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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prolonged neonatal seizures are often accompanied or exacerbated by hypoxemia. To determine the effects of hypoxemia on neonatal status epilepticus, we determined cerebral blood flow and cerebral metabolic state in groups of neonatal dogs subjected to hypoxia, to seizures during normoxia, or to seizures during hypoxia. The compensatory increase in cerebral blood flow was greatest in animals subjected to seizures during normoxia and somewhat less pronounced in animals made hypoxic. However, blood flow failed to increase in forebrain structures when animals were subjected to the combination of seizures and hypoxia. Accordingly, levels of adenosine triphosphate in forebrain (measured both by in vitro enzymatic analysis and by in vivo phosphorus-31 nuclear magnetic resonance spectroscopy) were depleted to the greatest degree in animals who were seizing while hypoxic. In addition, brain glucose was significantly reduced only in the seizure-hypoxia group. Systemic factors such as hypoxemia may play a critical role in the disruption of cerebral energy balance during neonatal status epilepticus.
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PMID:31P nuclear magnetic resonance study of the effect of hypoxemia on neonatal status epilepticus. 372 54

The neuronal regions affected and the neuropathologic features of ischemia and status epilepticus are similar. Experimentally, elevated plasma glucose levels, increasing brain lactate, are associated with more severe neuropathologic damage from cerebral ischemia. We therefore studied the cytologic features and cerebral content of lactate and glucose in the selectively vulnerable neurons of rat hippocampus after 2 hours of L-allylglycine-induced status epilepticus in rats with mean plasma glucose concentrations of 65, 250, and 480 mg/100 ml. Brain lactate concentration was elevated in status and maximal in the high-glucose group, but the maximum levels (8 mumol/g) were less than those thought to augment cell death in ischemia. Using multiple linear regressions, only time-in-status predicted neuropathologic damage.
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PMID:Hyperglycemia does not augment neuronal damage in experimental status epilepticus. 376 42

Poisoning is an uncommon manifestation of child abuse. The intentional administration of water to a child as a form of punishment has rarely been reported as the responsible substance among children who have been poisoned. We describe a case of a 5-year-old girl presenting with severe hyponatremia due to acute water intoxication. The patient was brought to the emergency room in status epilepticus. A history was obtained from the child's mother stating that the patient had been playing outside when she collapsed. She had had no known prior illnesses. Laboratory evaluation included a hemoglobin of 10.1 mg%, glucose of 60 mg%, serum sodium of 107 mEq/l, potassium of 3.2 mEq/l and chloride of 71 mEq/l. A CAT scan obtained approximately 1 h after admission revealed generalized cerebral edema. Careful examination of the skin revealed multiple linear ecchymosis of varying ages on the back and thighs and a hand print on the right flank. In addition, the child demonstrated severe failure to thrive with height, weight and bone age compatible with a 2.5-year-old girl. Appropriate therapy for severe hyponatremia was successfully instituted. For the next 12 h she was deeply somnolent, but the following morning was alert and conversant. She stated that she "would be good if she didn't have to drink any more water". The child's mother subsequently admitted that she frequently used water ingestion as a form of punishment. The child stabilized metabolically and demonstrated rapid in-hospital weight gain. She was placed in foster care at discharge and has had no further hyponatremia or seizures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyponatremic seizures as a presenting symptom of child abuse. 395 93

The regional influx of glucose across the blood-brain barrier and regional blood flow were studied simultaneously in conscious and restrained rats using the single pass bolus injection of [14C]butanol and [3H]D-glucose method. Glucose extraction by the cerebellum was about twice that of other brain regions. Thus, despite the lower cerebellar blood flow, the influx of glucose into the cerebellum was equivalent to that of the cerebral cortex and higher than that of the hippocampus over a wide range of plasma glucose concentrations. Because the local metabolic rate for glucose is higher in the cerebral cortex than in the cerebellum, the equal influx of glucose in these two regions means a relative oversupply of glucose to the cerebellum. In vivo analysis of blood to brain glucose transport kinetics showed similar plasma glucose concentrations at half-maximal transport (Kt) in brain regions that were studied. The values for Kt ranged between 4.4 and 5.1 mM. Maximal transport capability (Tmax), on the other hand, was similar in the cerebral cortex and cerebellum but significantly lower in the hippocampus (P less than 0.05). The higher ratio of glucose influx to glucose utilization in the cerebellum may explain the clinical and experimental findings of relative resistance of the cerebellum to hypoglycemia while the lower Tmax in the hippocampus may be the mechanism underlying its selective vulnerability during pathophysiologic conditions associated with marked increments in brain oxidative metabolism, such as status epilepticus.
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PMID:Regional comparisons of brain glucose influx. 397 Nov 56

With the six convulsants studied (Soman, intrahippocampal penicillin, bicuculline, pentylenetetrazol, picrotoxin and strychnine), the anatomical distribution of changes in local cerebral glucose utilization was related to the type of seizure observed. Strychnine induced a few very intense motor convulsions during the 2-deoxyglucose experimental period without having a major effect on brain local cerebral glucose utilization, in support of the view that its actions are predominantly in the spinal cord. Pentylenetetrazol and picrotoxin induced intermittent intense seizures and marked increases in local cerebral glucose utilization in the globus pallidus and substantia nigra. Soman, intrahippocampal penicillin and bicuculline all induced persistent status epilepticus associated with increases in local cerebral glucose utilization in many brain areas; those with striking increases in glucose use include: cortical areas, the limbic system, basal ganglia and substantia nigra. The glucose use changes produced by Soman, penicillin and bicuculline greatly exceeded those induced by pentylenetetrazol and picrotoxin. Activation of the substantia nigra and basal ganglia occurred with all centrally mediated convulsions and with status epilepticus there was also marked activation of cortical and limbic structures.
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PMID:Changes in local cerebral glucose utilization induced by convulsants. 399 Sep 60

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

Cardiovascular complications frequently occur during status epilepticus. To determine the changes in systemic and pulmonary arterial pressure, cardi output, and left ventricular contractility during seizures, 1-week-old pigs were intubated, paralyzed, mechanicall entilated, and catheterized with a Swan-Ganz catheter. Seizures were induced with intravenous bicuculline. Early changes consisted of significant systemic and pulmonary arterial hypertension. After 2 hours of seizures, the animals developed progressive systemic hypotension and decreased cardiac output. M-mode echocardiography disclosed a decrease in left ventricular contractility. Cardiac tissue frozen in situ showed a significant increase in lactate and reductions in glucose, triglyceride, and adenosine triphosphate levels. Prolonged seizures in the neonatal pig result in cardiac dysfunction, which may play a role in the development of epileptic brain damage.
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PMID:Cardiac dysfunction during status epilepticus in the neonatal pig. 405 58

Neuronal lesions in the brain occur in conditions associated with a reduced supply of oxygen (hypoxia and ischemia) and glucose (hypoglycemia) as well as in those associated with a pathologically enhanced neuronal activity (status epilepticus). In only two of these conditions (hypoxia and ischemia) are the lesions correlated to cellular oxygen lack, and gross energy failure is absent in one condition (status epilepticus). Although anaerobic mechanisms seem responsible for the cell injury in hypoxia and ischemia, oxidative mechanisms could operate in hypoglycemia and status epilepticus. Since the supply of oxygen has not ceased altogether in hypoxia and incomplete ischemia, and since reoxygenation/recirculation leads to a transient increase in tissue oxygen tensions, one cannot exclude the possibility that oxidative mechanisms contribute to the final damage following all types of cellular oxygen lack. We have failed to obtain evidence that peroxidative degradation of cellular constituents occurs in hypoglycemia and status epilepticus. Thus, there is neither a perturbation of the redox state of the glutathione pool of the tissue nor a measurable degradation of polyenoic phospholipid-bound fatty acids. It is emphasized that the cascade of events triggered by an accumulation of free polyenoic fatty acids, mainly arachidonic acid, may contribute to cell lesions by leading to cell edema and/or microcirculatory changes. During seizures, such an accumulation occurs even though energy failure is moderate and it may conceivably contribute to cell damage. In general, though, mechanisms of cell damage in the brain remain partly elusive.
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PMID:Neuronal cell damage in the brain: possible involvement of oxidative mechanisms. 693 2

The effects of a loading dose of 15 mg/kg phenytoin by iv infusion on the serum levels of insulin, glucagon, and glucose were investigated in five fasting healthy male volunteers between the ages of 23 and 35 years. Serum glucose concentrations rose immediately after the infusion of phenytoin followed by a significant increase in serum insulin values (P less than 0.05). A slight elevation in mean glucagon concentrations after the infusion was not statistically significant. Further studies are indicated to determine whether phenytoin as used in the treatment of status epilepticus may aggravate the hyperglycemia associated with seizures.
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PMID:Effects of single large doses of phenytoin on glucose homeostasis--a preliminary report. 704 Apr 99

The objective of the present experiments was to study metabolic correlates to the localization of neuronal lesions during sustained seizures. To that end, status epilepticus was induced by i.v. administration of bicuculline in immobilized and artificially ventilated rats, since this model is known to cause neuronal cell damage in cerebral cortex and hippocampus but not in the cerebellum. After 20 or 120 min of continuous seizure activity, brain tissue was frozen in situ through the skull bone, and samples of cerebral cortex, hippocampus, and cerebellum were collected for analysis of glycolytic metabolites, phosphocreatine (PCr), ATP, ADP, AMP, and cyclic nucleotides. After 20 min of seizure activity, the two "vulnerable" structures (cerebral cortex and hippocampus) and the "resistant" one (cerebellum) showed similar changes in cerebral metabolic state, characterized by decreased tissue concentrations of PCr, ATP, and glycogen, and increased lactate concentrations and lactate/pyruvate ratios. In all structures, though, the adenylate energy charge remained close to control. At the end of a 2-h period of status epilepticus, a clear deterioration of the energy state was observed in the cerebral cortex and the hippocampus, but not in the cerebellum. The reduction in adenylate energy charge in the cortex and hippocampus was associated with a seemingly paradoxical decrease in tissue lactate levels and with failure of glycogen resynthesis (cerebral cortex). Experiments with infusion of glucose during the second hour of a 2-h period of status epilepticus verified that the deterioration of tissue energy state was partly due to reduced substrate supply; however, even in animals with adequate tissue glucose concentrations, the energy charge of the two structures was significantly lowered. The cyclic nucleotides (cAMP and cGMP) behaved differently. Thus, whereas cAMP concentrations were either close to control (hippocampus and cerebellum) or moderately increased (cerebral cortex), the cGMP concentrations remained markedly elevated throughout the seizure period, the largest change being observed in the cerebellum. It is concluded that although the localization of neuronal damage and perturbation of cerebral energy state seem to correlate, the results cannot be taken as evidence that cellular energy failure is the cause of the damage. Thus, it appears equally probable that the pathologically enhanced neuronal activity (and metabolic rate) underlies both the cell damage and the perturbed metabolic state. The observed changes in cyclic nucleotides do not appear to bear a causal relationship to the mechanisms of damage.
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PMID:Metabolic changes in cerebral cortex, hippocampus, and cerebellum during sustained bicuculline-induced seizures. 729 97


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