title: Brain metabolite profiles of T1-hypointense lesions in relapsing-remitting multiple sclerosis.
abstract: OBJECTIVE
  Persistent T1-hypointense lesions ("black holes") are thought to represent permanent damage of brain parenchyma. We attempted to ascertain whether the metabolic profiles of these hypointense areas support this hypothesis and whether these profiles correlate with these hypointense findings.
  
  
  METHODS
  Four patients with relapsing-remitting multiple sclerosis and four matched control volunteers underwent MR imaging and 3D proton MR spectroscopy. Absolute levels of N-acetylaspartate (NAA), creatine, and choline (Cho) were obtained in 0.19 cm(3) voxels containing 14 T1-hypointense lesions (average volume, 0.4 cm(3); range, 0.2-1.0 cm(3)) in patients. Metabolite levels were analyzed, by using Pearson correlation, against their respective lesions' hypointensity relative to the surrounding normal-appearing white matter.
  
  
  RESULTS
  Moderate correlation, r = 0.56, was found between the NAA level and MR imaging hypointensity. Of the 14 lesions studied, 12 were deficient in NAA and 11 had excess Cho compared with corresponding brain regions in control volunteers. Only one lesion was significantly deficient in all three metabolites, indicative of total damage or matrix loss.
  
  
  CONCLUSIONS
  No relationship was found between the hypointensity of the lesions and their metabolic profile. Specifically, lesions with the same hypointensity on T1-weighted MR images were metabolically variable (ie, displayed disparate metabolite levels and behavior). Also, although 86% of the lesions exhibited abnormally low NAA, 71% also had increased Cho. This indicates that although neuronal damage had already occurred (lower NAA), these lesions were still "smoldering" with active membrane turnover (high Cho), most likely because of de- and remyelination, indicative of shadow plaques (remyelinated lesions). Consequently, relapsing-remitting hypointense lesions represent neither final-stage nor static pathologic abnormality.
authors.affiliation: Department of Radiology, New York University School of Medicine, New York, NY. University of California, San Francisco. VA Medical Center, San Francisco, CA.
authors.forename: Belinda S Y
authors.initials: BS
authors.lastname: Li
authors.forename: Juleiga
authors.initials: J
authors.lastname: Regal
authors.forename: Brian J
authors.initials: BJ
authors.lastname: Soher
authors.forename: Lois J
authors.initials: LJ
authors.lastname: Mannon
authors.forename: Robert I
authors.initials: RI
authors.lastname: Grossman
authors.forename: Oded
authors.initials: O
authors.lastname: Gonen
mesh_terms: D000328:Adult; D001224:Aspartic Acid / Q000031:analogs & derivatives* / Q000378:metabolism; D001921:Brain / Q000473:pathology / Q000503:physiopathology; D002794:Choline / Q000378:metabolism; D003401:Creatine / Q000378:metabolism; D004734:Energy Metabolism / Q000502:physiology*; D005260:Female; D006801:Humans; D007091:Image Processing, Computer-Assisted; D021621:Imaging, Three-Dimensional; D008279:Magnetic Resonance Imaging; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D020529:Multiple Sclerosis, Relapsing-Remitting / Q000175:diagnosis* / Q000503:physiopathology; D013223:Statistics as Topic
chemical_list: D001224:Aspartic Acid; C000179:N-acetylaspartate; D003401:Creatine; D002794:Choline