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

In order to assess the early regional changes in energy metabolism in bicuculline induced seizures, mice were injected and sacrificed before the onset of overt seizure activity, and shortly after clonic-tonic seizures began. The energy metabolites glucose, ATP, and phosphocreatine were measured in layers of the motor cortex and the cerebellar vermis. Results showed minimal metabolite changes in the cerebellum, whereas changes in energy metabolism in the motor cortex were largely localized to the layers containing pyramidal cells. These results are in agreement with previous studies showing a relative sparing of the cerebellum, and suggest early cortical changes occur in pyramidal cells.
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PMID:Regional cerebral energy metabolism in bicuculline induced seizures. 358 95

Effects of nicergoline on ischemic brain damages induced by bilateral carotid arterial ligation (BCAL) in ICR-strain mice and mongolian gerbils and lipid peroxide formation (LPOF) in normal brain homogenate of rats were compared with those of dihydroergotoxine (DHE). In mice, nicergoline (16 mg/kg, i.p.) significantly reduced the cumulative mortality rate after BCAL (from 80-83% in the control to 50-55%). In gerbils, nicergoline (32 mg/kg, i.p.) significantly prolonged the mean onset time of ischemic seizure following recirculation after the 30-min BCAL (from 45.8 min in the control to 94.9 min). DHE also showed protective effects in these animals. In the ischemic brain of mice, marked decreases of creatine-P, ATP, glucose and glycogen; a remarkable increase of lactate; and elevation of L/P ratio were observed 1 to 10 min after BCAL. Nicergoline (16 mg/kg, i.p.) slightly prevented these decreases and significantly suppressed the increase of lactate and the elevation of L/P ratio 2 min after BCAL. The inhibitory action of nicergoline (20-100 microM) on LPOF is more potent than those of alpha-tocopherol and DHE. These results suggest that nicergoline may have protective effects against ischemic brain damages due to its ameliorating action on cerebral energy metabolism and partially due to its inhibitory action of LPOF.
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PMID:[Pharmacological study of nicergoline. (II). Protective effect on ischemic brain damages in animals]. 375 14

The objective of this study was to evaluate changes in cortical energy metabolism in experimentally induced seizures in the primate. Cynamologus fascicularis monkeys were anesthetized, and a craniotomy was performed. Small samples from the motor cortex were removed for measurement of energy metabolites just prior to intravenous bicuculline infusion (0.6 mg/kg), 20 min after the onset of seizures, and 2 h after the second sample. Samples were also taken for electron microscopy. Results showed decreased phosphocreatine values 20 min after the onset of seizures, whereas ATP levels were normal. Two hours after the onset of seizures, phosphocreatine had returned to normal, but ATP levels were below normal. Examination of tissue by electron microscopy showed evidence of cell damage 2 h, 20 min after the onset of seizures. These findings are consistent with the concept that sustained seizures may lead to irreversible cell damage and that alterations in energy metabolism may contribute to the cell death.
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PMID:Status epilepticus-induced changes in primate cortical energy metabolism. 377 56

In vivo phosphorus 31 nuclear magnetic resonance (31P NMR) spectroscopy was used to evaluate changes in cerebral high-energy phosphate compounds in 8 infants with seizures. During the study 4 babies had seizures that caused a 50% decrease in the phosphocreatine to inorganic phosphate (PCr/Pi) ratio. Focal seizures caused lateralized decreases in the PCr/Pi ratio; generalized seizures caused bilateral decreases. Postictal spectra had increased PCr/Pi ratios, presumably due to postictal inhibition. Interictal 31P NMR spectra were normal. One patient's seizures were successfully treated with intravenously administered phenobarbital during NMR data acquisition, causing an immediate increase in the PCr/Pi ratio from 0.7 to 1.2. These studies indicate that cerebral PCr concentration decreases by approximately 33% and that oxidative metabolism increases by approximately 45% during neonatal seizures. Five babies had PCr/Pi ratios of less than 0.8 during seizures and subsequently developed long-term neurological sequelae, which suggests that neonatal seizures may cause or exacerbate cerebral injury by increasing cerebral metabolic demands above energy supply.
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PMID:Cerebral metabolic effects of neonatal seizures measured with in vivo 31P NMR spectroscopy. 378 67

The convulsant pentylenetetrazole was administered to the lower primate, the tree shrew. Shortly after the onset of seizures, the animals were killed using a microwave device at 25 Kw and 915 MHz. The energy metabolites glycogen, glucose, ATP, and phosphocreatine were measured in five layers of the cerebral cortex and three layers of the cerebellum. Results showed that, as compared with controls, seizing animals had decreased energy metabolites selective to certain layers. Glucose was decreased in all cortical layers, but only in the granular layer of the cerebellum. Phosphocreatine was decreased in the outer small pyramidal layer and the polymorphous layer of the cortex but was unchanged in the cerebellum. ATP was decreased only in the outer small polymorphous layer of the cortex. These changes are consistent with the concept that selective changes may occur during seizures and that these changes are localized to layers that contain pyramidal cells. Examination of whole cortex may mask more subtle regional changes.
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PMID:Pentylenetetrazole-induced changes in cerebral energy metabolism in Tupaia glis. 381 12

Female chicks carrying the lethal, sex-linked recessive paroxysmal (px) gene are susceptible to spontaneous and audiogenic seizures. Because seizure activity does not begin until 1 to 2 weeks posthatching - coincidental with disappearance of the yolk-sac - it is postulated that a contributing factor to seizure activity may be a developmental failure of the chick's ability to switch from lipid to carbohydrate as a primary energy source. In testing this hypothesis, three experiments were performed: 1) to evaluate cerebral energy reserves - adenosine triphosphate (ATP), phosphocreatine - of px and normal chicks; 2) to determine effects of energy source (ethanol, glucose, insulin, and glucose-insulin combined) on audiogenically-induced seizure activity and electrical seizure threshold; 3) to evaluate energy source utilization as estimated by the respiratory quotient (RQ). Brain ATP and phosphocreatine levels in px chicks were both decreased (P less than .05) as early as 10 days posthatching. Ethanol increased electrical seizure threshold in 50% of px chicks and provided protection from audiogenic stimulation. No consistent effect was found with any of the other substances. The RQ of px chicks were lower (P less than .05) than those of controls by 18 days posthatching.
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PMID:Energy metabolism in audiogenically seizure-prone chicks. 388 94

The objective of the present study was to assess metabolic changes in the neocortex and hippocampus of well-oxygenated or moderately hypoxic rats in which fluorothyl-induced seizures were sustained for 5 or 20 min, or which were allowed recovery periods of 5, 15, or 45 min following cessation of 20-min seizure activity by withdrawal of the convulsant gas. Sustained fluorothyl-induced seizures were found to cause metabolic alterations qualitatively and quantitatively similar to those previously observed with other commonly used convulsants. Thus, although the phosphorylation state of the adenine nucleotide pool remained only moderately perturbed, if at all, there were decreases in tissue concentrations of phosphocreatine and glycogen, and increases in those of cyclic AMP, lactate, and pyruvate, with a calculated fall in intracellular pH of about 0.15 units and a rise in the cytoplasmic NADH/NAD+ ratio. The enhanced metabolic rate was reflected in a marked reduction in the tissue-to-plasma glucose concentration ratio. Induced moderate hypoxia (arterial PO2 40-50 mm Hg) had no metabolic effect after 5 min of seizures but moderately increased lactate concentrations after 20 min (from about 10 to about 15 mumol X g-1). On cessation of seizure discharge cyclic AMP and phosphocreatine concentrations normalized already within 5 min, whereas glycogen and lactate concentrations normalized more slowly. In the neocortex (but not the hippocampus) postepileptic tissue-to-plasma glucose concentration ratios rose above control, probably reflecting metabolic depression. The results suggest that intracellular pH promptly returned to control, and that postepileptic alkalosis developed. They also suggest that some elevation of the NADH/NAD+ ratio persisted even after 45 min of recovery.
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PMID:Cerebral metabolic changes during and following fluorothyl-induced seizures in ventilated rats. 398 40

Graded transient cerebral hemispheral ischemia was produced in nitrous oxide-anesthetized Wistar rats by a procedure combining unilateral common carotid artery occlusion; elevation of intracranial pressure to 40-45 mm Hg by infusion of mock cerebrospinal fluid; and maintenance of arterial blood pressure at 100-110 mm Hg by controlled hemorrhage. Cerebral perfusion pressure was thus reduced into the ischemic range ipsilateral to carotid occlusion but remained 55-70 mm Hg contralaterally. Regional cerebral blood flow, measured autoradiographically, fell by 85-90% in the ischemic dorsolateral and lateral neocortex, hippocampus and lateral striatum, but remained at 71% of control or higher contralaterally. Metabolite assay revealed a gradient of energy depletion, with profound reductions in ATP and phosphocreatine and marked elevations of lactate in lateral neocortex, lateral striatum, hippocampus and lateral thalamus. Importantly, dorsolateral neocortex proved to be a penumbral zone, with marked lactate elevation comparable to that of lateral cortex, yet only intermediate degrees of ATP and PCr reduction. Contralateral structures were metabolically unaffected apart from mild increases in lactate. The advantages of this focal ischemia model include the consistent topographic distribution of ischemia and its regional gradations of intensity; the avoidance of painstaking intracranial microsurgery and of systemic complications; preservation of intact energy state of the contralateral hemisphere; ease of reversibility of ischemia; and lack of seizures. The consistent metabolic penumbral zone is a unique feature of the model.
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PMID:Graded focal cerebral ischemia in the rat by unilateral carotid artery occlusion and elevated intracranial pressure: hemodynamic and biochemical characterization. 400 62

The effects of prolonged bicuculline-induced seizures on cerebral blood flow and metabolism were determined in paralyzed, mechanically ventilated neonatal dogs. Transient changes occurring early in the course of status epilepticus included significant arterial hypertension, hypocarbia, elevation of plasma norepinephrine levels, and decline in brain glucose concentration. Cerebral blood flow remained elevated throughout the 45 minutes of seizure. Determination of cerebral metabolite values by in vivo phosphorus 31 nuclear magnetic resonance spectroscopy and by in vitro enzymatic analysis of frozen brain samples showed significant decreases in the level of phosphocreatine and relatively less change in ATP values. Progressive intracellular acidosis occurred, coincident with elevation of brain lactate concentrations. We conclude that the physiological and metabolic alterations that occur during prolonged seizures are not uniform, but change with time. Any hypothesis advanced to explain the mechanism of neuronal injury during prolonged seizures must take into account these temporally related changes.
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PMID:31P NMR study of cerebral metabolism during prolonged seizures in the neonatal dog. 403 47

The cerebral blood flow is lower in spontaneously hypertensive rats than in normotensive anaesthetized and mechanically ventilated rats during bicuculline-induced seizures, presumably due to the increase in vascular resistance in the hypertensive rats. This study investigates whether the hypertensive rats develop more severe derangement of the cerebral energy metabolites than normotensive rats because of the reduced cerebral blood flow. After 20 min of continuous seizure activity both normotensive and hypertensive rats had significantly decreased levels of phosphocreatine, ATP and glycogen as well as increased lactate and lactate/pyruvate ratio within the parietal cortex compared to controls. The metabolic disturbances were somewhat less pronounced in the hypertensive rats than in the normotensive rats. Thus, ADP was significantly increased in normotensive rats only and the lactate/pyruvate ratio was higher in the normotensive rats. We conclude that spontaneously hypertensive rats are not more prone than normotensive rats to derangement of cerebral energy metabolites during short term bicuculline-induced seizures and that insufficient blood flow is not the primary cause of the metabolic alterations.
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PMID:Cerebral energy metabolism during bicuculline-induced status epilepticus in spontaneously hypertensive rats. 406 Nov 12


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