(Sunday, 7/29/2018) 4:00 PM - 4:30 PM
Room: Exhibit Hall | Forum 8
Purpose: Traumatic brain injury (TBI) is a major cause of morbidity and mortality affecting ~1.7 million people annually in the US. Hydrogen-1 magnetic resonance spectroscopy (1H-MRS) can identify biochemical changes in the contralesional (CON) side of the primary and remote lesions connected to the striatum (STRI) and thalamus (THAL).
Methods: TBI was induced in rats (N=15) over the left somatosensory cortex (COR) using a pneumatic impactor (5.0 m/s). Rats were imaged at 1-3 hours & 2, 7, and 14 days post injury. T2-RARE MRI was used to track edema. 1H-MRS data were acquired at 7T using a STEAM sequence and metabolite concentrations were determined with jMRUI. Student’s t-tests were performed with p<0.05 deemed significant.
Results: Significant changes were seen in the CON COR, STRI and THAL. There was a significant increase in n-acetyl aspartate observed in the CON COR on day 2 (6.22+0.53 mmol/kg) versus baseline (4.63+0.23 mmol/kg) indicating impaired neuronal integrity. In the CON STRI there was a significant decrease in NAA on day 2 (3.46+0.17 mmol/kg) versus baseline (4.09 +/- 0.21 mmol/kg) indicating mitochondrial dysfunction. Choline (Cho) in CON COR significantly increased on day 2 (1.35+0.10 mmol/kg), day 7 (1.26+0.11 mmol/kg), and day 14 (1.29+0.07 mmol/kg) versus baseline (0.73+0.14 mmol/kg) suggesting inflammation in the CON COR. Myo-inositol significantly decreased in CON COR by day 14 (2.16+0.30 mmol/kg) compared to baseline (4.16+0.90 mmol/kg) indicating reactive glial proliferation. Glucose (Glc) decreased in CON STRI on day 0 (2.27+0.32 mmol/kg) versus baseline (3.50+0.14 mmol/kg) which could be due to increased metabolism, reduced supply of circulating Glc and/or uptake deficits. Creatine and GABA decreased in the THAL on day 14 (4.31+0.19, 2.30+0.22 mmol/kg) compared to baseline (5.79+0.17, 3.49+0 mmol/kg) indicating neurotransmission deficits.
Conclusion: 1H-MRS allowed quantificatin of the longitudinal changes to understand the pathophysiological mechanisms behind TBI for primary and remote lesions.
Funding Support, Disclosures, and Conflict of Interest: Funding Support from NIH TL1 Grant 5TL1TR001119-05
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