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

Nitrogen based fertilizers represent an important element in the farm economy, but their storage and use are associated with major risks to livestock and humans. An accidental ammonia exposure occurred at a Midwest county fair in Illinois. Six deaths occurred in show livestock; a Holstein cow, 3 Holstein heifers, a goat, and a lamb. Mortality was associated with consumption of water inadvertently contaminated with a liquid fertilizer containing ammonium nitrate and urea commonly used for irrigating agricultural crop fields and brought onto the fairgrounds by a tanker truck previously used to transport liquid fertilizer. The show animals that drank the contaminated water immediately became ill, developed seizures and died within a few hours. Postmortem findings were unremarkable to nonspecific. Rumen contents from the lamb, Holstein cow, and Holstein heifer had ammonia-nitrogen concentrations of l,000, 1,150 and 1,440 ppm, respectively. Water from the heifer's water bucket, the cow's water bucket, and the tanker truck, had nitrate levels of 6,336, 6,116, and 6,248 ppm, respectively. The ammonia toxicosis was attributed to the contaminated water brought onto the fairgrounds by the tankertruck that previously transported liquid ammonium nitrateand urea. This accident underscores the importance of meticulous observation of safety guidelines and measured working practices in agriculture and animal husbandry.
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PMID:Accidental ammonia exposure to county fair show livestock due to contaminated drinking water. 1236 Nov 12

Glutamine synthetase (GS) is a key enzyme in the regulation of glutamate neurotransmission in the central nervous system. It is responsible for converting glutamate to glutamine, consuming one ATP and NH3 in the process. Glutamate is neurotoxic when it accumulates in extracellular fluids. We investigated the effects of GS in both a spinal cord injury (SCI) model and normal rats. 0.1-ml of low (2- micro M) and high (55- micro M) concentrations of GS were applied, intrathecally, to the spinal cord of rats under pentobarbital anesthesia. Immediately after an intrathecal injection into the L1-L3 space, the rats developed convulsive movements. These movements initially consisted of myoclonic twitches of the paravertebral muscles close to the injection site, repeated tonic and clonic contractions and extensions of the hind limbs (hind limb seizures) that spread to the fore limbs, and finally rotational axial movements of the body. An EMG of the paravertebral muscles, fore and hind limbs, showed the extent of the muscle activities. GS (2- micro M) caused spinal seizures in the rats after the SCI, and GS (6- micro M) produced seizures in the uninjured anesthetized rats. Denatured GS (70 degrees C, 1 hour) also produced spinal seizures, although higher concentrations were required. We suggest that GS may be directly blocking the release of GABA, or the receptors, in the spinal cord.
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PMID:Glutamine synthetase induced spinal seizures in rats. 1261 85

Increased brain ammonia concentrations are a hallmark feature of several neurological disorders including congenital urea cycle disorders, Reye's syndrome and hepatic encephalopathy (HE) associated with liver failure. Over the last decade, increasing evidence suggests that hyperammonemia leads to alterations in the glutamatergic neurotransmitter system. Studies utilizing in vivo and in vitro models of hyperammonemia reveal significant changes in brain glutamate levels, glutamate uptake and glutamate receptor function. Extracellular brain glutamate levels are consistently increased in rat models of acute liver failure. Furthermore, glutamate transport studies in both cultured neurons and astrocytes demonstrate a significant suppression in the high affinity uptake of glutamate following exposure to ammonia. Reductions in NMDA and non-NMDA glutamate receptor sites in animal models of acute liver failure suggest a compensatory decrease in receptor levels in the wake of rising extracellular levels of glutamate. Ammonia exposure also has significant effects on metabotropic glutamate receptor activation with implications, although less clear, that may relate to the brain edema and seizures associated with clinical hyperammonemic pathologies. Therapeutic measures aimed at these targets could result in effective measures for the prevention of CNS consequences in hyperammonemic syndromes.
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PMID:Cell-selective effects of ammonia on glutamate transporter and receptor function in the mammalian brain. 1274

1. Increases in the concentrations of lactic acid and pyruvic acid in rat brain during acute dieldrin poisoning are associated with hyperactivity of the brain, whereas an increase in the cerebral alanine concentration occurs before the convulsions. Throughout the dieldrin-induced seizure pattern, fluctuations in the concentration of brain ammonia are out of phase with the actual convulsions. 2. Increases in the concentrations of alanine, ammonia and lactic acid in rat brain accompany picrotoxin-induced seizures; there is no increase in the concentration of glutamine. These changes are consistent with the inhibition of glutamine synthesis. 3. In addition to previously reported changes in the concentrations of intermediary metabolites of the brain after the administration of Telodrin (Hathway & Mallinson, 1964), increases have now been found in the alanine and lactic acid concentrations. Since increases in the alanine and glutamine concentrations occur before the convulsions, liberation of ammonia also occurs before the onset of convulsions and throughout their course. Ammonia-binding mechanisms later become inadequate and free ammonia accumulates in cerebral tissues. 4. An increase in the pyruvic acid concentration of the brain after the intraperitoneal injection of either dieldrin or Telodrin is endogenous in origin. 5. The parenteral administration of a small dose of glutamine increases the cerebral concentrations of alanine and glutamic acid. Some animals previously treated with glutamine resisted Telodrin convulsions. 6. Mechanisms for the disposal of ammonia liberated in brain are discussed.
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PMID:EFFECTS OF DIELDRIN, PICROTOXIN AND TELODRIN ON THE METABOLISM OF AMMONIA IN BRAIN. 1434 58

Nitrogen dissolves in the blood during dives, but comes out of solution if divers return to normal pressure too rapidly. Nitrogen bubbles cause a range of effects from skin rashes to seizures, coma and death. It is believed that these bubbles form from bubble precursors (gas nuclei). Recently we have shown that a single bout of exercise 20 h, but not 48 h, before a simulated dive prevents bubble formation and protects rats from severe decompression sickness (DCS) and death. Furthermore, we demonstrated that administration of N(omega)-nitro-l-arginine methyl ester, a non-selective inhibitor of NO synthase (NOS), turns a dive from safe to unsafe in sedentary but not exercised rats. Therefore based upon previous data an attractive hypothesis is that it may be possible to use either exercise or NO-releasing agents before a dive to inhibit bubble formation and thus protect against DCS. Consequently, the aims of the present study were to determine whether protection against bubble formation in 'diving' rats was provided by (1) chronic and acute administration of a NO-releasing agent and (2) exercise less than 20 h prior to the dive. NO given for 5 days and then 20 h prior to a dive to 700 kPa lasting 45 min breathing air significantly reduced bubble formation and prevented death. The same effect was seen if NO was given only 30 min before the dive. Exercise 20 h before a dive suppressed bubble formation and prevented death, with no effect at any other time (48, 10, 5 and 0.5 h prior to the dive). Pre-dive activities have not been considered to influence the growth of bubbles and thus the risk of serious DCS. The present novel findings of a protective effect against bubble formation and death by appropriately timed exercise and an NO-releasing agent may form the basis of a new approach to preventing serious decompression sickness.
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PMID:Exercise and nitric oxide prevent bubble formation: a novel approach to the prevention of decompression sickness? 1472 7

The opioid peptides were thought to be involved in specific types of seizures. Nociceptin/Orphanin FQ (NC) is the endogenous ligand of the nociceptin opioid peptide (NOP) receptor and may play a role in epilepsy. However, accumulated evidences indicated that NC had both anti- and pro-convulsive effects, and the direct effect of NC in modulating epilepsy in the hippocampus still remained unclear. In this study, we investigated the effect of NC on penicillin-induced seizures (PIS) in rats. Seizure model was produced by intra-hippocampus injection of penicillin in anesthetized rats. The electroencephalography (EEG) was then observed and estimated by power spectrum analysis. Pretreatment of NC (intracerebroventricular, i.c.v.) depressed PIS in a dose-dependent manner at doses of 0.055, 0.55 and 5.5 nmol in 2 microl saline, respectively. [Nphe1]Nociceptin(1-13)NH2, a selective NOP receptor antagonist reversed the effect of NC against PIS, and this antagonist was inactive to PIS itself. These results indicated that NC had a receptor-specific preventive effect against PIS.
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PMID:Inhibition of nociceptin/orphanin FQ on penicillin-induced seizures in rats. 1531 6

We evaluated the serum levels of lipids, lipoproteins, apolipoproteins, along with a number of minerals and trace elements such as Ca, Mg, Cu and Zn in a group of children after 6 months of valproic acid monotherapy. Thirty patients with seizures, mean age, 9.8+/-2.6 years and 79 healthy children (controls), mean age, 10.9+/-3.2 years, formed the two styd groups. The patient group was treated with valproic acid (27.9+/-14.8 mg/kg/24 hr). Patients underwent clinical and laboratory evaluations including liver function tests, NH3, lipid, mineral and selected trace element levels before and after six months on valproic acid treatment, whereas controls only one evaluation. Liver function data and NH3 levels were found to be elevated in the group of patients, whereas albumin level was reduced. Triglycerides, total cholesterol, HDL-C, apolipoprotein (ApoA)-1, Apo B and Ca concentrations were found relative to control values, LDL-C, VLDL-C, Mg, Cu, Zn, were measured significantly altered (P<0.0001) compared to controls. The ratios ApoA-1/ApoB, HDL-C/ApoA-1, LDL-C/Apo B, which were closely related to the size of LDL particles, where correlated with Zn/Cu (P<0.001). Serum lipid profile, especially LDL size, indirectly evaluated for the first time and metal levels were found to be significantly changed, after six months on valproic acid monotherapy, suggesting a possible risk of developing coronary heart disease. Since valproic acid is a long-term treatment, it could be recommended that the incorporation of measurements of lipids, lipoproteins, apolipoproteins and trace elements in the "follow up" laboratory testing could be a preventive measure.
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PMID:Lipids, lipoproteins, apolipoproteins, selected trace elements and minerals in the serum of children on valproic acid monotherapy. 1670 Aug 24

Citrullinemia is an inborn error of the urea cycle caused by deficient argininosuccinate synthetase, which leads to accumulation of L-citrulline and ammonia in tissues and body fluids. The main symptoms include convulsions, tremor, seizures, coma, and brain edema. The pathophysiology of the neurological signs of citrullinemia remains unclear. In this context, we investigated the in vitro effects of L-citrulline and ammonia in cerebral cortex from 30-day-old rats on oxidative stress parameters, namely thiobarbituric acid-reactive substances (TBA-RS), chemiluminescence, mitochondrial membrane protein thiol content, intracellular content of hydrogen peroxide, total radical-trapping antioxidant potential (TRAP), total antioxidant reactivity (TAR) as well as on the activities of the antioxidant enzymes (catalase, superoxide dismutase, and glutathione peroxidase). L-Citrulline significantly diminished TRAP (26%) and TAR (37%), while ammonia decreased TAR (30%). Ammonia increased SOD activity (65%) and L-citrulline did not affect the activities of any antioxidant enzymes. We also observed that L-citrulline and ammonia did not alter lipid peroxidation parameters, levels of hydrogen peroxide, and mitochondrial membrane protein thiol content. Taken together, these results may indicate that L-citrulline and ammonia decreased the antioxidant capacity of the brain, which may reflect a possible involvement of oxidative stress in the neuropathology of citrullinemia.
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PMID:Citrulline and ammonia accumulating in citrullinemia reduces antioxidant capacity of rat brain in vitro. 1677 71

Valproate-induced hyperammonemic encephalopathy is an unusual but serious complication that may occur in people with normal liver-associated enzyme levels, despite normal therapeutic doses and serum levels of valproate. Here, we describe an adolescent girl who had absence seizure and complained about progressive dizziness and general malaise several days after restarting valproate. Then, she presented vomiting and decreased consciousness three weeks after valproate use. Notably, her serum ammonia level was five times the upper limit of normal (184 micrommol/L), with normal liver-associated enzyme and supra-therapeutic valproate level. EEG showed continuous generalized slowing. The tandem mass analysis revealed carnitine deficiency. Consciousness improved after emergent hemodialysis. Ammonia level and EEG also returned to normal. Possible mechanisms, risk factors and the treatments of valproate-induced hyperammonemic encephalopathy are described. Physicians should consider this possibility when consciousness disturbance occurs in patients treated with valproate.
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PMID:Valproate-induced hyperammonemic encephalopathy treated by hemodialysis. 1879 59

Elevated concentrations of ammonia in the brain as a result of hyperammonemia leads to cerebral dysfunction involving a spectrum of neuropsychiatric and neurological symptoms (impaired memory, shortened attention span, sleep-wake inversions, brain edema, intracranial hypertension, seizures, ataxia and coma). Many studies have demonstrated ammonia as a major player involved in the neuropathophysiology associated with liver failure and inherited urea cycle enzyme disorders. Ammonia in solution is composed of a gas (NH(3)) and an ionic (NH(4) (+)) component which are both capable of crossing plasma membranes through diffusion, channels and transport mechanisms and as a result have a direct effect on pH. Furthermore, NH(4) (+) has similar properties as K(+) and, therefore, competes with K(+) on K(+) transporters and channels resulting in a direct effect on membrane potential. Ammonia is also a product as well as a substrate for many different biochemical reactions and consequently, an increase in brain ammonia accompanies disturbances in cerebral metabolism. These direct effects of elevated ammonia concentrations on the brain will lead to a cascade of secondary effects and encephalopathy.
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PMID:Identifying the direct effects of ammonia on the brain. 1910 24


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