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

The actions of adenosine in modulating amygdala kindling were examined using the stable adenosine analog 5'-N'-ethylcarboxamidoadenosine (NECA) and caffeine, an adenosine antagonist. Systemically administered NECA was found to significantly reduce the rate of postictal spiking and to significantly increase the duration of postictal EEG depression in amygdala kindled rats. In contrast, systemically administered caffeine significantly increased kindled seizure duration and reduced the duration of postictal EEG depression. Systemic administration of the methylxanthine derivative, 8-sulfophenyl theophylline (8-PST), failed to block the effects of NECA on kindling. Since systemically administered 8-PST blocks peripheral adenosine receptors, but has only limited CNS activity, the effects of NECA appear to be centrally mediated. These observations further demonstrate a role for adenosine in postictal phenomena and support the hypothesis that a release of endogenous adenosine contributes to the termination of ongoing seizure activity.
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PMID:Adenosine involvement in postictal events in amygdala-kindled rats. 227 40

A one-year-old white female ingested approximately two to three grams of caffeine (200-300 mg/kg). The patient survived the ingestion with a maximum caffeine concentration of 385 micrograms/ml four hours postingestion. The child developed ventricular arrhythmias, seizures, metabolic disturbances, and severe pulmonary edema. She survived without apparent long-term sequelae despite having reached a serum caffeine concentration that is the second highest reported level in a survivor.
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PMID:Presentation and management of an acute caffeine overdose. 229 Jul 30

Caffeine as well as the antiasthmatic drug theophylline can cause seizures when administered to humans or animals in excessive doses. Studies on rats have shown rapid development of functional tolerance to caffeine-induced seizures whereas repeated pretreatment with theophylline had no significant effect on the theophylline concentrations required to produce seizures. The purpose of this investigation was to determine whether chronic exposure to caffeine can affect susceptibility to the convulsant effect of theophylline. Rats received caffeine, 40 mg/kg, or solvent twice a day for 7 days as an intravenous injection. On the eighth day, theophylline was infused intravenously until the onset of maximal seizures. At this pharmacologic end point, rats pretreated with caffeine had significantly higher theophylline concentrations in the brain and cerebrospinal fluid than did control (solvent-pretreated) animals. Although the concentration differences were relatively small (approximately 11%), they demonstrate in principle the development of caffeine-induced tolerance to the neurotoxic effect of theophylline. Additional experiments showed that the caffeine effect on theophylline neurotoxicity is not acutely mediated by paraxanthine, a major metabolite of caffeine.
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PMID:Effect of chronic caffeine administration on theophylline concentrations required to produce seizures in rats. 230 23

Although pretreatment with intravenous caffeine is an effective technique for increasing seizure duration during a course of electroconvulsive therapy (ECT), little has been published regarding the use of this technique in patients with severe medical illness. The authors describe nine depressed inpatients with major cardiovascular or other medical disease or both whose ECT seizure durations declined despite maximal settings on the ECT device. In all cases, caffeine pretreatment lengthened seizures, and clinical improvement followed. The caffeine-modified ECT treatments were well tolerated and were associated with no clinically significant adverse cardiovascular effects.
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PMID:Caffeine-modified electroconvulsive therapy in depressed patients with medical illness. 232 78

The protective activity of carbamazepine (CBZ, 60 min before testing), phenobarbital (PB, 120 min), phenytoin (PHT, 120 min), and valproate (VPA, 30 min) alone or concurrent with methylxanthine derivatives was evaluated against maximal electroshock-induced seizures (MES) in male mice. All drugs were administered intraperitoneally (i.p.), and the protection offered by antiepileptic drugs (AEDs) was expressed as ED50 in mg/kg. Caffeine sodium benzoate in doses of 0.0595-0.476 mmol/kg (11.55-92.4 mg/kg) distinctly reduced the anticonvulsant efficacy of PB, in the highest dose tested with an increase in ED50 value from 19.5 to 38 mg/kg. This methylxanthine derivative in the dose range of 0.119-0.476 mmol/kg (23.1-92.4 mg/kg) also efficiently inhibited the protective action of PHT. When combined with caffeine (0.238 and 0.476 mmol/kg), the ED50 of PHT was raised from 12 to 17 and 24 mg/kg, respectively. In doses of 0.238 and 0.476 mmol/kg, caffeine also diminished the efficacy of CBZ and VPA, and at the highest dose tested the methylxanthine elevated the respective ED50s from 13 to 20.5 mg/kg and from 270 to 420 mg/kg. Generally caffeine sodium benzoate (up to 0.476 mmol/kg) did not affect the plasma levels of studied AEDs, and only at 0.476 mmol/kg did it significantly decrease the level of PHT. Among the other methylxanthines, pentoxifylline (0.238-0.476 mmol/kg; 66.3-132.5 mg/kg) and diprophylline (0.952 mmol/kg; 242.1 mg/kg) inhibited the protective potential of PHT and the respective ED50s were raised from 12 to 16.5, 15.5, and 14 mg/kg. No significant alterations in PHT plasma levels were observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of different methylxanthines on the anticonvulsant action of common antiepileptic drugs in mice. 234 49

The effect of adenosine agonist pretreatment on the seizure activity of caffeine was investigated in NIH Swiss mice. The seizure ED50 of caffeine alone was determined to be 223 mg/kg and this was reduced to 68 mg/kg following pretreatment with 0.30 mg/kg N-ethyl carboxamidoadenosine (NECA). Additionally, NECA dose-dependently increased the seizure potency of 100 mg/kg caffeine (a dose which is normally subconvulsant). A proconvulsant effect of NECA was also detected following intracerebroventricular administration of 2.5 ug NECA, however the same doses of N6-cyclohexyladenosine (CHA) and 2-chloroadenosine (2 C1-ADO) did not precipitate seizures. The data reveal proconvulsant actions of both peripherally and centrally administered NECA towards caffeine-induced seizures. Such actions need to be reconciled with the general anticonvulsant action of adenosine and adenosine agonists.
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PMID:Caffeine-induced seizures: apparent proconvulsant action of N-ethyl carboxamidoadenosine (NECA). 238 13

It has been hypothesized that the Long-Sleep and Short-Sleep mouse lines were bidirectionally selected for high and low brain excitability, and further, that these differences are mediated by the benzodiazepine/gamma-aminobutyric acid (GABA) receptor-chloride channel complex. Hence, mice from both lines were administered seven convulsants (bicuculline, pentylenetetrazol, 3-carbomethoxy-beta-carboline, picrotoxin, caffeine, flurothyl and strychnine) and myoclonic and clonic seizure latencies recorded. Supporting the original hypothesis, the results show that the two lines were differentiated by all of the convulsants and that in response to the drugs, three distinct convulsive patterns were found. Nevertheless, a simple genetic model accounting for these results was not evident. To further clarify these susceptibility patterns, a convulsant representing each of these patterns (bicuculline, pentylenetetrazol or caffeine) was administered in conjunction with the anticonvulsant-barbiturate phenobarbital or the benzodiazepine antagonist Ro 15-1788. Irrespective of the convulsant given, phenobarbital attenuated both myoclonus and clonus subsequent to all convulsants, while Ro 15-1788 had a more discrete anticonvulsant profile.
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PMID:Patterns of convulsive susceptibility in the long-sleep and short-sleep selected mouse lines. 250 42

The adenosine receptor antagonist, caffeine, transiently induced proto-oncogene c-fos mRNA in mouse brain in a dose-dependent fashion. In situ hybridization revealed that caffeine-induced c-fos expression was high in caudate-putamen and olfactory tubercle at both subconvulsive and convulsive doses. The pattern of c-fos mRNA distribution following caffeine administration differs from that reported after seizures induced by electroconvulsive shock (ECS) or other chemical convulsants, and closely parallels the distribution of adenosine A2 receptors. Furthermore, the potent adenosine A2 receptor agonist, 5'-N-ethylcarboxamide adenosine (NECA) blocked caffeine-induced c-fos expression whereas the adenosine A1 receptor ligand, N6-cyclohexyladenosine (CHA), had no effect. This study suggests that the caffeine-induced expression of c-fos mRNA may be mediated by the adenosine A2 receptor in mouse brain.
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PMID:Adenosinergic modulation of caffeine-induced c-fos mRNA expression in mouse brain. 251 Sep 4

Numerous case reports have documented that phenylpropanolamine (PPA) stimulates the central nervous system with symptoms ranging from anxiety and hallucinations to grand mal seizures produced by overdoses. Most of these reports have occurred following concomitant use of caffeine which in high doses is known to cause seizures and psychotic episodes. The purpose of this investigation was to determine if PPA could potentiate caffeine-induced seizures in the rat. First, the input rate dependence of caffeine-induced neurotoxicity was determined by infusing rats intravenously with caffeine at one of three different rates (1.65-8.12 mg/min) until the onset of maximal seizure. This occurred after an average of 12 to 60 min of infusion. The PPA concentrations in serum, brain, and cerebrospinal fluid (CSF) at this pharmacologic endpoint were independent of infusion rate. In another experiment, rats were pretreated with an anorexiant dose of PPA (30 mg/kg ip) either acutely or chronically for 6 d, while control animals received saline solution. All groups were then infused with caffeine at a rate of 4.18 mg/min until onset of seizures. Caffeine concentrations at that time in serum, brain, and CSF were significantly lower in the PPA-pretreated animals than in the control group. It is concluded that both acute and chronic pretreatment with PPA increases the sensitivity of rats to the neurotoxic effects of caffeine.
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PMID:Phenylpropanolamine potentiates caffeine neurotoxicity in rats. 261

Interaction of two well known methyl xanthines, aminophylline--an antiasthmatic agent--and caffeine--commonly present in beverages, on the seizure protective ability of carbamazepine (CBZ) against electrically and chemically induced seizures in rats was investigated. Aminophylline (75 mg/kg, ip) did not alter the activity of CBZ (10 mg/kg, ip; ED100) on maximal electroshock seizures while dose dependent antagonism of CBZ efficacy was seen at 100 and 150 mg/kg, ip. Similar effects were observed with caffeine (200 and 250 mg/kg, ip). At the highest tolerated doses, aminophylline (150 mg/kg, ip) and caffeine (250 mg/kg, ip) produced antagonism of CBZ protection against pentylenetetrazole seizures. These observations support the possibility that the antagonism due to the interaction of these drugs could be related to their action at adenosine receptor sites in the brain.
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PMID:Inhibition of anticonvulsant action of carbamazepine by aminophylline and caffeine in rats. 263 65


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