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

CNS oxygen (O2) toxicity is complex, and the etiology of its most severe manifestation, O2 convulsions, is yet to be determined. A role for depletion of the brain GABA pool has been proposed, although recent data have implicated production of reactive O2 species, e.g. H2O2, in this process. We hypothesized that the production of H2O2 and NH3 produced by monoamine oxidase (MAO) would lead to depletion of GABA and production of nitric oxide (NO.) respectively, and thereby enhance CNS O2 toxicity. In this study, rats treated with an MAO inhibitor (pargyline) or a nitric oxide synthase inhibitor (LNNA) were protected against O2-induced convulsions. Selected cerebral amino acids including arginine were measured in control and O2 treated rats (6 ATA, 20 min) with or without drug pretreatment. After O2 exposure, the cerebral pools of glutamate, aspartate, and GABA decreased significantly while glutamine content increased relative to control (P < 0.05). After treatment with either enzyme inhibitor, glutamine, glutamate and aspartate concentrations were maintained near control levels. Remarkably, GABA depletion by O2 was not prevented despite protection from seizures by both pargyline and LNNA. The NO. precursor, arginine, was increased significantly in the brain by toxic O2 exposure, but both pargyline and LNNA inhibited this effect. Simultaneous norepinephrine measurements indicated that its storage substantially decreased during hyperoxia (P < 0.05), but this effect too was blocked by either pargyline or LNNA. These data indicate that protection against O2 by these inhibitors is not related to preservation of the GABA pool. More importantly, O2 dependent norepinephrine metabolism and NO. synthesis appear to be interactive during CNS O2 toxicity.
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PMID:Cerebral amino acid, norepinephrine and nitric oxide metabolism in CNS oxygen toxicity. 846 4

Recent important technical developments in the field of surgery for congenital heart disease have included the Ross pulmonary autograft replacement of the aortic valve, video-assisted thoracoscopic surgery, and the double-switch and switch-Rastelli procedure for congenitally corrected transposition. Although the growth potential of the pulmonary autograft has been confirmed, an important incidence of late aortic regurgitation has been noted. Expanding indications for video-assisted thoracoscopic surgery have been described, including division of the vascular ring. Late hemodynamic assessment after the double-switch or switch-Rastelli procedure will encourage increased application of this repair. Both clinical and laboratory studies have focused on neurologic and developmental outcome after cardiac surgery. Perioperative seizures in young infants have been found to be associated with impaired psychomotor development at 1 year of age. In the area of perioperative management, the antifibrinolytic agents tranexamic acid, epsilon-aminocaproic acid, and aprotinin have been found to be useful in reducing postoperative hemorrhage. Nitric oxide is useful in reducing postoperative pulmonary hypertension. Late clinical follow-up studies of patients with single ventricle have revealed an important incidence of pulmonary arteriovenous malformations after a bidirectional Glenn shunt and atrial flutter after a Fontan procedure. Late assessment of patients after the arterial switch procedure for transposition has revealed preservation of ventricular function and an extremely low incidence of late arrhythmias.
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PMID:Advances in surgical care of infants and children with congenital heart disease. 854 59

The effect of N(G)-nitro-L-arginine (NNA), an inhibitor of nitric oxide (NO) synthase on L-cysteine- induced neurotoxicity was investigated in mice. When L-cysteine (1, 2.5, 5 or 10 micromol/brain) was injected intracerebroventricular (i.c.v.) in mice, severe tonic seizures were observed for over 20 s in the treated mice in a dose-dependent manner. However, the tonic seizures induced by L-Cysteine were prevented by pretreatment with N(G)-nitro-L-arginine. Although L-cysteine (0.5, 1, 2.5, 5, 10 micromol/brain, i.c.v.) also caused a wild running (WR), NNA did not affect behavior. These results suggest that an overproduction of NO may be involve in the development of tonic seizures but not WR induced by L-cysteine.
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PMID:Preventive effect of N(G)-nitro-L-arginine against L-cysteine-induced seizures in mice. 859 72

A review has been conducted of ongoing clinical and laboratory studies of hypothermic circulatory arrest (HCA) and low-flow cardiopulmonary bypass (LFB) at a children's hospital in Boston. A prospective randomized clinical trial of HCA versus LFB has shown a higher incidence of perioperative seizures in patients randomized to HCA. At 1 year of age, neurologic and developmental studies have shown an association between seizures and worse outcome. Longer duration of HCA is associated with a worse score on the Bayley scale assessment of gross and fine motor function in particular, as well as a higher probability of neurologic abnormality. A retrospective review of development after HCA for Senning procedure has shown a correlation between more alkaline pH (alpha-stat strategy) during cooling before HCA and lower developmental score relative to a more acidotic strategy (pH stat). The institutional change to alpha-stat was accompanied by several cases of choreoathetosis after HCA. Currently, patients are being randomized between alpha-stat and pH-stat. Laboratory studies have used a piglet model with assessment of cerebral blood flow and metabolism as well as high-energy phosphates and cerebral pH determined by magnetic resonance spectroscopy. High-energy phosphates are maintained by a flow rate of 50 mL/kg/min but are undetectable after approximately 35 minutes of HCS. A pH-stat is associated with more rapid recovery of high-energy phosphates after HCA than alpha-stat. Recent studies have examined the role of nitric oxide in the causation of brain injury after HCA as well as the potential utility of cerebroplegia in increasing the safe duration of circulatory arrest.
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PMID:Hypothermia, circulatory arrest, and the pediatric brain. 863 89

The freely diffusible gaseous compound nitric oxide (NO) has recently been discovered to be an important cellular messenger in many organ systems throughout the body. The importance of NO as an intermediary in cell communication in the brain is highlighted by the fact that the excitatory amino acid glutamate, the most abundant central neurotransmitter, is an initiator of the reaction that forms NO. In this article, background information about the discovery of NO, its biochemistry, and a brief summary of some of its peripheral and central actions are given to provide a complete picture of this remarkable novel second messenger. We also discuss how an improved understanding of NO pathway may lead to the identification of novel medications for the treatment of a number of neuropsychiatric conditions, including memory deficits, pain, drug addiction, seizures, bipolar disorder, psychosis, eating disorders, and the treatment of the sequelae of various brain injuries.
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PMID:The nitric oxide pathway: potential implications for treatment of neuropsychiatric disorders. 868 10

Tuberous sclerosis (Bourneville-Pringle's disease) is a rare, largely autosomal dominant neurocutaneous disease. The disease can also result from spontaneous mutations. Although strongly variable in its manifestation, manifestations are typically characterized by involvement of the central nervous system (early childhood seizures), skin (facial angiofibromas) and kidneys (angiomyolipomas). In the case described, a 67-year-old female patient complained exclusively of obstructed nasal breathing that was found to be due to angiofibromas in the nasal vestibule. Oral fibromas were asymptomatic, while fibromas in the facial region resulted in some cosmetic changes. This exclusively ENT manifestation of a patient with tuberous sclerosis has not been described previously. As treatment, the fibromas were ablated by an Nd:YAG laser under local anesthesia. Other therapeutic options are described. Additional clarification of all organ manifestations is advisable in view of numerous possible pathologies present. Genetic consultation is also recommended, particularly for patients with an oligosymptomatic variant.
HNO 1996 May
PMID:[Manifestation of tuberous sclerosis in the ENT area]. 870 32

Several hours after an hypoxic-ischemic injury to the developing brain, hyperemia, then seizures, edema, and infarction can develop. The roles of nitric oxide (NO) synthesis and excitotoxin accumulation during these later phases of injury are not known. The time course of extracellular levels of amino acids within the parasagittal parietal cortex were measured with microdialysis during and for 3 d after 30 min of cerebral ischemia in nine chronically instrumented near-term fetal sheep (119-133 d). Cortical electroencephalographic (EEG) activity and extracellular space (ECS) were quantified simultaneously with real-time spectral analysis and cortical impedance measurements, respectively. Amino acid concentrations were measured using HPLC. During ischemia, citrulline (by-product of NO synthesis), glutamate, glycine, and gamma-aminobutyric acid (GABA) concentrations rose to 147 +/- 18%, 180 +/- 20%, 290 +/- 50% and 4800 +/- 1300% of baseline respectively (p < 0.05). The excitotoxic index ([glutamate] x [glycine]/[GABA]) decreased to 15 +/- 8%. Upon reperfusion, the cytotoxic edema and amino acid accumulation largely resolved within 1 h, and the EEG was depressed. Citrulline began to rise again by 4 h (p < 0.05), reaching a maximum (273 +/- 21%) at 32 +/- 2 h. Seizure activity developed at 7 +/- 2 h, and impedance plus the excitotoxic index then rose progressively and peaked at 32 +/- 2 h (480 +/- 170%). At 72 h, there was severe neuronal loss and laminar necrosis within the parasagittal cortex. These data suggest that, several hours after a severe hypoxicischemic injury, NO synthesis increased, then seizures arose, and edema developed concomitantly with the accumulation of excitotoxins.
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PMID:Accumulation of cytotoxins during the development of seizures and edema after hypoxic-ischemic injury in late gestation fetal sheep. 872 30

The effects of N-nitro-L-arginine (NA), a nitric oxide (NO) synthase inhibitor, were investigated on the focal ictal-like seizure induced by 3-aminopyridine in rat neocortex in vivo. Intraperitoneal and intracerebroventricular (i.c.v.) injections of NA markedly facilitated propagation of epileptiform events. In addition, NA injected i.c.v. increased the number/hour of individual ictal periods while decreasing their duration. In the presence of NA and an N-methyl-D-aspartate (NMDA) receptor antagonist D(-)2-amino-5-phosphonovaleric acid (APV) the number of ictal periods increased while their duration synergically decreased. APV by itself did not change the number of ictal episodes but decreased their duration. Our results suggest that NO inhibits the induction and propagation of seizure activity. We cannot distinguish the proportion of neuronal and/or vascular NO involved in our experimental conditions, but these effects seem to be independent of the NMDA receptors.
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PMID:Nitric oxide synthase inhibitor facilitates focal seizures induced by aminopyridine in rat. 873 4

The pharmacological effects of a purified neurotoxin from king cobra (Ophiophagus hannah) venom were studied. Using the hot-plate test, it is shown that this neurotoxin increased latency time dose-dependently when administered i.p. Similar analgesic action was observed when it was administered p.o. or i.c.v. The rota-rod performance, which is a good index for neurological deficits including sedation, muscle relaxant and impairment of motor activity and coordination, was not significantly affected in the dose range of 16-32 ng/g that caused analgesia. The toxin did not increase the convulsion threshold in the dose range of 8-64 ng/g in the maximal electroshock seizure tests. These results demonstrated that this neurotoxin produced analgesia in the dose range of 16-32 ng/g (i.p.) without causing any neurological or muscular deficits. It is further shown that such analgesic action was blocked by naloxone and L-NG-nitro-arginine methyl ester, suggesting the possible involvement of the opioid and nitric oxide systems, respectively. In view of the source of this neurotoxin (O. hannah) and its potent analgesic action, it is proposed that this toxin be named hannalgesin.
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PMID:A novel analgesic toxin (hannalgesin) from the venom of king cobra (Ophiophagus hannah). 874 82

7-Nitro indazole (25-100 mg/kg i.p.), an inhibitor of neuronal nitric oxide (NO) synthase, attenuated the severity of pilocarpine (300 mg/kg i.p.)-induced seizures in mice. This indicates that the decreased neuroexcitability of the central nervous system (CNS) following administration of 7-nitro indazole may be due to inhibition of neuronal NO synthase, implying that NO acts as an excitatory and proconvulsant factor in the CNS.
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PMID:7-Nitro indazole, an inhibitor of neuronal nitric oxide synthase, attenuates pilocarpine-induced seizures. 874 39


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