title: Subcortical white matter metabolic changes remote from focal hemorrhagic lesions suggest diffuse injury after human traumatic brain injury.
abstract: OBJECTIVE
  We used positron emission tomographic studies to prospectively examine the relationship between glucose and oxidative metabolism in the subcortical white matter (WM) acutely after traumatic brain injury (TBI). The objective was to determine the nature, extent, and degree of metabolic abnormalities in subcortical brain regions remote from hemorrhagic lesions.
  
  
  METHODS
  Sixteen normal volunteers and 10 TBI patients (Glasgow Coma Scale score, 4-10; age, 17-64 yr; 6 with focal and 4 with diffuse injury) were studied. Each subject underwent dynamic positron emission tomographic studies using [(15)O]CO, (15)O(2), [(15)O]H(2)O, and fluorodeoxyglucose plus a magnetic resonance imaging scan acutely after TBI. Parametric images of the metabolic rate of oxygen and metabolic rate of glucose were generated, and a molar oxygen-to-glucose utilization ratio was calculated. Data from gray matter and WM remote from hemorrhagic lesions, plus whole brain, were analyzed.
  
  
  RESULTS
  There was a significant reduction in the subcortical WM oxygen-to-glucose utilization ratio after TBI compared with normal values (3.99 +/- 0.77 versus 5.37 +/- 1.00; P < 0.01), whereas the mean cortical gray matter and whole-brain values remained unchanged. WM metabolic changes, which were diffuse throughout the hemispheres, were characterized by a reduction in the metabolic rate of oxygen without a concomitant drop in the metabolic rate of glucose.
  
  
  CONCLUSIONS
  The extent and degree of subcortical WM metabolic abnormalities after moderate and severe TBI suggest that diffuse WM injury is a general phenomenon after such injuries. This pervasive finding may indicate that the concept of focal traumatic injury, although valid from a computed tomographic imaging standpoint, may be misleading when considering metabolic derangements associated with TBI.
authors.affiliation: Department of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California 90095-6901, USA.
authors.forename: Hsiao-Ming
authors.initials: HM
authors.lastname: Wu
authors.forename: Sung-Cheng
authors.initials: SC
authors.lastname: Huang
authors.forename: Naoya
authors.initials: N
authors.lastname: Hattori
authors.forename: Thomas C
authors.initials: TC
authors.lastname: Glenn
authors.forename: Paul M
authors.initials: PM
authors.lastname: Vespa
authors.forename: David A
authors.initials: DA
authors.lastname: Hovda
authors.forename: Marvin
authors.initials: M
authors.lastname: Bergsneider
mesh_terms: D000293:Adolescent; D000328:Adult; D001923:Brain Chemistry / Q000502:physiology; D020201:Brain Hemorrhage, Traumatic / Q000523:psychology*; D001930:Brain Injuries / Q000523:psychology*; D002540:Cerebral Cortex / Q000378:metabolism*; D019788:Fluorodeoxyglucose F18; D015600:Glasgow Coma Scale / Q000706:statistics & numerical data; D006801:Humans; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D008875:Middle Aged; D049268:Positron-Emission Tomography / Q000379:methods
chemical_list: D019788:Fluorodeoxyglucose F18