A wide variety of neurological and/or psychiatric disturbances has been reported in patients surviving the acute phase of carbon monoxide (CO) poisoning,after a period of apparent recovery. Postulated pathogenic mechanisms of these sequelae, usually referred to as ‘delayed neurological syndrome’(DNS) include: (1) hypoxic-ischemic stress related to defective oxygen transport to the cells and to impaired cardiovascular function; (2) CO interaction with intracellular targets (e.g. cytochromes) with impairment of mitochondrial electron transport; (3) brain lipid peroxidation; (4) excessive stimulation of excitatory amino acid receptors. Timely hyperbaric oxygen (HBO) treatment may interrupt the cascade of events leading to brain damage, and has been advocated as effective in preventing DNS. However, clinical studies comparing the efficacy of hyperbaric versus normobaric oxygen have generated conflicting results and controversies regarding both the causes of delayed CO neurotoxicity and the indications of HBO therapy. Additional clinical investigations and further basic research using appropriate animal models are needed.

Keywords:
Carbon monoxide, Delayed neurological syndrome, Brain diseases (chemically induced), Normobaric oxygen, Hyperbaric oxygen
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1995
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