Carbon monoxide (CO) poisoning may result in an anoxic-ischemic encephalopathy, with acute as well as delayed effects.


Carbon monoxide poisoning is mostly preventable with common causes including malfunctioning heating systems, improperly ventilated motor vehicles, and residential fires . It is also observed as an attempt to commit suicide.

Clinical presentation

Patients can present with :

  • acute symptoms of headache, dizziness, altered conscious state, seizures
  • chronic symptoms of cognitive decline, abnormal gait, fecal incontinence


The pathophysiology can be two fold:

  • carbon monoxide strongly binds to hemoglobin and the resultant carboxyhemoglobinin the bloodstream can cause profound hypoxic/anoxic injury
  • carbon monoxide is also a respiratory chain metabolism toxin that interferes with mitochondrial oxidative phosphorylation and activates polymorphonuclear leukocytes, which undergo diapedesis and cause brain lipid peroxidation; this results in the delayed effects of carbon monoxide poisoning

Radiographic features

Changes tend to be bilateral with the globus pallidus most commonly affected .


Classically seen as low attenuation in the globus pallidus region. Other features include diffuse hypoattenuation in cerebral white matter .


Regions of involvement are similar to CT. Signal characteristics include:

  • T1: affected areas are usually low signal, hemorrhagic areas can be high signal
  • T2/FLAIR: affected areas are high signal
  • T1 C+ (Gd): can show patchy peripheral enhancement in affected areas in the acute phase
  • DWI: affected areas show increased diffusion signal in the acute phase

Treatment and prognosis

Treatment consists of administering 100% oxygen which accelerates the elimination of carboxyhemoglobin .

Differential diagnosis

For involvement in and around the globus pallidus, consider:

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