Abstract
We report the neurobehavioral aspects of the delayed encephalopathy of carbon monoxide (CO) intoxication in a 29 year old woman and review the literature. Four weeks after CO poisoning, the patient developed a frontal lobe syndrome, visuoperceptual impairment, and diffuse white matter lesions with an otherwise normal neurological examination. In contrast, patients with the classical syndrome also have a parkinsonian state or an akinetic–mute state. The delayed encephalopathy of CO poisoning usually results from demyelination of subcortical white matter, necrosis of the globus pallidus, or both. The clinical aspects, risk factors, neurobiological features, and therapy and prognosis are discussed.
Highlights
Carbon monoxide (CO) is a powerful toxin
Similar to prior reports of apperceptive visual agnosia (Benson and Greenberg, 1969; Mendez, 1988), our patient could not immediately derive the global image from pictures or drawings and reverted to a slow, systematic analysis of visual details. She differed from most patients who develop the delayed encephalopathy of CO intoxication in the isolated behavioral presentation and the absence ofParkinsonian features or movement disorders (Choi, 1983; Lee and Marsden, 1994)
No specific risk factors reliably predict the development of the delayed encephalopathy of CO intoxication
Summary
Carbon monoxide (CO) is a powerful toxin. CO is a colorless, tasteless gas produced in large amounts by automobile exhausts, inadequately vented furnaces and other heating equipment, fires, and methylene chloride from paint removers (Ellenhorn and Barceloux, 1988). It is not surprising that CO is a common cause of poisoning. In addition to the effects of acute intoxication, a delayed encephalopathy may follow recovery from CO poisoning. After a lucid interval of 3 days to 6 weeks, up to 40% of survivors develop a neurobehavioral syndrome characterized by personality and cognitive changes, movement disorders, diffuse white matter changes, and lesions of the globus pallidus (Choi, 1983; Myers et ai., 1985). Clinicians may miss or misdiagnose this syndrome, in the absence of known CO exposure. The clinical manifestations of the delayed encephalopathy of CO intoxication are variable and can be limited to an isolated and potentially subtle behavioral disorder (Jefferson, 1976). We review the literature on this syndrome and describe a previously healthy patient
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