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

Blood-gas (pO2, pCO2) and pH-changes of venous (v.jugularis interna) and arterial (A.femoralis) blood samples, furthermore glucose utilization and lactate-, pyruvate-production of brain were investigated during electroconvulsive treatment in relaxation of 45 psychotic patients. The blood-gas values and substrate concentrations were statistically evaluated and represented in a function of the characteristic phases of the postconvulsive EEG-activity. A correlation was found between the glucose metabolism of the brain and the postconvulsive recovery of EEG. The restitution of postconvulsive brain metabolism runs discontinuously in the first 12 minutes of postconvulsive state. In the phase of electric silence and periodic delta-waves the brain metabolism was shifted to anaerobic direction. During the treatment no anoxic anoxia or acidosis takes place during the seizure activity and restitution, the measurable metabolic changes are moderate and supposedly play no important role in the "effect" of treatment.
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PMID:[EEG-restitution and brain metabolism during electroconvulsive treatment in relaxation (author's transl)]. 1 29

Rats with different levels of blood glucose concentration were exposed to 10 min of complete brain ischemia achieved by compression of neck vessels by a pneumatic cuff. All normoglycemic rats survived the ischemic period and made the best clinical recovery. Hyperglycemic rats died within 12 h. Seizure activity was observed in all animals in this group. Three of eight hypoglycemic rats died between 3 and 16 days. The clinical recovery was less complete than in the control group. Thus, recovery from cerebral ischemia depends upon preischemic blood glucose concentration. Hyper- and hypoglycemia hamper the clinical recovery after transient cerebral ischemia.
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PMID:Clinical restitution following cerebral ischemia in hypo-, normo- and hyperglycemic rats. 3 Feb 50

Both naturally occurring disease processes and experimental models of human disease in the Mongolian gerbil were reviewed. The gerbil was highly susceptible to cerebral infarction following unilateral ligation of one common carotid artery and was useful in studies of the pathogenesis of stroke. Spontaneous epileptiform seizures mimicked those of human idiopathic epilepsy, and both seizure-sensitive and resistant strains have been bred. Perhaps because of its more efficient nephron, the gerbil accumulated four to six times as much renal lead as the rat, and the gerbil has been proposed as an experimental model of lead nephropathy. On standard diets, about 10% of the animals became obese, and some showed decreased glucose tolerance, elevated serum immunoreactive insulin and diabetic changes in the pancreas and other organs. Some breeders exhibited hyperactivity of the adrenal cortex associated with hyperglycemia, hyperlipidemia and degenerative vascular disease. Although dietary supplements of cholesterol were toxic and did not induce atherosclerosis, the gerbil was useful in other studies of cholesterol absorption and metabolism. Spontaneous, insidious periodontal disease became evident after about 6 months on standard diets, and dental caries were induced by cariogenic diets or by pathodontic streptococci. Spontaneous neoplasia occurred in 8.4--24% of gerbils, usually after 2 years of life. Adrenal cortical, ovarian and cutaneous tumors were the most consistently reported neoplasms.
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PMID:The pathology of the Mongolian Gerbil (Meriones unguiculatus): a review. 9 95

Electrocorticographic (ECoG) and depth recordings have previously demonstrated the epileptogenic nature of surgical concentrations of the volatile anesthetic enflurane. We contrasted ECoG activity with local cerebral glucose uptake [( 14C]2-deoxyglucose autoradiography) in 23 brain structures in order to identify the epileptogenic foci. Autoradiograms were obtained from sectioned rat brain following a 30 min period of steady-state anesthesia at 1, 1.5, or 2 MAC (minimum alveolar concentration) enflurane. Pseudo-epileptiform ECoGs were obtained at 1 MAC where bursts of slow waves and sharp waves were evoked by peripheral sensory stimulation. At 1.5 MAC, the ECoG displayed frank, spontaneous epileptiform activity with large amplitude spike-wave complexes; repetitive auditory stimulation occasionally precipitated grand-mal seizures. At 2 MAC, spike complexes were less frequent and could not be repetitively driven. At 1 MAC enflurane, regional cerebral metabolism was generally depressed approximately 14% from the awake controls. However, metabolism in the dentate gyrus of the hippocampus and other subcortical structures in the limbic brain was increased. At 1.5 MAC this dichotomy in local cerebral metabolic rate was maximal; we observed increased metabolism in the hippocampus, habenula, habenulo-interpeduncular tract and interpeduncular nucleus and pineal. Metabolism in all other structures was significantly depressed (P less than 0.05) compared to awake values. At 2 MAC, metabolism was decreased in all structures. We conclude that the low seizure threshold hippocampus and related structures associated with the limbic system and its pathways are the epileptogenic foci for seizures induced with enflurane in the rat. At 1.5 MAC, epileptiform activity spreads throughout the visceral brain when seizure threshold is at a minimum.
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PMID:Local cerebral metabolism during enflurane anesthesia: identification of epileptogenic foci. 9 9

A previous study showed a strong relationship between human focal epilepsy and the presence in the cortex of "activated" astrocytes characterized by an intense activity of dehydrogenases (DH) involved in glucose metabolism and of glutamate DH. Using the semi-chronic model of cobalt-induced experimental focal epilepsy in the rat, we investigated a possible correlation between astrocyte modifications and the chronological development of the epileptic manifestations on the ECoG. After a few days the cobalt-implanted rats present spikes, then sharp waves followed by an electrical crisis and ultimately motor seizures. Activated astrocytes were found in each phase of this evolution. Their number increases with the intensity of the manifestations. There is a close relationship between activated astrocytes and focal epileptic phenomena. At this stage of our study it is clear that the presence of activated astrocytes is not a consequence of seizures. However, it is impossible to say whether the activation is secondary to the hyperactivity of the neurons or directly responsible for the constitution of the epileptic focus. In any case, activated astrocytes provide a new means of localizing an epileptogenic focus.
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PMID:Histochemical study of cobalt-induced focal epilepsy. 9 27

Changes in plasma glucose, nonesterified fatty acids, insulin, glucagon, cortisol, growth hormone, and prolactin have been studied in baboons during the course of generalized epileptic seizures induced by intravenous bicuculline. Plasma glucose rose to a peak at 25 min but fell to hypoglycemic levels after 60 min of seizure activity. This hypoglycemia was accompanied by a marked elevation in plasma insulin. Plasma glucagon rose to a peak at 14 min, then returned to normal. Plasma growth hormone levels were elevated after 60 min of seizure activity. Plasma prolactin and cortisol levels also rose during the seizure. These changes result from sequential interaction of (1) autonomic activation at seizure onset, (2) spread of neuronal activity to the hypothalamus leading to the liberation of releasing factors, and (3) indirect physiologic consequences of seizure activity.
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PMID:Endocrine factors and glucose metabolism during prolonged seizures in baboons. 11 9

In idiopathic or generalized epilepsy, serum glucose and cholesterol concentrations tend to be low, especially just before the seizure. Glucose tolerance curves are abnormal and variable. The electrolyte balance is disturbed, and epileptics tend to go readily into alkalosis. Serum [Na+] is usually unaffected, but [K+] is normal to low between attacks and increases during and after the seizure. Serum [Cl-] is usually high just before the seizure. Epileptics are generally mildly hypocalcemic, especially in the period before the seizure. Serum urea and nonprotein nitrogen values are low between paroxysms but increase after the seizure. Serum protein concentration is usually normal. Stress, which releases epinephrine and corticotropin, results in high serum citrate concentration, which probably contributes to decreased serum [Ca2+] just before a seizure. In the healthy individual, any increase in serum citrate is accompanied by increasing [Ca2+]. In the rabbit, convulsions can be induced with corticotropin, a result of increased serum citrate concentration coupled with a decrease in [Ca2+]. The net result is severe hypo-ionic-calcemia. A similar phenomenon has been reported in a few humans. Administration of insulin causes serum citrate concentrations to decrease. Apparently, the dynamic system that controls glucose and lipid metabolism, and thus electrolyte balance, through the hormones epinephrine, corticotropin, insulin, glucagon, calcitonin, and parathormone, is abnormal in the epileptic.
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PMID:Clinical biochemistry of epilepsy. I. Nature of the disease and a review of the chemical findings in epilepsy. 22 Nov 36

Twenty-three psychiatric patients were investigated during electroconvulsive treatment in relaxation. The blood gases, pH and serum bicarbonate levels in blood samples from the internal jugular vein and the femoral artery were measured radiometrically. The LDH fractions were separated electrophoretically and their activity, along with the activity of aldolase, was then determined on test materials. EEG recordings were made during the seizure and also during postconvulsive restitution. The following conclusions were drawn: (1) There was no evidence of anoxic anoxia in the brain during and after seizures. (2) A close relationship was found between the corresponding phases of electrical activity and brain metabolism as indicated by the blood gas changes during postconvulsive restitution. (3) On the basis of the increased glycolytic activity in the sera it is probable that glucose metabolism was shifted in the anaerobic direction during postconvulsive restitution of the brain tissues.
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PMID:Correlation between blood gases, glycolytic enzymes and EEG during electroconvulsive treatment in relaxation. 23 9

Experimental seizures were induced in mice by application of 50 mA for 0.2 sec via corneal electrodes. The reproducible conclusive behavior was characterized by a sequence of 2 sec of tonic flexion, 13 sec of tonic extension, and 8 sec of clonus followed by a postictal depressive stage. The animals were frozen and tissues were prepared for analysis according to Lowry and Passonneau [Lowry, O. H. & Passonneau, J. V. (1972) A Flexible System of Enzymatic Analysis (Academic, New York)]. Freeze-dried samples (1-10 ng) of pyramidal cell bodies and adjacent neuropil from the parietal cortex and of Purkinje cell bodies and adjacent neuropil from the cerebellum were analyzed for glucose, ATP, and P-creatine (0.01-0.05 pmol). There were marked decreases in these energy stores after the maximal electroshock in three of the areas examined. In the Purkinje cell bodies, however, the metabolic stress was dampened; glucose concentrations decreased, but the levels of ATP were maintained and, to a lesser extent, those of P-creatine. The results indicate that the output from the Purkinje cells is less than in the other regions examined in the excitable stages of the convulsion. The lesser energy debt probably reflects lower energy demand as well as a lower discharge intensity. The fact that Purkinje cells are spared from the metabolic stress imposed on other regions may be a partial explanation of the seizure activity. A diminished output from the Purkinje cells could be a situation that permits cortical convulsive activity.
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PMID:Sparing of metabolic stress in Purkinje cells after maximal electroshock. 28 34

The relation of endotoxicosis to insulin responsiveness was evaluated in male Holtzman rats. Salmonella enteritidis lipopolysaccharide at 0.5 or 1.0 mg per 300 g rat increased lethality in convulsive seizure deaths to 0.25, 0.50, or 1.0 U insulin sc. The hypoglycemic nadir induced by 0.05, 0.10, or 0.25 U of insulin sc was greater in rats rendered endotoxic with 1 mg of lipopolysaccharide IV. Oxidation of U-14C-D-glucose to 14 CO2 by endotoxic tissues in vitro was augmented in liver slices, epididymal fat pads, hemidiaphragms, and spleen slices; no pronounced glucose oxidation increases occurred in lung, heart, stomach, cerebrum, kidney, or whole blood. Epididymal fat pads from endotoxic rats (100 g) manifested increased basal glucose oxidation as well as an enhanced maximal response to incremental insulin doses of 0.01 to 25 mU/ml. It is suggested that altered tissue responsiveness in concert with hyperinsulinemia underlie the profound alterations in glucose homeostasis during endotoxicosis.
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PMID:Increased insulin responsiveness in endotoxicosis. 37 53


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