Carbon monoxide poisoning: neurologic aspects

K K Jain MD (Dr. Jain is a consultant in neurology and has no relevant financial relationships to disclose.)
Originally released June 6, 1997; last updated April 5, 2016; expires April 5, 2019

This article includes discussion of carbon monoxide poisoning: neurologic aspects and CO poisoning. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Overview

Carbon monoxide can produce several nonspecific symptoms and can mimic several diseases. Most of the signs and symptoms are due to hypoxia, which affects mainly the brain. The most significant neurologic and psychiatric manifestations of carbon monoxide poisoning are seen as subacute or late sequelae, often following a period of complete recovery from an acute episode. There is a possible interaction between nitric oxide, a ubiquitous molecule in the human body, and carbon monoxide. Carbon monoxide exposure initiates processes including oxidative stress that triggers activation of N-methyl-D-aspartate neuronal nitric oxide synthase, and these events are necessary for the progression of carbon monoxide–mediated neuropathology. The most important diagnostic test for carbon monoxide poisoning is the direct spectroscopic measurement of carboxyhemoglobin level in the blood. Brain imaging findings frequently correlate with clinical manifestations. Hyperbaric oxygen plays an important role in the management of carbon monoxide poisoning.

Key points

 

• Carbon monoxide poisoning can produce several nonspecific symptoms and can mimic several diseases.

 

• Most of the effects are due to hypoxia.

 

• Neurologic sequelae are significant and may be delayed in onset.

 

• Hyperbaric oxygen plays an important role in management of carbon monoxide poisoning.

Historical note and terminology

Human beings have been exposed to carbon monoxide ever since they first made fire inside sheltered caves. In 300 BC, Aristotle stated that, "coal fumes lead to heavy head and death." Obviously, this was a reference to carbon monoxide poisoning. In 1857 Claude Bernard showed that carbon monoxide produces hypoxia by reversible combination with hemoglobin (Bernard 1857), and in 1865 Klebs described clinical and pathologic findings in rats exposed to carbon monoxide (Klebs 1865). The classic bilateral lesions of the globus pallidus and diffuse subcortical demyelination were described and correlated with psychic akinesia by Pineas (Pineas 1924) and with parkinsonism by Grinker (Grinker 1925).

In 1895 Haldane showed that rats survived carbon monoxide poisoning when placed in oxygen at a pressure of 2 ATA (Haldane 1895). The effectiveness of hyperbaric oxygen in experimental carbon monoxide poisoning in dogs and guinea pigs was demonstrated in 1942 (End and Long 1942). In 1960 hyperbaric oxygen was first used successfully in treating human cases (Smith and Sharp 1960).

Carbon monoxide is produced in small amounts endogenously during the catabolism of heme, resulting in the coproduction of biliverdin and iron. Carbon monoxide is considered to be a signaling molecule because it shares some chemical and biological properties with nitric oxide. Carbon monoxide is a mediator in the autonomic nervous system. Inhalation of subtoxic concentrations of carbon monoxide may have a cytoprotective effect, which is being investigated currently. Actions of carbon monoxide in the nervous system, thus, range from the physiological to the pathological.

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