoid palsy followed the status of afebrile convulsion (AC) during ES. Twelve cases were clinically classified into four groups; (A) 2 patients in whom ACs were repeated as soon as the fever of ES had dropped, (B) 6 patients in whom frequent recurrences of febrile convulsion followed ES, showing epileptic EEG abnormalities, (C) 1 patient who had suffered from later epilepsy, (D) 3 patients who showed complex type of febrile convulsion only during ES without any EEG abnormalities. Except one patient in group (A), who showed residual hemiparesis on the left, 11 cases demonstrated normal psychomotor development, and in 5 of all 12 cases, the treatment with anti-convulsant drugs could be discontinued. Unless severe neurological sequelae are complicated, long-term prognosis is not so poor in children whose first febrile convulsion occurred during ES.

Anticonvulsants↗
PubMed1997

Involvement of nitric oxide and N-methyl-D-aspartate in acute hypoxic altitude convulsion in mice.

BACKGROUND: Altitude convulsion is a rather specific form of experimental convulsion which is induced by acute exposure to a hypobaric hypoxic condition. Several neurotransmitters have been shown to be involved in the mechanisms of altitude convulsions. However, their roles and interaction were not clear. HYPOTHESIS: The novel neurotransmitter nitric oxide (NO) may be involved in the mechanisms of altitude convulsion through its neuronal signalling roles in relation to the NMDA receptor. METHODS: There were 177 mice intraperitoneally administrated (i.p.) with several drugs. The altitude convulsion threshold (ACT) was used as an index to evaluate the acute hypoxic tolerance. RESULTS: NO synthesis precursor, L-arginine (20, 40, 200, 800 mg/kg), resulted in a dose-dependent decrease in the ACT in mice, while the NO synthase (NOS) inhibitor, NG-nitro-L-arginine-methyl ester (L-NAME, 1.25, 2.50, 5.00 mg/kg, i.p.) increased the ACT. Pretreatment with L-NAME (5.0 mg/kg) prior to L-arginine (200 mg/kg) administration prevented the effect of decreasing ACT caused by L-arginine. Similarly, N-methyl-D-aspartate (NMDA, 2.5, 10.0, 20.0 mg/kg, i.p.) yielded a decrease in the ACT in mice and this decrease in hypoxic tolerance caused by NMDA can be prevented by pretreatment with either NMDA receptor antagonist 2-amino-5-phosphovalerate (AP-5, 20.0 mg/kg, i.p.) or NOS inhibitor L-NAME (5.0 mg/kg, i.p.). CONCLUSIONS: These findings suggest an important signalling role for nitric oxide and NMDA in the development of altitude convulsion and further support the hypothesized relationship between NMDA-receptor mediated neurotoxicity and nitric oxide.

Acute Disease↗
PubMed1987

Pro-convulsant actions of theophylline and caffeine in the hippocampus: implications for the management of temporal lobe epilepsy.

The pro-convulsant actions of theophylline and caffeine have been investigated using the hippocampal slice preparation and rats administered kainic acid or Metrazol. Both theophylline and caffeine induced the generation of epileptiform activity in the CA3 region of the hippocampal slice with convulsive dose50 (CD50) values of 3 microM respectively. Kainic acid-induced bursting in hippocampal slices was enhanced by theophylline (0.3-30 microM) and caffeine (1-100 microM). Theophylline induced burst firing in response to electrical stimulation in hippocampal area CA3 but not area CA1. Theophylline (50 mg/kg) strongly potentiated the effect of the limbic convulsant kainic acid in vivo whilst a dose of 200 mg/kg was necessary to significantly lower the threshold dose of Metrazol required to induce generalized convulsions. We conclude that alkylxanthines, probably by antagonizing the effect of endogenous adenosine, exert a pro-convulsant action in the hippocampus which preferentially promotes limbic seizures.

Animals↗
PubMed1987

Direct microinjection of soman or VX into the amygdala produces repetitive limbic convulsions and neuropathology.

Rats were injected in the amygdala and other forebrain sites with nmolar amounts of the highly toxic organophosphate 'nerve agent' compounds soman or VX (O-ethyl-S-(2-diisopropylaminoethyl)-methylphosphonothioate) in an attempt to determine the mechanism(s) responsible for the permanent brain pathology that has been observed following systemic intoxication with these agents. Injections were performed using a stereotaxically guided microsyringe in animals maintained under halothane/oxygen anesthesia or using chronically implanted cannulae in conscious animals. Bilateral microsyringe injections of up to 11.0 nmol soman into the amygdala failed to evoke abnormal behavior or brain pathology. When rats were pretreated with lithium chloride, or when carbachol was coadministered, soman injections evoked repetitive clonic convulsions and neuropathology. Unilateral injections of 3.4 nmol of VX into the amygdala elicited convulsions and brain damage in 67% of the animals tested. Atropine pretreatment (15.0 mg/kg, i.p.) prevented the development of convulsions and brain damage. Neuropathology was observed only in animals that developed repetitive convulsions; the piriform and entorhinal cortex, amygdala, hippocampus and thalamus were the brain structures most consistently damaged. With unilateral injections, the damage was more severe on the side ipsilateral to the injection. The behavioral topography of the convulsions and the neuroanatomical distribution and nature of the subsequent pathology closely resemble that observed with systemic administration of these compounds. The results indicate that the nerve agents are not directly neurotoxic, that peripherally induced hypoxia or anoxia are unlikely mechanisms of the neuropathology, and that the brain damage produced by these compounds is primarily seizure-mediated.

Amygdala↗
PubMed1983

Increased release of [3H]acetylcholine in vitro from the mouse hippocampus by a convulsant barbiturate.

The effects of the convulsant barbiturate, 5-(2-cyclohexylidene-ethyl)-5-ethyl barbituric acid (CHEB), on the spontaneous release of [3H]acetylcholine (ACh) from mouse hippocampal slices in an in vitro superfusion system have been evaluated. The pattern of the release of [3H]ACh by a single treatment with CHEB or an elevated potassium concentration was similar, with the peak release occurring in the same fraction. A maximally effective concentration of CHEB (500 microM) caused a 177% stimulation of spontaneous release of [3H]ACh, while 50 mM KCl increased the release by 2100% above the baseline. The stimulation of the spontaneous release of [3H]ACh by CHEB was concentration-dependent with an EC50 of 180 microM. The pattern of release of [3H]ACh induced by multiple treatment with CHEB and elevated potassium appeared to differ, suggesting that different pools of [3H]ACh in the cholinergic neurons might be affected by these treatments. The action of CHEB on the spontaneous release of [3H]ACh was unique among some other convulsant drugs that were studied. Another convulsant barbiturate, S(+)-1-methyl-5-phenyl-5-propyl barbituric acid [S(+)-MPPB], pentylenetetrazol and a convulsant benzodiazepine 1,3-dihydro-5-methyl-2H-1,4-benzodiazepine-2-one (Ro-5-3663) did not affect the spontaneous release of [3H]ACh. The relationship between the stimulation of release of ACh and the convulsant action of the barbiturates is discussed.

Acetylcholine↗
PubMed1986

Anticonvulsant profile of drugs which facilitate GABAergic transmission on convulsions mediated by a GABAergic mechanism.

The effects of selected modulators of GABAergic transmission, either alone or in combination, were tested for their potency on the seizure pattern and mortality induced by convulsant drugs in rat. Pentobarbital and diazepam were effective against both tonic and clonic seizure components induced by bicuculline and picrotoxin. The anticonvulsant profile of ethanol closely resembled that of pentobarbital. Pentobarbital, diazepam and ethanol did not modify seizures induced by strychnine. In contrast, progabide, a central gamma-aminobutyric acid (GABA) receptor agonist, caused significant protection only against convulsions induced by strychnine and its lethality, but did not protect against seizures induced by bicuculline or picrotoxin. Data on interaction of drugs with subprotective doses of these agents clearly demonstrated potentiation of the anticonvulsant actions of these modulators. Thus, seizures induced by bicuculline were more sensitive to the inhibition by pentobarbital in combination with diazepam or ethanol, while pentobarbital with progabide was equally effective against convulsions induced by GABA antagonists. Diazepam, in combination with progabide, blocked only convulsions induced by picrotoxin. Ethanol, in combination with either pentobarbital or with diazepam, was effective against all the three convulsant drugs. These results are consistent with the concept that drugs which facilitate GABAergic transmission are effective against seizures related to an impairment of GABA transmission. Further, the present data indicate that tonic seizures are more susceptible to the actions of drugs than the clonic component. Smaller doses of these drugs, alone or in combination, modified the seizure patterns and mortality, whereas at larger doses, the possible involvement of a nonspecific depressant action cannot be ruled out.

Animals↗
PubMed1994

Regional expression of inducible heat shock protein-70 mRNA in the rat brain following administration of convulsant drugs.

Expression of inducible heat shock protein-70 mRNA (hsp-70 mRNA) was studied in the rat brain following systemic administration of different convulsant agents: an L-type voltage-dependent calcium channel agonist, (+/-)-BAY K 8644 (BAY-K); the excitotoxic glutamate agonists kainic acid and N-methyl-D-aspartic acid (NMDA); and the GABAA receptor complex antagonists pentylenetetrazole (PTZ) and lindane (gamma-hexaclorocyclohexane). BAY-K induced minimal hsp-70 mRNA expression in the hippocampus of convulsant rats, localized in the dentate gyrus and the pyramidal cell layer of Ammon's horn. Kainic acid treatment in rats, showing severe limbic convulsions, caused intense expression of hsp-70 mRNA and protein (HSP-70). Expression was localized in select cerebral regions, notably the pyramidal cell layer of the hippocampal CA3 field of Ammon's horn and the piriform cortex, and also the subicular complex and the amygdala, and, to a lesser extent, the entorhinal cortex, the pyramidal cell layer of CA1, several thalamic nuclei, and the parietal cortex. In contrast, systemic administration of NMDA, PTZ or lindane led to no detectable induction of hsp-70 mRNA in the rat brain, despite producing convulsions. Histological examination revealed cell injury only following kainic acid treatment. Damage was most apparent in the piriform and entorhinal cortices, pyramidal cell layer of the CA1 field, and cortical amygdaloid nuclei. BAY-K, NMDA, PTZ and lindane did not lead to any observable histopathological changes. These results show that convulsions of different aetiology do not inevitably induce hsp-70 mRNA expression or cell damage. Intense expression of hsp-70 mRNA was generally associated with regions that later showed variable degrees of nerve cell damage, although hsp-70 mRNA expression was not always predictive of subsequent cell death or survival.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1987

The effects of chemically and electrically-induced convulsions on [3H]nitrendipine binding in mouse brain.

The effects of chemically and electrically-evoked seizures on [3H]nitrendipine binding to voltage-dependent calcium channels in mouse brain were determined 30 and 60 min following the initiation of convulsions. While maximal electroconvulsive shock, pentylenetetrazol and strychnine exhibited either no or marginal effects, Ro 5-4864 produced a decrease (14%) in the Bmax of [3H]nitrendipine at 30 min but not 60 min. The convulsant dihydropyridine calcium channel activator, BAY K 8644, produced a significant increase in the Kd (31%) of [3H]nitrendipine at 30 min, and a significant increase in both the Bmax (21%) and Kd (28%) of [3H]nitrendipine 60 min following the initiation of convulsions. While maximal electroconvulsive shock, pentylenetetrazol and strychnine exhibited either no or marginal effects, Ro 5-4864 produced a decrease (14%) in the Bmax of [3H]nitrendipine at 30 min but not 60 min following the initiation of convulsions. These findings indicate that modulation of voltage-dependent calcium channels by certain convulsants may be important in the genesis of seizures or in post-ictal compensatory processes.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed2004

Characterization of the convulsant action of pregnenolone sulfate.

Pregnenolone sulfate (PS) is an endogenous neurosteroid synthesized by glial cells, which acts as a potent convulsant when injected intracerebroventricularly and intraperitoneally. PS is found in relatively high concentrations in the hippocampus. But its convulsant action in the hippocampus has not been characterized. A range of PS doses were infused directly into the right hippocampus of 42 rats, which were subsequently monitored for behavioral and electrographic seizures. At the highest dose (4 micromol), PS produced status epilepticus (SE) and severe behavioral convulsions. As the dose of PS was reduced, the fraction of rats having SE diminished (ED50 for SE = 2.7 micromol). At doses lower than 300 nmol, PS infusion produced discrete electrographic seizures (ED50 = 68 nmol) associated with mild behavioral seizures. Both the behavioral seizure score (BSS) and the total number of seizures during the observation period changed in a dose-dependent manner. In separate experiments in cultured hippocampal neurons, PS enhanced NMDA-evoked whole-cell currents (EC50 = 16 microM). The results demonstrate that the hippocampus is highly sensitive to the convulsant effects of PS and that the enhancement of NMDA currents could contribute to the convulsant action of PS.

Animals↗
PubMed2003

D,L-cis-2,3-Pyrrolidine dicarboxylate alters [3H]-L-glutamate binding and induces convulsions in mice.

This study investigated whether D,L-cis-2,3-Pyrrolidine dicarboxylate (D,L-cis-2,3-PDC), a new glutamate analogue, alters glutamate binding to cerebral plasma membranes and whether N-methyl-D-aspartate (NMDA) receptors are involved in the convulsant effect of this compound. D,L-cis-2,3-PDC reduced sodium-independent [3H]-L-glutamate binding to lysed membrane preparations from adult rat cortex and had no effect on sodium-dependent glutamate binding. Intracerebroventricular administration of D,L-cis-2,3-PDC (7.5-25 nmol/5 microl) induced generalized tonic-clonic convulsions in mice in a dose-dependent manner. The coadministration of MK-801 (7 nmol/2.5 microl), with D,L-cis-2,3-PDC (16.5 nmol/2.5 microl), fully protected the animals against D,L-cis-2,3-PDC-induced convulsions, while the coadministration of DNQX (10 nmol/2.5 microl) increased the latency to convulsions but did not alter the percentage of animals that had convulsions. These results suggest that D,L-cis-2,3-PDC-induced effects are mediated predominantly by NMDA receptors.

Animals↗
PubMed2004

Seizure susceptibility to various convulsant stimuli of knockout interleukin-6 mice.

In the present study, the susceptibility of knockout interleukin-6 (IL-6(-/-)) mice to various convulsant stimuli has been evaluated and compared with other three related mice strains. Animals were treated with chemical convulsants impairing the gamma-aminobutyric acid neurotransmission [pentylenetetrazole (PTZ), picrotoxin, bicuculline, methyl-6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate (DMCM), methyl-beta-carboline-3-carboxylate (beta-CCM)], enhancing glutamatergic neurotransmission [N-methyl-d-aspartate (NMDA), alpha-amino-3 hydroxy-5-methyl-4-isoxazolepropionate (AMPA) and kainic acid (KA)] or a K(+)channel blocker [4-aminopyridine (4-AP)]. The behavioural changes of such convulsant stimuli on IL-6(-/-) were observed and compared with those observed in C57, IL-6(+/+) and DBA/2 mice. The occurrence of clonic and/or tonic seizures was scored and statistically analysed to observe possible differences on seizure susceptibility. The IL-6(-/-) mice exhibited significantly higher seizure susceptibility to PTZ, beta-CCM, DMCM, NMDA, AMPA and KA than did the other mice strains, with the exception of DBA/2 mice. This study demonstrates that IL-6(-/-) mice possess an increased susceptibility to some convulsant stimuli. In particular, the major convulsant effects produced by NMDA, AMPA and KA suggest that the excitatory amino acid system is more active in the central nervous system (CNS) of IL-6(-/-) mice. The present data suggest that IL-6(-/-) mice might be a valid novel epileptic model for the study of pathophysiology and pharmacology of epileptic seizures.

Animals↗