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

The activities of lipoyl dehydrogenase, aspartate transaminase, and alanine transaminase, and levels of lactate were estimated in cerebral cortex, cerebellum, and brainstem of rats intoxicated acutely with tetraethyl lead and chronically with lead acetate. A significant inhibition of lipoyl dehydrogenase was observed in both groups of animals, whereas transaminase activities were increased in inorganic lead toxicity. Oxidative decarboxylation and anaplerosis of pyruvate was assessed in brain slices using [1-14C]pyruvate. Pyruvate dehydrogenase activity was decreased in both organic and inorganic lead toxicity, whereas labelling of aspartate and alanine was increased in inorganic lead toxicity. In studies in vitro, lead acetate showed a more significant effect than tetraethyl lead. The higher anaerobic metabolism in inorganic lead toxicity, as evidenced by increased anaerobic lactate production by brain slices, could either be an adaptive mechanism or be due to the delayed maturation of brain in the developing rat. Such a mechanism does not occur in acute organic lead toxicity, as the compound brings about massive and rapid degenerative changes in brain, resulting in convulsive seizures and death of the animals.
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PMID:Pyruvate metabolism in the brain of young rats intoxicated with organic and inorganic lead. 654 9

Rats injected intracranially with cholesterol precursors and subjected to electroconvulsive seizures showed significantly higher levels of deposition of [4-14C]cholesterol into brain cholesterol than controls. The degree of incorporation was cholesterol greater than mevalonic acid greater than sodium acetate; in each case convulsed animals exceeded unshocked animals. Enhanced turnover of brain cholesterol with incorporation of circulating sterol may be associated with the etiology of convulsive seizures.
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PMID:Increased deposition of cholesterol in brain after electroconvulsive seizure. 661 90

In normal and lissencephalic ferrets with chronically implanted electrodes, two antiepileptic drugs, (E)-2-[(amino)phenylmethylen]-benzo [b] thiophen-3(2H)-on (AF-CX 921 XX) and carbamazepine (CBZ), were compared. The variables included afterdischarges (AD) and seizures induced by cortical electrical stimulations (ES). Both drugs were given orally, 100 mg/kg of pure substance. ES was applied before and 1, 2, 3, 4, 5, and 24 h after drug administration. Lissencephaly was produced by a single intraperitoneal injection of 15 mg methylazoxymethanol acetate to pregnant animals. The administration of both drugs resulted in increases of the AD threshold current to 240% in the normal and to 170% in the lissencephalic ferrets, in comparison with control stimulations (the difference significant at p less than 0.001). Moreover, duration of the AD was shorter (p less than 0.01) than before the drugs. Seizure threshold also increased 170% after AF-CX 921 XX and 175% after CBZ in normal and 153% and 138% in lissencephalic ferrets, respectively. The difference between the two drugs was significant. However, in contrast to the threshold, duration of seizures during AF-CX 921 XX administration was significantly shorter (p less than 0.05) than during CBZ. In general, lissencephalic ferrets responded less than normal ferrets to both drugs, but AF-CX 921 XX had a greater inhibitory effect on the duration of seizures. The lissencephalic ferret is proposed as an animal model of epilepsy with diffuse developmental defects.
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PMID:Drug effects on afterdischarge and seizure threshold in lissencephalic ferrets: an epilepsy model for drug evaluation. 664 45

The influence of lead intoxication on the seizure state produced by amygdaloid kindling was studied in rats. Exposure to 1% lead (in the form of lead acetate) in drinking water for periods up to 4 weeks led to significant increases in lead content in the blood and various brain regions. Signs of lead intoxication, including behavioral depression, loss of body weight and decreased hematocrit were produced by this treatment regime. The intensity and nature of behavioral convulsions as well as the rate of development of amygdaloid kindled seizures did not appear to be affected by lead intoxication. However, lead exposure during kindling led to significant increases in an electrographic aspect of the seizure, i.e., the afterdischarge duration. Although pair-fed controls were not utilized and therefore definitive conclusions cannot be made, our data would seem to indicate that lead intoxication has a relatively minor ability to potentiate amygdaloid kindling in adult rats.
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PMID:Lead intoxication and the amygdaloid kindling model of epileptogenesis in the adult rat. 687 73

Large intramuscular doses of a water-miscible preparation of vitamin A (500,000 I.U. retinyl acetate/ml), vitamin E (50 I.U./ml) and vitamin D2 (50,000 I.U./ml) were administered to young monkeys (Macacus fascicularis) weighing 1-1.8 kg. At vitamin A doses equivalent to 200 mg retinol/kg or higher, early signs of acute toxicity included yawning, apparent drowsiness, nausea and vomiting, head shaking, neck hyperextension, motor hyperactivity and coordination. These immediate signs were first noted 3-35 minutes after injection. Following apparent recovery at 1-2 hrs, longer term signs of toxicity, such as decreased activity, malaise, drowsiness, loss of appetite, loss of weight, and itchiness of the skin, appeared within 1-6 days, depending on the dose. Monkeys receiving the highest lethal doses became progressively weaker, showed labored breathing, lapsed into a coma, lost simple reflexes and then died. Respiratory failure usually preceded the cessation of heart beat. In some monkeys on a lower but lethal dose, death was preceded by generalized convulsive seizures. The time of onset of the first sign and survival time were inversely proportional to the dosage, but in individual monkeys no correlation existed between onset time and survival time. Female monkeys seemed to succumb faster to a lethal dose than male monkeys. All animals receiving the equivalent of 300 mg retinol/kg died. Under the conditions used, the LD50 was estimated to be 168 mg retinol (560 000 I>U.) per body weight.
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PMID:A lethal hypervitaminosis A syndrome in young monkeys (Macacus fascicularis) following a single intramuscular dose of a water-miscible preparation containing vitamins A, D2 and E. 697 50

Mice, genetically selected for differences in brain weight were employed. Lead administration (0.5% lead acetate) from conception increased the proportion of 21 day old mice exhibiting seizures; total duration of observed seizures was also increased. Mice from the low brain weight line more frequently exhibited seizures than either mice from the high brain weight line or the Binghamton heterogeneous stock. Although genome and lead administration after bodyweight, the inability of bodyweight to predict seizure occurrence and/or total duration of seizure within conditions also was noted. Lead administration from conception through testing increased the probability and duration of transcorneally induced electroconvulsive seizures of 21 day old mice within all three genotypes, and both cocaine and amphetamine injections 15 min prior to ECS reduced the number of animals exhibiting seizures as well as the duration of seizures in both lead treated and control mice.
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PMID:Effect of amphetamine and cocaine on seizure in lead treated mice. 707 Oct 95

A 6-year-old girl developed generalized seizures followed by coma, five days after surgical removal of a craniopharyngioma. Low serum sodium levels and low serum osmolality with inappropriately high urinary sodium output confirmed the diagnosis of inappropriate antidiuretic hormone (ADH) secretion. Treatment with 3% hypertonic saline solution and repeated doses of furosemide (1 mg/kg) improved her clinical condition; serum sodium levels, however, rose slowly and urinary excretion remained high. Deoxycorticosterone acetate (DOCA), 4 mg/sq m/day, was added to the above regimen. A striking clinical improvement was noted. Serum sodium levels returned to normal with a concomitant sharp decline in urinary sodium output. The clinical course of this patient demonstrates the efficacy of the addition of deoxycorticosterone acetate to hypertonic saline and furosemide in the treatment of severe, life-threatening hyponatremia due to the syndrome of inappropriate antidiuretic hormone secretion.
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PMID:Combined treatment of severe hyponatremia due to inappropriate antidiuretic hormone secretion. 707 19

Male mice (25-30 g) were injected (ip) with either 0, 3.5 X 10(-6), 17.5 X 10(-6), or 26.25 X 10(-6) mol/kg of either tricyclohexyltin bromide (TCT) or triphenyltin acetate (TPhT) in a corn-oil vehicle. The mice were tested for maximal electroshock seizure (MES) at 0.5, 4, 24, and 96 h following exposure to the organotin compounds, and the durations of seizure phases were measured and used to assess seizure severity. No significant changes in seizure-grade distribution, as compared to controls, were observed in any of the TCT- or TPhT-treated groups at any of the time points examined. No significant changes in the duration of seizure phases, as compared to controls, were observed in animals dose with 3.5 X 10(-6) mol/kg of TCT or TPhT at any of the time points evaluated. At 0.5 h following exposure, the mice dosed with the two higher levels of TCT or TPhT exhibited increases in MES severity. At 4 and 24 h following exposures, the mice exposed to the two higher dose levels of TPhT exhibited decreases in MES severity, followed by a recovery of normal seizure severity at 96 h. Conversely, the animals dosed with the higher dose levels of TCT exhibited at increased MES severity at 4, 24, and 96 h following exposure. These results, in combination with those in the preceeding paper (Doctor and Fox, 1982), reveal that at equimolar doses TCT And TPhT possess a different spectrum of action than the tri-n-alkyltins.
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PMID:Effects of organotin compounds on maximal electroshock seizure (MES) responsiveness in mice. II. Tricyclohexyltin and triphenyltin. 713 89

Motor impairments and seizures are frequent neurologic sequelae of excess lead exposure in children. To evaluate the relative significance of such symptoms in an animal model, Long-Evans rats were lead-exposed from parturition to weaning by adulteration of the dams' drinking water with 0.02% or 0.2% lead acetate. Ontogeny of swimming ability from 6 through 24 days of age was not altered by postnatal lead exposure. Rotorod performance was tested on 21, 30, 60, 90, 150 and 440 days of age and was maximal in rats 30 through 150 days of age, with the poorest performance by 440-day-old rats. Rotorod performance was decreased by both levels of lead exposure and this effect was most evident at 60 and 150 days of age. Both levels of lead exposure increased kidney weights of dams at weaning and the 0.2% lead acetate exposure decreased hematocrit of dams. Kidney weights of lead-exposed pups were not increased at 10 days of age, but pups in the 0.2% lead acetate group had increased kidney weights at 20, 90 and 150 days of age. Hematocrit values of pups in the 0.2%, but not in the 0.02%, lead acetate exposure group were decreased at 20 days of age. No effects of lead exposure on hematocrits were found at 10, 90 or 150 days of age. Wet weight of brain, cerebellum, adrenals, spleen and thymus were not altered at any age by postnatal lead treatment. In a second study, Sprague-Dawley rats exposed to lead via dams drinking 0.2% lead acetate throughout gestation and lactation. Pre- and postnatal lead exposure did not alter the ontogeny of electro-shock seizure thresholds in rats tested on 8 through 20 days of age. The results suggest that the lead exposure levels used were at or near a no-effect level for several common neurobehavioral tasks and that kidney weight may be a more discriminative index of excess lead exposure than some simple neurobehavioral indices.
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PMID:Motor development, tissue weights and seizure susceptibility in perinatally lead-exposed rats. 720 May 84

The neurotransmitter gamma-aminobutyric acid is known to decrease preictally after administration of the potent convulsant methyoxypyridoxine, a competitive inhibitor of glutamate decarboxylase. An attempt was made to determine the effect of this gamma-aminobutyric acid decrease on the cholinergic system. Rabbits were immobilized and artificially ventilated in order to avoid hypoxidosis. Seizures were induced by intravenous injection of 100 mg kg-1 methoxypyridoxine; 40 minutes later the animals were decapitated and discrete brain areas removed. Tissue contents of acetylcholine and choline were estimated by gas chromatographic mass spectrometric analysis of the beta-dimethylaminoethyl acetate and propionate derivatives using deuterated internal standards. Gas chromatographic column optimization resulted in a considerable sensitivity gain. Computerized selected ion monitoring was carried out on the dimethylmethyleneimmonium ions using voltage switching. The use of a computer controlled solvent dump valve was implemented to increase precision. No significant difference was observed in the concentration of acetylcholine in the frontal cortex, cerebellar cortex, septum, hippocampus, or caudate of seizure versus control animals; septal choline increased, however. This suggests that the acetylcholine turnover could be increased during seizure.
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PMID:Selected ion monitoring determination of acetylcholine during methoxypyridoxine seizures. 722 35


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