Pathophysiology of brain injuries in acute carbon monoxide poisoning: a novel hypothesis.

Abstract

Acute carbon monoxide (CO) poisoning causes the neurologic symptoms and brain

lesions during both acute and delayed phase. We propose that catecholamine crises

in globus pallidus and deep white matter are the key pathophysiological factors

causing acute and delayed brain injuries respectively. Increased sympathetic

activities due to acute CO poisoning is followed by increases of catecholamine

levels in synapses or nerve terminals in organs including the brain, especially,

limbic system. A dopamine excess in the synaptic cleft of the mesolimbic system,

including globus pallidus, may cause the destruction of synapses and nuclei in

the globus pallidus. Consequently, the striatal lesion is affected in the acute

phase of CO intoxication. Moreover, an increase of catecholamine levels in

synapses of deep white matter can persist after the acute stage of CO

intoxication. A dopamine excess could lead to oxidative metabolism of dopamine,

serotonergic axonal injury, or secondary myelin damage.