Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Different causes of dizziness or vertigo can only be recognized by thorough anamnestic explorations. Following a classification in vestibular and nonvestibular causes for vertigo, a further differentiation is possible by defining different characteristic qualities of the symptoms involved. In addition to the classical vestibular forms of vertigo seen, dizziness currently results from drug overdosages, hypertension, polyneuropathy and--less commonly, but equally important--brief epileptic seizures. Psychosomatic and neurotic symptoms may also lead to unsteady gait, dizziness or vertigo, all of which are distinguished only with difficulty by the patient.
HNO 1978 May
PMID:[Diagnostic problems in dizziness or vertigo (author's transl)]. 35 Aug 16

A hypothesis is presented to explain the influence of alcohol on glutamate generated excitotoxicity. Chronic alcohol exposure is reported to increase glutamate-N-methyl-D-aspartate (NMDA) receptors and calcium ion channel activity, resulting in the neurotoxicity and seizure activity associated with alcohol withdrawal in certain persons. Recent information indicates that nitric oxide is responsible for the neurotoxicity associated with excessive glutamate stimulation of NMDA receptors. Thus, it is hypothesized that nitric oxide is involved in producing the neurotoxicity and cell disturbances associated with chronic alcohol exposure.
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PMID:Alcohol, nitric oxide, and neurotoxicity: is there a connection?--a review. 132 Aug 8

The effects of tacrine (5 mg/kg i.p.), a potent acetylcholinesterase inhibitor, were studied in rats pretreated (24 h beforehand) with a single dose (12 mEq/kg i.p.) of LiCl. Tacrine and LiCl were ineffective when given individually. Tacrine elicited seizures and brain damage in 90% of the rats treated. The intracerebroventricular microinfusion of N omega-nitro-L-arginine methyl ester (300 micrograms given 24 h after LiCl administration) significantly reduced the seizures and brain damage produced by tacrine (given 15 min later). These experiments suggest that the seizures and brain damage elicited by tacrine may be due, in part, to increased nitric oxide production in the brain.
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PMID:Tacrine-induced seizures and brain damage in LiCl-treated rats can be prevented by N omega-nitro-L-arginine methyl ester. 132 16

Although reactive O2 species appear to participate in central nervous system (CNS) O2 toxicity, the exact roles of different reactive O2 species are undetermined. To study the contribution of extracellular superoxide anion (O2-) to CNS O2 toxicity we constructed transgenic mice overexpressing human extracellular superoxide dismutase (ECSOD; superoxide:superoxide oxidoreductase, EC 1.15.1.1) in the brain. Remarkably, when exposed to 6 atm (1 atm = 101.3 kPA) of hyperbaric oxygen for 25 min, transgenic mice demonstrated higher mortality (83%) than nontransgenic litter-mates (33%; P < 0.017). Pretreatment with diethyldithiocarbamate, which inhibits both ECSOD and Cu/Zn superoxide dismutase (Cu/Zn SOD) activity, increased resistance to CNS O2 toxicity, in terms of both survival (100% in transgenics and 93% in nontransgenics) and resistance to seizures (4-fold increase in seizure latency in both transgenic and nontransgenic mice; P < 0.05). Thus, O2- apparently protects against CNS O2 toxicity. We hypothesized that O2- decreased toxicity by inactivating nitric oxide (NO.). To test this, we inhibited NO. synthase (EC 1.14.23) with N omega-nitro-L-arginine to determine whether NO. contributes to enhanced CNS O2 toxicity in transgenic mice. N omega-nitro-L-arginine protected both transgenic and nontransgenic mice against CNS O2 toxicity (100% survival and a 4-fold delay in time to first seizure; P < 0.05), as well as abolishing the difference in sensitivity to CNS O2 toxicity between transgenic and nontransgenic mice. These results implicate NO. as an important mediator in CNS O2 toxicity and suggest that ECSOD increases CNS O2 toxicity by inhibiting O2(-)-mediated inactivation of NO.
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PMID:Extracellular superoxide dismutase, nitric oxide, and central nervous system O2 toxicity. 132 5

In response to NMDA receptor activation, hippocampal, striatal and cerebellar neurons synthesize nitric oxide (NO), which in turn elevates cGMP levels via guanylate cyclase. NO is increasingly being considered as a transsynaptic retrograde messenger, involved in neuronal plasticity. The effect of an inhibitor of NO synthase, L-NG-nitroarginine (NOArg), was studied on amygdala kindling and on kindled seizures in rats. NOArg increased kindling rate, particularly in its initial period, but did not modify seizure severity in previously kindled rats, although we have no definitive explanation for this effect. However, an enhanced post-synaptic excitability could be attributed to the blockade of the negative feed-back exerted by NO on the NMDA receptor.
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PMID:A nitric oxide (NO) synthase inhibitor accelerates amygdala kindling. 138 71

Low doses of quinolinic acid (QUIN) administered intracerebroventricularly (ICV) to rats produced either no damage or mild to moderate damage in the pyramidal cell layer of the hippocampus and resulted in mild, limbic seizures in the majority of animals treated. The same dose of QUIN following ICV pretreatment with the nitric oxide synthase inhibitor N-nitro-L-arginine (NARG), produced extensive hippocampal lesions with complete loss of the pyramidal layer in 50% of the animals, and moderate damage with total neuronal loss in areas CA1 and CA3 in the remainder of the group. Animals treated with both NARG and QUIN also exhibited a greater incidence of severe convulsive behavior (9/11) and 3 deaths. Pretreatment with the nitric oxide-generating drug molsidomine attenuated the enhanced toxicity observed with combined NARG-QUIN treatment, resulting primarily in no detectable hippocampal damages and mild seizures resembling those produced by QUIN alone. Administration of NARG alone produced neither seizure activity nor histological evidence of neurotoxicity. We conclude that inhibition of nitric oxide production with NARG potentiates the neurotoxicity of quinolinic acid in the rat hippocampus.
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PMID:Potentiation of quinolinate-induced hippocampal lesions by inhibition of NO synthesis. 149 87

Sodium azide is a chemical of rapidly growing commercial importance with a high acute toxicity and an unknown mechanism of action. Although it has some chemical properties and biological effects in common with cyanide, its lethality does not appear to be due to inhibition of cytochrome oxidase. Unlike cyanide it is a potent vasodilator and inhibitor of platelet aggregation presumably by virtue of its conversion to nitric oxide in vivo and in isolated preparations of blood vessels and thrombocytes. It is not clear whether the high toxicity of azide is due to nitric oxide or to the parent anion. Of a number of possible azide antagonists tested in intact mice only phenobarbital in both anesthetic and subanesthetic doses afforded statistically significant protection against death. Diazepam, phenytoin, and an anesthetic dose of a ketamine/xylazine combination had no effect. Major motor seizures are sometimes seen in human azide poisoning, and these are a regular feature of azide poisoning in laboratory rodents. Solutions of nitric oxide given systemically to mice produced no signs of toxicity, but doses 1,000-fold lower placed in the cerebroventricular system of rats produced brief but violent tonic convulsive episodes. A dose of 0.61 mmol/kg azide as given systemically regularly produced convulsions whereas a dose of 6 mumol/kg given icv produced seizures in rats. The icv convulsive dose of azide was 50-fold larger than the icv dose of nitric oxide. These results suggest that azide lethality is due to enhanced excitatory transmission in the central nervous system perhaps after its conversion to nitric oxide.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute neurotoxicity of sodium azide and nitric oxide. 191 70

The role of nitric oxide (NO) in the genesis of motor and electrocortical seizures elicited by administration of excitatory amino acid agonists into the deep prepiriform cortex (DPC) has been evaluated. Motor and electrocortical seizures occurred in rats receiving unilateral microinjections into the DPC of either N-methyl-D-aspartate (NMDA, 5 and 10 nmol) or kainate (KA, 100 pmol). The selective NMDA receptor antagonist 2-amino-7-phosphonoheptanoate (APH), when microinjected into DPC, prevented the development of seizures induced by both NMDA and KA injected in the same site. In addition, methylene blue (20 nmol, which prevents activation of soluble guanylate cyclase) or NG-monomethyl-L-arginine (NMMA, 40 nmol; a specific inhibitor of nitric oxide synthesis), when microinjected into DPC 15 min prior to either NMDA or KA, significantly protected against seizures elicited by both excitatory amino acid agonists. These data confirm the role of excitatory amino acid transmission in the genesis of seizures elicited from the deep prepiriform cortex. They further suggest that activation of excitatory amino acid receptors within the DPC leads to the release of a substance which shares properties with EDRF/NO and contributes to the genesis of seizure activity in this area.
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PMID:Role of nitric oxide in the genesis of excitatory amino acid-induced seizures from the deep prepiriform cortex. 195 95

There are many drugs marketed for the purpose of altering vascular blood flow in various regions, especially of the central nervous system and in peripheral arterial insufficiency. More than 50 different methods are described for the treatment of sudden deafness. Considerations of the therapy of sudden deafness are influenced by the fact that the cause of the disease is unknown. The dysfunction of the hair-cells of the organ of CORTI is thought to be caused by a deficit of oxygen due to disorders of micro-circulation in the inner ear. The infusion of vaso-active drugs in the early state of disease can lead to a remarkable improvement of hearing whereas the prospect of improvement without treatment remains uncertain. Nevertheless it may be difficult to distinguish the beneficial effects of vasodilator agents from spontaneous improvement. Naftidrofuryl oxalate (dusodril) has been in use for many years and proved its therapeutic value in many studies. It is regarded as non-toxic and is used extensively in Europe. Side effects are only reported rarely, and include decrease of cerebral blood flow, abdominal distension, diarrhoea, oesophageal ulceration, epileptic seizures, aphasia, disturbances of consciousness, hypotension, hypertensive crisis, vertigo and dizziness, depression of cardiac conduction, thrombophlebitis, and allergy. This case report of allergic reaction in a young female patient demonstrates that the intravenous application of this drug may lead to severe complications.
HNO 1987 May
PMID:[Allergic reaction in therapy with naftidrofuryl (Dusodril). A case report]. 361 Jun 82

Electrical stimulation of the human olfactory mucosa was performed by means of an electrode, which was attached to a rhinoscope. Stimulations of the nasal mucosa did not evoke the sensation of smell, but suppressed smell sensations of presented odorants. When electrical stimulation followed the exposure to an odorant within a certain interval, the stimulus recalled the faded sensation of the preceding odorant. Electrical stimulation without prior natural stimulation produced unpleasant sensations in three patients with a history of temporal lobe seizures and olfactory auras, but not in patients with primary generalized or focal epilepsy.
HNO 1985 Jul
PMID:[Electric stimulation of the human olfactory nerve--an approach to short-term memory?]. 392 40


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