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

Ethanol (1.5 g/kg, IP) administered to kindled rats blocked the seizures normally elicited in these subjects by electrical stimulation of the amygdala. Tolerance to this anticonvulsant effect developed following a series of ethanol injections only when the amygdaloid stimulation was administered during the periods of ethanol intoxication. Control subjects stimulated each day prior to ethanol administration displayed no tolerance to ethanol's anticonvulsant effects. Such findings emphasize the important role of learning in the development of alcohol tolerance and support the view that tolerance develops more rapidly for responses that are affected by the alcohol exposure.
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PMID:Learned tolerance to the anticonvulsant effects of alcohol in rats. 663 61

A case of massive metoprolol poisoning (50 g) is described. Clinical signs included coma, seizures, hypoventilation, unmeasurable blood pressure, nodal bradycardia, and metabolic acidosis. Treatment comprised intubation, assisted ventilation, gastric lavage, atropine, bicarbonate, glucagon and repeated doses of prenalterol (a total of 160 mg over 15 hours). Prenalterol dosage was simple and could be guided by blood pressure response. Pacemaker treatment was not required. Ethanol concentration was 50 mmol/l (2.4%) on admission. Plasma metoprolol was 68 mumol/l (18 000 ng/ml) 2 hours after admission. The patient was awake after 15 hours.
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PMID:Massive metoprolol poisoning treated with prenalterol. 666 32

These experiments studied changes produced by a hypnotic dose of ethanol in the LS and SS lines of mice, which differ in ethanol sensitivity. In the first experiment, animals were injected either with ethanol or saline, and activity and seizure susceptibility measured 7-9 h later when blood levels of ethanol would have reached zero. Ethanol-treated mice of both genetic lines were less active in an open field test and more susceptible to clonic convulsions induced by flurothyl than saline-injected controls. There was no difference in the magnitude of these changes in the two lines. In the control condition SS (short-sleep) mice were more active than LS (long-sleep) mice, and more susceptible than LS mice to myoclonic but not to clonic seizures. The effect of the ethanol injection on body temperature was evaluated in separate groups of animals. LS mice showed a more pronounced hypothermia than SS mice when temperature was measured 2 h after injection. Six hours after injection, SS mice exhibited a small but statistically significant overshoot in temperature, after which they again became hypothermic with respect to controls; hyperthermia was not observed in LS animals.
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PMID:Withdrawal-like signs induced by a single administration of ethanol in mice that differ in ethanol sensitivity. 677 54

From 1977 to 1981, the intravenous use of a pentazocine/tripelennamine combination (T's and Blues) has become a major drug abuse problem in the city of St. Louis, Missouri, U.S.A. There has been a continuous increase in the involvement of these drugs in (a) sudden and violent deaths (62 homicides, 7 fatal intoxications), (b) emergency room visits (137 in 1980), (c) admissions to drug treatment programs (7.7% in 1978 up to 64% in 1981), and (d) police laboratory cases (100 in 1977 - 78 up to 700 in 1981). Initial popularity of the drugs was related to the decline in the quality of street heroin (2.5% in 1977 reduced to 0.5% by 1979) and the lack of strict legal controls. Serious adverse reactions include clonic-tonic seizures and pulmonary foreign body granulomatosis. Ethanol and diazepam were present in 53% and 10% of T's and Blues medical examiner's cases, respectively (n = 70). Addicts are usually black males, 20 - 30 years old, from impoverished areas of the city. The drugs are available to the illicit trade through theft or diversion from legitimate sources.
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PMID:Pentazocine/tripelennamine (T's and blues) abuse: a five year survey of St. Louis, Missouri. 716 38

The effects of withdrawal from chronic ethanol administration on locomotion and rearing frequencies of rats and mice were studied. Ethanol withdrawal induced a significant increase in animal's activity. In mice a positive correlation was found between locomotion plus rearing frequencies and audiogenic-induced seizures susceptibility 25 hr after ethanol removal. Results show that general activity evaluated through the open-field method might be used as a simple, non-drastic and reliable procedure to detect ethanol withdrawal symptoms in laboratory animals.
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PMID:The open field: a simple method to show ethanol withdrawal symptoms. 719 42

Phenytoin kinetics during long-term alcohol use and withdrawal were studied in 11 male alcoholics with a history of withdrawal seizures and no evidence of chronic liver disease. Ethanol, 20% v/v, was given for 6 days after admission to maintain the blood alcohol level between 500 and 800 mg/l and phenytoin suspension, 150 mg, was given orally or intravenously (on three occasions) every 12 hr for 20 days. The mean (+/- SD) total phenytoin clearance in 9 of 11 subjects was 0.023 +/- 0.006 l/kg/hr during the alcohol ingestion period. Clearance rose to 0.033 +/- 0.013 l/kg/hr (P less than 0.05) during alcohol withdrawal. Total steady-state concentration after 3 wk ranged from 3.4 to 29.9 mg/l, while the weight-corrected dose range was only 3.7 to 5.5 mg/kg/day. Inter- and intra-subject variation in bioavailability was small (0.93 to 1.03). Phenytoin free fractions ranged from 9.09% to 17.75% and changes in total and free phenytoin concentration correlated (r2 = 0.92, P less than 0.001). The data are compatible with the hypothesis that increased phenytoin clearance during alcohol withdrawal is due to the increased metabolic rate of the drug secondary to enzyme induction by ethanol, which becomes unmasked on cessation of drinking. In most alcoholics standard-dose phenytoin (300 mg/l) will induce lower than usual plasma concentrations.
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PMID:Effect of short- and long-term alcohol use on phenytoin kinetics in chronic alcoholics. 727 3

Ethanol, acutely, is a potent inhibitor of the function of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor. After chronic exposure of animals to ethanol, however, the NMDA receptor in brain is upregulated. This upregulation is associated with the occurrence of ethanol withdrawal seizures. When cultured cerebellar granule neurons are exposed chronically to ethanol, the resulting upregulation of NMDA receptor function renders the cells more susceptible to glutamate-induced neurotoxicity. The present studies show that chronic ethanol exposure produces an increase in NMDA receptor number in the cells, measured by ligand binding to intact cells. Glutamate-induced excitotoxicity, both in control and ethanol-exposed cells, is blocked by the same NMDA receptor antagonists previously shown to block ethanol withdrawal seizures in animals. In addition, glutamate neurotoxicity is blocked by acute (2-hr) pretreatment of cells with ganglioside GM1 or by chronic (3 days) treatment with the ganglioside. Acute ganglioside treatment does not interfere with the initial rise in intracellular calcium caused by glutamate, whereas this response is downregulated after chronic ganglioside treatment. These results suggest that therapeutic agents can be developed to block both ethanol withdrawal signs and the neuronal damage that accompanies ethanol withdrawal. Furthermore, chronic ganglioside treatment during ethanol exposure has the potential to prevent changes in the NMDA receptor that lead to withdrawal seizures and enhanced susceptibility to excitotoxicity.
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PMID:Attenuation of glutamate-induced neurotoxicity in chronically ethanol-exposed cerebellar granule cells by NMDA receptor antagonists and ganglioside GM1. 757 99

Ethanol is present in a large number of pharmaceuticals, cosmetics, detergents and beverages. Without adequate safety measures, the accidental ingestion of such products by children is possible. Ethanol ingestion by children is known to cause various metabolic and neurologic disorders, including hypoglycemia, metabolic acidosis, seizures or coma. In Taiwan, little information has been published regarding the effects of ethanol ingestion by children. This is a report of a 5-year-old boy who became hypoglycemic after ingestion of rice wine. Admitted in a coma, the boy regained consciousness within 30 min after slow administration of 5% dextrose. His initial plasma glucose level was extremely low and hypokalemia was also found. Blood ethanol was 159 mg/dL, 3 h after the alcohol ingestion. He was discharged in good health the following day. Ethanol-induced hypoglycemia may be easily overlooked as symptoms of adrenaline excess are frequently absent. Prompt recognition and treatment with intravenous glucose are essential and may be life-saving. Pediatricians need to be aware of the devastating impact of ethanol. Preventive measures, such as child-proof packaging and parent education, are required if ethanol intoxication in children is to be avoided.
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PMID:Hypoglycemia following ethanol ingestion in children: report of a case. 761 61

Prolonged alcohol consumption leads to the development of tolerance to and dependence on ethanol, resulting in a decreased response to the sedative/hypnotic effects of ethanol, and by negative symptomatology following abrupt termination of use. One symptom associated with ethanol withdrawal in humans, as well as laboratory animals, is enhanced susceptibility to seizures. This study investigated the effects of the neurosteroid, 3 alpha-hydroxy-5 alpha-pregnan-20-one (3 alpha-5 alpha-THP), on alterations in seizure sensitivity associated with ethanol withdrawal. 3 alpha-5 alpha-THP is a potent anxiolytic and anticonvulsant agent that acts via selective interactions with GABAA receptors. Extensive evidence suggests that some aspects of ethanol dependence and withdrawal are mediated by alterations in GABAA receptor function. Withdrawal from chronic ethanol exposure elicited dramatic increases in seizure susceptibility in male and female rats. Administration of 3 alpha-5 alpha-THP just before seizure threshold determinations blocked the increased seizure susceptibility induced by ethanol withdrawal. Ethanol-withdrawn animals were protected by 3 alpha-5 alpha-THP at a dose that had no effect on control animal seizure thresholds. Moreover, male and female rats displayed differential responses to the seizure-threshold lowering effects of ethanol withdrawal, as well as the protection by 3 alpha-5 alpha-THP pretreatment. These findings suggest that there are gender differences associated both with ethanol withdrawal as well as the protection by 3 alpha-5 alpha-THP in ethanol-dependent rats.
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PMID:The neurosteroid, 3 alpha-hydroxy-5 alpha-pregnan-20-one, protects against bicuculline-induced seizures during ethanol withdrawal in rats. 762 68

Ethanol dependence was achieved in male, Long-Evans rats after 8 days on a balanced liquid diet that supplied 4.5% ethanol. After 1-h access to a solution of 10% ethanol (95%)/5% sucrose, the rats were deprived of food, water, and ethanol for 9 h. Following 30-s key jingling, about 80% of the animals exposed to ethanol experienced tonic-clonic seizures. Neurochemical analyses of striatal tissues revealed a significant (p < 0.05) increase in dopamine (DA) and a significant decrease in serotonin (5-HT) in the ethanol-exposed rats that had seizures compared to control rats. Homovanillic acid concentrations of the ethanol-treated rats with seizures were significantly higher than the levels found in ethanol-treated animals that had experienced no seizures. Daily average ethanol intake of the rats that had seizures vs. those that did not was almost the same at 16 g/kg/day. The findings indicate that rats experiencing ethanol withdrawal-induced seizures manifest opposite alterations in dopaminergic and serotoninergic activity compared to controls. The present results do not reveal if the striatal changes are caused by ethanol rather than by the seizures.
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PMID:Simultaneous changes in striatal dopamine, serotonin, and metabolites after withdrawal seizures in rats from dependence on alcohol. 763 60


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