Carbon monoxide poisoning : Anoxic-ischemic encephalopathy, usually with bilateral lesions, caused by inhalation of carbon monoxide (CO) gas

Etiology of CO poisoning

• Hypoxic theory
  • CO : combine with Hb (affinity about 250time of oxygen)
         → carboxyhaemoglobin(COHb)
         → reduce the oxygen-carrying capacity of blood
• Cellular theory
  • CO : inhibits the mitochondrial electron transport enzyme system
         → brain lipid peroxidation
         → leading to the delayed effects of CO poisoning
• Neurons are most vulnerable to hypoxic–ischemic insult (oxygen and glucose demands↑)
             → predominantly involving the gray matter

Key imaging finding of carbon monoxide poisoning

➔Necrosis of the Globus pallidus

• Most common site of involvement in CO poisoning
• The damage usually occurs immediately
• hypotensive effects of CO poisoning in the watershed territory of the arterial supply
• CO binding to the iron-rich globus pallidus
• Imaging findings
  • CT : symmetric hypodensity.
  • MRI
    • T1WI : Both hypointensity (likely due to necrosis) and hyperintensity (likely duye to hemorrhage) are reported
  • • T2WI : Ischemia/Infarct of globus pallidus
      • Cerebral hemispheric WM : Bilateral confluent hyperintense WM (periventricular/centrum semiovale)Cortical hyperintensity (commonly temporal lobe)Medial temporal lobe hyperintensity (uncommon despite frequent pathologic findings)
    • T1CE(+) : patchy or peripheral enhancement in the necrotic areas
    • DWI and ADC maps : restriction of water diffusivity due to cytotoxic edema from acute tissue necrosis

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