Serial assessments of delayed encephalopathy after carbon monoxide poisoning using magnetic resonance spectroscopy and diffusion tensor imaging on 3.0T system

Eur Neurol. 2008;59(1-2):55-61. doi: 10.1159/000109262. Epub 2007 Oct 4.


To elucidate the still unclear mechanism of delayed encephalopathy after carbon monoxide (CO) poisoning, we serially performed single-voxel proton magnetic resonance spectroscopy ((1)H-MRS) and diffusion tensor imaging (DTI) on a 3.0T system and intelligence tests in 2 patients, while they were undergoing hyperbaric oxygenation therapy. The chronological changes in (1)H-MRS- and DTI-derived parameters indicated the following: (1) White matter demyelination, aerobic metabolism inhibition, and cytotoxic edema persisted for at least 3 months even after starting the hyperbaric oxygenation therapy; (2) the axonal function and structural integrity of the white matter were initially severely impaired and then gradually and partially improved for 5 months, showing changes similar to those in the scores of the intelligence tests. The results demonstrated that brain damage after CO poisoning may persist longer than expected, and that the (1)H-MRS- and DTI-derived parameters are good indicators of the clinical progress of a patient. The combination of (1)H-MRS and DTI on a 3.0T system is useful for monitoring the changes in brain damage and the clinical symptoms of patients with delayed encephalopathy after CO poisoning.

Publication types

  • Case Reports
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Aspartic Acid / analogs & derivatives
  • Carbon Monoxide Poisoning / complications*
  • Choline / metabolism
  • Diffusion Magnetic Resonance Imaging / methods*
  • Electroencephalography / methods
  • Female
  • Humans
  • Lactic Acid / metabolism
  • Magnetic Resonance Spectroscopy / methods*
  • Neurotoxicity Syndromes / diagnosis*
  • Neurotoxicity Syndromes / etiology*


  • Aspartic Acid
  • Lactic Acid
  • N-acetylaspartate
  • Choline