Macromolecular‐Suppressed GABA‐Edited MR Spectroscopy in the Posterior Cingulate Cortex of Patients With Acute Mild Traumatic Brain Injury

Background Mild traumatic brain injury (mTBI) causes a number of molecular and cellular alterations. There is evidence of an imbalance between the main excitatory (glutamate, Glu) and the main inhibitory (gamma‐aminobutyric acid [GABA]) neurotransmitters following mTBI. In vivo human GABA–Glu balance studies following mTBI are sparse. Purpose To investigate the effect of acute mTBI on the GABA concentration measured in the posterior cingulate cortex (PCC) of pediatric patients by using the macromolecular (MM)‐suppressed GABA J‐editing technique. Study type Prospective patient and phantom. Participants A total of 14 pediatric patients (mean age 16.0 ± 1.7) with acute mTBI (<3 days after trauma; Glasgow Coma Scale 15) and 16 healthy volunteers (mean age 16.9 ± 2.8). Phantom: 524 cm 3 sphere containing 10 mM glycine, 10 mM GABA. Field Strength/Sequence A 3 T, MEGA‐PRESS pulse sequence. Assessment GABA spectra were processed in Gannet software. MM‐suppressed GABA editing efficiency was derived from the phantom study. Absolute GABA and glutamate + glutamine (Glx) concentrations were quantified using different types of correction and compared between groups. N ‐acetyl aspartate (NAA) and choline (Cho) levels relative to tCr were also compared. Statistical tests Shapiro–Wilk test, Mann–Whitney U test, Student t ‐test, Pearson or Spearman correlations. P < 0.01 was considered statistically significant. Results The MM‐suppressed GABA editing efficiency was 0.63. GABA signal fit error was <16% for all participants. The GABA concentration in the PCC of the mTBI group was significantly different from that in healthy controls: GABA/tCr was higher by 27%, absolute GABA concentration with different types of correction was higher by ≈17%. No significant differences were observed in Glx concentrations ( P ≥ 0.32) or in Glx/tCr ( P ≥ 0.1), NAA/tCr ( P = 0.55), and Cho/tCr levels ( P = 0.85). Data conclusion We report an increase in the GABA concentration in the PCC region in acute mTBI pediatric patients. This may suggest activation of GABA synthesis and impairment of the GABAergic system after acute mTBI. Evidence Level 3 Technical Efficacy Stage 1