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PubMed1993

Modification of intravenous lidocaine-induced convulsions by epinephrine in rats.

We studied intravenous lidocaine-induced convulsions in rats to determine whether added epinephrine influences the provocation of lidocaine toxicity. Wistar rats (200-250 g) were divided into three groups of ten, depending on the concentration of epinephrine added to lidocaine. Group 1: plain 1.5% lidocaine; Group 2: 1.5% lidocaine with 1:200,000 epinephrine; Group 3: 1.5% lidocaine with 1:100,000 epinephrine. After surgical preparation and recovery from anaesthesia, all rats received a continuous i.v. infusion of lidocaine (15 mg.ml-1) at a rate of 4.0 mg.kg-1 x min-1 until generalized convulsions occurred. The epinephrine-treated animals developed acute hypertension after one minute of lidocaine infusion (105 +/- 2 to 141 +/- 2 mmHg in Group 2 and 103 +/- 2 to 151 +/- 2 mmHg in Group 3). The PaO2 values in the epinephrine groups at the onset of convulsions were decreased significantly (88.3 +/- 1.0 to 84.0 +/- 1.5 mmHg in Group 2 P < 0.05 and 86.9 +/- 1.2 to 78.1 +/- 2.4 mmHg in Group 3 P < 0.01). However, these values were still within physiological ranges. Serum potassium concentrations in all groups were decreased P < 0.05, (4.24 +/- 0.09 to 3.52 +/- 0.12 mEq.L-1 in Group 1, 4.02 +/- 0.09 to 3.63 +/- 0.17 mEq.L-1 in Group 2, and 4.15 +/- 0.10 to 3.69 +/- 0.17 mEq.L-1 in Group 3).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2004

[70-year-old patient with convulsive syncope].

BACKGROUND: Syncope is a frequent reason for hospital admissions or emergency department visits with a broad differential diagnosis. Convulsive syncope is often falsely interpreted as an epileptic disorder. However, due to cerebral hypoperfusion, all forms of syncope can be associated with convulsions. In elderly patients with coronary heart disease or hypertension, "neurocardiogenic" causes, especially the carotid sinus syndrome, should be searched for. In general, cardiac pauses > or = 3 s after massage of the carotid sinus are required for the diagnosis of inhibitory carotid sinus syndrome. CASE REPORT: In the patient presented here, massage of the right carotid sinus provoked sinus bradycardia with pauses of 2,2 s and subsequent convulsive syncope. CONCLUSION: Additive factors such as coronary heart disease, arteriosclerosis, heart failure, and antihypertensive therapy may result in early symptoms of the inhibitory carotid sinus syndrome. This underlines the multifactorial pathogenesis of syncope, especially in the elderly patient.

Age Factors↗

PubMed1998

Cyamemazine decreases ethanol intake in rats and convulsions during ethanol withdrawal syndrome in mice.

The effect of cyamemazine a dopamine D2 receptor antagonist on voluntary ethanol consumption in rats and on ethanol withdrawal in mice was examined. Male Sprague-Dawley rats were tested in a free choice (water and 10% ethanol) experiment and consumed 5 g/kg ethanol daily. Rats were treated daily IP with cyamemazine (0.5, 1, or 2 mg/kg) or acamprosate (100 mg/kg) during 2 weeks. Both acamprosate and 1 mg/kg cyamemazine significantly decreased ethanol intake by 45% without affecting either fluid or food intake. The lowest dose of cyamemazine had no effect on alcohol intake but increased food intake. The highest dose had no effect on any variables. During the post-treatment period, only 1 mg/kg cyamemazine decreased both ethanol and fluid intakes. Mice were made dependent on alcohol using a chocolate fluid diet containing increasing concentrations of alcohol and withdrawn after 9 days. Mice were treated with cyamemazine (1 or 0.5 mg/kg, respectively) or with the same doses of lorazepam acutely on the day of withdrawal or chronically (during alcohol treatment). Both chronic and acute cyamemazine and lorazepam treatments decreased convulsions during ethanol withdrawal. Both acute treatments decreased locomotor activity in control and alcohol dependent mice. Chronic treatment had no effect on locomotor activity. We suggest that cyamemazine could reduce alcohol consumption by antagonizing the activation of the dopaminergic pathways during the induction of alcohol dependence. The action of cyamemazine on 5-HT3 receptors could also explain its effect on alcohol convulsions during withdrawal convulsions.

Alcohol Deterrents↗

PubMed2000

[Neurocardiogenic convulsive syncope--differential diagnosis, pathophysiology and therapy based on a case report].

Neurocardiogenic convulsive syncope as a disease at the border between cardiovascular and neurologic dysfunction can pose considerable diagnostic challenges. We report on the case of a 19 year-old female patient with recurrent neurocardiogenic convulsive syncope where the time from the onset of symptoms to the correct diagnosis and initiation of an effective therapy spanned more than three years. Based on this case report, we discuss differential diagnosis, pathophysiology and therapy of this disorder of autonomic cardiovascular regulation. Neurocardiogenic convulsive syncope should be considered whenever a patient has both syncope that exhibits a typical cardiovascular pattern (e.g., fainting of short duration with rapid reorientation phase) and prolonged loss of consciousness with characteristic neurological features (e.g., cerebral seizures with postictal state of confusion). Head-up tilt testing, introduced into clinical practice in 1986, is an efficient tool to diagnose neurocardiogenic syncope with comparatively high sensitivity in patients with recurrent syncope of unknown origin. Besides orthostatic training and pharmacotherapy, permanent dual-chamber cardiac pacing has gained increasing importance as treatment for cardioinhibitory forms of neurocardiogenic syncope.

Adult↗

PubMed2005

Cyclosporin A aggravates electroshock-induced convulsions in mice with a transient middle cerebral artery occlusion.

1. To test whether an ischemic insult increases the susceptibility to cyclosporine A (CsA)-induced neurotoxicity, we examined the effect of CsA on the minimal electroshock-induced convulsions in mice treated with a transient middle cerebral artery occlusion (MCAO) for a short period (2 h). 2. This MCAO produced small to mid-sized infarcted regions in the cerebral hemisphere with increasing post-operative days. In MCAO mice, CsA (30 mg/kg, i.p.) elevated the incidence of minimal electroshock-induced convulsions to 90-100% over that in sham mice (20-30%) at 1-7 days but not 14 days post-surgery. 3. In light of these findings, the possibility that CsA increases the risk of convulsions in patients with cerebral infarction and/or at an early stage following focal cerebral ischemia would have to be considered.

Animals↗

PubMed2006

Rofecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor potentiates the anticonvulsant activity of tiagabine against pentylenetetrazol-induced convulsions in mice.

Numerous studies have implicated prostaglandins as potential modulators in seizure activity. The objective of the present study was to elucidate the effect of rofecoxib (selective COX-2 inhibitor) alone or in combination with newer antiepileptic drug tiagabine (gamma-amino acid reuptake inhibitor) against pentylenetetrazol (PTZ) (80 mg/kg, i.p.)-induced chemoconvulsions in mice. Rofecoxib or tiagabine was administered 45 min prior to the PTZ challenge. In combination study, rofecoxib was administered 10 min before tiagabine and after 35 min the animals were challenged with convulsive dose of PTZ. Mean onset time of jerks, clonus and extensor phases following PTZ challenge was noted. Pretreatment with rofecoxib (1-5.0 mg/kg, i.p.) or tiagabine (1-10 mg/kg, i.p.) dose dependently protected the animals against PTZ-induced convulsions. The mean onset time of jerks, clonus and extensor phase were increased. A subeffective dose of rofecoxib (0.5 mg/kg, i.p.) potentiated the effect of subprotective dose of tiagabine (0.5 mg/kg, i.p.). The results of the present study suggested that the protective effect of rofecoxib, a COX-2 inhibitor against PTZ-induced convulsions may be possibly through the GABAergic modulation. Rofecoxib may have a place as adjuvant therapy with standard antiepileptic drugs such as tiagabine in the treatment of epilepsy.

Animals↗

PubMed1999

Convulsive Status Epilepticus.

Generalized convulsive status epilepticus (GCSE) is a medical emergency that must be treated rapidly and aggressively to prevent neuronal damage. Treatment should be initiated with intravenous lorazepam, 0.1 mg/kg, given at a rate of no more than 2 mg/min. If convulsions persist for more than 10 minutes or recur more than 20 minutes after lorazepam therapy is started, then fosphenytoin (20 mg of phenytoin equivalents per kilogram) should be infused at a rate of no more than 150 mg/min. If convulsions still continue, intravenous general anesthesia with pentobarbital, benzodiazepine drip, or propofol should be initiated after respiratory support has been established. All patients with GCSE who do not recover consciousness should be monitored with electroencephalography (EEG), and any residual epileptiform activity on EEG, including periodic epileptiform discharges (PEDs), should be considered evidence of continuing GCSE and treated aggressively.

Journal Article↗

PubMed1980

Decreased convulsant potency of picrotoxin and pentetrazol and enhanced [3H]flunitrazepam cortical binding following stressful manipulations in rats.

Various stressful manipulations in rats (cold-water swim, electric foot-shock administration, imparied access to food reward) were found to reduce the convulsant potency of drugs which interfere with GABA or benzodiazepine central processes. The convulsant threshold dosages of picrotoxin (0.4 mg/ml) or pentetrazol (10 mg/ml) administered after the stress by infusion (0.2 ml/min) via a vein of the tail were enhanced. The onset of generalized seizures induced by isoniazid (800 mg/kg) or by thiosemicarbazide (64 mg/kg) i.p. was delayed after cold-water swim. However, convulsant threshold dosages of bemegride or strychnine perfused at 2 and 0.2 mg/ml respectively were not changed by stress. Cold-water swim increased the number of cortical (but not cerebellar) [3H]flunitrazepam binding sites (+ 24%) but failed to alter cortical [3H]muscimol binding. This post-stress enhancement of binding sties, although suppressed by bicuculline (10(-4) M) seems not to be dependent on GABAergic mechanisms. Indeed cold-water stress did not reduce the ability of muscimol (10(-6) and 10(-5) M) and GABA (5 x 10(-6) and 5 x 10(-5) M) to increase flunitrazepam binding. Finally, this post-stress enhancement of benzodiazepine binding was not found to be paralleled by changes in the protective effects of diazepam against picrotoxin- or pentetrazol-induced seizures.

Animals↗

PubMed1982

The effects of convulsant and anticonvulsant drugs on the release of radiolabeled GABA, glutamate, noradrenaline, serotonin and acetylcholine from rat cortical slices.

A possible presynaptic site of action of convulsant and anticonvulsant drugs has been evaluated by studying their effect on depolarization-induced transmitter release using radiolabeled GABA, glutamate, noradrenaline, serotonin and acetylcholine. The antiepileptic diphenylhydantoin (DPH) inhibited the release of noradrenaline and serotonin at concentrations that are antiepileptic in vivo. The release of the other transmitters was affected only with higher concentrations. Phenobarbital (PhB) reduced the release of all transmitters studied at concentrations much above the levels that are considered antiepileptic in vivo. Comparison with the anesthetic barbiturate pentobarbital (PB) further indicated that the presynaptic effects of PhB were related to its sedative rather than antiepileptic properties. Diazepam and sodium valproate had little effect; only GABA release was slightly reduced with diazepam at the highest concentration studied. The convulsants penicillin and pentylenetetrazole both increased the release of glutamate at concentrations that induce epileptiform activity in vivo or in vitro. Other transmitter systems were differentially affected by the two convulsants. A small increase of noradrenaline and serotonin release was observed with penicillin, but not with pentylenetetrazole. A presynaptic site of action for some, but not all, epileptogenic and antiepileptic drugs probably exists in addition to other, postsynaptic mechanisms. Glutamate is probably a major excitatory neurotransmitter in the brain and many physiological studies have suggested a role of excitatory pathways in the generation of epileptiform activity. The observed increase of glutamate release in the presence of two epileptogenic drugs observed in this in vitro study is in agreement with such a hypothesis.

Acetylcholine↗

PubMed1986

Supernumerary locus coeruleus neurons as a determinant of inherited epilepsy in the convulsive mutant mouse quaking.

In quaking mice (a genetic model of epilepsy with an increased number of noradrenergic neurons) bilateral electrolytic coagulation of locus coeruleus (LC) in adult mice inhibited the convulsions elicited by somatic stimulations while neonatal 6-hydroxydopamine (6-OHDA) treatment remained ineffective upon the convulsions. Biochemical effects of the two treatments differed only in the brainstem where electrolytic lesion decreased while 6-OHDA treatment increased noradrenaline (NA) and 3-methoxy 4-hydroxyphenylethyleneglycol (MHPG) levels. Our results suggest that supernumerary LC neurons mediate the convulsions of the mutants through an action presumably restricted to the brainstem.

Animals↗

PubMed1991

Genetic factors influence changes in sensitivity to the convulsant properties of cocaine following chronic treatment.

Repeated administration of doses of cocaine below the threshold for seizure induction results in the development of an increased susceptibility to cocaine-induced seizures (cocaine-kindling). Genetic differences in susceptibility to cocaine-kindled seizures were evaluated in 4 inbred mouse strains and compared with susceptibility to seizures induced by acute administration of cocaine. The acute administration of cocaine produced convulsant activity in mice from all 4 genotypes, however, there were significant differences in the dose of cocaine required to induce seizures. C57 mice were highly susceptible and SJL mice highly resistant to convulsions induced by acute administration of cocaine, while BALB and DBA mice showed an intermediate degree of seizure susceptibility. The repeated administration of subconvulsant doses of cocaine resulted in rapid sensitization to cocaine-induced seizures. The 4 strains differed in the rate at which sensitization to cocaine-induced seizures developed, with the SJL strain being most sensitive and the C57 strain the least sensitive to the cocaine-kindling process. The susceptibility of the 4 strains to cocaine kindling was virtually opposite to their susceptibility to seizures induced by the acute administration of cocaine, suggesting that different mechanisms may be involved in the control of acute and kindled seizures did not persist upon further exposure to cocaine. Following a period of increased sensitivity to cocaine-induced seizures, tolerance to the convulsant properties of cocaine developed among C57, BALB and DBA mice. Only among the SJL mice did the development of a kindled state persist upon repeated exposure to cocaine. These differences emphasize the potential importance of inheritance in determining the effects of cocaine and suggest novel approaches to understanding the the mechanisms underlying the effects of cocaine.

Animals↗

PubMed1992

Patterns of glucose use after bicuculline-induced convulsions in relationship to gamma-aminobutyric acid and mu-opioid receptors in the ventral pallidum--functional markers for the ventral pallidum.

Bicuculline-induced convulsions increased glucose use throughout the brain and sharply demarcated the ventral pallidum and globus pallidus. Glucose use in the nucleus accumbens also increased after bicuculline-induced convulsions, except for a circumscribed region in the dorsomedial shell. Since the projection from the nucleus accumbens to the ventral pallidum contains gamma-aminobutyric acid (GABA) and the opioid peptide, enkephalin, the pattern of increased glucose use in the ventral pallidum and nucleus accumbens after bicuculline-induced convulsions was compared to the topography of GABAA and mu-opioid receptors. The pattern of glucose use in the nucleus accumbens and ventral pallidum resembled the topography of GABAA, but differed from that of mu-opioid receptors. Bicuculline may disinhibit GABAergic efferents to the ventral pallidum resulting in a dramatic increase in glucose use within striatopallidal synaptic terminals as well as in local terminals of the pallidal projection neurons.

Animals↗

PubMed1993

Sensitivity to N-methyl-D-aspartic acid-induced convulsions is genetically associated with resistance to ethanol withdrawal seizures.

Mice genetically selected to be resistant (withdrawal-seizure resistant, WSR) or prone (withdrawal-seizure prone, WSP) to handling-induced convulsions during ethanol withdrawal were tested for sensitivity to convulsions induced by timed intravenous (i.v.) infusion of N-methyl-D-aspartic acid (NMDA). WSR mice displayed convulsions at infused doses of NMDA that averaged 20% lower than WSP mice. This result was present in both genetically independent replicates of the WSR and WSP mice and provides strong evidence for an involvement of the NMDA system in the difference in withdrawal seizures present in these lines.

Animals↗

PubMed1976

Picrotoxin convulsions and GABA metabolism after injection of anticonvulsants in chicks.

Two clinically effective anticonvulsants, phenobarbitone and diazepam, protected 5-day old chicks against picrotoxin convulsions without reducing brain GABA-transaminase activity or raising brain GABA concentration. Ethanolamine-O-sulphate and amino-oxyacetic acid, in doses which inhibited GABA-transminase by at least 63% and approximately doubled brain GABA concentration, did not significantly affect the ED50 for picrotoxin convulsions. The ED50 for picrotoxin convulsions was significantly raised by di-n-propylacetate (800 mg/kg) which inhibited GABA transaminase activity by 6% and elevated brain GABA concentration by 26%.

4-Aminobutyrate Transaminase↗

PubMed1983

Brain content of immunoreactive [Leu5]enkephalin and [Met5]enkephalin after pentylenetetrazol-induced convulsions.

Wistar rats were injected daily with convulsant doses of PTZ (40 mg/kg). The brain content of immunoreactive (IR) enkephalins was measured after repetitive clonic convulsions and after the 'kindling' state was reached. In both instances we found a significant increase of IR [Leu5]enkephalin and IR [Met5]enkephalin in septum, striatum and amygdala 24 h after PTZ administration. These results support the suggestion that the peptide increase occurs with repetitive convulsions and not only after the 'kindling' state is reached.

Animals↗

PubMed1993

Effect of thioperamide, a histamine H3 receptor antagonist, on electrically induced convulsions in mice.

The effect of thioperamide, a histamine H3 receptor antagonist, on electrically induced convulsions was studied in mice. Thioperamide significantly and dose dependently decreased the duration of each phase of convulsion and raised the electroconvulsive threshold. Its anticonvulsant effects were prevented by pretreatment with (R)-alpha-methylhistamine, a histamine H3 receptor agonist. These findings suggest that the effect of thioperamide on electrically induced convulsions is due to an increase in endogenous histamine release in the brain, an effect mediated by histamine H3 receptors. The anticonvulsant effect of thioperamide was antagonized strongly by mepyramine (or pyrilamine), a centrally acting histamine H1 receptor antagonist, but not by zolantidine, a centrally acting histamine H2 receptor antagonist. Thus, the blockade by mepyramine of the thioperamide-induced decrease in seizure susceptibility indicates that histamine released by thioperamide from the histaminergic nerve terminals interacts with the histamine H1 receptors of postsynaptic neurons. These findings support the hypothesis that the central histaminergic system is involved in the inhibition of seizures.

Animals↗

PubMed1989

The convulsant effects of kainic acid microinjections into cerebral cortex are concentration but not laminar dependent.

The direct excitatory glutamate analog, kainic acid, when injected into different layers of the cat visual cortex, has two effects on this tissue that are fundamentally different from those exerted by the disinhibitory agents penicillin, bicuculline, and strychnine. First, both concentration-dependent suppression and convulsant activity was seen. Second, these concentration-dependent influences were produced effectively in each cortical layer challenged despite a reported preferential localization of kainic acid receptors to layer 6. In contrast, the disinhibitory agents generally produce only convulsant effects, do so in a laminar-specific manner, and at significantly lower concentrations in intact brain (i.e., 50 microM vs 15 mM). These results suggest that kainic acid, in the concentrations employed here, has a generalized excitatory effect on all cortical circuitry and that it's convulsant influences are nonspecific and less potent than those of the inhibitory blockers. Further, a common neural trait shared by these different modes of epileptogenesis is discussed.

Animals↗

PubMed1988

Responsiveness of genetically epilepsy-prone rats to intracerebroventricular morphine-induced convulsions.

The sensitivity to intracerebroventricular morphine-induced convulsions was determined in members of the severe seizure (GEPR-9) and moderate seizure (GEPR-3) colonies of genetically epilepsy-prone rats as well as in non-epileptic control rats. GEPR-9s were more sensitive to morphine-induced wet-dog shakes, rearing with bilateral forelimb clonus and generalized clonus than controls of GEPR-3s. GEPR-3s were less sensitive to morphine-induced wet-dog shakes and rearing with bilateral forelimb clonus than controls. Both high and extremely low doses of morphine in GEPR-9s elicited tonic extensor convulsions resembling the characteristic sound-induced convulsion of GEPR-9s. The results suggest that opiotergic systems may contribute to the pathophysiology of the seizure-prone condition in GEPR-9s. Further, differences in responsiveness of opiotergic systems in GEPR-3s and GEPR-9s may partially account for differences in seizure severity in the characteristic sound-induced seizures of these two types of GEPRs.

Animals↗