A 67-year-old man living alone was admitted for acute disturbance of consciousness during winter. He presented with semicoma, a decorticate posture, and exaggerated tendon reflexes of the limbs, but brainstem reflexes were intact. The
carboxyhemoglobin (COHb) level was normal in arterial blood gas on admission, and
protein in cerebrospinal fluid was increased without
pleocytosis. Brain MRI showed diffuse T2 high intensities in the deep white matter bilaterally without a contrast effect and abnormal T1 intensity in the pallidum. (1)H-MR spectroscopy (MRS) of the white matter lesion demonstrated findings suggesting
demyelination as an increased
choline peak, enhanced anaerobic metabolism as increased
lactate and
lipids peaks, and reduced neurons as a decreased
N-acetylaspartate peak, which corresponded to delayed
encephalopathy due to the interval form of
carbon monoxide (CO)
poisoning. The possibility of CO exposure due to
coal briquette use 2 weeks before the symptomatic onset was indicated by his family, so he was diagnosed with CO
poisoning. His consciousness slightly improved with
corticosteroid therapy and repetitive
hyperbaric oxygen therapy, but brain MRI and MRS findings did not improve. Characteristic MRS findings of
leukoencephalopathy are helpful for diagnosing the interval form of CO
poisoning in the case of a normal COHb level.