Metabolic and cognitive response to human traumatic brain injury: A quantitative proton magnetic resonance study

Citation
Wm. Brooks et al., Metabolic and cognitive response to human traumatic brain injury: A quantitative proton magnetic resonance study, J NEUROTRAU, 17(8), 2000, pp. 629-640
Citations number
35
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROTRAUMA
ISSN journal
08977151 → ACNP
Volume
17
Issue
8
Year of publication
2000
Pages
629 - 640
Database
ISI
SICI code
0897-7151(200008)17:8<629:MACRTH>2.0.ZU;2-G
Abstract
Proton magnetic resonance spectroscopy (H-1-MRS) offers a unique insight in to brain cellular metabolism following traumatic brain injury (TBI). The ai m of the present study was to assess change in neurometabolite markers of b rain injury during the recovery period following TBI. We studied 19 TBI pat ients at 1.5, 3, and 6 months postinjury and 28 controls. We used H-1-MRS t o quantify N-acetylaspartate (NAA), creatine (Cre), choline (Cho), and myoi nositol (mIns) in occipitoparietal gray matter (GM) and white matter (WM) r emote from the primary injury focus. Neuropsychological testing quantified cognitive impairment and recovery. At 1.5 months, we found cognitive impair ment (mean z score = -1.36 vs. 0.18,p < 0.01), lower NAA (GM: 12.42 mM vs. 13.03, p = 0.01; WM: 11.75 vs. 12.81, p < 0.01), and elevated Cho (GM: 1.51 vs. 1.25, p < 0.01; WM: 1.98 vs. 1.79, p < 0.01) in TBI patients compared with controls. GM NAA at 1.5 months predicted cognitive function at outcome (6 months postinjury; r = 0.63, p = 0.04). GM NAA continued to fall by 0.4 6 mM between 1.5 and 3 months (p = 0.02) indicating continuing neuronal los s, metabolic dysfunction, off both. Between 3 and 6 months, WM NAA increase d by 0.55 mM (p = 0.06) suggesting metabolic recovery. Patients with poorer outcomes had elevated mean GM Cho at 3 months postinjury, suggesting activ e inflammation, as compared to patients with better outcomes (p = 0.002). H -1-MRS offers a noninvasive approach to assessing neuronal injury and infla mmation following TBI, and may provide unique data for patient management a nd assessment of therapeutic efficacy.