Specific Imaging Findings

The globus pallidus is the most common and characteristic site of brain involvement in acute carbon monoxide (CO) poisoning and CT usually shows symmetric hypodensity. On MRI, the pallidi demonstrate low T1 and high T2 signal with reduced diffusion. T1 hyperintensity and a rim of low T2 signal are sometimes seen, reflecting hemorrhagic necrosis. Patchy or peripheral contrast enhancement may occur in the acute phase. Similar MRI findings are occasionally seen in the substantia nigra, hippocampus and cerebral cortex. In patients who develop a delayed leukoencephalopathy, bilateral symmetric confluent areas of high T2 signal are found in the periventricular white matter and centrum semiovale, along with mildly reduced diffusion. Diffuse white matter involvement may also be present.

Pertinent Clinical Information

Symptoms of mild CO poisoning can include headache, nausea, vomiting, myalgia, dizziness, or neuropsychological impairment. Severe exposures result in confusion, ataxia, seizures, loss of consciousness, or death. Long-term low-level CO poisoning may cause chronic fatigue, affective conditions, memory deficits, sleep disturbances, vertigo, neuropathy, paresthesias, abdominal pain, and diarrhea. On physical examination, patients may demonstrate cherry red lips and mucosa, cyanosis, or retinal hemorrhages. Suspected CO poisoning can be confirmed with blood carboxyhemoglobin levels. Delayed encephalopathy associated with CO toxicity typically occurs 2–3 weeks after recovery from the acute stage of poisoning and is characterized by recurrence of neurologic or psychiatric symptoms. Characteristic symptoms include mental deterioration, urinary incontinence, and gait disturbances.