Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

Intravenous infusions of three levels of 2-deoxy-D-glucose (2DG) were made through chronically implanted jugular and portal cannulas in rats. Food and water intakes were unaffected by 100 mg/kg 2DG, enhanced by 200 and 400 mg/kg 2DG, and unrelated to the route of administration. Drug-induced drinking occurred as readily when food was present as in its absence. Infusions of 2DG also produced stupor and ataxia whose severity was proportional, as was feeding and drinking, to the dose administered. Drinking induced by 2DG is inconsistent with the glucoprivic theory of feeding, and it was proposed that the consummatory and aberrant behaviors elicited by 2DG may result from hypoglycemia-induced seizures in limbic structures of the brain.
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PMID:Drinking and feeding induced by jugular and portal infusions of 2-deoxy-D-glucose. 119 Mar 12

Fifteen patients were treated in a Phase I study of intracarotid carboplatin (200-400 mg/m2) in 5% dextrose and water infused over 15 to 30 minutes through a transfemoral catheter with a 0.2-micron inline filter. This study was done because intravenous carboplatin has less neurotoxicity than cisplatin and is active against brain tumors. Eleven men and four women ranging in age from 37 to 72 years (median, 59 years) were treated. The Eastern Cooperative Oncology Group performance status was 1 in 3, 2 in 4, and 3-4 in 8 patients. Eight patients had one to three previous chemotherapy regimens; previous radiotherapy had failed in 13 patients. The response of patients in the Phase I study follows: glioblastoma, 6 failed; not evaluated because of early death from pulmonary embolus, 1; recurrent Grade II and III glioma, 1 stable (minor response with neurologic improvement) and 2 failed; malignant oligodendroglioma, 1 failed; brain metastases from nonsmall cell lung cancer, 1 partial remission, 1 stable (minor response), and 1 failed; brain metastases from unknown primary, 1 stable (minor response with neurological improvement). Median survival was 9 weeks. Nausea was mild to moderate. One patient had granulocytopenia, and 2 had thrombocytopenia (mild). At 200 mg/m2 (2 patients), 1 had a focal seizure. At 300 mg/m2 (9 patients), 2 with abnormally small arteries had severe pain early in the treatment and posttreatment ipsilateral conjunctival edema, decreased vision, and cerebral edema (with partially reversible increased hemiparesis); 1 other had mild decrease in ipsilateral vision and 1 had transient aphasia on removal of the catheter (possibly the result of a vascular spasm).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phase I study of intracarotid administration of carboplatin. 131 64

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

We performed interictal 18F-2-fluoro-2-deoxy-D-glucose positron emission tomography (18FDG-PET) studies in 57 patients with complex partial epilepsy (CPE), not controlled by medical treatment and considered for surgical resection of their epileptic focus. A precise localization of the epileptic focus was obtained in 37 of these patients with a combination of subdural and depth electrodes. We visually inspected the metabolic images; we also measured glucose consumption in a number of brain regions and compared the values with those obtained in 17 normal controls. Eighty-two percent of the 57 patients had an area of glucose hypometabolism on the 18FDG-PET images. Six patients had a frontal epileptic focus, 3 of them had a frontal lobe hypometabolism. Twenty-six patients had a unilateral temporal lobe focus and all of them displayed a temporal lobe hypometabolism. The asymmetry was more pronounced in the lateral temporal cortex (-20%) than in the mesial part of the temporal lobe (-9.6%). In each cortical brain region on the side of the epileptic focus (except the sensorimotor cortex), glucose consumption rate was lower than in the contralateral region or than in controls. No differences could be found between patients with a seizure onset restricted to the hippocampus and patients with a seizure onset involving the hippocampus and the adjacent neocortex. Divergent metabolic patterns were obtained in 5 patients with bilateral temporal seizure foci. Combined with other non invasive techniques (EEG, neuroradiology), PET contributes increasingly to the selection of patients with CPE who could benefit from surgical treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional brain glucose metabolism in patients with complex partial seizures investigated by intracranial EEG. 139 38

This report is a retrospective review of the perioperative management of 56 children who underwent craniofacial surgical procedures. The use of a combination of 5% dextrose in normal saline or 5% dextrose in Ringer's lactate and normal saline resulted in postoperative sodium values in a normal range. In patients receiving a combination of 5% dextrose and electrolyte No. 48 and normal saline, the mean postoperative sodium level was 130 mEq/l with 9 of 18 patients below 130 mEq/l. Two patients in the series suffered clinical seizures on postoperative day 1 as a result of serum sodium levels of 122 and 121 mEq/l, respectively. We recommend that only solutions with a sodium content between 77 and 154 mEq/l be used routinely in the perioperative management of craniofacial patients.
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PMID:Fluid, blood, and blood product management in the craniofacial patient. 141 42

Classification, management and prevention of seizures in children are summarized for clinicians in Papua New Guinea. Seizures are classified as febrile with or without underlying brain pathology, and afebrile, including neonatal fits, infantile spasms, myoclonic jerks, akinetic seizures, tonic clonic fits, petit mal, benign focal, and psychomotor seizures. In all cases the first step is to secure the airway, then do a fingerstick and treat hypoglycemia, and finally stop the fit if it is prolonged with paraldehyde, diazepam, phenobarbitone or phenytoin. A cause for the seizure should be sought: physical exam, especially tympanic membranes and throat, blood slide for malaria, lumbar puncture for signs of meningitis, blood culture, serum calcium, and other chemistries. Some empirical treatments to use for negative findings include: dextrose, calcium gluconate, magnesium SO4, pyridoxine, quinine and Fansidar. Hyperthermia in a febrile child can be reversed with cool sponging. The author recommends prescribing phenobarbitone to prevent subsequent simple febrile seizures if the child has 3 or more, then slowly withdrawing the drug if the child is seizure free for a year. Drug therapy for the various other types of seizures available in Papua New Guinea include sodium valproate by special order, and phenobarbitone, phenytoin, carbamazepine, nitrazepam, ethosuximide, and prednisolone. A table is provided to help select the drug for each seizure type, e.g. ethosuximide for petit mal, prednisolone for infantile spasms, and carbamazepine for various types of focal and psychomotor seizures.
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PMID:Convulsions in children. 150 14

The case of a non diabetic 6-year-old boy affected by Down's syndrome, who developed hyperosmolar hyperglycemic non-ketotic coma following the infusion of hypertonic dextrose solution during general anesthesia for a surgical procedure for cryptorchidism is reported. Following surgery, the patient remained deeply comatose and generalized seizures occurred. Hyperosmolarity due to hyperglycemia and acidosis were reduced by administration of insulin at low rate, hypotonic saline and sodium-bicarbonate solutions. The patient's clinical conditions promptly improved following normalization of blood glucose levels. An oral glucose tolerance test performed three months later was normal. The authors emphasize the potential risk of hyperosmolar hyperglycemic non-ketotic coma also in non diabetic patients treated with hypertonic dextrose solutions, during surgery events.
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PMID:A case of hyperglycemic hyperosmolar non-ketotic coma during anesthesia: a possible cause of failed re-awakening. 168 69

An eleven year old boy was referred because of sudden loss of consciousness, muscular weakness, poor general health, severe hypoglycemia with seizures and hepatomegaly. Response to oral glucose and galactose increased blood lactic acid and glucose at different times. Fasting values of blood lactic was normal, but glucose was found at 33 mg/dl. Similar test made up two hours after feeding revealed hyperlactatemia (35-50 mg/dL) and hyperglycemia (129 mg/dL). Glucagon did not result in a rise of glucose at fasting or feeding. Hepatic glycogen content was found 15 gm/100 mg of tissue. The enzyme activities revealed a deficiency of the liver debranching enzyme while leukocytes had normal enzyme activity. Hepatic biopsy showed liver fibrosis. The present case had the clinical characteristics of severe form of glycogen storage disease. A low carbohydrate and high protein diet was indicated in order to increase the gluconeogenic precursors. Although debranching enzyme deficiency is almost always benign a high carbohydrate diet induced a more severe expression of the disease.
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PMID:Diet therapy in severe clinical expression of debrancher deficiency. 184 14


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