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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A potential antiepileptic drug, loreclezole, was studied in rats of 7, 12, 18, 25 and 90 days old. Metrazol-induced motor phenomena served as a model. Loreclezole did not consistently influence isolated myoclonic jerks or minimal metrazol seizures (predominantly clonic with preserved righting ability). Major metrazol seizures, i.e., generalized tonic-clonic seizures, were suppressed by loreclezole in a dose-dependent manner in all age-groups, except in the 7 day old group where outlined changes did not reach statistical significance. Severity of seizures was significantly diminished at all developmental stages studied. Loreclezole exhibits nearly the same profile of action as phenytoin and carbamazepine in this model.
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PMID:Effects of loreclezole on metrazol-induced phenomena in developing rats. 224 26

Although transient increases in heart rate typically occur, bradycardia has infrequently been noted in association with partial seizures. Five patients with temporal lobe epilepsy are described in whom sinus bradyarrhythmias and syncope were prominent manifestations of seizure activity. Partial improvement occurred in one of two patients in whom a permanent pacemaker was implanted before a diagnosis of epilepsy was established. Treatment with phenytoin or carbamazepine resulted in nearly complete resolution of symptoms in all five patients. Because pacemaker implantation does not prevent recurrent symptoms, but anticonvulsant therapy does, this experience underscores the importance of considering the diagnosis of partial epilepsy in selected patients with sinus bradyarrhythmias and syncope.
J Am Coll Cardiol 1990 Mar 15
PMID:Bradycardia and syncope as manifestations of partial epilepsy. 230

Homocysteine thiolactone (HTL) elicits seizures in mice at a dose of 850 mg/kg (95-100% of animals) with an average latency time of 19.5 min. These seizures are reversed by both 5' N-ethylcarboximide adenosine (NECA) and flunitrazepam, with respective ED50 doses of 0.025 and 0.20 mg/kg. NECA was approximately four-fold more potent as an inhibitor of HTL-induced seizures than of seizures induced by pentylenetetrazol (PTZ, 75 mg/kg). Flunitrazepam was equipotent in both seizure paradigms. The purine precursor 5-amino-4-imidazole carboxamide riboside, (AICAr), although virtually ineffective against PTZ-induced seizures at doses greater than 1 g/kg, was able to inhibit HTL-induced seizures with an ED50 of approximately 350 mg/kg. The anticonvulsant effect of AICAr was dose and time dependent. The anticonvulsant potency of AICAr was increased by simultaneous administration of the adenosine uptake blocker Mioflazine, whereas the central nervous system (CNS)-impermeable adenosine uptake blocker dipyridamole had no effect. The ability of AICAr to permeate the blood-brain barrier (BBB) is limited (less than 1%) and may explain its low potency as an anticonvulsant. AICAr also has very low potency at brain adenosine A1 and A2 receptors as well as adenosine uptake sites (IC50 greater than 10(-3) M), suggesting that its anticonvulsant properties are not mediated by direct action at these sites. The results indicate that AICAr does have frank anticonvulsant effects and further suggest that HTL-induced seizures may represent a useful paradigm for evaluation of adenosinergic agents. AICAr or more potent derivatives thereof may represent a new class of anticonvulsants with the ability to target seizure foci selectively.
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PMID:Adenosinergic modulation of homocysteine-induced seizures in mice. 234 40

The anticonvulsant effects of D-alpha-tocopherol (vitamin E) were studied in 4 animal seizure models: the Metrazol threshold model (MET), the maximal electroshock model (MES), the kindling model (well-established seizures), and the ferrous chloride model. Vitamin E failed to antagonize seizures in the MES, MET, or the kindling models. It was, however, able to significantly delay the onset of electrographic seizures in the intracerebral ferrous chloride model. Thus, vitamin E shows activity in the ferrous chloride model, but not in the animal models commonly used to screen for anticonvulsant drug actions.
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PMID:An evaluation of the anticonvulsant effects of vitamin E. 235 52

AHR-11748, the desmethyl metabolite of fluzinamide (an effective antiepileptic), was active in preventing maximal seizures induced in mice or rats by electroshock and threshold seizures induced in mice by Metrazol, bicuculline, and picrotoxin. The compound showed a profile of anticonvulsant activity similar to those of phenobarbital and valproic acid and different from those of phenytoin and ethosuximide. ED50s were less than those of valproic acid, but greater than those of phenobarbital. Analysis of plasma and whole brain homogenates of mice indicated that AHR-11748 has an apparent terminal half-life (t1/2, beta) of 1.0 h. The brain:plasma ratio of AHR-11748 was 3.4:1 from 0.5 h to 6 h.
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PMID:Pharmacodynamics and pharmacokinetics of AHR-11748, a new antiepileptic agent, in rodents. 238 74

The antiseizure activity of the glia-selective GABA uptake inhibitor, 5,6,7,8-tetrahydro-4H-isoxazolo[4,5-c]azepin-3-ol (THAO), was evaluated in rats in models of acute chemoconvulsion. In these experiments, intracerebroventricular administration of the drug 30 min prior to testing in doses between 100-750 micrograms provided protection against maximal pentylenetetrazol seizures and increased the latency to isonicotinic acid hydrazide seizures. Pentylenetetrazol seizure thresholds, in contrast, were not significantly elevated. The ability of THAO to suppress tonic but not generalized minor seizures suggests that it may block seizure spread.
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PMID:Anticonvulsant activity of the glial GABA uptake inhibitor, THAO, in chemical seizures. 253 4

Pentylenetetrazol (PTZ)-induced convulsion were studied in control, chronic ethanol-maintained, and ethanol-withdrawal rats. The convulsive doses of PTZ varied among the different groups of rats. Ethanol-maintained rats required higher doses of PTZ to produce convulsions, compared to control and ethanol-withdrawal rats. The partially negative ligands for benzodiazepine binding sites, Ro 15-4513 (2 mg/kg, i.p.) and FG 7142 (20 mg/kg, i.p.) produced proconvulsant effect in saline (control) and ethanol-withdrawal rats as they potentiated the effect of subconvulsive dose of PTZ. A higher dose of Ro 15-4513 (4 mg/kg, i.p.), but not FG 7142 (up to 80 mg/kg, i.p.), also produced proconvulsant effect in ethanol-maintained rats. Furthermore, Ro 15-4513 (5, 10 mg/kg, i.p.), but not FG 7142 (up to 80 mg/kg, i.p.), produced clonic-tonic seizures of short duration in ethanol-withdrawal rats. These effects of Ro 15-4513 and FG 7142 were reversed by diazepam (2 mg/kg, i.p.), as well as by the GABA-neutral Ro 15-1788 (10 mg/kg, i.p.), thereby, indicating the involvement of central benzodiazepine receptors in the action of Ro 15-4513 and FG 7142. These observations suggest that chronic ethanol treatment selectively alters the receptor sensitivity to Ro 15-4513, an ethanol antagonist and partially negative ligand for BZ sites, and this observation supports the notion that ethanol effects are more susceptible to reversal by the imidazobenzodiazepine as compared to other negative ligand for BZ binding sites.
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PMID:Chronic ethanol treatment alters the behavioral effects of Ro 15-4513, a partially negative ligand for benzodiazepine binding sites. 254 9

Tuberous sclerosis is a neurologic disease affecting various organs with a triade: sebaceum adenoma, mental retardation and seizures. This report presents a case of a patient with tuberous sclerosis and third degree A-V block with complete invasive and non-invasive evaluation. The patient had sincope and complete A-V block with QRS complexes showing right bundle branch block morphology. The echocardiogram showed dilated cardiomyopathy with diffuse left ventricular dysfunction and had normal coronary arteriography. The eletrophysiologic evaluation showed complete infra-hisian A-V block and QRS with left bundle branch block pattern with normal sinus nodal and A-V nodal function. It was not possible to induce ventricular tachtyarrhythmias up to two extrastimuli. Histologic study showed normal myocardium under light and electronic microscopy. After permanent VVI pacemaker implant, the patient in follow-up for 16 years. This case seems to be the first in the international medical literature of tuberous sclerosis with complete heart block.
Arq Bras Cardiol 1989 Oct
PMID:[Total A-V block due to tuberous sclerosis. A case report]. 262 81

Kindling was induced in male wistar rats (280-320 g) by daily ip injections of PTZ in subthreshold doses (30 mg/kg). Repeated administration of PTZ to animals resulted in developing of enhanced seizures and also enhanced seizure susceptibility which could be sustained for a long time (6 months) after last seizure paroxysm. The lesioned hippocampus retarded the manifestation of PTZ kindling, where as lesioned caudate nuclei increased the seizure kindling development. Results also revealed hippocampus as a determinant structure in PTZ kindling formation, which stabilize the epileptic manifestations and make them chronic, at the same time caudate nuclei retarded the epileptic seizures stabilization. This role may be only antiepileptic, and not anti-kindling as is known for caudate nuclei.
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PMID:Pentylenetetrazol (PTZ)-kindling development in intact and subcortical structure lesioned rats. 263 5

Hereditary atrioventricular conduction defect is an uncommon cause of acquired complete heart block in children. We report a father and son, both of whom presented with seizures as the initial manifestation of acquired complete heart block and required permanent pacemaker implantation. A review of the variations of this entity and the histopathological findings of previously reported cases is presented. Family members of patients with acquired heart block of uncertain etiology should be examined for the presence of conduction abnormalities that may progress to complete heart block.
Pediatr Cardiol 1989
PMID:Hereditary atrioventricular conduction defect in a child. 270 52


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