 The mechanism that is thought to have a significant influence on delayed effects involves formed blood cells and chemical mediators , which cause brain lipid peroxidation ( degradation of unsaturated fatty acids ) . Carbon monoxide causes endothelial cell and platelet release of nitric oxide , and the formation of oxygen free radicals including peroxynitrite . In the brain this causes further mitochondrial dysfunction , capillary leakage , leukocyte sequestration , and apoptosis . The result of these effects is lipid peroxidation , which causes delayed reversible demyelinization of white matter in the central nervous system known as Grinker myelinopathy , which can lead to edema and necrosis within the brain . This brain damage occurs mainly during the recovery period . This may result in cognitive defects , especially affecting memory and learning , and movement disorders . These disorders are typically related to damage to the cerebral white matter and basal ganglia . Hallmark pathological changes following poisoning are bilateral necrosis of the white matter , globus pallidus , cerebellum , hippocampus and the cerebral cortex . 
