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

To define the time course of the metabolic acidosis that follows a single grand-mal seizure, we obtained serial blood samples from eight consecutive patients. Immediately after a seizure, the mean (+/- S.E.M.) venous lactate concentration was 12.7 +/- 1.0 meq per liter, the mean carbon dioxide content 17.1 +/- 1.1 mmol per liter, and the mean arterial pH 7.14 +/- 0.06. Sixty minutes later their values were 6.6 +/- 0.7 meq per liter (P less than 0.005), 23.6 +/- 1.1 mmol per liter (P less than 0.005) and 7.38 +/- 0.04 (P less than 0.005) respectively. The spontaneous resolution of the acidosis was due, in large part, to the metabolism of lactate and to the concomitant removal of hydrogen ion. There was no change in the serum potassium concentration, despite the development of a severe systemic acidemia and the subsequent return to normal of the pH. We suggest that the patient with seizures may serve as a unique model of lactic acidosis.
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PMID:Natural history of lactic acidosis after grand-mal seizures. A model for the study of an anion-gap acidosis not associated with hyperkalemia. 1 2

We propose than an alarm mechanism is operative in animals, designed to regulate neuromuscular irritability by regulating [Ca2+]. Epinephrine or corticotropin (ACTH), injected intramuscularly into animals, causes a hypercitricemia, resulting in decreased [Ca2+]. This increases muscular excitability to facilitate escape. To avoid over reaction, [Cl-] is shifted into the plasma without a concomitant shift of Na+, thus generating an acidosis and an increase in ionization of Ca. Plasma pH, pCO2, total CO2, and [K+] decrease, and [Mg2+] increases. The acidosis, decrease in K+, and increase in [Mg2+] serve to counteract the effect of the decrease in [Ca2+], to protect against tetany. In the rabbit the hypercitricemia observed upon ACTH administration is accompained by a severe hypocalcemia and drop in blood pressure, resluting in tetanic convulsions. This seems to indicate calcitonin release, independent of the hypercitricemia. Thyroidectomized rabbits show only mild hypocalcemia when given ACTH, but develop a severe acidosis and typical grand mal epileptiform seizures. Administration of ACTH and then calcitonin to the goat, an animal resistant to the effects of ACTH alone, simulates the effect observed in the rabbit with respect to changes in blood components and blood pressure. Changes in the blood in the goat and rabbit resemble those in humans before an epileptic seizure. alpha-Melanotropin, containing a portion of the ACTH sequence, reacts in a manner similar to ACTH but more rapidly.
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PMID:Clinical biochemistry of epilepsy. II. Observations on two types of epileptiform convulsions induced in rabbits with corticotropin. 22 Nov 37

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

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

The author discusses some mechanisms, conditioning the double role of carbon dioxide in the genesis of epileptical activity, first as a provocative factor, when carbon dioxide is a background against which the epileptical seizure appears and then as arresting the sequalae during the administration of CO2 during a seizure. It was demonstrated that the different action of CO2 was due to different phases in the changed functional state of the brain. The study was accomplished on 80 rabbits of the chenchille breed. The evalution of phases in changes of the functional state of the brain was performed with the aid of the encephalographic method.
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PMID:[Carbon dioxide gas provoking and stopping an epileptic seizure]. 69 5

The diffusion permeability to water of the rat blood-brain-barrier (BBB) was studied. Preliminary data obtained with the Oldendorf tissue uptake method (Oldendorf 1970) in seizure experiments suggested that the transfer from blood to brain of labelled water is diffusion-limited. More definite evidence of such a limitation was obtained using the single injection technique of Crone (1963). 14-C-labelled sucrose was used as intravascular reference substance and tritium-labelled water as test substance. The non-exchanging (transmitted) fraction, I-E equals T, of labelled water during a single passage increased from 0.26 to 0.67 when the arterial carbon dioxide tension was changed from 15 to 85 mm Hg, a change increasing the cerebral blood flow about sixfold. This finding suggests that water does not pass the blood-brain barrier as freely as lipophilic gases.
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PMID:The diffusion permeability to water of the rat blood-brain barrier. 114 83

EEG, end-tidal CO2, neck muscle EMG, eye movements, and ECG were recorded in 17 children undergoing enflurane anesthesia combined with N2O and O2. All subjects were classified in the lowest risk group and had normal pre-anesthetic EEG recordings. Eleven subjects were breathing spontaneously and six were under controlled ventilation. Thirteen subjects were hyperventilated for short periods. As previously reported for adults, various signs of increased central nervous excitability appeared. At the enflurane concentration of 4% all three cases with PaCO2 below 32 mmHg showed generalized high voltage epileptic activity of grand mal type followed by several minutes of postictal slowing. One of these subjects also showed motor manifestations of the electrographic seizure activity. At 3% enflurane, three out of eight subjects showed electrographic seizure activity of poly-spike-suppression type. One of these children also had motor manifestations during this type of seizure activity at a PaCO2 of 31 mmHg. The results indicate that electrographic seizure activity is common among children with moderate hypocapnia at enflurane concentrations of 3% or more.
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PMID:Electroencephalographic activity in children under enflurane anesthesia. 121 Oct 75

Zinc is a potent inducer of the 72 kD heat shock protein (HSP72). In brain, pathological conditions such as ischemia and seizures increase extracellular zinc. The present study examines the effect of zinc on HSP72 expression in rat primary cortical astrocyte culture. Astrocytes were grown to confluence and exposed to zinc chloride in CO2-equilibrated Earle's buffered salt solution. Expression of HSP72 was examined using immunocytochemistry. HSP72 was induced with zinc concentrations of 5 to 100 microM after 4 h exposures, or 200 to 300 microM after 15 min exposures. At the lower concentrations expression occurred in small clusters of contiguous cells. At concentrations high enough to cause cell death, HSP72-positive astrocytes formed a continuous margin around patches of dead cells. These patterns of HSP72 expression are similar to the patterns seen after cerebral ischemia in vivo. Exposure to zinc at 100 microM for 4 h or 400 microM for 15 min caused greater than 90% cell death. Increases in extracellular zinc may contribute to HSP72 induction and astrocyte death under ischemia and other pathological conditions in brain.
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PMID:Zinc toxicity and induction of the 72 kD heat shock protein in primary astrocyte culture. 133 69

pH regulatory mechanisms in primary cultures of astrocytes from the cerebral cortex of neonatal audiogenic-seizure-susceptible DBA/2J (DBA) and genetically controlled C57BL/6J (C57) mice were studied with [14C]dimethyloxazolidine-2-4-dione (DMO) and [3H]-methyl-D-glucose (MDG). Effects of changing the concentration of Na+, K+, HCO3- or Cl- in medium, and/or of different transport blockers and metabolite inhibitor on intracellular pH (pHi) of cultured astrocytes were also studied. In nominal HCO3(-)-free HEPES-buffered Hanks' balanced salt solution (HEPES HBSS), when the pH of medium (pHo) was maintained at 7.4, the steady-state pHi of cultured astrocytes from DBA mice was 6.98 +/- 0.03, and that from C57 mice was 7.01 +/- 0.03. When the cells were incubated in HBSS containing 25 mM HCO3- and equilibrated with 5% CO2 (HCO3- HBSS, pHo = 7.4), pHi of both DBA and C57 astrocytes was approximately 0.1-0.15 pH units higher than that in HEPES HBSS. Reducing the pH or the Na+ concentration in media (pHo, [Na+]o) of either HEPES HBSS or HCO3- HBSS, pHi of both DBA and C57 astrocytes decreased markedly (0.25-0.45 pH units lower than the controls). The decrease in pHi was greater in HEPES HBSS than in HCO3- HBSS. Reducing the Cl- concentration ([Cl-]o) in either HEPES or HCO3- HBSS, pHi of astrocytes increased by 0.05-0.1 pH units. Increasing the K+ concentration ([K+]o) of or adding Ba2+ to the media increased the pHi of both DBA and C57 astrocytes accordingly. SITS, an anion transport inhibitor, decreased the pHi of both DBA and C57 astrocytes in HCO3- HBSS but not in HEPES HBSS. It enhanced the response of pHi to reduction in pHo. Amiloride, a Na(+)-H+ exchange inhibitor, decreased the pHi of both DBA and C57 astrocytes more in HEPES HBSS than in HCO3- HBSS. It enhanced the response of pHi to reduction in pHo and [Na+]o. Ouabain, an Na+,K(+)-ATPase inhibitor, decreased the pHi of cultured astrocytes in HEPES HBSS, but not in HCO3- HBSS. It also enhanced the response of pHi to changing pHo and [Na+]o in HEPES HBSS. Acetazolamide, a carbonic anhydrase inhibitor, decreased the pHi of astrocytes in both HEPES and HCO3- HBSS. Both bumetanide, an Na+,K+/Cl- cotransport blocker, and KCN, a metabolic inhibitor, produced no significant effect on the steady-state pHi or the response of pHi to changing ionic concentration in media in both DBA and C57 astrocytes.
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PMID:Studies on pH regulatory mechanisms in cultured astrocytes of DBA and C57 mice. 139 16

The topography of CO2 vasoreactivity during hyperventilation in 8 patients with complex partial seizure (CPS) was visualized using the regional cerebral blood flow (rCBF) as measured by H(2)15O-PET (positron emission tomography) and compared with that of 10 normal volunteers. In the normal volunteers, the vascular response to CO2 (VrCO2 = delta CBF%/delta PaCO2) in the temporal lobe was 2.46 +/- 0.56 (%/mmHg). In the patients with CPS, VrCO2 in the temporal lobe of the affected side was 2.08 +/- 0.40 (%/mmHg), while VrCO2 on the contralateral side was 2.30 +/- 0.46 (%/mmHg). There was a significant difference in VrCO2 between the affected side of the temporal lobes and the temporal lobes of the normal volunteers. Furthermore, there was a tendency for VrCO2 to be lower in the affected than in the contralateral side of the temporal lobe in patients with CPS. As CO2 is the main regulator of CBF, this impaired vasoreactivity may reflect the brain dysfunction in the seizure focus and adjacent areas.
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PMID:Temporal lobe CO2 vasoreactivity in patients with complex partial seizures. 143 64


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