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PubMed1981

Ketamine: convulsant or anti-convulsant?

Ketamine hydrochloride in doses producing narcotic-cataleptic effects (50--100 mg/kg, IP) reduced the intensity of picrotoxin convulsions and eliminated seizures caused by metrazol administration. Subcataleptic doses (5--20 mg/kg) increased the duration of mitigated convulsive symptoms (abortive grand mal fits, jerks) especially those evoked by picrotoxin. Narcotic-cateleptic doses of ketamine considerably increased the duration of the period of single and multiple jerks produced by picrotoxin administration. Both convulsants transformed 1--2 Hz "ketamine complexes" into 2--4 Hz Wave spike discharges which appeared in a quasi-periodic fashion alternating with periods of relatively suppressed electrocortical activity. Electroencephalographic grand mal patterns were typically dissociated from behavioral manifestations under 50--100 mg/kg of ketamine, followed by a short period of postictal depression and a rapid recovery of preseizure electrographic patterns. Findings suggest that mechanisms involved in seizure alleviation may be responsible for sustaining mitigated convulsive phenomena. Neuro-chemical processes underlying antiepileptic ketamine potency remain unknown.

Animals↗

PubMed1996

The effects of a single neonatally induced convulsion on spatial navigation, locomotor activity and convulsion susceptibility in the adult rat.

The effect of a single neonatal convulsion on subsequent behaviour was investigated in the male rat. Convulsions were induced by heat or pentylenetetrazol on days 1, 10 or 21. As adults, locomotor activity, spatial ability and convulsion susceptibility were measured. Significant differences were seen in some measures and some groups but a single neonatal convulsion did not induce a consistent and significant pattern of behavioural change, despite the persistent change in hippocampal physiology shown in a previous study.

Aging↗

PubMed1984

Effect of convulsions of the synthesis of heterogeneous nuclear RNA associated with polyadenylate and oligoadenylate sequences from El mouse brain as a convulsive strain.

Animals from the El (susceptible to seizures) and ddy (nonsusceptible) mouse strains were subjected to vestibular stimulation by tossing. After convulsions in the El mice, both the stimulated El mice and ddY mice were intracranially injected with [14C]- and [3H]adenosine, respectively. In the control experiment, nonstimulated El and ddY mice received radioactive adenosines in the same manner. The rate of incorporation of adenosine into brain nuclear RNA, expressed as a percentage of the 3H; 14C ratio, was reduced to an average of 68% at 15 min after convulsions, then increased and reached a control value at 5 h. This reduction in nuclear RNA synthesis was not due to alteration of the adenosine triphosphate pool. Gel electrophoresis of RNA revealed no obvious differences in the labeling distribution between El and ddY mice, but the synthesis of RNA species larger than 35S in heterogeneous nuclear RNA (HnRNA) was impaired in convulsed El mice. Nuclear resistant segments of HnRNA with both T1 RNase and RNase A, were chromatographed with poly(U)-Sepharose followed by urea-polyacrylamide gel electrophoresis. The ologo(A) and poly(A) segments consisted of 29, 19, and 11, and 203, 135, and 69 nucleotides, respectively. The convulsions of El mice reduced the incorporation of radioactive adenosines into oligo(A) and poly(A) segments, suggesting that they inhibited transcription as well as polyadenylation within HnRNA.

Adenine Nucleotides↗

PubMed1984

Amino acid metabolism in the brain with convulsive disorders. Part I: Free amino acid patterns in the brain of E1 mouse with convulsive seizure.

To clarify the biochemical mechanism of convulsions from a view point of the amino acid metabolism, the free amino acid patterns in brains of El mice were investigated. The free amino acid levels in the brain excluding the cerebellum were measured by an amino acid autoanalyzer. 1) In the convulsion group, the free aspartic acid and serine levels in brains increased compared to the preconvulsion group. 2) In the postconvulsion group, an increase of glutamine and alanine levels in brains and a decrease of cystathionine level were found compared to the convulsion group. 3) It was found that in the preconvulsion group, the cystathionine and ornithine levels were high and the serine, alanine and GABA levels were low compared to the postconvulsion group. These results suggest that the free amino acid balance in the brain of this mouse should play an important role in the inducing mechanism of convulsions.

Alanine↗

PubMed2000

Febrile convulsions: acute seizure characteristics and anti-convulsant therapy.

A descriptive study using data from the medical records of 448 children with febrile convulsion was carried out to determine the seizure characteristics and use of anti-convulsant therapy for febrile convulsions in a Malaysian hospital. There was a higher incidence of multiple seizures and a lower incidence of focal seizures in the local population than in studies done among Western populations. The majority of initial seizures occurred within 24 h of fever onset. Transient neurological abnormalities following an acute seizure were common. A quarter of children referred by general practitioners had been given anti-convulsants prior to referral but up to 20% of general practitioners had used ineffective routes for administering diazepam. However, diazepam used in the hospital was found to be effective in controlling acute febrile seizures.

Acute Disease↗

PubMed1990

[Involvements of neuropeptides in pentylenetetrazol-induced convulsion in rats and effects of TRH and ceruletide on the convulsion].

To study the possible involvements of neuropeptides in the occurrence of convulsion, pentylenetetrazol (PTZ) was given to male Wistar rats weighing 250-350 g, and the concentration of neurotensin (NT), and the maximal number of binding sites (Bmax) and dissociation constant (Kd) of NT receptor in the frontal cortex were measured. The effect of the pretreatment of thyrotropin-releasing hormone (TRH) or ceruletide (CER) on the convulsion was also studied. NT was extracted from the homogenates of rat frontal cortex by boiling, and measured by radioimmunoassay. Membrane fractions were incubated with increasing concentrations of 125I-NT. Nonspecific binding was determined in the presence of unlabeled NT and subtracted from total binding to obtain the specific binding. The Bmax and Kd were calculated by Scatchard analysis. Generalized convulsion appeared after intraperitoneal administration of 50 mg/kg PTZ with a latency of 68.2 +/- 4.4 sec. One hour after the administration, neurotensin-like immunoreactivity (NTLI) concentration was reduced from 4.7 +/- 0.6 to 2.3 +/- 0.1 ng/g wet wt (p less than 0.01) and the Bmax of NT receptor from 17.2 +/- 2.8 to 10.8 +/- 1.1 fmol/mg protein (p less than 0.01). However no significant changes were observed in somatostatin-like immunoreactivity (SSLI) concentration and the Bmax and Kd of SS receptor. These facts indicate that PTZ stimulates the release of NT resulting in down regulation of NT receptor. Pretreatment with intracerebroventricular (icv) administration of 30 micrograms/10 microliters NT 30 min before the 50 mg/kg PTZ administration shortened the duration of the convulsion from 135.0 +/- 42.8 to 11.5 +/- 11.9 sec (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Regional changes in brain 2-14C-deoxyglucose uptake induced by convulsant and non-convulsant doses of lindane.

Lindane-induced dose- and time-related changes in regional 2-14C-deoxyglucose (2-DG) uptake were examined in 59 discrete rat brain structures using the 2-DG autoradiographic technique. At different times (0.5-144 hr) after administration of a seizure-inducing single dose of lindane (60 mg/kg), 2-DG uptake was significantly increased in 18 cortical and subcortical regions mainly related to the limbic system (e.g., Ammon's horn, dentate gyrus, septal nuclei, nucleus accumbens, olfactory cortex) and extrapyramidal and sensory-motor areas (e.g., cerebellar cortex, red nucleus, medial vestibular nucleus). There was also a significant increase in superior colliculus layer II. In addition, significant decreases occurred in a group of 6 regions (e.g., auditory and motor cortices). Non-convulsing animals treated with the same dose of lindane showed a regional pattern of 2-DG uptake less modified than the convulsant group. A non-convulsant single dose of lindane (30 mg/kg) also modified significantly the 2-DG uptake (0.5-24 hr) in some brain areas. Although the various single doses of lindane tested produced different altered patterns of brain 2-DG uptake, some structures showed a similar trend in their modification (e.g., superior colliculi and accumbens, raphe and red nuclei). Repeated non-convulsant doses of lindane produced defined and long-lasting significant elevations of 2-DG uptake in some subcortical structures (e.g., dorsal cochlear nucleus, dentate gyrus). Considering the treated groups all together, 2-DG uptake increased significantly in 26 of the 59 regions examined but only decreased significantly in 9 of them during the course of lindane effects. This fact can be related to the stimulant action described for this neurotoxic agent. The observed pattern provides a descriptive approach to the functional alterations occurring in vivo during the course of lindane intoxication. These results may be linked to the proposed mechanism of lindane neurotoxicity postulating an initial action on the GABAA receptor-chloride channel sites.

Animals↗

PubMed1985

Pro- and anti-convulsant drug effects in combination with the convulsant benzodiazepine Ro 5-4864.

The effects of several compounds believed to act at the GABA-benzodiazepine receptor complex and which have anticonvulsant or proconvulsant properties when administered in combination with picrotoxin and pentetrazol (leptazol, pentylenetetrazole) were investigated in combination with the convulsant benzodiazepine Ro 5-4864. Tracazolate (25-100 mg kg-1) failed to affect convulsions induced by Ro 5-4864; however, they were prevented by treatment with CL 218,872 (20 mg kg-1). Compounds having proconvulsant activity in combination with a subthreshold dose of Ro 5-4864 were: CL 218,872 (5 mg kg-1), and CGS 8216 (20 mg kg-1) and FG 7142 (40 mg kg-1), two compounds characterized as 'inverse agonists' at benzodiazepine receptors. The phenylquinolines PK 8165 and PK 9084, originally believed to have anxiolytic properties, had no significant effect in combination with Ro 5-4864 (25-100 mg kg-1). The convulsant profile of Ro 5-4864 is compared with that of picrotoxin and pentetrazol.

Animals↗

PubMed1994

Benign infantile familial convulsions are not an allelic form of the benign familial neonatal convulsions gene.

Benign infantile familial convulsions (BIFC) and benign familial neonatal convulsions (BFNC) are two forms of familial convulsions having an age of onset within the first year of life. The gene responsible for BFNC has been mapped to chromosome 20q in the close vicinity of D20S19 and D20S20 markers. We performed linkage analysis between BIFC and D20S19-D20S20 in eight families in order to know whether the BFNC gene is also implicated in BIFC. Several apparent obligate crossovers between affected members were detected. The data here presented demonstrate that the BFNC gene is not responsible for BIFC.

Age of Onset↗

PubMed2006

Vagus nerve stimulation does not affect spatial memory in fast rats, but has both anti-convulsive and pro-convulsive effects on amygdala-kindled seizures.

Vagus nerve stimulation (VNS) is an adjunctive treatment for refractory epilepsy. Using a seizure-prone Fast-kindling rat strain with known comorbid behavioral features, we investigated the effects of VNS on spatial memory, epileptogenesis, kindled seizures and body weight. Electrodes were implanted in both amygdalae and around the left vagus nerve of 17 rats. Following recovery, rats were tested in the Morris water-maze utilizing a fixed platform paradigm. The VNS group received 2 h of stimulation prior to entering the Morris water-maze. Rats were then tested in the kindling paradigm wherein the VNS group received 2 h of stimulation prior to daily kindling stimulation. Finally, the abortive effects of acute VNS against kindling-induced seizures were determined in fully kindled rats by applying VNS immediately after the kindling pulse. Body weight, water consumption and food intake were measured throughout. Memory performance in the Morris water-maze was not different between control and vagus nerve stimulation rats. Similarly, kindling rate was unaffected by antecedent VNS. However, pro-convulsive effects (P<0.05) were noted, when VNS was administered prior to the kindling pulse in fully kindled rats. Yet, paradoxically, VNS showed anti-convulsant effects (P<0.01) in those rats when applied immediately after the kindling stimulus. Body weight was significantly lower throughout kindling (P<0.01) in VNS-treated rats compared with controls, which was associated with reduced food intake (P<0.05), but without difference in water consumption. VNS appears to be devoid of significant cognitive side effects in the Morris water-maze in Fast rats. Although VNS exhibited no prophylactic effect on epileptogenesis or seizure severity when applied prior to the kindling stimulus, it showed significant anti-convulsant effects in fully kindled rats when applied after seizure initiation. Lastly, VNS prevented the weight gain associated with kindling through reduced food intake.

Amygdala↗

PubMed2001

Linkage of benign familial infantile convulsions to chromosome 16p12-q12 suggests allelism to the infantile convulsions and choreoathetosis syndrome.

The syndrome of benign familial infantile convulsions (BFIC) is an autosomal dominant epileptic disorder that is characterized by convulsions, with onset at age 3-12 mo and a favorable outcome. BFIC had been linked to chromosome 19q, whereas the infantile convulsions and choreoathetosis (ICCA) syndrome, in which BFIC is associated with paroxysmal dyskinesias, had been linked to chromosome 16p12-q12. BFIC appears to be frequently associated with paroxysmal dyskinesias, because many additional families from diverse ethnic backgrounds have similar syndromes that have been linked to the chromosome 16 ICCA region. Moreover, one large pedigree with paroxysmal kinesigenic dyskinesias only, has also been linked to the same genomic area. This raised the possibility that families with pure BFIC may be linked to chromosome 16 as well. We identified and studied seven families with BFIC inherited as an autosomal dominant trait. Genotyping was performed with markers at chromosome 19q and 16p12-q12. Although chromosome 19q could be excluded, evidence for linkage in the ICCA region was found, with a maximum two-point LOD score of 3.32 for markers D16S3131 and SPN. This result proves that human chromosome 16p12-q12 is a major genetic locus underlying both BFIC and paroxysmal dyskinesias. The unusual phenotype displayed by one homozygous patient suggests that variability of the ICCA syndrome could be sustained by genetic modifiers.

Age of Onset↗

PubMed1996

Prolonged nonepileptic twilight state with convulsive manifestations after febrile convulsions: a clinical and electroencephalographic study.

EEGs were obtained from 14 infants during behavior clinically diagnose d as prolonged febrile seizures. The clinical manifestations during EEG recordings resembled complex partial seizures (CPS) with convulsive manifestations, but the accompanying EEG waveforms were not epileptiform. Rather, two types of slow wave activity occurred: One was continuous diffuse delta (CDD) waves; the other was diffuse rhythmic theta (DRT) waves. I have termed these clinical states "nonepileptic twilight states with convulsive manifestations" (NETC). Because the CDD and DRT activity was similar to childhood arousal responses, I hypothesized that NETC might be a prolonged arousal state with increased muscle tone induced by a preceding febrile convulsion.

Arousal↗

PubMedDate not supplied

[Effect of serotoninergic and antiserotoninergic preparations on convulsions induced by the endogenous convulsants kynurenine and quinolinic acid].

Serotoninergic drugs DL-5-hydroxytryptophan, 5-methoxytryptamine (mexamine) and 5-hydroxytryptamine (serotonin) were found to reduce clonic convulsions induced by intracerebroventricular administration of DL-kynurenine sulfate in mice. Serotonin antagonist deseril weakened the antikynurenine effect of DL-5-hydroxytryptophan and mexamine. Quinolinic acid-induced convulsions could be attenuated only by DL-5-hydroxytryptophan. Deseril and metergoline and destruction of the cerebral serotoninergic neurons by 5,6-dihydroxytryptamine potentiated the convulsant effect of quinolinic acid but not kynurenine. The serotoninergic protective anticonvulsant mechanism is probably better developed against kynurenine rather than quinolinic acid.

Animals↗

PubMedDate not supplied

[The role of mediators in the genesis of convulsive activity. Biogenic monoamine content of the brain of rats with various predispositions to audiogenic convulsions].

Content of serotonin, tryptophane, adrenaline, noradrenaline, dopamine, DOPA and tyrosine in was studied in cerebellum, truncus cerebri, hypothalamus and brain hemispheres of rats with various predisposition to audiogenic convulsions. Distinct decrease in content of brain serotonin, noradrenaline and increase in dopamine content was noted in rats with high level of audiogenic convulsive activity. The data obtained suggest that the increase in dopamine and decrease in serotonin and noradrenaline content in brain tissue may be among the factors responsible for elevation of potential convulsive activity of central nervous system.

Acoustic Stimulation↗

PubMed1977

[Influence of convulsive and pre-convulsive components of an audiogenic seizure on the process of consolidation of temporary connections].

In comparing the seizures of different severity in rats an amnestic effect of the convulsive phases of the audiogenic attacks on the short-term (in difference from the long-term) memory and the process of consolidation of temporary associations was revealed. Without behavioristic seizures the audiogenic attacks almost failed to derange the short-term memory. The results obtained confirmed the authors' results obtained earlier on different nature of the convulsive and preconvulsive phases of the motor activity during the audiogenic attack in rats. The preconvulsive phase is regarded only as a peculiar motor aura of the audiogenic attack without any convulsive components.

Acoustic Stimulation↗

PubMed1991

Effects of convulsants on handling-induced convulsions in mice selected for ethanol withdrawal severity.

Withdrawal seizure-prone (WSP) mice were genetically selected to express severe handling-induced convulsions (HIC) upon cessation of chronic ethanol vapor inhalation. The HIC is a sensitive measure of CNS excitability, and the current paper compares the effects of eleven convulsant drugs on the HIC in WSP and WSR (withdrawal seizure-resistant) mice, the latter selected for minimal alcohol withdrawal HIC. If WSP and WSR mice were differentially sensitive to a subset of the tested drugs, a common mechanism of action for that subset would imply that genes influencing that mechanism were important in determining ethanol withdrawal severity. All drugs significantly enhanced HIC in WSP mice. The magnitude of enhancement was small for N-methyl-D-aspartate (NMDA), kainic acid, BAY K 8644, Ro 15-4513, and strychnine; greater enhancement in WSP mice was seen after nicotine, and the direct and indirect gamma-aminobutyric acid (GABA) antagonists bicuculline, 3-mercaptopropionic acid, picrotoxin, t-butylcyclophosphorothionate (TBPS), and pentylenetetrazol. Only two drugs, picrotoxin and pentylenetetrazol, had a marked effect on WSR mice: maximal effect of these drugs was equivalent in WSP and WSR mice. However, picrotoxin and pentylenetetrazol were more potent in WSP than in WSR mice. Three other GABA antagonists, bicuculline, 3-mercaptopropionic acid, and TBPS, had a very small effect in WSR mice: these drugs also seemed to be more potent in WSP than in WSR mice. For all other tested drugs, maximal effect in WSP mice was much greater in WSP than in WSR mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholism↗

PubMedDate not supplied

Urinary excretion of phenobarbital and its metabolite p-hydroxyphenobarbital in convulsing and non-convulsing patients.

As part of an investigation of phenobarbital (PB) pharmacokinetics in patients with status epilepticus (SE), urinary excretion of PB and its main metabolite, hydroxyphenobarbital (HPB), was studied in patients who had an episode of SE, as well as in non-convulsing ones. Eleven in-patients were studied:(group 1) five patients (4 M + 1 F; 48 +/- 28 years old; 64 +/- 6 kg body weight; mean +/- SD) with convulsive status epilepticus, and (group 2) six patients (5 M + 1 F; 37 +/- 13 years old; 71 +/- 15 kg body weight) with epilepsy, seizure-free at the moment of PB administration and without established anti-epileptic therapy. All subjects received a single intravenous dose of PB (15 mg/kg) at a rate of 100 mg/min. PB and HPB concentrations were measured by high performance liquid chromatography with UV detection at 220 nm in urine samples collected throughout 24 h. The comparison of pharmacokinetic parameters of urinary excretion of PB and HPB showed a statistically significant difference in the values of recovery of HPB and total barbiturate (higher values in the patients with SE) in 24 h urine. Differences in the excretion of PB between the two groups of patients--higher values in the patients who had had an episode of SE, and in urine flow--slightly elevated volumes in the same group, failed to reach statistical significance, probably due to the small number of participants in the study.

Adult↗

PubMed1985

Convulsive and non-convulsive ethanol withdrawal behaviour in rats with lesions of the noradrenergic locus coeruleus system.

The ascending noradrenergic pathways from the locus coeruleus were lesioned bilaterally in 10 rats by intracerebral 6-hydroxydopamine injections. Ten rats were sham-operated. All animals were subjected to a 4-day ethanol intoxication period using intragastric intubation. Intoxication and withdrawal assessments were performed blindly. The 6-hydroxydopamine lesions did not appear to affect tolerance to ethanol. During withdrawal, however, lesioned animals showed minor, but statistically significant changes in scores of certain non-convulsive withdrawal signs, but incidence and intensity of spontaneous and audiogenic convulsive seizures were not different between the groups.

Acoustic Stimulation↗