title: Magnetization transfer imaging and proton MR spectroscopy in the evaluation of axonal injury: correlation with clinical outcome after traumatic brain injury.
abstract: OBJECTIVE
  Current imaging does not permit quantification of neural injury after traumatic brain injury (TBI) and therefore limits both the development of new treatments and the appropriate counseling of patients concerning prognosis. We evaluated the utility of magnetization transfer ratio (MTR) and proton MR spectroscopy in identifying patients with neuronal injury after TBI.
  
  
  METHODS
  Thirty patients with TBI (21-77 years old; mean age, 42 years; admission Glasgow Coma Scale (GOS) scores 3-15; mean score, 11) were studied on a 1.5-T system with magnetization transfer imaging and MR spectroscopy of the splenium. Magnetization transfer imaging was also performed in the brain stem in all patients, and other areas of the brain were sampled in one patient. The splenium of the corpus callosum and brain stem were studied because these are often affected by diffuse axonal injury. Scans were obtained 2 to 1129 days after injury (median, 41 days). MTR was considered abnormal if it was more than 2 SD below normal. Proton MR spectroscopy was used to calculate the N-acetylaspartate (NAA)/creatine (Cr) ratio. GOS was determined at least 3 months after injury.
  
  
  RESULTS
  In 10 patients with a GOS of 1 to 4, the mean NAA/Cr was 1.24 +/- 0.28; two of these patients had abnormal MTR in normal-appearing white matter (NAWM). In 20 patients with a GOS of 5, the mean NAA/Cr was 1.53 +/- 0.37 (P < .05); four of these patients had abnormal MTR in NAWM. MTR abnormalities in NAWM were identified in six patients, but these changes did not correlate with GOS or MR spectroscopy changes.
  
  
  CONCLUSIONS
  MTR and MR spectroscopy can quantify damage after TBI, and NAA levels may be a sensitive indicator of the neuronal damage that results in a worse clinical outcome.
authors.affiliation: Department of Neurosurgery, University of Pennsylvania School of Medicine, Philadelphia 19104, USA.
authors.forename: G
authors.initials: G
authors.lastname: Sinson
authors.forename: L J
authors.initials: LJ
authors.lastname: Bagley
authors.forename: K M
authors.initials: KM
authors.lastname: Cecil
authors.forename: M
authors.initials: M
authors.lastname: Torchia
authors.forename: J C
authors.initials: JC
authors.lastname: McGowan
authors.forename: R E
authors.initials: RE
authors.lastname: Lenkinski
authors.forename: T K
authors.initials: TK
authors.lastname: McIntosh
authors.forename: R I
authors.initials: RI
authors.lastname: Grossman
mesh_terms: D001224:Aspartic Acid / Q000031:analogs & derivatives* / Q000378:metabolism; D001369:Axons / Q000473:pathology*; D015415:Biomarkers; D001921:Brain / Q000378:metabolism / Q000473:pathology*; D001930:Brain Injuries / Q000175:diagnosis* / Q000378:metabolism / Q000503:physiopathology; D001933:Brain Stem / Q000473:pathology; D003337:Corpus Callosum / Q000473:pathology; D003401:Creatine / Q000378:metabolism; D015600:Glasgow Coma Scale; D008279:Magnetic Resonance Imaging; D009682:Magnetic Resonance Spectroscopy; D013997:Time Factors
chemical_list: D015415:Biomarkers; D001224:Aspartic Acid; C000179:N-acetylaspartate; D003401:Creatine