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

Sodium cyanide was infused intravenously in 11 lightly anaesthetised and spontaneously breathing M. mulatta. In most, the EEG, ECG, respiratory rate, blood pressure, cerebral venous sinus pressure, end-tidal pCO2 and body temperature were recorded. Blood gases, pH, lactate and pyruvate were estimated in arterial and venous sinus blood samples. There was an initial hyperventilation with tetany in all animals. A rapid rate of cyanide infusion led to apnoea. An isoelectric or near-isoelectric EEG was usually precipitated by bradycardia often with additional hypotension. Neither epileptic seizures nor their EEG concomitants were seen at any stage. Three animals died of early heart failure. Brain damage was seen in 4 animals surviving up to 98 hr. White matter was involved in all. Ischaemic neuronal alterations, restricted to the striatum of one animal, were attributed to major circulatory complications. It was concluded that under these experimental conditions there is no evidence for hypoxic neuronal damage of purely histotoxic type.
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PMID:Cyanide intoxication in Macaca mulatta. Physiological and neuropathological aspects. 1 59

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

A 39-year-old woman ingested 59 mL of Super Nail Nail Off (American International Industries, Hollywood, CA) (containing 99% acetonitrile) in a suicide attempt. Following a latent period of approximately 12 hours, the patient developed cyanide poisoning with severe metabolic acidosis, seizures, and shallow respirations. She responded to the administration of sodium nitrite and sodium thiosulfate, although the administration of nitrite produced bradycardia and hypotension. She developed several relapses over the course of her hospitalization and each time responded to sodium thiosulfate administration. The patient developed hypernatremia from the sodium load given to her; hemodialysis and charcoal hemoperfusion were initiated to correct the hypernatremia and to attempt to remove cyanide, thiocyanate, and acetonitrile. On the fifth hospital day, the patient was fully recovered and was discharged.
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PMID:Severe cyanide poisoning from the ingestion of an acetonitrile-containing cosmetic. 201

A patient presented without symptoms 30 minutes after ingesting acetonitrile, also known as methylacyanide. He had prompt gastric lavage and activated charcoal administration. Hours later, the onset of clinical toxicity was heralded by mental status abnormalities and vomiting prior to a generalized seizure. Following administration of sodium thiosulfate, the patient made an uneventful recovery. A blood cyanide level drawn shortly after presentation, but reported after the patient had been discharged, documented significant exposure. During hospitalization, cyanide toxicity was inferred from the history of ingestion of acetonitrile, plus a significant absence of venous blood hemoglobin desaturation. Because even small amounts can be harmful and toxicity is delayed, all acetonitrile ingestions should be presumed dangerous. Patients should be observed and repeatedly evaluated for at least 24 hours. In the absence of cyanide level determinations, lethargy, vomiting, seizures, and the lack of normal venous blood hemoglobin desaturation are clues to cyanide toxicity.
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PMID:Cyanide toxicity from acetonitrile-containing false nail remover. 201 1

A 23-year-old man survived a suicide attempt in which he had swallowed 1500 mg potassium cyanide. Initially there were cerebral seizure and marked lactacidosis. Six hours after hospital admission the cyanide blood level was 6 mg/l. The poisoning having at first not been recognized he at that time merely received supportive treatment to counteract the acidosis, as well as assisted ventilation with hyperventilation and hyperoxigenation. Afterwards, sodium thiosulphate was given additionally for 24 h at a dosage of 1 g per hour. The clinical course underlines the great importance of supportive measures in the treatment of cyanide poisoning. In the individual case the balance between risk and value of an intrinsically toxic antidote administration must be critically assessed.
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PMID:[Cyanide poisoning: treatment with hyperoxygenation and sodium thiosulphate]. 237 41

The effects of acute exposure to acrylonitrile (ACN), 10, 20, or 40 mg/kg by gavage, on the ability of metrazol (MTZ) to induce seizures was studied in adult, male Sprague-Dawley rats. The frequency of seizure occurrence and the frequency of a lethal seizure was greater when the high ACN dosage was given in combination with metrazol. This dosage of ACN was not lethal when given alone. Examination of brain tissue in these animals revealed no difference in cyanide levels when MTZ was combined with ACN. However, brain cytochrome c was significantly lower in animals given ACN+MTZ and brain cholinesterase was significantly higher. These results suggest that the enhanced lethality occurring in animals exposed to the combination of ACN+MTZ is not due to cyanide, a metabolic product of ACN, but rather to a potentiation of other effects of ACN perhaps involving cholinergic neurotransmission.
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PMID:Effect of acute acrylonitrile exposure on metrazol induced seizures in the rat. 298 62

A 34 year old, 73 kg man ingested a 1 gram potassium cyanide pellet in a suicide attempt. Within one hour, coma, apnea, metabolic acidosis, and seizures developed. Sodium nitrite and sodium thiosulfate were administered. Dramatic improvement in the clinical condition occurred by the completion of antidote infusion. Methemoglobin level was 2% immediately after nitrite administration. Serial whole blood cyanide levels were obtained, documenting a highest measured level of 15.68 mcg/mL. Estimations of toxicokinetic parameters including terminal half-life (t 1/2) (19 hours), clearance (163 mL/minute), and volume of distribution (Vd) (0.41 L/kg) were calculated. The nitrite/thiosulfate combination was clinically efficacious in this case and resulted in complete recovery.
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PMID:Nitrite/thiosulfate treated acute cyanide poisoning: estimated kinetics after antidote. 358 82

Two cases of unresectable intra-cranial arterio-venous malformation (AVM) are reported, treated by direct intra-operative embolization. A 50% mixture of Butyl-2-Cyano-Acrylate and Mono-Iodo-Stearate of Ethyle (Duroliopaque) was used after catheterization of some of the feeding cortical arteries. No intra-operative angiography was performed. The first patient, admitted after subarachnoid hemorrhage and presenting with a mild transient right hemiparesia and aphasia, showed evidence of a left temporal AVM with a left middle cerebral artery supply and contribution from the left cerebral posterior artery. The AVM was embolized with 3 cc of the mixture. A mild aphasia occurred after surgery and completely recovered after two weeks. Roughly half of the AVM was occluded on the postoperative angiograms. The second patient suffering from a long history of seizures had a huge right frontal AVM, with a right middle cerebral artery and right anterior cerebral artery supply, and contribution from a right lenticulostriate artery, the left anterior cerebral artery and the right posterior cerebral artery. The AVM was embolized with 7 cc of the mixture. A complete palsy of the left upper limb occurred after surgery, with complete recovery after two weeks. On the post-operative angiograms, more than three fourth of the AVM was occluded.
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PMID:[Intra operative embolization of unresectable cerebral arterio-venous malformations. Occlusion attempt by means of a delayed polymerization mixture. Report of two cases (author's transl)]. 626 18

The purpose of this study was to investigate the possible importance of adenosine in cerebrocortical vasodilatation accompanying brain activation (epileptic seizures and direct electrical stimulation) and hypoxia (arterial hypoxia and cyanide poisoning of the brain cortex). In chloralose-anesthetized cats a circumscribed area of the brain cortex was treated with adenosine deaminase (Type III; Sigma), which potently deaminates adenosine to the nonvasoactive inosine. Cerebrocortical vascular volume and fluorescence of reduced nicotinamide adenine dinucleotide were measured in vivo by surface fluororeflectometry. The responses of small pial and intracortical vessels to brain activation and hypoxia were studied in brain cortices superfused with artificial (mock) CSF and 5 U/ml adenosine deaminase. It was found that superficially applied adenosine deaminase readily diffuses onto the brain cortex. Prolonged pretreatment of the brain cortices with 0.025 U/ml adenosine deaminase eliminated almost completely the vasodilative effect of 10(-7) mol/ml adenosine. The inhibitory effect of the enzyme on adenosine-induced cortical vasodilatation was specific, because 5 U/ml adenosine deaminase did not attenuate the vasodilative potency of 10(-8) mol/ml 2-chloroadenosine. Adenosine deaminase (5 U/ml) pretreatment of the brain cortices did not diminish the cerebrocortical vascular volume, which increased with arterial hypoxia, topical cyanide poisoning, and direct electrical stimulation. However, it slightly decreased the vasodilative effect of epileptic seizures. On the basis of these results, it seems very unlikely that adenosine is a critical factor in the control of cerebrovascular tone during arterial hypoxia and brain activation.
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PMID:Effect of topical adenosine deaminase treatment on the functional hyperemic and hypoxic responses of cerebrocortical microcirculation. 647 59

Excitatory amino acid (EAA)-like and excitotoxic properties of the secondary metabolite of cyanide, 2-iminothiazolidine-4-carboxylic acid, (2-ICA) were evaluated because of its possible role in cyanide-induced neurotoxicity. Intracerebroventricular (i.c.v.) injections of 2-ICA in mice produced wild-running seizures that were qualitatively and quantitatively similar to seizures observed with glutamate. 2-ICA, kainate and proline seizures were prevented by both the NMDA and non-NMDA antagonists, MK-801 and CNQX, respectively. In contrast, NMDA-induced seizures were prevented by MK-801, but not CNQX. When infused i.c.v. in rats over a seven day period, 2-ICA produced extensive and selective loss of CA-1 pyramidal neurons of the hippocampus. In hippocampal slices preloaded with D-[3H]aspartate, 2-ICA superfusion did not evoke release nor significantly augment potassium stimulated release of the radiolabeled transmitter. These findings indicate 2-ICA has excitotoxic properties and its role in cyanide neurotoxicity deserves further study.
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PMID:Seizures and selective CA-1 hippocampal lesions induced by an excitotoxic cyanide metabolite, 2-iminothiazolidine-4-carboxylic acid. 760 31


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