Introduction: Delayed encephalopathy can occur after 2 to 4-week asymptomatic period following clinical remission of acute carbon monoxide (CO) poisoning. The patient with delayed encephalopathy suffered from serious disabilities including cognitive impairment, psychiatric symptoms and gait impairment. Up to the present time, there have not been effective treatments in delayed encephalopathy, so the prognosis is poor. We report a case about nearly complete recovery of delayed encephalopathy with multimodal therapy.
Case Report: A 39-year-old man was admitted to the acute local hospital after attempting suicide using burning artificial coal. Upon admission, the patient was diagnosed with acute CO poisoning and had been treated with hyperbaric oxygen (HBO) therapy. He was discharged 8 days later without any disturbance of consciousness, cognition and movement disorders.
About 20 days after discharge from acute local hospital, he began to experience amnesia, cognition deficit, and balance impairment, which worsened within a few days. He was hospitalized again to our department at 38 days after the CO poisoning. On examination, he demonstrated a retardation of thought, irrelevant thinking and cognitive impairment and also cannot walk independently. He had a Mini-Mental State Examination (MMSE) score of 8/30 and an intelligence quotient (IQ) score of 41. He exhibited akathisia, and balance impairment with Berg balance scale score of 36/56. Sensory disturbance and muscle weakness were not detected. Brain MRI showed high-intensity lesions in the white matter of the frontal, temporal, and parietal lobes on a T2-weighted image (T2WI) and a diffusion-weighted image (DWI) (Fig. 1).
The patient was administered initially high dose steroid, and cerebrolysin for about three weeks and maintained with memantine and vitamins. HBO therapy (1.5 atm, 60 minutes, every day) was administered concurrently and continued over 21 subsequent sessions. However, these therapeutic regimens appeared only mild or transient effects. After cessation of steroid therapy, he has been treated with a repetive-transcranial magnetic stimulation (rTMS) (to left prefrontal cortex facilitation, 5 days a week) therapy.
After the multimodal therapy, he showed improvement of cognition (MMSE score 21) and also improvements in gait disturbance (Berg balance score 54) at discharge.
One month later from discharge (4months after acute CO poisoning), he could perform nearly complete ADL independently and return to work with good cognitive function (IQ score of 98) and normal gait(berg balance scale 56). Follow up Brain MRI showed much disappearance of high intensity areas on frontal, parietal, and also temporal areas. (Fig. 2)
Conclusion: We report a patient with great improvement as a result of multimodal therapy on delayed encephalopathy following CO poisoning. Further investigation would be needed on the mechanism associated with these improvements.
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