Delayed onset generalised dystonia after cyanide poisoning

Borgohain, Rupam; Singh, Ajay Kumar; Radhakrishna, H; Rao, V. Chalapathi; Mohandas, Sukhada

doi:10.1016/0303-8467(95)00029-j

Cited by 35 publications

(11 citation statements)

References 7 publications

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“…These data demonstrate that cyanide affects complex neural behaviors in zebrafish. Collectively, these data on cardiac, neuronal, and metabolic physiology and on survival parallel known human responses to cyanide, suggesting that the zebrafish is a useful in vivo model of cyanide intoxication (3–5).…”

Section: Resultsmentioning

confidence: 72%

Chemical and metabolomic screens identify novel biomarkers and antidotes for cyanide exposure

et al. 2013

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Exposure to cyanide causes a spectrum of cardiac, neurological, and metabolic dysfunctions that can be fatal. Improved cyanide antidotes are needed, but the ideal biological pathways to target are not known. To understand better the metabolic effects of cyanide and to discover novel cyanide antidotes, we developed a zebrafish model of cyanide exposure and scaled it for high-throughput chemical screening. In a screen of 3120 small molecules, we discovered 4 novel antidotes that block cyanide toxicity. The most potent antidote was riboflavin. Metabolomic profiling of cyanide-treated zebrafish revealed changes in bile acid and purine metabolism, most notably by an increase in inosine levels. Riboflavin normalizes many of the cyanide-induced neurological and metabolic perturbations in zebrafish. The metabolic effects of cyanide observed in zebrafish were conserved in a rabbit model of cyanide toxicity. Further, humans treated with nitroprusside, a drug that releases nitric oxide and cyanide ions, display increased circulating bile acids and inosine. In summary, riboflavin may be a novel treatment for cyanide toxicity and prophylactic measure during nitroprusside treatment, inosine may serve as a biomarker of cyanide exposure, and metabolites in the bile acid and purine metabolism pathways may shed light on the pathways critical to reversing cyanide toxicity.

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Section: Resultsmentioning

confidence: 72%

Chemical and metabolomic screens identify novel biomarkers and antidotes for cyanide exposure

et al. 2013

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“…The patient’s findings are not unique in terms of cyanide exposure, but to our knowledge, brain sequelae resulting from inhalation of cyanide produced by fire smoke have not been previously documented. The principal differences between the patterns of damage by cyanide and carbon monoxide seem to be the sparing of the hippocampi in cyanide intoxication29 and the early occurrence of haemorrhagic necrosis of the basal ganglia in cyanide poisoning.…”

Section: Discussionmentioning

confidence: 97%

Cyanide: an unreported cause of neurological complications following smoke inhalation

Baud

Boukobza²,

Borron³

2011

Case Reports

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“…Consequently, there is a dearth of literature describing the pattern of clinical and neurocognitive features in survivors. In most of the patients reported, neurological sequelae including parkinsonism, dystonia and dyskinesia have been commonly noted, reflective of the involvement of structures within the BG 3 5. The striatum has been noted to be particularly vulnerable to cyanide-mediated neurotoxicity attributable to high glucose and oxygen utilisation within these structures, as well as region-specific considerations such as a higher local distribution of cytochrome oxidase 4…”

Section: Discussionmentioning

confidence: 99%

Surviving acute cyanide poisoning: a longitudinal neuropsychological investigation with interval MRI

Mohan

Lee²,

Sachdev

2014

BMJ Case Reports

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SUMMARYWe report the case of a 22-year-old woman who presented with self-poisoning by cyanide ingestion. We have elected to pay particular attention to describing the neuropsychological sequelae of cyanide poisoning, and the evolution of these deficits over a 6-month period. Prominent deficits in episodic memory were noted from an early stage, which were consistent with the findings noted on structural neuroimaging. These deficits remained persistent, although improving in severity over the follow-up period. No focal neurological deficits or abnormal involuntary movements emerged, and the patient's overall functional status remained satisfactory. The patient's psychiatric presentation and background history are briefly discussed. BACKGROUND

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Delayed onset generalised dystonia after cyanide poisoning

Cited by 35 publications

References 7 publications

Chemical and metabolomic screens identify novel biomarkers and antidotes for cyanide exposure

Chemical and metabolomic screens identify novel biomarkers and antidotes for cyanide exposure

Cyanide: an unreported cause of neurological complications following smoke inhalation

Surviving acute cyanide poisoning: a longitudinal neuropsychological investigation with interval MRI

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