Neurological Sequelae of Carbon Monoxide Poisoning: Role of Hyperbaric Oxygen

A wide variety of neurological and/or psychiatric disturbances has been reported in patients surviving the acute phase of carbon monoxide (CO) poi soning, after a period of apparent recovery. Postulated pathogenic mecha nisms of these sequelae, usually referred to as 'delayed neurological syndrome' (DNS) include: (1) hypoxic-ischemic stress related to defective oxygen trans port 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 compar ing the efficacy of hyperbaric versus normobaric oxygen have generated con flicting results and controversies regarding both the causes of delayed CO neu rotoxicity and the indications of HBO therapy. Additional clinical investiga tions and further basic research using appropriate animal models are needed.