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PubMed1990

Dopamine D1 receptor modulation of pilocarpine-induced convulsions.

The contribution of dopaminergic mechanisms to the generalization of epileptic activity was studied in rats given pilocarpine after pretreatment with selective dopamine agonists. At the dose of 200 mg/kg, pilocarpine produced limbic stereotypes but not convulsions or seizure-related brain damage. Pilocarpine, 200 mg/kg, following pretreatment with the D1 agonist (RS)-2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3 benzazepine, but not its (S)-enantiomer, induced convulsive activity as revealed by behavioral, electroencephalographic alterations and widespread brain damage. These features were identical to those produced by a higher, convulsant dose of pilocarpine (400 mg/kg). On the other hand, pretreatment with the D2 agonist 4,4a,5,6,7,8,8a,9-octahydro-5-n-propyl-2H-pyrazolo-3,4-g-quinoline failed to induce convulsions. Furthermore, the D1 receptor antagonist (R)-(+)-8-chloro-2,3,4,5-n-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepine -7-ol prevented the convulsive activity induced by both 2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3 benzazepine plus pilocarpine (200 mg/kg) and pilocarpine (400 mg/kg), given alone. However, neither dopamine agonists nor antagonists altered the limbic stereotypes induced by pilocarpine, suggesting a dopamine system involvement primarily in the mechanisms of epilepsy generalization. The results suggest that pharmacological manipulation of dopaminergic transmission may provide an alternative approach to therapy of secondarily generalized epilepsy.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1995

Corticosteroids enhance convulsion susceptibility via central mineralocorticoid receptors.

Recently, interest in the roles of central nervous system mineralocorticoid receptors (MR) and glucocorticoid receptors (GR) has increased. In vitro results have implicated MR in the enhancing effects of corticosteroids and GR in the suppressing effects of corticosteroids on hippocampal excitability. Although indirect evidence exists suggesting that opposing actions of central MR and GR occur in vivo, direct evidence from studies employing receptor agonists and antagonists is only beginning to emerge. Work in our laboratory suggests that increased corticosterone levels are associated with increased severity of ethanol, pentobarbital, and diazepam withdrawal. Further work with chemical convulsants suggests that MR mediate excitatory effects of corticosteroids on convulsion susceptibility. The circadian rhythm in convulsion susceptibility varies with the circadian rhythm of plasma corticosterone levels and MR binding. The types of convulsions affected by manipulations of MR activity are believed to be of limbic origin, suggesting that limbic convulsions may be alleviated by the use of specific MR antagonists. In addition, because MR are substantially bound at rest and maximally occupied during the circadian peak in corticosteroid levels and during stressor exposure, these receptors are implicated in the maintenance of and in changes in the arousal state of animals.

Alcohol Withdrawal Delirium↗
PubMed1989

The effective agent in electroconvulsive therapy: convulsion or coma?

The ability of electrically-induced convulsions to alleviate at least some symptoms of mental illness was first reported in the literature 50 years ago; however, the cerebral mechanisms responsible for such therapeutic effects have thus far escaped elucidation. It is thus interesting to note that those seeking explanations for the therapeutic effects of electroconvulsive therapy (ECT) have focused their attention on the convulsion produced by ECT, as opposed to the coma. The present hypothesis emphasizes the coma following the convulsion as a potential explanation of the effectiveness of ECT and other convulsive therapies. It is postulated that the primary effect of the convulsion is to cause the release of adenosine (ARN) from neuronal tissue and that the subsequent depressant effect of ARN on neuronal activity results in the clinical effect observed. Thus hypothesis suggests that chemically-induced coma, particularly coma induced by benzodiazepines, may offer a safe, effective and more acceptable alternative to ECT.

Adenosine↗
PubMedDate not supplied

Effects of chloroquine on pentylenetetrazol-induced convulsions in mice.

The effects of chloroquine pretreatment were investigated on pentylenetetrazol-induced clonic-tonic convulsions in mice. The results demonstrated that lower doses of chloroquine (1.0-5.0 mg kg-1) significantly induced a delay in onset time to the clonic component of convulsions and reduced the incidence of the tonic phase of convulsions and mortality. In contrast, at a higher dose range (10.0-50.0 mg kg-1) chloroquine had opposite effects. This study points out the biphasic action of chloroquine on clonic-tonic PTZ convulsions and its preferential effect against the tonic phase of convulsions.

Animals↗
PubMed2004

Serum and cerebrospinal fluid nitrite/nitrate levels in patients with rotavirus gastroenteritis induced convulsion.

Nitric oxide (NO) is a highly reactive free radical that is involved in a variety of different biological process. In recent reports, the putative role of NO in the neuropathogenesis of brain inflammation has been demonstrated. And then the relation between neuronal NO and convulsive seizures induced by virus has been suggested. However, there are few reports about NO in vivo under viral neurological infections. In order to evaluate the relation between NO production and neurological disorders induced by viral infection, sixty-six cases including 11 patients with rotavirus gastroenteritis admitted for convulsions were examined in this study. NO metabolites (NOx) levels in both serum and cerebrospinal fluid obtained from rotavirus gastroenteritis patients with convulsion were much higher than in those of patients with purulent meningitis, encephalitis, febrile convulsion or in the control group. There was a relative correlation between IL-6 and NOx in some cases. These results indicated that NO may have a pathophysiological role in convulsions associated by rotavirus infection either through indirect or direct effects of NO. Consequently, NOx inhibitors might be helpful for the treatment of rotavirus encephalopathy.

Child, Preschool↗
PubMed2004

Involvement of NO in the convulsive behavior and oxidative damage induced by the intrastriatal injection of methylmalonate.

Acute intrastriatal administration of methylmalonic acid (MMA) induces convulsions through NMDA receptor-mediated mechanisms and increases production of end products of oxidative damage. Although it has been demonstrated that nitric oxide (NO) production increases with NMDA receptor stimulation and contributes to the oxidative damage observed in several neurodegenerative disorders, the role of NO in MMA-induced convulsions has not been investigated to date. In the present study we investigated the effects of the intrastriatal injection of N(omega)-nitro-L-arginine methyl ester (L-NAME: 10(-4) to 10(0) nmol/0.5 microl) on the convulsions and striatal protein carbonylation induced by the intrastriatal injection of MMA (4.5 micromol/1.5 microl). l-NAME (10(-3) to 10(-1)nmol) protected against MMA-induced convulsions and protein carbonylation ex vivo. These results suggest the involvement of NO in the convulsive behavior and protein carbonylation elicited by MMA.

Animals↗
PubMed2006

Electroencephalographic and convulsant effects of the delta opioid agonist SNC80 in rhesus monkeys.

Non-peptidic delta opioid receptor agonists are being evaluated for a wide range of clinical applications; however, the clinical utility of piperazinyl benzamide delta agonists such as SNC80 may be limited by convulsant activity. The purpose of the present study was to evaluate the electroencephalographic and convulsant activity produced by a high dose of 10 mg/kg SNC80 IM in rhesus monkeys. EEG and behavioral activity were examined in four adult male rhesus monkeys after IM administration of SNC80. Monkeys were seated in a standard primate restraint chair, and EEG activity was recorded using an array of 16 needle electrodes implanted subcutaneously in the scalp in a bipolar (scalp-to-scalp) montage in a longitudinal direction, with bilateral frontal, central, temporal, and occipital leads. Behavior was recorded using video monitoring equipment. Initially, all monkeys were tested with 10 mg/kg SNC80, which is a relatively high dose 3-10-fold greater than doses necessary to produce a variety of other behavioral effects. Behavioral convulsions and EEG seizures were observed in one of the four monkeys. In this monkey, neither behavioral convulsions nor EEG seizures were observed when a lower dose of 3.2 mg/kg was administered nine weeks later or when the same dose of 10 mg/kg SNC80 was administered one year later. These results suggest that IM administration of SNC80 is less potent in producing convulsant effects than in producing other, potentially useful behavioral effects (e.g. antinociception) in rhesus monkeys.

Animals↗
PubMedDate not supplied

Delayed convulsions and brief contralateral hemiparesis after retrobulbar block.

OBJECTIVE: This case report describes convulsions and hemiparesis after retrobulbar injection with good outcome in a patient undergoing outpatient cryocoagulation of his right eye. CASE REPORT: We report a young man in which localized convulsions of the ipsilateral face occurred 9 minutes after retrobulbar injection followed shortly by convulsions of the contralateral arm and leg. After the convulsions, the patient experienced left-sided hemiparesis resolving approximately 1 hour after the injection. There was no hemodynamic instability during this period. It was difficult to determine the exact cause of convulsions and hemiparesis. CONCLUSIONS: We believe these complications occurred because of unintentional injection of local anesthetic agent into the subarachnoid space without affecting the brainstem. Possible mechanisms of spread of local anesthetic agent into the central nervous system after retrobulbar block are discussed.

Adult↗
PubMed1997

Involvement of the claustrum in the convulsive evolution of temporal limbic seizure in feline amygdaloid kindling.

The effects of unilateral lesioning of the claustrum (CL) either prior to or following completion of amygdaloid (AM) kindling was examined in cats. CL lesioning ipsilateral to the kindling or the kindled AM caused the emergence of a mirror image pattern of expected or established AM onset convulsive seizure originating in the contralateral hemisphere. This finding suggests that: (1) the CL is involved in the convulsive evolution of AM onset non-convulsive limbic seizure; (2) an alternative transhemispheric route is available for the convulsive evolution of AM onset limbic seizure when the ipsilateral CL is disrupted; and (3) the CL is not critical for secondary convulsive generalization.

Amygdala↗
PubMed2003

Evidence for the involvement of GABA(A) receptor blockade in convulsions induced by cephalosporins.

There is accumulating evidence that most beta-lactam antibiotics (i.e., cephalosporins and penicillins) have some degree of convulsive activity, both in laboratory animals as well as in clinical settings. The proposed mechanism is suppression of inhibitory postsynaptic responses, mainly mediated by gamma-amino butyric acid (GABA)(A)-receptors (GABA(A)-R). However, comprehensive studies on the convulsive activities of various beta-lactam antibiotics in vivo and in vitro have not been performed. We have therefore examined the convulsive activities of seven different cephalosporins using both in vivo and in vitro models: intracerebroventricular (ICV) administration in mouse; [(3)H]muscimol binding assay (BA) in mouse brain synaptosome; and inhibition of recombinant mouse alpha1beta2gamma2s GABA(A)-Rs in Xenopus oocyte (GR). The rank orders of convulsive activities in mouse (cefazolin>cefoselis>cefotiam>cefpirome>cefepime>ceftazidime>cefozopran) correlated with those of inhibitory potencies on [(3)H]muscimol binding and GABA-induced currents of GABA(A)-R in vitro, with correlation coefficients of ICV:GR, ICV:BA and BA:GR of 0.882, 0.821 and 0.832, respectively. In contrast, none of the antibiotics had affinities for N-methyl-D-aspartate (NMDA) receptors nor facilitatory actions on NMDA receptor-mediated current in oocytes. These results clearly demonstrate that the mechanism of cephalosporin-induced convulsions is mediated predominantly through the inhibition of GABA(A)-R function and not through NMDA receptor modulation.

Animals↗
PubMed1999

Characterization of quinolone antibacterial-induced convulsions and increases in nuclear AP-1 DNA- and CRE-binding activities in mouse brain.

The quinolone antibacterials enoxacin and norfloxacin (2.5 mg/kg, i.v.) provoked clonic convulsions in mice treated concomitantly with biphenylacetic acid (BPAA, 100 mg/kg, i.p.), a major metabolite of the nonsteroidal anti-inflammatory drug fenbufen. Gel-shift assays showed that enoxacin-induced convulsions resulted in increases in nuclear activator protein 1 (AP-1) DNA- and cyclic AMP responsive element (CRE)-binding activities in the cerebral cortex and hippocampus, but not in other regions, such as the cerebellum and thalamus. In contrast, ofloxacin and levofloxacin, at the same doses, in the presence of BPAA did not evoke convulsions or increase these DNA-binding activities. Administration of these quinolones and BPAA alone elicited neither convulsions nor increases in these DNA-binding activities. These results suggest that the increased nuclear AP-1 DNA- and CRE-binding activities in the cerebral cortex and hippocampus induced by quinolones with BPAA correlated with seizure activities and that these brain regions play pivotal roles in quinolone-induced convulsions.

Animals↗
PubMed2000

Prevention of cocaine-induced convulsions and lethality in mice: effectiveness of targeting different sites on the NMDA receptor complex.

N-methyl-D-aspartate (NMDA) receptors appear to be involved in the behavioral toxic effects of cocaine. Therefore, different classes of NMDA receptor antagonists were compared for their ability to attenuate cocaine-induced convulsions and lethality in male, Swiss Webster mice. The mice were pre-treated (i.p.) with vehicle or an antagonist from one of the following classes: NMDA/glycine site antagonist (7-chlorokynurenic acid, ACEA-1021, ACEA-1031, ACEA-1328, DCQX, R(+)-HA-966), competitive antagonist (CPP, D-AP7), channel blocker (MK-801, memantine), or allosteric modulator (ifenprodil, CP-101,606, Co 101022, haloperidol). After a 15 min pre-treatment period, the mice were administered a convulsive (60 mg/kg, i.p.) or lethal (125 mg/kg, i.p.) dose of cocaine, equivalent to the calculated ED/LD97 values. Pre-treatment with competitive or NMDA/glycine site antagonists dose-dependently attenuated cocaine-induced convulsions and lethality (P<0.05). Pre-treatment with channel blockers or allosteric modulators of the NMDA receptor protected against cocaine-induced convulsions (P<0.05), but were ineffective or less effective than the competitive and glycine site antagonists in preventing death. The glutamate release inhibitor riluzole failed to prevent both the convulsions and lethality induced by cocaine. Significantly, post-treatment with NMDA/glycine site antagonists (ACEA-1021, ACEA-1031, ACEA-1328) after a cocaine overdose prevented death in a significant number of animals. The data suggest that NMDA receptors are involved in the pathophysiology of a cocaine overdose.

Animals↗
PubMed1984

Anticonvulsive effects of endogenous prostaglandins formed in brain of spontaneously convulsing gerbils.

Seizures were induced in a strain of epileptic gerbils by moderate environmental stress. Concentrations of five different cyclooxygenase products (PGD2, PGF2 alpha, PGE2, 6-keto-PGF1 alpha and thromboxane B2) were measured in brain by specific radioimmunoassays before and at different time intervals after the onset of clonic-tonic convulsions. All prostanoids markedly increased subsequent to the convulsions. Maximal concentrations were reached after about 15 min. The major compound detected was PGD2, followed by PGF2 alpha and lower concentrations of the other cyclooxygenase products. Indomethacin completely prevented the convulsion-induced formation of prostanoids. Fifteen min after a first seizure almost all animals proved to be protected against a second convulsion. Indomethacin pretreatment markedly reduced the number of convulsion-resistant animals. These findings are compatible with the hypothesis that endogenous prostaglandins exert anticonvulsive effects.

Animals↗
PubMed2003

The effect of N-nitro-L-arginine methyl ester posttreatment on the anticonvulsant effect of phenobarbitone and diazepam on picrotoxin-induced convulsions in rats.

The present study has investigated the effect of posttreatment of the nonspecific inhibitor of nitric oxide (NO) synthase (NOS), N-nitro-L-arginine methyl ester (L-NAME), on the anticonvulsant effect of phenobarbitone and diazepam on picrotoxin-induced convulsions in rats. Phenobarbitone, which is known to inhibit convulsions by potentiating gamma-aminobutyric acid (GABA) activity in the brain, did not inhibit the convulsive action of picrotoxin in L-NAME-posttreated animals. L-NAME produced no such interaction with diazepam, which inhibits convulsions through GABA potentiation as well as by a GABA-independent mechanism. L-arginine, the precursor of NO, increased the protective effect of both phenobarbitone and diazepam. These results suggest that a decreased synthesis of NO in the brain by the nonspecific inhibitors of NOS is likely to result in an impairment of the anticonvulsant effect of antiepileptics that inhibit convulsions solely by potentiating GABA activity in the brain.

Animals↗
PubMed2001

Glufosinate ammonium induces convulsion through N-methyl-D-aspartate receptors in mice.

Glufosinate ammonium, a broad-spectrum herbicide, causes convulsion in rodents and humans. Because of the structural similarities between glufosinate and glutamate, the convulsion induced by glufosinate ammonium may be ascribed to glutamate receptor activation. Three N-methyl-D-asparate (NMDA) receptor antagonists, dizocilpine, LY235959, and Compound 40, and an alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)/kainate receptor antagonist, NBQX, were coadministrated with glufosinate ammonium (80 mg/kg, intraperitoneally) in mice. Statistical analyses showed that the NMDA receptor antagonists markedly inhibited the convulsions, while the AMPA/kainate receptor antagonist had no effect on the convulsion. These results suggest that the convulsion caused by glufosinate ammonium is mediated through NMDA receptors.

Aminobutyrates↗
PubMed1983

Benign familial neonatal convulsions.

A pedigree of so-called benign familial neonatal convulsions was reported. Nine members experienced convulsions in the neonatal period and/or in early infancy. All members except one had good prognosis. One member had mild mental retardation and epilepsy with rolandic EEG foci. It was suggested that some common genetic factors may be involved in the etiology of benign familial neonatal convulsions, convulsions of unknown etiology in infancy (Fukuyama) and epilepsy with rolandic EEG foci. A review of literature revealed that about 14% of cases with benign familial neonatal convulsions eventually developed epilepsy.

Adolescent↗
PubMedDate not supplied

Opposite effects of ethanol and nitrendipine on nicotine-induced emesis and convulsions.

The effects of ICV injections were investigated in unanesthetized cats of ethanol alone and in combination with the dihydropyridine calcium antagonist, nitrendipine, on emesis and the convulsions produced by nicotine, which was similarly injected by the ICV route. In the first series of experiments, short lasting convulsions and emesis were the most prominent symptoms after the ICV injection of nicotine in a dose of 1.0 mg. In the second series of experiments the pretreatment of cats with ethanol given ICV in doses of 0.03, 0.2, and 0.3 ml reduced the emesis and prevented the convulsions induced by 1.0 mg dose of ICV nicotine. In the third series of experiments, the ICV injection of nitrendipine in doses of 0.024, 0.16, and 0.24 mg incorporated in the solution of ethanol, given in volumes of 0.03, 0.2, and 0.3 mt, respectively, blocked emesis but not the convulsions induced by the 1.0 mg dose of nicotine given ICV. The results suggest, therefore, that at least two different mechanisms underlie these phenomena. First, the synergistic effects at the neuronal nicotinic ionophores in the brain would act to underlie the antagonistic action of ethanol and nitrendipine on the emetic response. Second, conformational changes brought about by ethanol at voltage-dependent calcium channels in the brain may antagonize the inhibitory effect of the dihydropyridine calcium antagonist, producing the reversal of convulsions.

Animals↗
PubMed2004

Outcome after prolonged convulsive seizures in 186 children: low morbidity, no mortality.

Prolonged convulsive seizures are a common neurological emergency and a potential cause of neuronal damage and functional sequelae. We explored the role of seizure duration and various background factors for neurological sequelae in children with prolonged convulsive seizures. The population-base of this study was all children (age < 16 years) who had been admitted to the Tampere University Hospital, Finland between 1993 and 1999 with convulsive seizures lasting more than 5 minutes. Patients were followed up individually (mean length of follow-up 2 years 1 month, range 0 to 7 years 8 months). All available data on the prolonged seizure episodes and clinical follow-up were analyzed retrospectively by a detailed review of all medical charts and records. In 186 children (94 males, 92 females; mean age 4 years 5 months, SD 3 years 10 months, range 1 month to 15 years 4 months) there were 279 separate convulsive seizure episodes lasting over 5 minutes, yielding an annual incidence of 47.5 out of every 100000 episodes. Seizure aetiology was idiopathic in 26.2% of episodes, febrile in 41.9%, remote symptomatic in 28%, and acute symptomatic in 3.9% of episodes. Mean duration of all seizure episodes was 42.5 minutes (SD 46.1 minutes) and was significantly correlated with the aetiology: shortest in the febrile group (mean 35.4 minutes) and longest in the acute symptomatic group (mean 88.6 minutes; p < 0.001). There was no mortality related directly to these acute seizure episodes. The most common sequela was an onset of epilepsy in 40 children (22%). Permanent neurological sequelae were noted in only four patients (2.2%; mean seizure duration 16 minutes) and non-permanent sequelae in six patients (3.2%; mean seizure duration 38 minutes). Neurological sequelae of prolonged convulsive seizures in children are rare and are related to aetiological factors rather than the duration of a single seizure. The role of acute seizures in the evolution of epilepsy in children remains obscure.

Adolescent↗