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

We studied the effects of parenteral magnesium sulfate (MgSO4) administration on electroencephalographic seizures induced by hyperbaric oxygen (HBO) in awake rats. Sixteen rats chronically implanted with electrocorticographic electrodes were preinjected i.p. with either vehicle or 3 mmol/kg MgSO4 (the latter resulted in serum levels of 3.5-5.5 mmol/liter) and then exposed to 6 ATA O2 in a pressure chamber. The time to develop an electric ichtal seizure was measured and compared to that in the same animal receiving the alternate treatment 3 days later. Mean and median times after the magnesium treatment were almost double those of vehicle administration. A central anticonvulsive action of magnesium, which should be investigated over the entire HBO range, is indicated.
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PMID:Magnesium sulfate suppresses electroencephalographic manifestations of CNS oxygen toxicity. 231 59

Both generalized and focal seizures dissociate brain polyribosomes and severely inhibit brain protein synthesis. This effect is found in freely convulsing animals and in animals that have been paralyzed and oxygen-ventilated in order to prevent hypoxemia, cerebral hypoxia, and other systemic changes associated with convulsions. Recent autoradiographic studies have shown that generalized seizures can result in striking focal inhibition of brain protein synthesis in adult rats and newborn marmoset monkeys. Local cerebral glucose metabolism and local cerebral blood flow were also studied in newborn marmosets by autoradiography. Although flow and metabolism are closely matched in control marmosets, seizures result in large local increases in 2-deoxyglucose metabolism, with lesser or no increases in local cerebral blood flow resulting in a relative mismatch. Those regions in which protein synthesis was most severely inhibited were those in which the relative mismatch between blood flow and metabolism was most marked. The molecular mechanisms regulating protein biosynthesis are not known. Translational regulation during seizures appears to be exerted, in large part, at the initiation step. A likely mechanism is the inhibition of ternary complex formation, one of the early steps in the initiation process, by increases in the intracellular ratio of [GDP]:[GTP]. This ratio is related to the cells' energy charge. Reduced levels of ATP during seizures can lead to an increased ratio of [GDP]:[GTP] via of the enzyme nucleoside diphosphate kinase (E.C. 2.7.4.6) and to inhibition of protein synthesis initiation. Regulation of protein biosynthesis during seizures is likely to be complex and exerted at many sites; some of these possibilities are discussed.
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PMID:Brain protein metabolism in epilepsy. 242 96

Hyperacute intracerebral hematomas were successfully created in five cats by injecting a prepared blood sample in which the oxygen (O2) saturation ranged from 0-80%. T1- and T2-weighted spin-echo sequences and T2-weighted gradient refocused scans were obtained 2.5-10 hr after injection on a 1.5-T imaging system. Detailed histology or electron microscopy was performed on each brain to confirm the presence of intact red blood cells in a retracted clot matrix. Areas of the hematoma were hypointense relative to brain in all five cats on the gradient refocused scans. The hematoma was isointense relative to brain on the T1- and T2-weighted spin-echo scans in all cats except one, which suffered a seizure/respiratory arrest and died during the scanning procedure. Portions of the hematoma in this animal had a hypointense T2-weighted signal and a hyperintense T1-weighted signal, which corresponded to the predicted MR properties of intracellular methemoglobin. We hypothesize that acute (less than 10 hr old) hematomas that contain virtually 100% intracellular deoxyhemoglobin may not appear hypointense relative to brain on T2-weighted scan sequences at 1.5 T unless surrounding tissue hypoxia and/or anoxia promote additional changes, one of which may be the formation of intracellular methemoglobin.
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PMID:MR imaging of hyperacute intracranial hemorrhage in the cat. 250 98

Administration of recombinant erythropoietin (r-HuEPO) is an effective treatment for the anaemia of chronic renal failure, but in some patients it has been accompanied by elevated blood pressure. This study focuses on seven patients with end-stage renal failure, managed on haemodialysis, who developed probable hypertensive encephalopathy with seizures during treatment with r-HuEPO. All made a full recovery. The events were not clearly related to the haemoglobin concentrations achieved, and four patients have subsequently been restarted on r-HuEPO therapy at a reduced dose, resulting in a slower increase in haemoglobin with no recurrence of episodes of severe hypertension. Close attention needs to be paid to blood pressure in patients commencing erythropoietin therapy, and it seems prudent to aim for a gradual increase in haemoglobin concentration to allow the circulation to adapt to changes in oxygen delivery and haematocrit.
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PMID:Seizures in haemodialysis patients treated with recombinant human erythropoietin. 251 27

Hyper- but not normoglycemic cats exposed to 8 min of anoxia show neurologic signs (fasciculations, myoclonic jerks, seizures) that develop after a symptom-free period. We examined brain mitochondrial function and metabolite concentrations at 0, 1, 3, and 5 h following exposure to anoxia, to correlate biochemical findings with the presence ("symptomatic") or absence ("presymptomatic") of neurologic signs. Brain mitochondria isolated postexposure only from symptomatic cats showed markedly decreased (-50%), state 3 (ADP-stimulated), and uncoupler-stimulated respiration rates with NAD- and FAD-linked substrates. Respiratory control and ADP/oxygen (ADP/O) ratios remained unchanged, indicating, respectively, that coupling and efficiency of ATP synthesis were preserved. Thus, inhibition of electron transport chain function, not phosphorylative activity, may be rate limiting for respiration. During anoxia, hyperglycemic cats showed higher brain lactate levels (26 versus 20 mumol/g), but similar ATP and phosphocreatine concentrations, compared with normoglycemic cats. After exposure, in all animals lactate and phosphocreatine were restored to control levels, whereas ATP remained at 85%. Cats that became symptomatic demonstrated four- to sixfold increases in lactate and 50% reductions in phosphocreatine. At 3 and 5 h postexposure, symptomatic animals showed significant reductions in ATP concentrations. We conclude that although initially asymptomatic, hyperglycemic cats exposed to anoxia undergo a neurologic deterioration over several hours following reoxygenation that is correlated with inhibition of mitochondrial respiration, increases in tissue lactate, and decreases in energy state.
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PMID:Delayed neurologic deterioration following anoxia: brain mitochondrial and metabolic correlates. 256 72

High pressures affect the physiology of the central nervous system. For a better understanding of this effect, we examined the hippocampal activity in the rat under high pressures (91 bars) of helium-oxygen. Effects of high pressure on hippocampal physiology are: an abnormally sustained 5-8 Hz pattern of spontaneous activity, followed, in some cases, by seizures; a marked decrease in the responses of CA1 pyramidal cells to stimulation of their commissural afferents; and a 50% decrease in the afterdischarge threshold. On the basis of the relatively well understood hippocampal physiology in normobaric conditions, our observations suggest that high pressures induce hypoexcitability of afferents and/or target cells.
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PMID:A study of spontaneous and evoked activity in the rat hippocampus under helium-oxygen high pressure. 257 37

A new thin-film, multisensor probe was used to determine tissue oxygen tension, tissue temperature, and electrical activity at two depths below the brain surface in chloral hydrate- or nitrous oxide/halothane-anesthetized rats. Brain tissue temperature at both depths was found to be lower than core temperature by 1-2 degrees C. Electrical activation, spreading depression, and pentylenetetrazol seizures all resulted in transient increases of brain tissue temperature of a few tenths degree centigrade. Vasodilation, induced by hypercapnia or hypoxia, caused a warming of brain tissue. Near-maximum oxygen metabolism, reached upon reoxygenation after severe hypoxia, was accompanied by tissue temperature rises of greater than 1 degree C. It was concluded that brain tissue temperature in the anesthetized rat is lower than core temperature due to extensive radiative and conductive heat loss to the environment through the head. Transient increases in tissue temperature during activation are caused by vasodilation and increased metabolism.
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PMID:Stimulus-activated changes in brain tissue temperature in the anesthetized rat. 260 41

Three children were observed to have extensive liver injury following protracted seizures. Two recovered with supportive care and one died from central nervous system complications. When first measured, the levels of aminotransferases were minimally elevated, but they increased to 250 to 8,000 times normal within 12 to 24 h after the seizure episode. They fell to near normal over the next 8 to 11 days in the survivors, and to one sixth of the peak level by 4 days in the patients who died. A percutaneous liver biopsy from one child demonstrated centrolobular necrosis consistent with severe ischemic injury. Common causes for liver dysfunction, including viral hepatitis, drug hepatitis, and Reye syndrome, were excluded on clinical, serologic, and histologic grounds. We reason that hepatic injury resulted from ischemia. We speculate that prior treatment with anticonvulsants, which are capable of inducing mixed-function oxidases in the liver, aggravated the ischemia-reperfusion injury by increasing the production of reactive oxygen intermediates and reducing cytoprotective mechanisms. Prevention of such injury should be directed toward control of seizures and early respiratory support when seizures occur, not restructuring medication regimens.
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PMID:Acute liver injury after protracted seizures in children. 262 20

We evaluated the newborn lamb's cerebral cellular activity and metabolism following acute insulin-induced hypoglycemia. Eleven animals received an insulin bolus followed by a continuous infusion to maintain a plasma glucose of 1 mM/l for 2 h, while 8 other animals received an equivalent dose of saline. Following the induction of hypoglycemia, the animals became quiet and transient seizures were observed in 3 animals. A significant increase in heart rate (p less than 0.01), and a decrease in arterial PaCO2 at 30 min (p less than 0.01), and pH at 2 h (p = 0.02), following hypoglycemia, were observed in the experimental group. Hypoglycemia did not significantly alter the cerebral blood flow, mitochondrial respiratory control ratio or the state-3 activity. The cerebral arteriovenous difference (CAVD) for oxygen did not change, while the glucose CAVD was significantly reduced from 0.47 +/- 0.21 to 0.24 +/- 0.16 mM/l (p less than 0.05) at the end of the hypoglycemia period, suggesting consumption of alternate substrates of energy by the brain. Insulin-induced hypoglycemia was associated with a significant increase in arterial lactate (p less than 0.01), and a significant correlation (p less than 0.01) between arterial and CAVD for lactate and beta-hydroxybutyrate (BOB) was observed. Cerebral consumption of alternate substrates of energy was inconsistent, and only observed for lactate in 5 and for BOB in 3 experimental animals following hypoglycemia. These data indicate that the newborn lamb's cerebral cellular activity is not affected by the degree of hypoglycemia achieved in these studies.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral metabolic response and mitochondrial activity following insulin-induced hypoglycemia in newborn lambs. 265 16

In spite of significant advances made in the technology to image the intracranial contents and to measure the metabolic activity of discrete brain sites, the factor(s) responsible for the death of ischemic neurons remains unresolved. Several potential culprits have been tried: (1) "energy failure", or depletion of high-energy phosphates, occurs very quickly after ischemia, but energy metabolites recover even in tissues where functional return does not occur; (2) "tissue lactacidosis" enhances ischemic cell necrosis, but this factor is not the indispensable cause of neuronal necrosis because acidosis is minimal or nonexistent under conditions of hypoglycemia and seizures; (3) "impairment of the microcirculation" may be a contributing factor, but such microcirculatory impairment cannot be the initiating event as it is known that irreversible neuronal injury precedes the development of microcirculatory abnormalities; (4) the effects of "excitatory neurotransmitters", especially glutamate, may explain the "delayed neuronal death" or the protracted necrosis of neurons in the CA1 sector of the hippocampus; (5) ionic pump alterations: studies of experimental myocardial ischemia tend to support a contributory role of Ca2+ in the aggravation of cell necrosis; however, lack of an experimental model in which steady-state conditions can be maintained has left unresolved the potential participation of calcium ions in ischemic cell necrosis; (6) the same statement, concerning the lack of an experimental model, can be made about the role of free-radical species; oxygen free radicals and superoxides are abundant in the reperfusion stage of ischemic injury, but it is unclear how significant their contribution might be as initiators of ischemic necrosis; and (7) the "ischemic penumbra" is a zone or portion of brain tissue that is sufficiently hypoperfused as to be functionless, but where the cells are likely to recover once normal perfusion is reestablished. Further understanding of the "penumbra" may prove crucial in future studies of brain ischemia.
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PMID:Physiopathology of cerebral ischemia. 265 39


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