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February 11, 2014; 82 (6) Article

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, Yvonne W. Lui
First published January 8, 2014, DOI: https://doi.org/10.1212/WNL.0000000000000105
Andrea S. Kierans
From the Department of Radiology, New York University School of Medicine, NY.
MD
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Ivan I. Kirov
From the Department of Radiology, New York University School of Medicine, NY.
PhD
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Oded Gonen
From the Department of Radiology, New York University School of Medicine, NY.
PhD
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Gillian Haemer
From the Department of Radiology, New York University School of Medicine, NY.
BSc
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Eric Nisenbaum
From the Department of Radiology, New York University School of Medicine, NY.
BSc
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James S. Babb
From the Department of Radiology, New York University School of Medicine, NY.
PhD
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Robert I. Grossman
From the Department of Radiology, New York University School of Medicine, NY.
MD
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Yvonne W. Lui
From the Department of Radiology, New York University School of Medicine, NY.
MD
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Citation
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, Yvonne W. Lui
Neurology Feb 2014, 82 (6) 521-528; DOI: 10.1212/WNL.0000000000000105

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Abstract

Objective: To 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 (1H-MRS) and to compare these measurements against normal healthy control subjects.

Methods: This study approved by the institutional review board is Health Insurance Portability and Accountability Act compliant. T1-weighted MRI and multi-voxel 1H-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.

Results: Quantitative 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.

Conclusion: Increased 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.

GLOSSARY

ANCOVA=
analysis of covariance;
Cho=
choline;
Cr=
creatine;
FLAIR=
fluid-attenuated inversion recovery;
FOV=
field of view;
GCS=
Glasgow Coma Scale;
Glx=
glutamate plus glutamine;
1H-MRS=
proton magnetic resonance spectroscopy;
IS=
inferior-superior;
mI=
myoinositol;
MP-RAGE=
magnetization-prepared rapid-acquisition gradient echo;
mTBI=
mild traumatic brain injury;
NAA=
N-acetylaspartate;
ROI=
region of interest;
TBI=
traumatic brain injury;
TE=
echo time;
TR=
repetition time;
VOI=
volume of interest

Footnotes

  • Go to Neurology.org for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the article.

  • Received June 26, 2013.
  • Accepted in final form November 1, 2013.
  • © 2014 American Academy of Neurology
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