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Effects of postnatal caffeine exposure on seizure susceptibility in developing rats.
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Postnatal caffeine treatment of rats can influence brain excitability during development. To study the mechanism involved in the alterations of seizure susceptibility, we used an animal model that corresponds to the infants treated with caffeine for apnea of prematurity. Seizure susceptibility to
Use of caffeine to lengthen seizures in ECT.
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During a course of ECT, seizure duration may become too brief for clinical benefit. Use of higher-energy stimuli may lengthen seizures but may also increase the risk of toxicity, and it is not possible when maximum settings are reached. The authors present the cases of six drug-free depressed
Different genes specify hyporesponsiveness to seizures induced by caffeine and the benzodiazepine inverse agonist, DMCM.
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Two strains of inbred mice differed significantly in their susceptibility to tonic seizures induced by caffeine and the benzodiazepine inverse agonist, methyl 6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate (DMCM). The hyporesponsive strain, SWR, was not less susceptible to the convulsant action
Different effects of postnatal caffeine treatment on two pentylenetetrazole-induced seizure models persist into adulthood.
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BACKGROUND
Postnatal treatment with caffeine from P7 to P11 (10 or 20 mg/kg daily) resulted in transient changes in two pentylenetetrazole (PTZ)-induced models of epileptic seizures characterized by spike-and-wave EEG rhythm in immature rats. To know if some changes persist into adulthood we studied
Caffeine augmentation of electroconvulsive seizures.
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Caffeine has been used clinically to increase seizure length in electroconvulsive treatment (ECT). The present study was designed to establish an animal model of caffeine-augmented seizures for further study of mechanisms and effects of pharmacological manipulation of seizure length. Increasing
Caffeine modification of kindled amygdaloid seizures.
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Rats were kindled during exposure to caffeine (50 mg/kg) or saline given IP twenty minutes before daily electrical stimulation of the amygdala until 3 kindled amygdaloid seizures (KAS) occurred. They were then stimulated for 3 days without drug pretreatment followed by 5 additional days with drug
Hippocampal neurons are damaged by caffeine-augmented electroshock seizures.
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Caffeine-augmented electroconvulsive therapy has been introduced into medical practice without experimental confirmation that such seizure modification does not result in neuronal injury. In this report rats pretreated with caffeine prior to a series of nine electrically induced convulsions showed
Rapid development of functional tolerance to caffeine-induced seizures in rats.
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The concentration and time dependence of caffeine-induced neurotoxicity was determined by infusing rats intravenously with caffeine at a rate of about 5, 12.5, and 25 mg kg-1 min-1 until the onset of generalized seizures which occurred at about 82, 28, and 11 min, respectively. The concentration of
Phencyclidine (PCP) reduces the intensity of caffeine-induced convulsions in rats.
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The effects of phencyclidine (PCP) on the threshold and intensity of caffeine-induced convulsions in rats were examined. There was a dose-dependent effect of PCP on convulsion intensity with significant reduction in intensity at 4.0 and 8.0 mg/kg PCP. At 16.0 mg/kg PCP, convulsant intensity was
Epileptic seizure during aspirin and caffeine withdrawal in a drug induced headache.
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A 45-year-old female migraineur with a long-standing history of drug-induced headache is described. She had been abusing caffeine (250 mg/day) and aspirin (5 gr/day). On the third day after discontinuation a withdrawal syndrome characterized by headache and a generalized tonic-clonic seizure
Grand mal seizure in a postpartum patient following intravenous infusion of caffeine sodium benzoate to treat persistent headache.
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A 27-year-old parturient developed a severe headache after placement of a labor epidural catheter. A presumptive diagnosis of an occult postdural puncture headache (PDPH) was made, and the patient was treated with an intravenous (IV) infusion of 500 mg of caffeine sodium benzoate (CSB) to
[Optimization of electroconvulsive therapy. Strategies for an adequate convulsion: role of caffeine].
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The Electroconvulsive Therapy is a widely used technique in psychiatry as a treatment for several mental disorders with particular indications. To produce therapeutic effect it's necessary to induce a convulsion which is considered adequate if its duration lasts more than 20 seconds. Considerations
Caffeine blocks absence seizures in the tottering mutant mouse.
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The neurological tottering mutant mouse is characterized by frequent "absence" seizures accompanied by bilateral synchronous spike and wave EEG bursts. Under anesthesia, adult homozygous tottering mice were implanted with permanent epidural electrodes, and at least 7 days elapsed before
[The remote effects of neonatal injections of caffeine and piracetam on audiogenic seizure susceptibility in mice of three genotypes].
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Neonatal DBA/2J, 101/HY and CBA/Lac/Sto mice (2-7-day-old) were subcutaneously injected with caffeine (200 mg/kg), piracetam (50 mg/kg) or distilled water. At the age of 1 month, they were tested for audiogenic seizure susceptibility (SS). The neonatal injections changed SS in 1-month-old mice in a
Effects of early postnatal caffeine exposure on seizure susceptibility of rats are age- and model-dependent.
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Repeated caffeine treatment during early postnatal period led to a decreased sensitivity to convulsant action of drugs interfering with inhibitory systems. To know if it is a general effect we studied convulsant action of agonists of glutamate receptors N-methyl-d-aspartate (NMDA) and kainic acid
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