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.