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PubMed1992

Technetium-99m hexamethylpropylene amine oxime single photon emission tomography in febrile convulsions.

We report our initial experience with technetium-99m hexamethyl propylene amine oxime (99mTC-HMPAO) brain single photon emission tomography (SPET) in the investigation of 19 children presenting with febrile convulsions. Two patients with complex febrile convulsions showed focal SPET lesions contralateral to the neurological deficit. However, in 9 out of 17 patients with simple febrile convulsions, focally disturbed perfusion was shown. In 4 out of 6 patients with electroencephalogram (EEG) abnormalities on admittance, SPET revealed at least 2 focal lesions. The temporofrontal region was the one most commonly involved. The SPET findings presented here also suggest a temporal relationship with the febrile convulsions, with markedly fewer lesions if examined after 12 days. In our initial experience, perfusion SPET did not show any particular pattern helpful in the differential diagnosis of the child presenting with febrile convulsions. Physiopathologically, our findings may support the hypothesis that brain tissue is regionally more vulnerable to fever, in patients presenting with febrile convulsions.

Brain↗
PubMed1989

Time-course of malaoxon-induced alterations in brain regional inositol-1-phosphate levels in convulsing and nonconvulsing rats.

The potential of a single dose of malaoxon (26.2 or 39.2 mg/kg i.p.) to produce convulsions and to increase cerebral levels of inositol-1-phosphate (Ins1P), an intermediate in phosphoinositide (PI) cycle, was followed for 1, 4, or 72 hr. The lower dose of malaoxon did not produce convulsions whereas the higher dose induced convulsions in 60% of the exposed rats. Malaoxon caused a dose-dependent, at most 2-fold, increase in brain regional Ins1P levels in nonconvulsing rats as compared to controls. At the higher dose of malaoxon, in convulsing rats, the Ins1P-levels increased 4-fold above the control Ins1P-levels. In nonconvulsing rats, the Ins1P-levels reached their maximum 1-4 hr after the administration of malaoxon, whereas in convulsing rats the levels increased for 72 hr. The results suggest that PI-signalling is associated with convulsions produced by malaoxon.

Animals↗
PubMed1995

Serum sodium levels and probability of recurrent febrile convulsions.

UNLABELLED: In a prospective study of 69 children with febrile convulsions, serum sodium levels were often lower than normal (52% had levels < 135 mmol/l). The mean level (134.4 +/- 0.4 mmol/l) was significantly lower as compared to a group of children without fever (140.6 +/- 0.4 mmol/l, n = 23) and as compared to a group with fever but without convulsions (137.6 +/- 0.6 mmol/l, n = 31). The probability of a repeat convulsion within the same febrile period appeared to be significantly related to the serum sodium level. CONCLUSION: Measurement of the serum sodium is a valuable investigation in the child with a febrile convulsion. The lower the serum sodium level, the higher the probability of a repeat convulsion. This knowledge may be of practical value in deciding whether to admit the child or allow it to return home and in advising parents or carers of the risk of a repeat convulsion.

Case-Control Studies↗
PubMedDate not supplied

Risk factors for recurrence of febrile convulsions.

A cohort of hundred children with febrile convulsions, in the age group of 3 months to 5 years were followed up prospectively for one year to study the natural course of the illness, and to determine if specific factors would increase the risk of recurrence of febrile convulsions. The risk factors studied were age of onset under one year, long duration of convulsion (more than 15 minutes), family history of febrile convulsion or epilepsy and combination of two or all of the above factors. Four groups of children with different risk factors were followed up for recurrence of convulsion, after the first attack. A group of children without any risk factor was considered as control and they were also followed up for recurrence of convulsions. Though all the groups with the risk factors, showed a trend towards a higher recurrence rate when compared to controls, the difference observed clinically was not significant statistically. This could be due to the small sample size of each group. A larger study could throw light on the predictive value of these risk factors and narrow down the use of long term anticonvulsant prophylaxis.

Age Factors↗
PubMed1991

The effects of sevoflurane on lidocaine-induced convulsions.

The influence of sevoflurane on lidocaine-induced convulsions was studied in cats. The convulsive threshold (mean +/- SD) was 41.4 +/- 6.5 mg. l(-1) with lidocaine infusion (6 mg.kg(-1).min(-1)), increasing significantly to 66.6 +/- 10.9 mg. l(-1) when the end-tidal concentration of sevoflurane was 0.8%. However, the threshold (61.6 +/- 8.7 mg. l(-1)) during 1.6% sevoflurane was not significant from that during 0.8% sevoflurane, indicating a celling effect. There was no significant difference in the convulsive threshold between sevoflurane and enflurane. The rise in blood pressure became less marked when higher concentrations of sevoflurane or enflurane were administered and the blood pressure at convulsions decreased significantly in 1.6% sevoflurane, and in 0.8% and 1.6% enflurane. However, there was no significant difference in the lidocaine concentrations measured when the systolic blood pressure became 70 mmHg. Apamin, a selective blocker of calcium-dependent potassium channels, was administered intracerebroventricularly in rats anesthetized with 0.8% sevoflurane to investigate the mechanism of the anticonvulsive effects. Apamin (10 ng) had a tendency to decrease the convulsive threshold (21.6 +/- 2.2 to 19.9 +/- 2.5 mg. l(-1)) but this was not statistically significant. It is suggested that sevoflurane reduces the convulsive effect of lidocaine toxicity but carries some risk due to circulatory depression.

Journal Article↗
PubMed1984

Differential behavioral effects induced by intrathecal microinjection of opiates: comparison of convulsive and cataleptic effects produced by morphine, methadone, and D-Ala2-methionine-enkephalinamide.

Intrathecal (i.t.) microinjection of 400 micrograms of morphine in rats induces convulsive activity restricted to the hindlimbs. This activity is potentiated rather than antagonized by naltrexone, is potentiated in animals pretreated over 6 days with increasingly higher systemic doses of morphine, and is potentiated and prolonged by high thoracic spinalization . Similar to morphine, convulsive spinal activity could also be elicited with i.t. injection of the non-opiate convulsant penthylenetetrazol (PTZ). However, methadone, D-ala2-methionine-enkephalinamide (DALA), or naltrexone, injected i.t. at equimolar doses with morphine did not produce similar convulsive behavior. DALA and methadone rather produced pronounced spinal catalepsy. It was concluded: that the spinal convulsive action of morphine is not mediated by specific opiate receptors; and that the spinal cord may be one of the sites where high doses of systemically administered morphine may produce convulsions.

Animals↗
PubMed1988

Measurement during convulsions of guanidino compound levels in cerebrospinal fluid collected with a catheter inserted into the cisterna magna of rabbits.

An easy method for collecting cerebrospinal fluid (CSF) was developed using a catheter inserted into the cisterna magna of rabbits. Levels of guanidino compounds in CSF collected by this method were measured. Levels of guanidinoacetic acid and creatinine increased at the onset of a pentylenetetrazol (PTZ)-induced convulsion. These levels normalized 2 h after the convulsion. The arginine level started to decrease 2 h after the convulsion, continued to decrease gradually and normalized 4 days after the convulsion. These results suggest that guanidinoacetic acid and creatinine are related to the initiation of PTZ-induced convulsions, and that 4 days are required for the metabolism of guanidino compounds to return to normal after a convulsion in rabbits.

Animals↗
PubMed1995

Alpha 2-adrenoceptor agonist, dexmedetomidine, protects against kainic acid-induced convulsions and neuronal damage.

Kainic acid (KA)-induced convulsions are accompanied by histopathological changes that are most prominent in the temporal lobe structures. In the present study, we investigated whether a selective alpha2-adrenoceptor agonist, dexmedetomidine could attenuate KA-induced epileptic convulsions and subsequent neuronal damage in the rat hippocampus. Rats were pretreated 30 min before KA injection (9 mg/kg, i.p.) with dexmedetomidine (3 micrograms/kg, s.c.). The behavior of animals was observed for at least 3 h. Dexmedetomidine suppressed the development (p < 0.001), generalization (p < 0.05) and severity (p < 0.01) of convulsions. In addition, histological analysis revealed that dexmedetomidine-treated animals without convulsions or with only partial convulsions had no neuronal damage in the principal cell layers of the hippocampus. A selective alpha2-antagonist, atipamezole (1 mg/kg, s.c.) potentiated KA-induced convulsions and increased the mortality in status epilepticus. In conclusion, the present study demonstrated that dexmedetomidine, in addition to possessing anticonvulsant properties, has a neuroprotective effect in the KA model of status epilepticus.

Adrenergic alpha-Agonists↗
PubMed1976

Changes in regional brain acetylcholine levels during drug-induced convulsions.

Acetylcholine (ACh) levels were determined in the brain of rats killed by decapitation or focussed microwave radiation during drug-induced convulsions. During metrazol or strychnine-induced convulsions a diffuse decrease in ACh levels was found in rats killed by decapitation. When the rats were killed by radiation and the brain was only divided into three large regions, strychnine caused no changes in ACh levels; metrazol caused a decrease in the cerebral cortex and lower brainstem. When discrete brain regions were investigated in rats killed by radiation, metrazol-induced convulsions were associated with a decrease in ACh level in all regions dissected and strychnine-induced convulsions with a decrease in the hippocampus and caudate nucleus only. Picrotoxin-induced convulsions were associated with a decrease in ACh level in the cerebral cortex, hippocampus, midbrain and medulla-pons, those induced by bicuculline with an increase in ACh level in the frontal cortex, hippocampus, midbrain and medulla-pons, by dimefline with an increase in the frontal cortex, midbrain and medulla-pons and a decrease in the caudate nucleus. The experiments show that each type of convulsant affects ACh levels in discrete brain regions in a different way.

Acetylcholine↗
PubMed1985

Inhibition of intrathecally administered picrotoxin- and bicuculline-induced convulsions in mice by pipecolic acid or GABA.

Pipecolic acid (PA) is an alicyclic amino acid and putative neurotransmitter which may modulate GABAergic transmission in the central nervous system. The present study was designed to investigate the anticonvulsant effect of intrathecally (i.t.) injected PA on picrotoxin- and bicuculline-induced convulsions which are thought to be produced by interactions with GABAergic systems. Intrathecal injections of picrotoxin and bicuculline in mice produced convulsions which were characterized by a rapid onset and short duration. Coadministration of GABA with either bicuculline or picrotoxin, but not strychnine, attenuated the severity of the convulsions. Coadministration of PA also protected against bicuculline- and picrotoxin-induced convulsions. Intrathecal injections of PA produced a dose-related increase in the latency to the onset of these convulsions as well as a decrease in their duration, however PA failed to inhibit the duration of strychnine-induced seizures. The D isomer of PA was found to be more effective than the L isomer as an anticonvulsant in this study. When administered in a high dose (500 micrograms i.t.), the D isomer produced flaccid paralysis while injection of high doses (100-500 micrograms i.t.) of the L isomer actually elicited convulsions. These results further support an interaction between PA and GABAergic activity.

Animals↗
PubMed1988

Anticonvulsive activity of several excitatory amino acid antagonists against barbital withdrawal-induced spontaneous convulsions.

Several excitatory amino acid antagonists were tested for an ability to prevent spontaneous convulsions seen during the barbital abstinence syndrome in rats. Barbital-dependent animals were continuously infused intracerebroventricularly (i.c.v.) for the first 48 h following barbital withdrawal with either saline, 2-amino-7-phosphonoheptanoic acid (APH), magnesium sulfate, glutamyldiethyl ester (GDEE) or cis-2,3-piperidine dicarboxylic acid (PDA) using the highest dosages which did not affect normal behavior of the rats. All animals were observed continuously from 12 to 48 h postwithdrawal and the number of spontaneous convulsions observed in each animal was recorded. After this time, animals were killed by focused microwave irradiation and the cerebellas were collected for determination of cyclic guanosine monophosphate (cGMP) levels. While both APH and MgSO4 dramatically prevented convulsions, only APH prevented the withdrawal-induced elevation of cerebellar cGMP. PDA and GDEE had no statistically significant effect on either cerebellar cGMP levels or on convulsive activity. Although the effect of GDEE was not statistically significant, the number of convulsions was reduced to 1/3 those seen in control animals. These data implicate N-methyl-d-aspartate (NMDA) receptor-mediated pathways in seizure activity associated with the barbital abstinence syndrome and show that the withdrawal-induced elevation of cerebellar cGMP can occur without the induction of convulsions.

Amino Acids↗
PubMed1990

Evidence for a role of glycine in area tempestas for triggering convulsive seizures.

An epileptogenic region of the deep prepiriform cortex, area tempestas (AT), triggers convulsive seizures in response to the focal application of GABA antagonists, muscarinic agonists and excitatory amino acid agonists. In all cases, activation of N-methyl-D-aspartate (NMDA)-sensitive receptors in AT is required for triggering convulsions from this site. To determine whether glycine is involved in the activation of NMDA-sensitive receptors in AT, we evaluated the effects of 7-chlorokynurenic acid (7-CLKYN); kynurenic acid (KYN) and 3-amino-1-hydroxy-2-pyrrolidone (HA-966) on convulsions evoked by focal application of bicuculline methiodide (118 pmol) into AT. Significant anticonvulsant effects were obtained with 1.25 nmol of 7-CLKYN, 6.25 nmol of KYN and 60 nmol of HA-966 in AT. 7-CLKYN in AT also blocked the convulsant effects of carbachol (273 pmol) and kainic acid (117 pmol) injected into AT. When injected into the lateral ventricle, high doses (50-100 nmol) of 7-CLKYN were required in order to attenuate AT-evoked convulsions and these doses produced marked ataxia. In contrast, no ataxia was observed following 7-CLKYN application into AT at anticonvulsant doses. Our results implicate glycine antagonism as a mechanism for preventing convulsions triggered via NMDA receptor activation in AT and demonstrate that a different anatomical site of action is responsible for the motor impairment produced by glycine antagonism.

Animals↗
PubMed1991

Diazepam-atenolol combination antagonizes aminophylline-induced convulsions and lethality in mice.

The present study was undertaken to identify protective drugs against aminophylline (240 mg/kg i.p.)-induced convulsions and lethality in mice. Diazepam (10 mg/kg) and valproic acid significantly prevented the convulsions, but were not effective in preventing mortality. Phenytoin, atropine, carbamazepine and atenolol were ineffective in protecting against convulsions and death. Ketamine gave partial protection against convulsions, but was not effective in preventing mortality. Diazepam (10 mg/kg) and atenolol (5 mg/kg) administered together gave total protection against convulsions and death. These results show that aminophylline-induced convulsions are relatively resistant to antiepileptic drugs, and that a combination of diazepam and a beta-blocker (atenolol) has potential as an anti-aminophylline agent.

Aminophylline↗
PubMed1983

Potentiation of hyperthermia-induced convulsions in the developing rat by previous treatment with pentylenetetrazol.

Infant rats were subjected to pentylenetetrazol-induced convulsions on alternate days from 5 to 13 days of age. At 17 days of age, their susceptibility to the convulsant effects of hyperthermia was examined. It was found that previous pentylenetetrazol-induced convulsions caused a significant facilitation in the development of hyperthermia-induced convulsions. The development of hyperthermia-induced convulsions was also facilitated in rat pups of a similar age after acute pretreatment with a subconvulsive dose of pentylenetetrazol. The results of this study indicate that cross sensitization between convulsant agents is possible in the developing rat. In addition, although the nervous system of the immature rat is not fully developed, the central substrates of this process evince adultlike characteristics.

Animals↗
PubMed1992

The effect of convulsions on the rectification of central nervous system disorders in epileptic mice.

Abnormal behavior in epileptic mice (El mice) may be rectified after convulsive seizures. This mechanism was investigated behaviorally through measurements of ethanol-induced sleeping time and locomotor activity, as well as immunohistochemically using a microphotometry system. Decreased ethanol-induced sleeping time and increased ethanol-dependent locomotor activity in El mice as compared to ddY mice (the mother strain of El mice) were rectified by convulsions as well as the intraventricular (IVT) administration of CaCl2, dopamine, or serotonin. Also, the lower dopamine levels in the neostriatum and nucleus accumbens septi in El mice as compared to ddY mice were improved by convulsions as well as the IVT administration of CaCl2. We have previously observed that a lower level of serum calcium in El mice causes a decrease in central biogenic amine synthesis through a calmodulin-dependent system. This may increase the susceptibility to epileptic convulsions and induce abnormal behavior. Combining the present results with our previous observations, we suggest that the convulsions in El mice will be induced when the balance of physiological functions is lost, as may be seen when the biogenic amine syntheses are decreased. The serum calcium level in El mice is increased by convulsions, and an elevated serum calcium level enhances brain biogenic amine synthesis through a calmodulin-dependent system. Subsequently, biogenic amines rectify physiological disorders in El mice.

Animals↗
PubMed1981

Studies on prostaglandin F2 alpha formation caused by pentametylenetetrazol-induced convulsions in rat brain.

Prostaglandin F2 alpha formation caused by pentametylenetetrazol convulsions was studied as a function of the duration, the doses of the convulsant and the intensity of the seizures. It was shown by the statistical analysis of the results in the case of clonic convulsions that the amount of synthetized PGF2 alpha did not depend on the doses of convulsant, while close relation existed between the duration and the PGF2 alpha production. At the same time, during tonic convulsions lasting longer than 50 sec, no more increase in the PGF2 alpha content of the brain was observed. An experimental model is suggested to study in vivo the mechanisms regulating the brain's prostaglandin biosynthesis. Pretreatment of the animals with reserpine did not affect the rate of convulsion-induced PGF2 alpha-formation.

Animals↗
PubMed1984

Evidence of reduced uptake of convulsant in brain following prostaglandin E2.

The toxic and convulsant effects of the acetylcholinesterase (AChE) inhibitor Soman, were examined in mice pretreated with various doses of prostaglandin E2 (PGE2), administered by either intraperitoneal injection (i.p.) or by intracerebroventricular (i.c.v.) infusion. PGE2 (i.p.) reduced the lethal effects of Soman slightly. PGE2 (i.p. and i.c.v.) delayed the onset and reduced the severity of cholinergically-induced convulsions, resulting from Soman. Whole brain AChE was measured at various times after Soman or Soman preceded by PGE2. PGE2 (i.p. or i.c.v.) reduced the rate at which Soman inhibited brain AChE, which appeared to be related to the increased time to onset of convulsive activity. Repeated injections of PGE2 did not delay convulsions indefinitely nor were convulsions terminated once they had started. The results suggest that the anticonvulsant properties of PGE2 may have been due, in part, to decreased cerebral circulation with subsequent reduction in the access of the convulsant to the brain and in part to direct neuronal effects.

Acetylcholinesterase↗
PubMedDate not supplied

Possible involvement of nitric oxide in quinolinic acid-induced convulsion in mice.

Quinolinic acid (QA) induced clonic and tonic convulsions in mice when it was injected into the cerebral ventricle. Pretreatment with L-arginine (L-Arg), a substrate of nitric oxide (NO) synthase (NOS), and/or 5,6,7,8-tetrahydrobiopterin (THB), cofactor of NOS, tended to potentiate QA-induced convulsion. NG-monomethyl-L-arginine (NMMA), a competitive NOS inhibitor, diminished QA-induced convulsion. This effect of NMMA was attenuated by coadministration of L-Arg or THB. Sodium nitroprusside (SNP), which spontaneously releases NO, did not potentiate, but diminished QA-induced convulsion. These findings suggest that an endogenous NO may be involved, at least in part, in QA-induced convulsion in mice, and that an exogenous NO released from SNP may cause downregulation of N-methyl-D-aspartate (NMDA) receptor activity, and thereby prevent the excessive excitation of NMDA receptors and subsequent convulsion caused by QA.

2-Amino-5-phosphonovalerate↗