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Delayed postanoxic encephalopathy after carbon monoxide poisoning
  1. O Y Kwon1,
  2. S P Chung2,
  3. Y R Ha3,
  4. I S Yoo2,
  5. S W Kim2
  1. 1Department of Anatomy, College of Medicine, Chungnam National University, Daejeon, Republic of Korea
  2. 2Department of Emergency Medicine, Chungnam National University Hospital, Daejeon, Republic of Korea
  3. 3Department of Emergency Medicine, Daejin Medical Centre, Pundang Jesaeng General Hospital, Kyunggido, Republic of Korea
  1. Correspondence to:
 Dr S W Kim
 Department of Emergency Medicine, Chungnam National University Hospital, Daejeon, 301-721, Republic of Korea;


Delayed postanoxic encephalopathy causes deterioration and relapse of cognitive ability and behavioural movement a few weeks after complete recovery from initial hypoxic injury. A case is reported of delayed postanoxic encephalopathy after carbon monoxide poisoning, which was diagnosed with diffusion weighted magnetic resonance imaging. The literature is also reviewed.

  • carbon monoxide
  • poisoning
  • magnetic resonance imaging
  • postanoxic encephalopathy
  • ED, emergency department
  • CO, carbon monoxide
  • DPE, delayed postanoxic encephalopathy
  • DWMRI, diffusion weighted magnetic resonance imaging

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A 65 year old man was admitted to the emergency department (ED) with memory impairment and movement disturbance. One month previously he had presented to our ED with a drowsy mental status because of carbon monoxide (CO) poisoning after he had attempted suicide by a briquette fire. However, he had recovered with normobaric oxygen therapy that resulted in a decrease in the blood carboxyhaemoglobin level from 30.5% on arrival to 2.3% just before discharge. On his second presentation, he had no other remarkable medical history. His blood pressure was 120/80 mm Hg, heart rate 82/min, and respiratory rate 24/min. He was alert, comparatively well coordinated, but slightly disoriented with regard to time and person. He showed no neurological abnormality apart from parkinsonian movement.

Diffusion weighted magnetic resonance imaging (DWMRI) showed diffuse high signal intensity in both periventricular and deep white matter (fig 1). He was admitted to the neurology ward for supportive care, and discharged on the 17th hospital day without significant improvement. Two months after the second discharge, his symptoms were slightly improved, but mild rigidity and gait disturbance still remained.

Figure 1

Diffusion weighted magnetic resonance imaging shows abnormal high signal intensity in both periventricular and deep white matter.


Many cases of CO poisoning, whether incidental or accidental, initially visit the ED. Most of them recover well without any complication with hyperbaric or high oxygen therapy. But 10% to 30% of them revisit hospital with delayed neuropsychiatric sequelae, symptoms such as cognitive and personality changes, incontinence, dementia, and psychosis.1 Parkinsonism is also one of the features of delayed CO encephalopathy, and has been reported to occur in 9.5% of CO poisoned patients.2 The exact mechanism is uncertain, but a magnetic resonance spectroscopic study revealed white matter damage that was reversible in accordance with complete recovery from parkinsonism.3 The diagnosis is easily made by typical symptoms such as short step gait, hypokinesia, masked face, and increased muscle tone.2

We performed the DWMRI in this case to confirm the diagnosis of DPE. The DWMRI is a new generation magnetic resonance imaging sequence based on the translational movement of water. It is becoming more common in the ED because of high sensitivity for acute ischaemic stroke as well as short scanning time.4 The DWMRI showed hyperintense signals in the periventricular and deep white matter, and the high signal intensity means cytotoxic oedema may be differentiated from apoptosis and triggered by hypoxia.5 We could not obtain a follow up DWMRI after improvement. But a serial imaging study showed gradual normalisation of the high signal lesion.5

The recovery from DPE after CO poisoning occurs in 50%–75% within one year.6 It seems that no specific treatment is required for DPE. Levodopa and anticholinergic drugs have been reported ineffective to reverse the parkinsonian feature.2 It has been reported in a small randomised trial that the hyperbaric oxygen treatment for acute CO poisoning could decrease the incidence of delayed neuropsychiatric sequelae.7 But, a recent animal study failed to demonstrate the neuroprotection effect as compared with the normobaric oxygen therapy.8 Clinical status or carboxyhaemoglobin level on initial CO poisoning could not predict the occurrence of DPE. The most common computed tomography finding in several cases of CO poisoning was low density in the cerebral white matter followed by lesions of the globus pallidi. Some investigators reported that there was significant correlation between the cerebral white matter changes in the initial CT scan and the development of delayed neurological sequelae after acute CO poisoning.9

Most CO poisoning patients present to the ED. Thus emergency doctors should be familiar with the possibility of DPE after apparent complete recovery from acute CO poisoning.