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AJNR - American Journal of Neuroradiology

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American Journal of Neuroradiology 28:907-913, May 2007
© 2007 American Society of Neuroradiology

BRAIN

Proton MR Spectroscopy and MRI-Volumetry in Mild Traumatic Brain Injury

B.A. Cohen^a, M. Inglese^a, H. Rusinek^a, J.S. Babb^a, R.I. Grossman^a and O. Gonen^a

^a From the Department of Radiology, New York University School of Medicine, New York, NY

Address correspondence to Oded Gonen, PhD, Department of Radiology, New York University School of Medicine, 650 First Ave, 6th floor, New York, NY 10016; e-mail: oded.gonen{at}med.nyu.edu

BACKGROUND AND PURPOSE: More than 85% of brain traumas are classified as "mild"; MR imaging findings are minimal if any and do not correspond to clinical symptoms. Our goal, therefore, was to quantify the global decline of the neuronal marker N-acetylaspartate (NAA), as well as gray (GM) and white matter (WM) atrophy after mild traumatic brain injury (mTBI).

MATERIALS AND METHODS: Twenty patients (11 male, 9 female; age range, 19–57 years; median, 35 years) with mTBI (Glasgow Coma Scale score 13–15 with loss of consciousness for at least 30 seconds) and 19 age- and sex-matched control subjects were studied. Seven patients were studied within 9 days of TBI; the other 13 ranged from 1.2 months to 31.5 years (average and median of 4.6 and 1.7 years, respectively) after injury. Whole-brain NAA (WBNAA) concentration was obtained in all subjects with nonlocalizing proton MR spectroscopy. Brain volume and GM and WM fractions were segmented from T1-weighted MR imaging and normalized to the total intracranial volume, suitable for intersubject comparisons. The data were analyzed with least squares regression.

RESULTS: Patients with mTBI exhibited, on average, a 12% WBNAA deficit that increased with age, compared with the control subjects (p < .05). Adjusted for age effects, patients also suffered both global atrophy (–1.09%/year; P = .029) and GM atrophy (–0.89%/year; P = .042). Patients with and without visible MR imaging pathology, typically punctate foci of suspected shearing injury, were indistinguishable in both atrophy and WBNAA.

CONCLUSION: WBNAA detected neuronal/axonal injury beyond the minimal focal MR-visible lesions in mTBI. Combined with GM atrophy, the findings may provide further, noninvasive insight into the nature and progression of mTBI.

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