Experimental Carbon Monoxide Leucoencephalopathy in the Cat

Horita, N.; Ando, Susumu; Seino, Shoichi; Hagiwara, I.

doi:10.1097/00005072-198003000-00008

Cited by 20 publications

(8 citation statements)

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“…These results suggest that early changes of membrane metabolism had already occurred around 2 weeks after CO inhalation, regardless of clinical behaviour. This is to be expected, as previous studies in animal models have documented histological changes to myelin sheaths within 1 week after CO inhalation 29. Some authors have mentioned the occurrence of inflammation in association with demyelination of the CNS in the acute phase among CO poisoned patients 8 9.…”

Section: Discussionsupporting

confidence: 56%

1H-magnetic resonance spectroscopy indicates damage to cerebral white matter in the subacute phase after CO poisoning

Beppu

Nishimoto

Fujiwara

et al. 2011

Journal of Neurology, Neurosurgery & Psychiatry

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Section: Discussionsupporting

confidence: 56%

1H-magnetic resonance spectroscopy indicates damage to cerebral white matter in the subacute phase after CO poisoning

Beppu

Nishimoto

Fujiwara

et al. 2011

Journal of Neurology, Neurosurgery & Psychiatry

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“…The cerebral white matter lies in a deep cerebral area; therefore, the decrease of systemic arterial blood flow in acute CO poisoning would easily diminish oxygen delivery and accelerate the hypoxic brain damage of the cerebral white matter. 15,16 Therefore, cerebral hypotension along with hypoxia in acute CO poisoning may produce a hypoxic-ischemic leukoencephalopathic damage to the region where the local blood flow decreases.…”

Section: Discussionmentioning

confidence: 99%

“…20 Therefore, CO can be accumulated easily, and the globus pallidus can be damaged seriously compared with other cerebral areas. Horita et al 16 reported that CO may have a direct toxic effect on myelin sheaths, causing acute demyelination to the nerve cells and increased cerebral white matter damage. The hypoxic-ischemic leukoencephalopathic damage may be enhanced extensively by the direct CO effect on the region.…”

Section: Discussionmentioning

confidence: 99%

An Autopsy Case of Acute Carbon Monoxide Poisoning After a Long-Term Vegetative State

Sato

Tanaka

Kasai

et al. 2012

American Journal of Forensic Medicine &Amp; Pathology

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A 23-year-old woman was rescued from an accidental fire in a state of cardiopulmonary arrest. Based on the diagnosis of carbon monoxide (CO) poisoning, she received hyperbaric oxygen therapy and survived in a vegetative state. After 1 and a half years, she died without recovering from the vegetative state. At autopsy, the brain was observed to be moderately softened with a severely atrophied appearance and ventricular enlargement. In addition, a characteristic damage of hypoxic-ischemic leukoencephalopathy was also observed clearly in both the bilateral globus pallidus and cerebral white matter, which are typical findings of past acute CO poisoning. A long-term vegetative state causes the brain to soften and liquefy because of reactive gliosis and autolytic change. The cause of death becomes difficult to diagnose only from the autopsy findings in general. This case is rare in that the past acute CO poisoning could be diagnosed from the remaining typical cerebral findings even after a long-term vegetative state.

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“…16 The pathogenesis of this is unclear, but studies suggest the damage is localized to the white matter of the brain, 17,18 and some studies support a demyelination process. 19…”

Section: Smoke Inhalationmentioning

confidence: 99%

Toxic Inhalational Exposures

Chen

Malli

Maslove

et al. 2012

J Intensive Care Med

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Respirable toxicants are a spectrum of irritant and nonirritant gases, vapors, fumes, and airborne particles that can be entrained into the body through the respiratory tract, resulting in exposures that cause pulmonary injury and/or systemic disease. Sources of respirable toxicants include structural fires, industrial accidents, domestic mishaps, and intentional releases of injurious agents on the battleground (warfare) or in civilian settings (acts of terrorism). Acute toxic inhalational exposures may result in respiratory failure, multisystem organ dysfunction, and death. Management of victims includes assessment and protection of the airway, monitoring and treatment of systemic toxicity, and delivery of exposure-specific and nonspecific therapies that improve outcomes. Treatments may include antidotes, hyperbaric oxygen, and other nonspecific life-supporting interventions.

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Experimental Carbon Monoxide Leucoencephalopathy in the Cat

Cited by 20 publications

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1H-magnetic resonance spectroscopy indicates damage to cerebral white matter in the subacute phase after CO poisoning

1H-magnetic resonance spectroscopy indicates damage to cerebral white matter in the subacute phase after CO poisoning

An Autopsy Case of Acute Carbon Monoxide Poisoning After a Long-Term Vegetative State

Toxic Inhalational Exposures

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