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PubMed1982

Long-term deficits in passive avoidance responding following experimental febrile convulsions during infancy.

Human infantile febrile convulsions are occasionally associated with later deficits in cognitive and motor performance. In the present report, experimental febrile convulsions during various stages of infancy in the rat were investigated. Infant rats that were subjected to a single hyperthermia-induced convulsion at 10, 15, or 20, but not 5, days of age required more trials than controls to acquire a step-down passive avoidance response when tested as adults (50-60 days of age). Although rats that were subjected to a series of convulsions during infancy also evinced deficits in passive avoidance responding at adulthood, the magnitude of the effect was not appreciably greater than that following a single convulsion. The present results indicate that a single experimental febrile convulsion during infancy can have long-term effects on subsequent behavior.

Age Factors↗

PubMedDate not supplied

Sex-specific distinctions in audiogenic convulsions exhibited by severe seizure genetically epilepsy-prone rats (GEPR-9s).

The severe seizure genetically epilepsy-prone rat (GEPR-9) is characterized by a broad-based seizure predisposition and is increasingly recognized as a useful model of epilepsy. When sound stimulated, members of the GEPR-9 colony exhibit complete tonic extensor convulsions. Female GEPR-9s appear to experience a higher frequency of more severe seizures than males when they are sound stimulated. The purpose of this report is to examine and document this observation. Convulsive behavior was evaluated in approximately 4400 GEPR-9s. Each of these animals was sound stimulated 3 times at weekly intervals. Audiogenic response score (ARS), latency to wild running and latency to convulsion were recorded for each animal in each of the 3 tests. For the first 2 weekly tests, females exhibited a significantly higher incidence of complete tonic convulsions, a significantly higher ARS and significantly shorter latencies to wild running and convulsions than did males. The significant differences in latencies persisted through the 3 tests, whereas an increase in the incidence of complete tonic convulsions among males led to a diminution of the differences between males and females in the other parameters. The possible underlying biochemical differences that are responsible for this sex difference in seizure severity are, as yet, unknown.

Acoustic Stimulation↗

PubMedDate not supplied

Audiogenic convulsions in moderate seizure genetically epilepsy-prone rats (GEPR-3s).

The moderate seizure genetically epilepsy-prone rat (GEPR-3) typically exhibits a generalized clonic convulsion upon acoustical stimulation. The purpose of this report is to document sex-specific distinctions in the seizure characteristics as well as the effect of prior seizure experience on sensitivity to acoustically induced seizures in members of the GEPR-3 colony. Convulsive behavior was evaluated in approximately 3300 GEPR-3s. Each of these animals was stimulated with sound 3 times at weekly intervals. Audiogenic response score (ARS), latency to the onset of wild running and latency to convulsion were recorded for each animal in each of 3 tests given at 1 week intervals. Statistical analysis revealed that compared to their male littermates, females exhibited significantly shorter latencies to onset of running and convulsion for the last of the 3 weekly tests. Also, in both sexes, a significantly higher incidence of clonic convulsions, an increase in audiogenic response scores and a reduction in latencies to running and convulsion were observed in each succeeding audiogenic stimulation test. The mechanism of this increased seizure facilitation with prior seizure experience may have at least some similarity to that of kindling. The factors responsible for sex-specific distinctions in seizure severity are unknown at the present time.

Acoustic Stimulation↗

PubMed2006

Genetic interactions among cortical malformation genes that influence susceptibility to convulsions in C. elegans.

Epilepsy is estimated to affect 1-2% of the world population, yet remains poorly understood at a molecular level. We have previously established the roundworm Caenorhabditis elegans as a model for investigating genetic susceptibilities to seizure-like convulsions in vivo. Here we investigate the behavioral consequences of decreasing the activity of nematode gene homologs within the LIS1 pathway that are associated with a human cortical malformation termed lissencephaly. Bioinformatic analysis revealed the nud-2 gene, encoding the worm homolog of mammalian effectors of LIS1, termed NDE1 and NDEL1. Phenotypic analysis of animals targeted by RNA interference (RNAi) was performed using a pentylenetetrazole (PTZ) exposure paradigm to induce convulsions. Worms depleted for LIS1 pathway components (NUD-1, NUD-2, DHC-1, CDK-5, and CDKA-1) exhibited significant convulsions following PTZ and RNAi treatment. Strains harboring fluorescent markers for GABAergic neuronal architecture and synaptic vesicle trafficking were employed to discern putative mechanisms accounting for observed convulsion behaviors. We found that depletion of LIS1 pathway components resulted in defective GABA synaptic vesicle trafficking. We also utilized combinations of specific genetic backgrounds to create a sensitized state for convulsion susceptibility and discovered that convulsion effects were significantly enhanced when LIS-1 and other pathway components were compromised within the same animals. Thus, interactions among gene products with LIS-1 may mediate intrinsic thresholds of neuronal synchrony.

Animals↗

PubMed2005

Scopolamine-induced convulsions in fasted mice after food intake: effects of glucose intake, antimuscarinic activity and anticonvulsant drugs.

The present study was performed to further evaluate the contribution of antimuscarinic activity and hypoglycaemia to the development of scopolamine-induced convulsions in fasted mice after food intake. The effects of anticonvulsant drugs on convulsions were also evaluated. Antimuscarinic drugs atropine (3 mg/kg) and biperiden (10 mg/kg) were given intraperitoneally (i.p) to animals fasted for 48 h. Like scopolamine, both drugs induced convulsions after animals were allowed to eat ad libitum. Another group of animals was given glucose (5%) in drinking water during fasting. These animals, although they had normoglycaemic blood levels after fasting, also developed convulsions after treated with scopolamine i.p. (3 mg/kg), atropine (3 mg/kg) or biperiden (10 mg/kg) and allowed to eat ad libitum. Among the drugs studied, only valproate (340 mg/kg), gabapentin (50 mg/kg) and diazepam (2.5 and 5 mg/kg) markedly reduced the incidence of scopolamine-induced convulsions. The present results indicate that antimuscarinic activity, but not hypoglycaemia, underlies these convulsions which do not respond to most of the conventional anticonvulsant drugs.

Animals↗

PubMed2004

Infantile convulsions and paroxysmal choreoathetosis in a consanguineous family.

Infantile convulsions and paroxysmal choreoathetosis is a rare autosomal-dominant disorder characterized by variable presentation of benign infantile seizures and paroxysmal dyskinesia. The disease gene was mapped to chromosome 16p12-q12. We report a consanguineous Turkish family with three individuals affected by infantile convulsions and paroxysmal choreoathetosis. Two siblings whose parents were first cousins had benign infantile convulsions and paroxysmal choreoathetosis. Whereas their father presented only paroxysmal choreoathetosis. The siblings displayed an earlier age of onset and increased frequency of the paroxysmal symptoms than their father. We genotyped the pedigree with polymorphic microsatellite markers, spanning the pericentromeric region of chromosome 16. Construction of the haplotypes demonstrated the segregation of the disease with the infantile convulsions and paroxysmal choreoathetosis locus. The disease was inherited as an autosomal-dominant trait with incomplete penetrance. The affected father was heterozygous for the disease haplotype. However, the two affected siblings manifested homozygosity for the disease haplotype. By haplotype analysis, we confirmed the assignment of the locus for infantile convulsions and paroxysmal choreoathetosis to chromosome 16p12-q12 in this family, and our results also demonstrate that homozygotes for infantile convulsions and paroxysmal choreoathetosis may have a more severe form of the disease than heterozygotes.

Adolescent↗

PubMed2001

Pharmacological evidence that alpha-ketoisovaleric acid induces convulsions through GABAergic and glutamatergic mechanisms in rats.

Neurological dysfunction is common in patients with maple syrup urine disease (MSUD). However, the mechanisms underlying the pathophysiology of this disorder are poorly known. In the present study we investigated the effect of intrastriatal administration of the alpha-keto acids accumulating in MSUD on the behavior of adult rats. After cannula placing, rats received unilateral intrastriatal injections of alpha-ketoisocaproic acid (KIC, 8 micromol), alpha-ketoisovaleric acid (KIV, 8 micromol), alpha-keto-beta-methylvaleric acid (KMV, 6 micromol) or NaCl. KIV elicited clonic convulsions in a dose-response manner, whereas KIC and KMV did not induce seizure-like behavior. Convulsions provoked by KIV were prevented by intrastriatal preadministration of muscimol (46 pmol) and MK-801 (3 nmol), but not by the preadministration of DNQX (8 nmol). These results indicate that among the keto acids that accumulate in MSUD, KIV is the only metabolite capable of causing convulsions in the present animal model and indicates that KIV is an important excitatory metabolite. Moreover, the participation of GABAergic and glutamatergic NMDA mechanisms in the KIV-induced convulsant behavior is suggested, since KIV-induced convulsions are attenuated by muscimol and MK-801. The authors suggest that KIV may play an important role in the convulsions observed in MSUD, and highlight its relevance to the understanding of the pathophysiology of the neurological dysfunction of MSUD patients.

Animals↗

PubMed2003

Ammonia potentiates methylmalonic acid-induced convulsions and TBARS production.

Hyperammonemia is a common finding in children with methylmalonic acidemia, an inherited metabolic disease characterized by mental retardation, convulsions, and accumulation of methylmalonic acid (MMA). Although it has been suggested that MMA induces convulsions through succinate dehydrogenase (SDH) inhibition, very little is known about the contribution of hyperammonemia to the development of convulsions in these patients. In the present study we investigated the effects of ammonium ions on the convulsant action of MMA, MMA-induced inhibition of striatal succinate dehydrogenase, and the striatal content of thiobarbituric acid-reactive substances (TBARS). Adult rats were injected with ammonium acetate (1.5 mmol/kg, sc) or sodium acetate (1.5 mmol/kg, sc), followed 5 min later by buffered MMA (3 micromol/microl) or NaCl (4.5 micromol/microl) injected into the striatum. The animals were observed in an open field for the appearance of convulsive episodes. After 30 min of behavioral evaluation, the animals were sacrificed and had their striatal TBARS content measured. Ammonium acetate pretreatment caused no behavioral effects per se, but potentiated MMA-induced convulsions and increased basal TBARS content and MMA-induced TBARS production in the striatum. Ammonium chloride had no effect on basal succinate dehydrogenase activity and did not alter MMA-induced inhibition of SDH in vitro. These results suggest that ammonia potentiates MMA-induced behavioral effects through a mechanism that does not involve further succinate dehydrogenase inhibition, but may involve facilitation of MMA-induced oxidative damage and provide evidence that ammonia and MMA may have mutually additive toxicity.

Acetates↗

PubMed2003

Kainic acid-induced convulsions cause prolonged changes in the chondroitin sulfate proteoglycans neurocan and phosphacan in the limbic structures.

Systemic administration of kainic acid induces repeated convulsive seizures (KA convulsions) that result in neuropathological changes similar to temporal lobe epilepsy and the appearance of spontaneous recurrent seizures (SRS). The appearance of SRS is considered a result of the remodeling of neuronal networks following neuronal degeneration. We investigated the changes in chondroitin sulfate proteoglycans (CSPGs) in the limbic structures after KA convulsions in the rat using monoclonal antibodies 1G2, which recognizes full-length neurocan and the C-terminal half of neurocan, neurocan C, and 6B4, which recognize phosphacan and protein tyrosine phosphatase zeta. After KA convulsions, full-length neurocan appeared by 24 h and reached a peak by 48 to 72 h, whereas phosphacan decreased within 24 h in the hippocampus. In immunohistochemistry, neurocan increased in the limbic structures coincident with the appearance of reactive astrocytes. Phosphacan decreased coincident with pyramidal cell loss in the hippocampus, and the number of phosphacan-positive perineuronal nets around parvalbumin neurons decreased, whereas parvalbumin neurons were relatively conserved. In contrast, phosphacan increased in the entorhinal and piriform cortices in correlation with the severity of neuronal loss. Both neurocan and phosphacan recovered to the control level by 8 weeks after KA convulsions in some rats, but the changes in neurocan and phosphacan described above still persisted in more than half the rats. The results indicate that KA convulsions induce prolonged changes in neurocan and phosphacan similar to those in the developing rat brain and suggest a role of these CSPGs in the remodeling of neuronal networks related to the establishment or enhancement of epileptogenesis.

Animals↗

PubMed2000

The role of serotonin(2) receptors in mediating cocaine-induced convulsions.

Previous research in our laboratory suggests that serotonin (5-HT) neurotransmission mediates the expression of cocaine-induced convulsions. The role of 5-HT in mediating this toxic effect of cocaine appears to be due to activation of 5-HT(2) receptors, because cocaine-induced convulsions are blocked by the 5-HT(2) antagonists cinanserin, ketanserin, and pirenperone. The present study utilized a number of compounds that display a high affinity for 5-HT(2) receptors to further examine the role of these sites in mediating this toxic effect of cocaine. Cocaine-induced convulsions were observed following pretreatment with various doses of the following 5-HT(2) antagonists: mianserin, metergoline, MDL 11939, and methiothepin. In addition, 1-(2-methoxyphenyl)-4-[4-(2-phthalimido)butyl]piperazine (NAN 190) was tested to examine the influence of 5-HT(1) sites and the agonist compound 1-(3-triflurormethylphenyl)piperazine (TFMPP) was examined to further explore the role of 5-HT(1) and 5-HT(2) sites. Each 5-HT(2) antagonist attenuated cocaine-induced convulsions. Conversely, NAN 190 did not alter this toxic effect of cocaine. In addition, TFMPP significantly potentiated cocaine-induced convulsions. The results from this study support the hypothesis that 5-HT neurotransmission, acting primarily at 5-HT(2) receptors, plays an important role in mediating cocaine-induced convulsions.

Animals↗

PubMedDate not supplied

Elevated prodynorphin expression associated with ethanol withdrawal convulsions.

The hypothesis that kappa-opioid system activity may in part mediate convulsions exhibited during ethanol withdrawal was tested by exposing Withdrawal Seizure-Prone (WSP) and Withdrawal Seizure-Resistant (WSR) mice to chronic ethanol. Whole brain was harvested for RNA isolation and prodynorphin mRNA steady-state levels in whole brain were examined using Northern blot analysis. The data revealed significantly increased levels of prodynorphin mRNA expression in mice susceptible to ethanol withdrawal convulsions after withdrawal, with no corresponding increase in prodynorphin steady-state levels in mice resistant to ethanol withdrawal convulsions. These findings were not due to basal differences in prodynorphin expression between the WSP and WSR mice. To verify that the differences observed were not due to an ethanol-induced global alteration in gene transcription, mRNA levels of the housekeeping gene glyceraldehyde-3-phosphate dehydrogenase were measured. Glyceraldehyde-3-phosphate dehydrogenase expression was unchanged following both chronic exposure to ethanol and chronic exposure followed by withdrawal. These results extend our understanding of prodynorphin's role in generalized seizure activity to include ethanol withdrawal-induced convulsions. Our findings suggest that prodynorphin expression is modulated during ethanol withdrawal convulsions, or alternatively, prodynorphin may mediate the severity of ethanol withdrawal convulsions.

Administration, Inhalation↗

PubMed2003

Creatine protects against the convulsive behavior and lactate production elicited by the intrastriatal injection of methylmalonate.

Methylmalonic acidemias are metabolic disorders caused by a severe deficiency of methylmalonyl-CoA mutase activity, which are characterized by neurological dysfunction, including convulsions. It has been reported that the accumulating metabolite, L-methylmalonic acid (MMA), inhibits succinate dehydrogenase leading to ATP depletion in vitro, and that the intrastriatal injection of MMA induces convulsions through secondary NMDA receptor stimulation. In this study we investigated the effect of creatine (1.2, 3.6 and 12.0 mg/kg, (i.p.), [DOSAGE ERROR CORRECTED] succinate (1.5 micromol/striatum) and MK-801 (3 nmol/striatum) on the convulsions and on the striatal lactate increase induced by MMA (4.5 micromol/striatum) in rats. The effect of creatine on the striatal phosphocreatine content and on MMA-induced phosphocreatine depletion was also evaluated. Creatine, succinate and MK-801 pretreatment decreased the number and duration of convulsive episodes and the lactate increase elicited by MMA. Creatine, but not succinate, prevented the convulsions and the lactate increase induced by the direct stimulation of NMDA receptors. Acute creatine administration increased the total striatal phosphocreatine content and prevented MMA-induced phosphocreatine depletion. Our results suggest that MMA increases lactate production through secondary NMDA receptor activation, and it is proposed that the anticonvulsant effect of creatine against MMA-induced convulsions may be due to an increase in the phosphocreatine content available for metabolic purposes.

Animals↗

PubMed2001

Acetylcodeine, an impurity of illicitly manufactured heroin, elicits convulsions, antinociception, and locomotor stimulation in mice.

Acetylcodeine is one of the major impurities present in illicitly manufactured heroin (diacetylmorphine). Data on its pharmacology and toxicology are limited and its ability to alter the toxic effects of diacetylmorphine is not known. The first objective of the present study was to compare the acute pharmacological and toxicological effects of acetylcodeine to those of codeine and diacetylmorphine in mice by assessing nociception in the tail-flick test, locomotor stimulation, and convulsive behavior. The second goal of this study was to determine whether acetylcodeine would alter the convulsant effects of diacetylmorphine. The antinociceptive potencies of acetylcodeine and codeine were similar, as reflected by their ED50 (95% confidence limits) values of 35 (29-44) and 51 (40-65) micromol/kg, respectively. Acetylcodeine was somewhat less potent than codeine in stimulating locomotor behavior, with ED50 values of 28 (22-37) and 12 (6-24) micromol/kg, respectively. Diacetylmorphine was considerably more potent than the other two drugs, producing antinociception and locomotor stimulation at ED50 values of 2.4 (1.4-4.1) and 0.65 (0.36-1.2) micromol/kg, respectively. On the other hand, the convulsant effects of acetylcodeine (ED50=138 (121-157) micromol/kg) and diacetylmorphine (ED50=115 (81-163) micromol/kg) were similar in potency and both were more potent than codeine (ED50=231 (188-283) micromol/kg). Finally, a subthreshold dose of acetylcodeine (72 micromol/kg) decreased the convulsant ED50 dose of diacetylmorphine to 40 (32-49). These findings suggest that the convulsant effects of acetylcodeine are more potent than predicted by its effects on locomotor activity and antinociception. The observation that acetylcodeine potentiated the convulsant effects of diacetylmorphine suggests a mechanism for some of the heroin-related deaths reported in human addicts.

Analgesics, Opioid↗

PubMed1981

Febrile convulsions and rolandic discharges.

Clinical and electroencephalographic assessments were performed on 39 children with febrile convulsions showing EEG evidence of rolandic discharges and 23 epileptic children showing rolandic discharges with a preceding history of febrile convulsions. Ten families in which EEGs from the proband and his (or her) sibling or cousin demonstrated rolandic discharges were also described. The results of these studies stress a close genetic relationship between febrile convulsions with rolandic discharges and focal seizures or generalized convulsions that occur during sleep, namely, benign epilepsy of childhood with rolandic discharges. This indicates that the febrile convulsions with rolandic discharges constitute a particular subtype of febrile convulsions.

Asphyxia Neonatorum↗

PubMed1983

Prognostic factors of convulsive disorders in the first year of life.

Prognostic factors for mental and physical development and seizure control were investigated in 194 patients with convulsive disorders in the first year of life, excluding infantile spasms, neonatal convulsions and occasional convulsions. Thirty-three patients with febrile convulsions were included in the study. All patients were followed up to age six or older. The cases were subdivided into five etiologic groups; prenatal, perinatal, postnatal, doubtful and cryptogenic. Those with delayed development before the onset of seizures, or neurological abnormalities at the first visit had significantly less chance of being seizure-free and attaining normal mental and physical development. The prognosis for seizures and mental and physical development was much better in the patients with brief, symmetric, generalized tonic and/or clonic convulsions. This was also true with cryptogenic cases. There was a significant correlation between the initial EEGs and the long-term prognosis for mental and physical development and seizure control. Normal EEG was associated with a good prognosis. From these data, the neurodevelopmental status before the onset, the clinical features of convulsions and EEG findings in the infantile period were demonstrated to be important prognostic factors in addition to etiology.

Electroencephalography↗

PubMed1997

Scopolamine-induced convulsions in food given fasted mice: effects of physostigmine and MK-801.

We recently reported that scopolamine pretreated mice fasted for 48 h developed clonic convulsions soon after they were allowed to eat a small amount of food for 30 s. The present experiments were performed to determine whether animals also develop convulsions when they were allowed to eat ad libitum and to find some evidence for the contribution of the cholinergic and/or glutamatergic systems in the underlying mechanism(s) of convulsions. Animals fasted for 48 h were treated with 3 mg/kg scopolamine or saline. Twenty minutes later, they were allowed to eat either ad libitum or a small portion of food for 30 s. Scopolamine pretreated animals after starting to eat ad libitum or a small amount in a restricted time developed convulsions in a few minutes, the incidence being 76 and 54%, respectively. Pretreatment of 0.17 mg/kg MK-801, the noncompetitive NMDA antagonist, decreased the incidence of scopolamine-induced convulsions (22%) without affecting latency to the onset of seizures. Pretreatment of 0.1 mg/kg physostigmine, the cholinesterase inhibitor, changed neither the incidence (90%) nor latency to the onset of scopolamine-induced convulsions.

Animals↗

PubMed2003

[Convulsive syncope: characteristics and reproducibility using the tilt test].

OBJECTIVES: To establish the main clinical characteristics of convulsive syncope and the usefulness of the tilt test in its diagnosis. METHODS: A total of 317 patients (aged 5-18 years old) under clinical suspicion of neurocardiogenic syncope underwent a multiparametric tilt test. Our tilt test protocol includes continuous noninvasive measurement of heart rate, blood pressure, and arterial oxygen saturation, as well as continuous noninvasive measurement of cerebral oxygen saturation by near-infrared spectrophotometry. In selected patients, simultaneous electroencephalogram (EEG) was performed. RESULTS: The tilt test was positive in 216 patients (68.1 %). Of these, 25 (11.6 %) showed seizures during the test (convulsive syncope). Convulsions were asymmetric-tonic in 15 patients (60 %), generalized tonic in 5 (20 %), and tonic-clonic in 5 (20 %). In all patients, convulsive episodes lasted less than 30 seconds and spontaneously ceased upon placing the patient in a horizontal or Trendelenburg position. When simultaneous EEG was performed, diffuse brain wave slowing was observed, without paroxysmal activity. CONCLUSIONS: Convulsive syncope is not an uncommon event in children and is easily elicited by means of the tilt test. Pediatricians should be aware of this finding in order to avoid the frequently established unidirectional association between seizures and epileptic disorders. Consequently, the tilt test should be considered an essential tool in the differential diagnosis between convulsive syncope and epilepsy.

Adolescent↗

PubMed1975

Split-brain rat: transfer and interference of kindled amygdala convulsions.

Rats were subjected to varying degrees of commissurotomy, followed by implantation of a bipolar electrode into each amygdala. After the kindling of six convulsions at one electrode (primary site), the procedure was applied to the contralateral amygdala (secondary site). Convulsions were observed to develop more rapidly, independent of the degree or kind of transection. After 6 secondary site convulsions, the primary site was re-tested and convulsion-triggering was blocked, except in animals with transection of the rostral portion of the corpus callosum (CC). Collectively, the data indicate: (i) amygdala kindling develops a lasting trace which operates through the midbrain or brainstem; (ii) kindling from a second site utilizes this trace; (iii) a series of 6 convulsions produces negative after-effect which manifests itself at the convulsion level via the anterior CC; (iv) the anterior CC is important in determining the laterality of the forelimb clonus; and (v) the inter-amygdala propagation of after-discharge is blocked by the combined sectioning of the anterior CC and the anterior commissure.

Amygdala↗