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

Intracerebroventricular administration of 10--20 microgram of steroid-O-sulfates induced hypermotility, agitation, salivation, EEG abnormalities, stereotypies, wet dog shakes and seizures. Equivalent effects resulted from 30--200 microgram morphine sulfate (H2SO4 salt), 50 microgram EGTA or 300--400 microgram of sodium sulfate or phosphate, but not chloride, nitrate or acetate. Non-steroid sulfates, steroid glucuronides and steroid phosphates were inactive. Naloxone, previously found to antagonize the excitatory effects of androsterone sulfate, failed to antagonize those of cortisol sulfate, sodium sulfate or EGTA. These findings suggest a role for extracellular calcium ions and for sulfate derived from circulating steroids in central responses to opiates.
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PMID:Opiate-like excitatory effects of steroid sulfates and calcium-complexing agents given cerebroventricularly. 21 60

Eight group-living male monkeys received cocaine (0 to 3.0 mg/kg) individually or as a group. Cocaine suppressed social affiliative behaviors, eating, and drinking (of both alcohol and control solutions). It induced bizarre stereotypies, hypervigilance, panic-like fleeing, enhancement and then suppression of locomotion, and a seizure. Cocaine had little effect on aggressiveness or sexual behavior. Proportion of time spent lying or sitting changed significantly. Cocaine produced severe behavioral abnormality in this social setting.
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PMID:Cocaine, social behavior, and alcohol-solution drinking in monkeys. 155 26

The orally active competitive N-methyl-D-aspartate (NMDA) receptor antagonists CGP 37849 (DL-[E]-2-amino-4-methyl-5-phosphono-3-pentenoic acid) and its ethyl ester CGP 39551 were evaluated in amygdala-kindled rats, a model for complex partial and secondarily generalized seizures. Anticonvulsant and behavioral effects of these novel compounds were compared with those of the noncompetitive NMDA receptor antagonist MK-801 [(+)-5-methyl-10,11-dihydroxy-5H-dibenzo(a,d)cyclohepten-5,10-imin e] and the antiepileptic drug carbamazepine, one of the major drugs for treatment of partial and generalized seizures in humans. For comparative evaluation, the compounds were injected i.p. at the following doses: 1 to 10 mg/kg (CGP 37849 or CGP 39551), 0.05 to 0.3 mg/kg (MK-801) and 20 to 40 mg/kg (carbamazepine), respectively. In contrast to carbamazepine, CGP 37849, CGP 39551 and MK-801 exerted only weak anticonvulsant effects in fully kindled rats and did not increase the focal seizure threshold. The weak anticonvulsant effects of the NMDA receptor antagonists in kindled rats were associated with profound untoward behavioral effects. The behavioral syndrome induced by the NMDA receptor antagonists in kindled rats was characterized by marked ataxia, hyperactivity and, in case of CGP 37849 and MK-801, stereotypies, such as head weaving. The low or absent effectiveness of the novel NMDA receptor antagonists against kindled seizures suggests that these compounds will not be clinically useful antiepileptics against partial and secondarily generalized seizures. Furthermore, in view of the recent clinical findings on psychotomimetic effects of MK-801 in epileptic patients, the similarities in the excitatory effects produced by CGP 39551, CGP 37849 and MK-801 in kindled rats may indicate that competitive NMDA receptor antagonists may also produce psychotomimetic effects in humans.
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PMID:Anticonvulsant and behavioral effects of two novel competitive N-methyl-D-aspartic acid receptor antagonists, CGP 37849 and CGP 39551, in the kindling model of epilepsy. Comparison with MK-801 and carbamazepine. 167 93

Autism is one of the behaviorally defined developmental disorders of brain function. It has a variety of genetic and nongenetic etiologies, with etiology being unknown in the majority of children. Boys are more frequently affected than girls. Manifest in the preschool years, autism always affects sociability, communication, and the child's repertoire of activities and interests. Autism encompasses children with a broad range of severities and a variety of other signs of brain dysfunction. These include motor signs, notably stereotypies; abnormal responses to a variety of sensory stimuli; and disorders of affect and attention. A significant proportion of autistic children experience epileptic seizures and have abnormal EEGs. Neuroimaging, preferably magnetic resonance imaging, discloses abnormalities of brain development in a minority of autistic persons. The level of intelligence may range from profound mental deficiency to giftedness. The pattern of cognitive skills is likely to be uneven, typically with better nonverbal than verbal skills. In the preschool years, all autistic children have a developmental language disorder. Verbal expression may range from total lack of language to verbosity with echolalia; comprehension and language use are invariably impaired. While there is no specific pharmacologic agent to mitigate the fundamental disorder, children may benefit from drugs to treat specific symptoms such as attention disorder and seizures. Although autistic behaviors are the consequence of a static disorder of brain function, their character changes with maturation and appropriate intervention. Communication skills and sociability remain deficient but improve in all but the most severely affected children. Outcome is a function of both innate cognitive competence and the effectiveness of early intervention focused on the development of appropriate social skills and meaningful communication. Intelligent autistic adults may be educable, employable, and able to live independently, while more severely handicapped ones require a lifelong protected environment.
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PMID:Autistic children: diagnosis and clinical features. 170 91

The effect of selective dopamine receptor blockade on epileptic activity was tested in rats, using the lithium-pilocarpine seizure model. One day after lithium pretreatment, systemic administration of the dopamine D1 antagonist, SCH 23390, prevented the convulsive activity induced by either 10 or 15 mg/kg of pilocarpine in a dose-dependent manner as revealed by behavioral and electroencephalographic alterations. No anticonvulsant effect was observed when SCH 23390 was injected at the same time as lithium and 24 h prior to pilocarpine. Furthermore, the D2 antagonists, raclopride and haloperidol, potently reduced the threshold for convulsions induced by 10 mg/kg of pilocarpine, following lithium pretreatment. Neither dopamine D1 nor D2 antagonists altered the limbic stereotypies induced by pilocarpine, supporting the view that the dopamine system is primarily involved in the mechanisms of convulsion generation and seizure spreading. These results indicate that dopamine receptor subtypes exert opposite functions on the regulation of convulsive activity.
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PMID:Dopamine D1 and D2 receptors mediate opposite functions in seizures induced by lithium-pilocarpine. 182 82

Memantine (1-amino-3,5-dimethyladamantane) has previously been shown to attenuate or block chemically or electrically induced seizures in rodents at doses of 5-20 mg/kg i.p., suggesting that the drug might have potential utility in the treatment of seizures. In the present study, the effects of memantine were examined in amygdala-kindled and non-kindled rats. In fully kindled rats, i.e. a model of focal seizures with secondary generalization, memantine exerted no effects on seizure parameters at 5 mg/kg i.p., but reduced seizure severity and duration at 10 mg/kg. The threshold for induction of afterdischarges recorded from the amygdala was not altered after administration of 10 mg/kg. At 20 mg/kg, memantine induced spontaneous motor seizures in amygdala-kindled rats. No motor seizures were observed in non-kindled rats, but in both kindled and non-kindled animals memantine, 20 mg/kg, induced spikes in the electroencephalogram. Additional dose-dependent behavioural alterations observed after memantine included hyperactivity, ataxia and stereotypies, which may relate to the dopaminomimetic properties of the drug. The results demonstrate that kindled rats are more sensitive to central nervous system stimulating effects of memantine than non-kindled rats, which could relate to an impairment of inhibitory processes and/or alterations in synaptic transmission mediated by excitatory amino acids in the kindled brain.
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PMID:High doses of memantine (1-amino-3,5-dimethyladamantane) induce seizures in kindled but not in non-kindled rats. 236 81

The effects of chronic carbamazepine on cocaine-kindled seizures and behavioral sensitization were examined in this study. Rats were fed a diet containing carbamazepine or no drug and then repeatedly administered cocaine (40 and 50 mg/kg intraperitoneally [IP] [117.6 and 147.0 mumol/kg, respectively]). Carbamazepine markedly decreased the development of cocaine-kindled seizures and their associated lethality, but did not affect the development of sensitization of behavioral stereotypies. Carbamazepine consistently decreased the peak stereotypy ratings at the 40 mg/kg but not 50 mg/kg dose. In a 2-day sensitization paradigm chronic carbamazepine did not affect acute cocaine-induced hyperactivity (day 1; 40 mg/kg), nor did it affect sensitization to a low dose challenge of cocaine (day 2; 10 mg/kg [29.4 mumol/kg]). Sensitization of stereotypy and locomotor activity are thought to be related to the psychomotor stimulant properties of cocaine, while seizures may be associated with cocaine's local anesthetic effects. Our data suggest that carbamazepine is inhibiting mechanisms associated with local anesthetic kindling and only minimally affecting the psychomotor stimulant effects of cocaine.
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PMID:Carbamazepine retards the development of cocaine-kindled seizures but not sensitization to cocaine-induced hyperactivity. 240 May 45

Chronically implanted rats were injected either with somatostatin (SST) lumbar intrathecally (i.t.) (100 micrograms, n = 5), into the fourth ventricle (3 micrograms, n = 5; 10 micrograms, n = 6; 30 micrograms, n = 5) or into the lateral ventricle (10 micrograms, n = 6; 30 micrograms, n = 6), or received an injection of the substance P (SP) analogue, [D-Pro2, D-Trp7,9]SP into the fourth ventricle (0.3 micrograms, n = 2; 1 micrograms, n = 4; 3 micrograms, n = 4; 10 micrograms, n = 1) or lateral ventricle (3 micrograms, n = 3). A dose-dependent EEG depressant effect was observed following fourth and lateral ventricular injections of SST and of the SP analogue. Acute death due to respiratory depression was observed following i.t. and fourth ventricular injection of SST, and fourth ventricular injection of the SP analogue. Prominent motor behavior (barrel rotation, circling, cranial stereotypies) was observed, without signs of EEG seizure activity, following intraventricular injection of both drugs. Present findings indicate neurotoxic effects of SST and SP analogue at the cerebral level.
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PMID:Electroencephalographic and behavioral assessment of intracerebroventricular somatostatin and a substance P analogue. 247 57

Focal, limbic seizures were produced by systemically administered pilocarpine (200 mg/kg, i.p.); as previously described this dose produces limbic stereotypies but neither convulsions nor seizure-related brain damage. The pretreatment, 5 minutes prior pilocarpine, with the D-1 agonist SKF 38393 (-ED50 = 1 mg/kg; i.p.) induced convulsions similar to those produced by a higher, convulsant dose of pilocarpine. On the other hand, the pretreatment with the D-2 agonist LY 171555 failed to induce convulsions. The D-1 receptor antagonist SCH 23390 prevented the convulsions induced by SKF 38393 plus pilocarpine (200 mg/kg). This study indicates that D-1, but not D-2, receptor stimulation converts subconvulsant doses of pilocarpine into convulsant ones.
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PMID:D-1 dopamine agonist administration reduces the threshold for convulsions produced by pilocarpine. 257 May 98

Kainic acid (KA, 8-15 ng) was injected into the amygdala of conscious freely moving rats via chronically implanted fused silica cannulas. At 15-25 min after the injection, most rats suffered a limbic seizure attack of short duration, consisting of mastication, forelimb clonus, and raising on hind limbs, behaviorally indistinguishable from kindled seizures. Typically, the attack was followed by stereotypies, intense exploration, and by 1 or 2 more attacks. About 60 min after the injection, most rats appeared normal again and histopathological changes in their brains did not exceed those seen in vehicle-injected rats. In 3 cases, however, recurrent seizures culminated in behavioral status epilepticus 60-90 min after the injection. The status epilepticus was stopped by i.p. injection of diazepam (10 mg/kg) after a duration of 10 min (1 case) and 30 min (2 cases), respectively. After 10 min status epilepticus, we observed marginal neuronal damage with slight gliosis in both hippocampi (CA3 and CA1); after 30 min, hippocampal histopathology was more pronounced, with additional necrosis of the ipsilateral piriform cortex. After 0.8 microgram KA, a hundredfold higher dose, the incidence of limbic seizures during the first 40 min was not significantly higher (9/12) than after the lower KA doses (13/19). However, a significantly higher proportion of rats exhibited long-lasting seizure activity, associated with confluent destruction of CA3 pyramidal cells and additional seizure-related brain damage. Our results show that limbic motor seizures do not inevitably lead to histopathological changes in the brain, provided they do not culminate in a state of permanent seizure activity.
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PMID:Limbic seizures without brain damage after injection of low doses of kainic acid into the amygdala of freely moving rats. 274 56


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