Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies have demonstrated that the dentate granule and the CA3 pyramidal cells of the rat hippocampal formation are neuronal populations vulnerable to the toxic effects of ethanol. It also has been shown that the resulting alterations do not end after withdrawal from ethanol. As the neurons in the dentate hilus are heavily interconnected with the dentate granule cells, the authors decided to examine the fate of the hilar neurons after chronic alcohol consumption and withdrawal, inasmuch as the hilar somatostatin-immunoreactive (SS-I) neurons were found to be sensitive to cerebral ischemia and to seizures. The following groups of adult rats were studied: (1) alcohol-fed for 6 and 12 months; (2) alcohol-fed for 6 months and then switched to water for a further 6 months; (3) pair-fed controls; and (4) controls fed ad libitum. The authors determined the numerical density of hilar neurons and the number of its SS-I subpopulation. These were found to be significantly reduced in both the alcohol-fed and withdrawal groups when compared with the respective age-matched controls. The consequent loss of the integrative action of the hilar neurons, including the SS-Is, could explain some of the alcohol-related functional deficits as well as their persistence after withdrawal.
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PMID:Effects of chronic alcohol consumption and withdrawal on the somatostatin-immunoreactive neurons of the rat hippocampal dentate hilus. 136 47

Withdrawal seizure prone (WSP) and withdrawal seizure resistant (WSR) mice were treated with 5 mg/kg lorazepam for 7 days via implanted osmotic mini pumps. Following chronic drug treatment, brains were assayed for GABA-mediated chloride flux (GABA-Cl-). Under control (drug naive) conditions, brain membranes prepared from WSP and WSR lines did not differ in flunitrazepam or ethanol stimulation of GABA-mediated 36Cl- uptake, but the WSP lines were more sensitive to inhibition of 36Cl- flux by the inverse agonist, FG-7142. Membranes from lorazepam tolerant WSP and WSR mice were resistant to flunitrazepam- and ethanol-stimulation of GABA-Cl-. Withdrawal from chronic treatment, by an acute injection with the benzodiazepine antagonist RO15-1788, returned flunitrazepam stimulation of GABA-Cl- to near control levels in WSR membranes but not in WSP membranes and restored ethanol modulation of the channel to control levels in both lines. Inhibition of chloride flux by the benzodiazepine partial inverse agonist, FG-7142 was greater in membranes from WSP mice compared with WSR mice. Tolerance to lorazepam increased sensitivity of the WSR membranes to FG-7142 without altering the response in the WSP line. Again, withdrawal restored the Cl- flux response to FG-7142 back to near control levels. Lorazepam tolerance lowered [3H]-flunitrazepam binding affinity slightly only in the WSR strain with no change in binding number. Withdrawal from chronic lorazepam treatment produced no significant change in binding affinity or number. The initial genotypic differences in benzodiazepine inverse agonist sensitivity, may be related to the selection for withdrawal seizure severity. Chronic administration of lorazepam reduces the coupling between the benzodiazepine agonist site and the chloride channel and concomitantly increases coupling between the channel and the inverse agonist site, while withdrawal resets the receptor coupling back to control response levels. However, for the WSP line, this drug environment dependent shift in channel coupling bias appears to be deficient compared with the WSR line.
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PMID:Effects of lorazepam tolerance and withdrawal on GABAA receptor operated chloride channels in mice selected for differences in ethanol withdrawal severity. 138 57

The effects of alcohol on the central nervous system can be subdivided into three main categories: the effects of acute intoxication (drunkenness, acute encephalopathy, stroke), the effects of tolerance and ethanol withdrawal (delirium tremens, seizures) and the delayed manifestations of chronic alcohol consumption (cerebellar degeneration, Wernicke's encephalopathy, dementia).
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PMID:[Main involvement of the central nervous system in alcoholism]. 141 Sep 80

This study shows inhibition of the increase in locomotor activity induced by ethanol (2 g/kg i.p.) in mice by a low dose (0.1 mg/kg i.p.) of the non-opioid beta-endorphin fragment ORG 5878 (des-enkephalin-gamma-endorphin). ORG 5878 (0.1 mg/kg i.p.) also significantly antagonised the large increase in electroshock seizure threshold produced by ethanol (1.5 g/kg i.p.). In contrast, the hypothermia induced by ethanol (2 g/kg i.p.) was not altered by ORG 5878 (0.1 mg/kg i.p.). The effects of ORG 5878 showed an abnormal dose-response relationship, in that a high dose (1 mg/kg i.p.) did not significantly suppress any of the behavioural effects of ethanol examined although there was some indication that it attenuated the stimulant action of ethanol. ORG 5878 (0.1, 1 mg/kg i.p.) did not have any intrinsic effects on locomotion, seizure threshold or body temperature in mice. These results are the first demonstration that ORG 5878 may act as an ethanol antagonist in some paradigms.
Alcohol Alcohol 1992 Jul
PMID:Attenuation of the behavioural effects of ethanol in mice by des-enkephalin-gamma-endorphin (ORG 5878). 141 12

The outcome in 165 subjects with either an unknown (n = 93) or an alcohol-related (n = 72) seizure etiology, admitted to the emergency room of a general hospital in 1977-1978, was assessed after 10 years on the basis of subsequent hospital records and death-certificate-based mortality data. Alcohol and/or drug poisoning was the most frequent cause of death in the group with alcohol-related seizures. Sixty-four percent of the deaths in this group were directly related to alcohol abuse. The crude mortality was 45.8 (expected 8.6)/100 persons/10 years in the group with alcohol-related seizures and 15.1 (expected 6.0)/100 persons/10 years in the other group, the odds ratio between the groups being 4.8. Twenty percent of those with an unknown seizure etiology were found to show alcohol-related seizures, while the seizure etiology remained unknown in 59%, and a specific etiology other than alcohol abuse was revealed in 21% during the follow-up period. We conclude that alcohol abuse is an important, though often undetected, seizure etiology carrying a poor prognosis. The difference in mortality between the groups was due more to alcoholism than to seizures. There was no difference in mortality between those with a first alcohol-related seizure and those with previous alcohol-related seizures.
Alcohol Clin Exp Res 1992 Oct
PMID:Outcome in subjects with alcohol-provoked seizures. 144 34

The influence of ethanol on the single-dose kinetics of carbamazepine (400 mg syrup) was assessed in 7 alcoholics after a debauche (mean daily consumption 240 g ethanol) and after 9 days of controlled abstinence, and in 8 healthy volunteers after intake of the drug with and without a single dose of ethanol (25 g). Twelve h after the first test dose of carbamazepine the alcoholics were treated with the drug for 4 days (200 mg tablet b.d.). Carbamazepine was then withheld until a single test dose was given on day 9. Serum levels of carbamazepine and its 10,11-epoxide metabolite were measured by liquid chromatography. Carbamazepine absorption appeared to be delayed in alcoholics, both after debauche and withdrawal, but its bioavailability did not seem to be reduced. Carbamazepine levels were higher and those of its metabolite lower in alcoholics after a debauche than after 9 days of controlled abstinence, but neither was changed in healthy volunteers after the ingestion of carbamazepine together with a single dose of ethanol. The difference may have been due to inhibition of carbamazepine metabolism by ethanol at the high levels attained in alcoholics but not in volunteers. However, it could also be an expression of the unmasking of enzyme induction after ethanol withdrawal. None of the alcoholics had any withdrawal seizures. Despite similar carbamazepine levels, side effects occurred in all volunteers but in none of the alcoholics, indicating that long-term ethanol exposure may promote central nervous adaptation to the acute untoward effects of carbamazepine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Carbamazepine kinetics and adverse effects during and after ethanol exposure in alcoholics and in healthy volunteers. 145 19

Kainic acid (KA 4-14 mg/kg) administered intraperitoneally (i.p.) produces automatisms (scratching until third postnatal week, "wet dog" shakes thereafter), and clonic and tonic-clonic seizures in rats aged 7, 12, 18, 25, and 90 days. Administration of carbamazepine (CBZ) i.p. (25 or 50 mg/kg), phenobarbital (PB 20-80 mg/kg), clonazepam (CZP 0.2 or 1 mg/kg), or valproate (VPA 200 mg/kg) influenced neither incidence nor latency of automatisms. Clonic seizures that are regularly observed after the third postnatal week in controls were either abolished or substantially suppressed by any of the aforementioned antiepileptic drugs (AEDs). Tonic-clonic seizures observed in the first 3 postnatal weeks were suppressed only by solvent [including propyleneglycol (PEG), ethanol, and water]; the effect of AEDs on tonic-clonic seizures was proconvulsant instead. The automatisms were most resistant to AED therapy. These results induce some doubts about the adequacy of the KA model for identifying AEDs effective against complex partial seizures, but forthcoming AEDs that suppress automatisms in the KA rat model might also be active against human complex partial seizures.
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PMID:Action of antiepileptic drugs against kainic acid-induced seizures and automatisms during ontogenesis in rats. 146 81

It is thought that certain actions of ethanol involve an interaction with endogenous opioids, including proopiomelanocortin-derived peptides such as beta-endorphin. To examine this possibility, we used a sensitive and specific assay for proopiomelanocortin mRNA to obtain an estimate of the activity of the endorphinergic system in the mediobasal hypothalamus and the pituitary of rats exposed for 10 days in an inhalation chamber to either ethanol or water. This protocol causes dependence in the ethanol-exposed group, as demonstrated by the presence of withdrawal seizures after cessation of treatment. While ethanol treatment did not affect proopiomelanocortin mRNA levels in the pituitary, the level in hypothalamus was significantly lower in the ethanol-treated animals than in controls. These results suggest that some effect of ethanol may involve the hypothalamic endorphinergic system.
Alcohol Clin Exp Res 1992 Dec
PMID:Proopiomelanocortin messenger RNA is decreased in the mediobasal hypothalamus of rats made dependent on ethanol. 147 70

Abnormal behavior in epileptic mice (El mice) may be rectified after convulsive seizures. This mechanism was investigated behaviorally through measurements of ethanol-induced sleeping time and locomotor activity, as well as immunohistochemically using a microphotometry system. Decreased ethanol-induced sleeping time and increased ethanol-dependent locomotor activity in El mice as compared to ddY mice (the mother strain of El mice) were rectified by convulsions as well as the intraventricular (IVT) administration of CaCl2, dopamine, or serotonin. Also, the lower dopamine levels in the neostriatum and nucleus accumbens septi in El mice as compared to ddY mice were improved by convulsions as well as the IVT administration of CaCl2. We have previously observed that a lower level of serum calcium in El mice causes a decrease in central biogenic amine synthesis through a calmodulin-dependent system. This may increase the susceptibility to epileptic convulsions and induce abnormal behavior. Combining the present results with our previous observations, we suggest that the convulsions in El mice will be induced when the balance of physiological functions is lost, as may be seen when the biogenic amine syntheses are decreased. The serum calcium level in El mice is increased by convulsions, and an elevated serum calcium level enhances brain biogenic amine synthesis through a calmodulin-dependent system. Subsequently, biogenic amines rectify physiological disorders in El mice.
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PMID:The effect of convulsions on the rectification of central nervous system disorders in epileptic mice. 148 41

The "transurethral resection of prostate" syndrome (TURPS) is the clinical manifestation of the resorption into the patient's body of a large amount of glycocolle-containing irrigating fluid used for this procedure. The full clinical picture, which is seldom seen, consists of dyspnoea, nausea, arterial hypertension, an increased central venous pressure, cerebral oedema, cardiogenic shock and renal failure. Improved surgical techniques, as well as incomplete and atypical forms of the syndrome could explain this low incidence. Absorption into the blood stream may be rapid, by way of the prostatic venous plexi, or slower, from the spaces around the prostate and under the peritoneum. The present-day pathophysiological theory explains this syndrome by an acute hyponatraemia, sometimes dissociated from the hypoosmolality, the toxicity of glycocolle, and the neurological effects of hyperammonemia. Acute hyponatraemia, with blood sodium concentrations below 115 to 120 mmol.l-1, should be considered as potentially serious. The different mechanisms involved may act alone or together, thus explaining that the minor forms of the syndrome mostly consist of a neurological picture. The emergency treatment depends on the natraemia. It includes diuretics and progressive reloading of the patient with sodium in case of severe hyponatraemia with seizures. The best prevention is a correct surgical indication and technique. The resection should not last for more than 90 to 120 min. The major problem remains the early diagnosis of TURPS. Carrying out this surgery under regional anaesthesia is helpful for this purpose, but, in the near future, the best means might be the monitoring of expired ethanol concentrations.
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PMID:[Prostate transurethral resection syndrome]. 150 91


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