ABSTRACT
Monoxide-Induced Encephalopathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 464 21.7 Discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 471 21.8 Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 473 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 474
It has been established in this book and earlier books in this series, that carbon monoxide (CO) poisoning is an insidious cause of death and disability in the United States and throughout the world.1 Tissue anoxia is most commonly implicated as the underlying pathophysiologic mechanism of toxic CO exposure as a result of its displacement of oxygen from hemoglobin forming carboxyhemoglobin (COHb). In addition, CO has been shown to have a direct effect on several key biochemical
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cytochrome oxidase, and cytochrome p 450 and other key enzymes in the oxidative metabolic process.2,3 Furthermore, it has been shown that CO binds directly to the heme iron in the globus pallidus in substantia nigra.4 Among the various types of neurotoxins, CO produces a unique clinical syndrome in which, after survival of an acute intoxication, a lucid period of variable duration can ensue followed by the onset of delayed neurological symptoms (DNS) in sequelae or a fraction of patients.4 The mechanism for the delayed a fraction effects of CO poisoning is not well understood, but involves elements of reperfusion injury, vascular oxidative stress by generation of reactive oxygen species, lipid peroxidation,5 neuronal exitotoxicity, and apoptosis.6,7 When these molecular changes affect large enough areas of neural tissue, they may be visualized by various neuroimaging techniques. We will see later how the pattern, distribution, and nature of these induced neuropathalogic changes may provide characteristic neuroimaging clues associated with CO poisoning. The role of specific neuroimaging modalities during the various stages of CO poisoning will be reviewed.
