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

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 doses of caffeine (0-200 mg/kg, IP) were given before electroconvulsive stimulation (ECS) in rats and resulting seizure lengths were quantified by timing of classical tonic-clonic convulsive movements. With this paradigm, caffeine led to a dose-dependent increase in seizure duration. This proconvulsant action of caffeine was detectable within 1 min after dosing, persisted for at least 230 min and was reversible. The results suggest that seizure length is a practicable measure in pharmacological modification of electroconvulsive seizures. They also suggest that pharmacologically-modified ECS can be modeled effectively in animals.
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PMID:Caffeine augmentation of electroconvulsive seizures. 787 Oct 71

Past research focused on characterizing the cognitive deficits caused by ECT, understanding their causes, and defining ways of ameliorating the deficits. Future research includes the following recommendations. IN CHARACTERIZING THE DEFICITS: more accurately defining the time course to recovery; finding out whether specific memory tasks and specific patients show long-lasting effects; and defining specific components of memory and non-memory deficits (e.g., associative memory, incidental everyday memory, inattention). IN UNDERSTANDING THE CAUSES: determining whether seizure activity in certain brain structures is associated with specific cognitive deficits; finding out in which ways electric dose, electrode placement, seizure duration, and seizure threshold interact in causing the deficits; evaluating the effects of mediating variables such as blood pressure rise; and assessing the influence of background variables such as age, sex, and brain abnormality. IN AMELIORATING THE DEFICITS: continuing the search for effective medication; defining ways of reducing the number of treatments (twice weekly ECT, caffeine or thyroxine modified treatment); and manipulating dose in relation to electrode placement.
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PMID:Neuropsychology and ECT: past and future research trends. 787 83

In an elevated plus-maze indole-3-pyruvic acid (IPA, 100-200 mg/kg), an endogenous metabolite of tryptophan, possesses in mice an activity typical of anxiolytics. IPA increased the ratio of the number of entries into open arms over the total number of entries into open and closed arms and the time spent in open arms. Similar effect was observed for diazepam, a standard anxiolytic. Pretreatment with IPA attenuated the anxiogenic effect of caffeine (50 mg/kg) and 3-hydroxykynurenine (1.2 micrograms, i.c.v.) but not that of pentylenetetrazole (10 mg/kg), or phenylethylamine (5 and 10 mg/kg). Pretreatment with IPA (50-200 mg/kg) did not attenuate pentylenetetrazole- or phenylethylamine-induced seizures in contrast to diazepam which prevents both types of seizures. The data suggest that IPA is an endogenous anxiolytic with novel profile.
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PMID:Anxiolytic effect of indole-3-pyruvic acid (IPA) in mice. 790 63

Caffeine lengthens electroconvulsive therapy (ECT) seizures but has not been demonstrated to lower seizure threshold, nor to directly improve treatment outcome. We examined the effects of caffeine upon three recently proposed physiologic measures of seizure quality or impact: electroencephalography voltage suppression ratios, seizure regularity, and heart rate. None of these measures differed significantly in depressed inpatients randomly pretreated with either i.v. caffeine or saline on successive treatments during a course of right unilateral ECT. Newly defined measures of seizure impact may help identify ECT seizures of differing clinical efficacy, but these measures did not discriminate our caffeine and placebo conditions.
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PMID:Effects of caffeine pretreatment on measures of seizure impact. 755 56

Optimizing the safety and the efficacy of a treatment course has been a persistent goal of ECT practice since its introduction sixty years ago. Muscle relaxants, barbiturate anesthesia, and oxygenation were developed to reduce the risks of fracture, fear, and cognitive deficits. Unilateral electrode placement elicited fewer cognitive complaints and was reported as clinically effective as bilateral placement. Seizure duration monitoring, first by cuff and then by EEG, was introduced to define "an effective seizure". Caffeine pre-treatment lengthened seizure durations. Brief pulse square wave currents replaced sinusoidal currents to reduce cognitive effects. Twice weekly treatments were shown to be as effective as three treatments weekly, although the latter was more rapidly effective. Continuation ECT became a feature of practice. The safety and efficacy of psychoactive drugs combined with ECT were clarified so that antipsychotic drugs now are generally continued; benzodiazepines, lithium, and anticonvulsants are withdrawn; and the continuation of antidepressant drugs is optional. In recent studies, the minimal energy needed to elicit a seizure was determined and energy dosing is suggested as 2.5 times [or other multiple] of the threshold. Others find that age or half-age dosing methods are satisfactory and with less risk to patients. The definition of an "effective seizure" as one that is 25 seconds or longer in motor convulsive activity is questioned and EEG criteria are examined as substitutes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Optimizing ECT. 808 32

The effects of long-term caffeine treatment on N-methyl-D-aspartate (NMDA)-induced seizures in mice were studied. Caffeine was added (0.3 g/l) to drinking water for 14 days and the mice ingested 60-70 mg/kg/day. During the treatment, the plasma concentrations of methylxanthines (caffeine, theophylline and/or paraxanthine, theobromine) were measured. NMDA (150 mg/kg i.p.) was administered to control mice and to mice during and after the caffeine administration. A1 adenosine receptor density in the gyrus dentatus of hippocampus, measured by quantitative receptor autoradiography with [3H]cyclohexyl adenosine as the ligand, was not significantly altered after long-term caffeine treatment. NMDA-induced clonic seizures, wet dog shakes and mortality were significantly reduced at the end of long-term caffeine treatment but returned towards control at 1 and 2 days after withdrawal. At the end of caffeine treatment, tonic seizures were also absent. These results show that long-term treatment with caffeine in a dose that gives plasma levels of 6-10 microM decreases the effects of NMDA on e.g. seizure susceptibility, and that this effect cannot be ascribed to changes of A1 adenosine receptor density.
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PMID:Long-term caffeine treatment leads to a decreased susceptibility to NMDA-induced clonic seizures in mice without changes in adenosine A1 receptor number. 833 Feb 5

Caffeine lengthens ECT seizures, perhaps by lowering the convulsive threshold. The authors assessed the impact of caffeine on the convulsive threshold and seizure duration. The convulsive threshold and seizure durations of 12 inpatients receiving right unilateral ECT were determined with and without caffeine pretreatment. Caffeine did not change the convulsive threshold, but it did lengthen seizure duration. Caffeine's lengthening of seizure duration without affecting the convulsive threshold is an uncertain benefit in right unilateral ECT.
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PMID:A reappraisal of the role of caffeine in ECT. 809 53

Apneic episodes, quite common in newborns, are considered rare after age 1 month, when gastroesophageal reflux, cardiac arrhythmias, idiopathic central apnea, and seizures become included in differential diagnosis. Determining the cause of apnea is important as treatment differs significantly and can be harmful; Caffeine given for presumed idiopathic central apnea is reported to have precipitated seizures in 2 patients with apneic seizures. Two cases of partial seizures presenting as apnea in infants were studied. Interictal EEG was normal in 1 and showed focal spikes in the other. Video EEG monitoring (16 channel) showed focal ictal discharge originating from temporal areas clearly preceding onset of apnea in both patients. Because therapeutic options are sometimes diametrically opposite and interictal EEGs are particularly unreliable for diagnosis, we recommend video-EEG monitoring if there is any doubt about the diagnosis before starting treatment in patients with apneic episodes.
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PMID:Partial seizures presenting as life-threatening apnea. 840 44

We tested the effect of caffeine, on hyperoxia-induced seizures. Thirty-seven rats with chronic cortical electrodes were injected i.p. with caffeine (1.25, 2.5, and 10 mg/kg) or vehicle before exposure to 0.5 MPa oxygen and 17 rats to oxygen with 5% CO2 at 0.5 MPa. EEG monitoring and spectral analysis of EEG activity were carried out. Caffeine significantly prolonged the latent period to the onset of seizures (P < 0.05 in ANOVA), in a dose-related manner. Our results suggest that caffeine may be used in low doses for protection against hyperoxia-induced seizures.
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PMID:Caffeine attenuates CNS oxygen toxicity in rats. 857 77

Early developmental exposure to caffeine in rats results in decreased susceptibility to certain chemically-induced seizures in the adult. To determine whether this effect first appears in adulthood or is present during preceding developmental stages, we exposed neonatal rats to caffeine and determined seizure thresholds in animals 28, 42 and 70-90 days of age. Rats were unhandled or received either vehicle (water) or caffeine (15-20 mg/kg/day) by gavage (0.05 ml/10 g) over postnatal days 2-6. At 28, 42, or 70-90 days of age, rats were infused intravenously with picrotoxin (PIC), bicuculline (BIC), pentylenetetrazol (PTZ), caffeine (CAFF), strychnine (STR), or kainic acid (KA). Seizure thresholds for each compound were analyzed as a function of neonatal treatment, sex, and age. At 28 days, neonatally caffeine-exposed rats had a higher seizure threshold only for PTZ (P < 0.03). At 42 days, neonatally caffeine-exposed rats had higher seizure thresholds for PIC (P < 0.0007) and PTZ (P < 0.0001) than did controls. These results at 28 and 42 days are compared with previously reported data that demonstrated that in adulthood, rats neonatally exposed to caffeine have higher thresholds for seizure induction with CAFF, PTZ, and KA. Thus, early developmental exposure to caffeine results in decreases in seizure susceptibility that are agent specific and may result in a delay in the decrease in seizure threshold that occurs for many agents between late juvenile ages and adulthood.
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PMID:Neonatal caffeine exposure alters seizure susceptibility in rats in an age-related manner. 857 85


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