• Neurology · Feb 2014

    Myoinositol and glutamate complex neurometabolite abnormality after mild traumatic brain injury.

    • Andrea S Kierans, Ivan I Kirov, Oded Gonen, Gillian Haemer, Eric Nisenbaum, James S Babb, Robert I Grossman, and Yvonne W Lui.
    • From the Department of Radiology, New York University School of Medicine, NY.
    • Neurology. 2014 Feb 11;82(6):521-8.

    ObjectiveTo obtain quantitative neurometabolite measurements, specifically myoinositol (mI) and glutamate plus glutamine (Glx), markers of glial and neuronal excitation, in deep gray matter structures after mild traumatic brain injury (mTBI) using proton magnetic resonance spectroscopy ((1)H-MRS) and to compare these measurements against normal healthy control subjects.MethodsThis study approved by the institutional review board is Health Insurance Portability and Accountability Act compliant. T1-weighted MRI and multi-voxel (1)H-MRS imaging were acquired at 3 tesla from 26 patients with mTBI an average of 22 days postinjury and from 13 age-matched healthy controls. Two-way analysis of variance was used to compare patients and controls for mean N-acetylaspartate, choline, creatine (Cr), Glx, and mI levels as well as the respective ratios to Cr within the caudate, globus pallidus, putamen, and thalamus.ResultsQuantitative putaminal mI was higher in patients with mTBI compared with controls (p = 0.02). Quantitative neurometabolite ratios of putaminal mI and Glx relative to Cr, mI/Cr, and Glx/Cr were also higher among patients with mTBI compared with controls (p = 0.01 and 0.02, respectively). No other differences in neurometabolite levels or ratios were observed in any other brain region evaluated.ConclusionIncreased putaminal mI, mI/Cr, and Glx/Cr in patients after mTBI compared with control subjects supports the notion of a complex glial and excitatory response to injury without concomitant neuronal loss, evidenced by preserved N-acetylaspartate levels in this region.

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