Neurological sequelae after acute carbone monoxide poisoning: from physiology to clinical presentation

Abstract

Neuropsychiatric sequelae of carbon monoxide (CO) poisoning occur in up to 50% of all patients presenting with toxic CO levels. Neurological abnormalities include persistent (PNS) and delayed neurological sequelae (DNS) that occur after an asymptomatic period. Multiple hypotheses explain the mechanisms by which CO toxicity leads to cerebral injury including prolonged hypoxemia and dysfunction of intracellular mitochondrial cytochrome oxydase. Neurological examination shows impairments in memory and concentration as well as parkinsonism. Urinary and fecal incontinences represent common problems in severely CO-poisoned patients. No neuroprotective agents have yet demonstrated efficacy in preventing or improving delayed post-anoxic encephalopathy. Data on the effects of hyperbaric oxygen are conflicting because of the absence of any consensual protocol to treat CO poisonings.