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

Thirteen juvenile monkeys were taught two visual discrimination tasks. After 12 to 24 hours of food deprivation, ten underwent 14-minute episodes of cardiac arrest. Three served as controls. Five of the ten arrested animals survived and were tested in the discrimination box. All continued to perform color and pattern discrimination tasks with one to eight days' delay. All appeared neurologically intact, while brain pathologic examination after 11 to 64 days' survival showed either intact brains or injury restricted to nuclear structures in the brain stem, cerebellar Purkinje cells, and hippocampus. Five animals died 4 to 36 hours after they were resuscitated. Two required prolonged cardiac massage and, despite return of adequate cardiovascular function, died early. A third animal dislodged its arterial catheter and exsanguinated. The remaining two animals, who received infusions of glucose just prior to arrest, developed widespread fasciculations and myoclonic seizures. They became decerebrate and opisthotonic and were killed after 10 and 36 hours. Their brains showed mild edema and widespread necrosis of cortex and basal ganglia. Thus, food-deprived monkeys tolerate 14 minutes of circulatory arrest well and show minimal neurologic and pathologic changes, while administration of glucose just before arrest markedly augments the severity of brain injury and alters its distribution.
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PMID:Nervous system effects of cardiac arrest in monkeys. Preservation of vision. 40 27

The effect of electrically induced seizures on the permeability of the rat blood-brain barrier was investigated. The small radioactive tracers sodium (24Na+), chloride (36Cl-) carbon labelled thiourea (14C-thiourea) and glucose (14C-D-glucose) were studied in indicator dilution experiments with indium labelled diethylenetriaminepenta-acetic acid (113mIn-DTPA) as reference substance. This method allows a quantitative estimate of the transcapillary loss of solutes, the extraction (E), during a single passage through the brain. Passage of macromolecules was studied using as marker substance Evans Blue which binds to plasma albumin. In the resting state ENa, ECl, Ethiourea and Eglucose were 2.9, 4.8, 9.3 and 12.5%, respectively. During seizures and during shortlasting hypercapnia E glucose decreased while E for the other tracers was unchanged. As cerebral blood flow increased, there must be an increased transfer of test substances into the brain. This finding is in agreement with recent human studies [15]. When Evans Blue was injected intravenously prior to electroshock, there was no staining of brain tissue after one electroshock but following repeated electroshocks some staining was observed. In an attempt quantify this transcapillary loss of albumin by means of indicator dilution, 51Cr-labelled erythrocytes were used as intravascular reference substance against 113mIn-DTPA (a plasma tracer). However, the albumin loss (by pinocytosis or otherwise) occurring after ten electroshocks could not be detected during a single passage through the brain.
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PMID:Blood-brain barrier during electroshock seizures in the rat. 40 65

A 10 month old female infant was evaluated for severe lactic acidosis. Clinically she was well nourished and had a substantial amount of adipose tissue despite recurrent episodes of acidosis. Her psychomotor development was retarded, her movements were dystonic and generalized seizures punctuated her course. Metabolic abnormalities included elevated blood concentrations of lactate, pyruvate, beta-hydroxybutyrate, acetoacetate, alanine, proline and glycine, decreased blood concentrations of glutamine, aspartate, valine and citrate, and intermittent elevations of serum cholesterol. A trial on a high-fat diet worsened the clinical condition and intensified the ketoacidosis and hyperalaninemia. Analysis of hepatic tissue obtained by open biopsy revealed increased concentrations of lactate, alanine, acetyl-CoA and other short-chain acyl-CoA esters, and decreased concentrations of oxaloacetate, citrate, alpha-ketoglutarate, malate and aspartate. The blood and tissue metabolic perturbations reflected a deficiency of hepatic pyruvate carboxylase. The apparent Km of hepatic citrate synthase for oxaloacetate was 4.6 micrometer. Calculated tissue oxaloacetate concentrations were 0.50--0.84 micrometer suggesting that tricarboxylic acid cycle activity was severely limited by the decreased availability of this substrate. An iv glucose tolerance test resulted in the paradoxical synthesis of ketone bodies. This observation, coupled with the intermittent hypercholesterolemia and the increased tissue acetyl-CoA concentrations, suggests that pyruvate carboxylase is important in modulating the fractional distribution of intracellular acetyl-CoA between the tricarboxylic acid cycle, the beta-hydroxy-beta-methyl-glutaryl-CoA cycle (and the synthesis of cholesterol and ketone bodies), and fatty acid synthesis. Treatment in future cases might be directed toward increasing tissue concentrations of oxaloacetate.
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PMID:The clinical and biochemical implications of pyruvate carboxylase deficiency. 41 60

Two initially healthy infants developed acute encephalopathic illnesses characterized by stupor, seizures, cerebrospinal fluid (CSF) erythrocytic and monocytic pleocytosis, increased CSF protein, and decreased CSF glucose and progression to chronic decerebration. In one case, herpes simplex virus was recovered from cutaneous lesions. The initial computed tomography (CT) scan revealed widespread subcortical increased attenuation with further increase after contrast medium injection and patchy areas of decreased attenuation in the deep cerebral white matter. Subsequent CT scans demonstrated progressive cortical calcifications and persistence of low attenuation areas. Autopsy revealed multiple cystic encephalomalacia. The second infant had similar clinical, CSF, and CT findings but remains in a chronic decerebrate state at 14 months of age. The CT abnormalities seen in these patients have not been encountered in any of 13 other infants with the clinical diagnosis of meningitis or encephalitis. Multiple cystic encephalomalacia of infancy is a rare condition with a uniformly bleak prognosis. Computed tomography may prove useful in the early diagnosis, thereby aiding clinicians in counseling and in the acute and long-term management of patients with this lesion.
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PMID:Multiple cystic encephalomalacia of infancy: computed tomographic findings in two cases with associated intracerebral calcification. 42 99

Four patients with pathologically documented polycystic cavitation of the brain had an acute illness characterised by stupor, seizures, CSF erythrocytic and monocytic pleocytosis, increased CSF protein, and diminished CSF glucose. The acute phase was followed by chronic decerebation, disappearance of the CSF abnormalities, and radiological evidence of polycystic cavitation of the brain. In one patient Herpes simplex was isolated from a cutaneous vesicle. The CSF abnormalities in the disorder have received scant attention, and have not previously been correlated with the acute and chronic stages. Clearly some cases are associated with Herpes simplex virus. The clinical profile should now be sufficiently distinctive to permit future identification of the aetiology in more neonates.
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PMID:Neonatal polycystic encephalomalacia: four new cases and review of the literature. 42 63

To evaluate the effects of substrate deficiency on cerebral function, metabolism, and blood flow during seizures, rats were injected intravenously with bicuculline (1.2 mg.kg-1) following a 24-hour period of starvation. During the course of seizures, blood glucose concentrations fell, and when they were reduced to below about 3 mumol.gm-1, cerebral function, metabolism, and blood flow altered. Changes in function involved the transition of an electroencephalographic pattern of bursts and suppression into one of frequent or sparse single spikes. Oxygen consumption, which initially increased at least twofold, fell toward normal or subnormal values in the single-spike period. Cortical blood flow was markedly reduced, and there was an attenuated response to carbon dioxide administration. Simultaneously, a small but clear fall was detected in the cerebral phosphorylation potential, and concentrations of glycolytic metabolites (including lactate) and citric acid cycle intermediates were reduced. Changes in amino acids and ammonia were somewhat similar to those observed in insulin-induced hypoglycemia, but since the amino acid pool did not fall, the experiments failed to give evidence that amino acids serve as oxidative substrates. The perturbation of cerebral energy state (and of levels of carbohydrate substrates and amino acids) was reversed by glucose administration; but since neither this procedure nor additional bicuculline injections could cause resumption of continuous seizure activity, the results suggest that cellular substrate depletion may have given rise to a sustained disturbance of synaptic transmission.
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PMID:Effects of bicuculline-induced seizures on cerebral metabolism and circulation of rats rendered hypoglycemic by starvation. 42 77

Seventy-two children who survived septic meningitis were reevaluated after 3 to 11 years. Thirty-four (52%) of 65 children were found to have neurological sequelae. Of the 34, 15 had major sequelae and 19 showed evidence of only minimal brain dysfunction--namely, hyperkinetic behavior, organic learning disturbances and minor motor disabilities. Acute-phase findings that were significantly associated with the rate of neurological sequelae were age, time between onset and admission, seizures, spinal fluid glucose level and the number of polymorphonuclear cells. In view of the high frequency of late neurological sequelae, it is advisable that children who survive septic meningitis have long-term follow-up in order to detect evidence of minimal brain dysfunction. An early diagnosis will help in proper management.
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PMID:Neurological sequelae of septic meningitis. A follow-up study of 65 children. 45 84

The onset of susceptibility to audiogenic seizures (AGS) coincides with the draining of the ear canal at about 14 to 16 days of age. This is also when the mouse brain has almost attained its maximal size and weight, and also about the time of weaning from the dam's high-fat milk to the beginning of dietary self-sufficiency. During suckling, the brain is primarily dependent on ketone-body utilization as a source for brain energy; weaned mice use glucose. It is suggested that in AGS-prone mice, there may be a developmental lag in the onset of a sufficient rate of glycolysis in brain to provide adequate immediately available energy reserves to last through a brief period of an external-stimulus-induced large energy expediture until energy repletion processes can begin. As a results, ATP levels might fall below an hypothesized lower limit to subserve organized neural activity in some inhibitory area of the brain, resulting in the onset of an AGS.
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PMID:Sources of energy for the brain and susceptibility to audiogenic seizures. 45 95

In order to determine the effects of acetate on signs and symptoms of hypoglycemic seizures, Swiss Webster albino mice were injected intraperitoneally with solutions of NaCl, NaHCO3, NH4Cl, Na-acetate, or NH4-acetate, followed by subcutaneous injection of 7 U of insulin/kg body wt. Administration of Na- or NH4-acetate delayed and reduced the incidence of hypoglycemic reactions. Reinjection with Na-acetate or repeated injections with NH4-acetate caused a return to normal behavior patterns for 60 and 75%, respectively, of the affected hypoglycemic experimental animals. Injections of control animals with NaHCO3 or NH4Cl showed that the results were not due to alkalosis or acidosis. Acetate administration significantly increased plasma acetate and citrate, but not glucose, lactate, beta-hydroxybutyrate, or acetoacetate concentrations. The results indicate that intraperitoneal administration of acetate directly acted to prevent signs of hypoglycemia from occurring and reversed its manifestations when they were present. The protective effect of acetate suggests that it may serve as a fuel for the brain.
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PMID:Effect of acetate on hypoglycemic seizures in mice. 48 41

Progressive cerebral ischemia was induced by blood pressure (BP) reduction in rats during status epilepticus, and the sequence of cerebral functional (EEG, extracellular K+ activity) and metabolic (levels of high energy phosphates, glucose, glucose-6-phosphate, lactate, pyruvate, alpha-ketoglutarate) changes were determined. Very moderate reductions of BP were accompanied by tissue lactate accumulation and a decrease of the rate of re-uptake of K+ extruded during discharges. These changes were pronounced at BP about 50 mm Hg, when also the energy state showed some deterioration, and the EEG activity changed from one of bursts and suppressions into single spikes. At BP about 30 mm Hg EEG activity was abolished, but not until a slightly lower BP level was there a severe energy depletion and a massive K+ release, indicating generalized membrane depolarization. The results show an increased susceptibility to ischemia during seizures with changes of membrane pump function, and energy metabolism appearing at moderate reductions of BP. Concomitant decrease of seizure activity delayed to some extent the development of massive energy failure and membrane depolarization.
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PMID:Effects of reduced cerebral blood flow upon EEG pattern, cerebral extracellular potassium, and energy metabolism in the rat cortex during bicuculline-induced seizures. 49 17


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