Posttraumatic stress disorder (PTSD) patients have low cortical
concentrations of γ-aminobutyric acid (GABA) and elevated glutamate (Glu)
as measured by proton magnetic resonance spectroscopy (1H MRS).
Alcohol use disorder (AUD) is highly comorbid with PTSD, but the neurobiological
underpinnings are largely unknown. We wanted to determine if PTSD patients with
AUD have normalized cortical GABA and Glu levels in addition to metabolite
alterations common to AUD. We compared brain metabolite concentrations in 10
PTSD patients with comorbid AUD (PAUD) with concentrtations in
28 PTSD patients without AUD and in 20 trauma-exposed controls
(CON) without PTSD symptoms. We measured concentrations of GABA, Glu,
N-acetylaspartate (NAA), creatine- (Cr) and
choline-containing metabolites (Cho), and myo-Inositol (mI) in three cortical
brain regions using 1H MRS and correlated them with measures of
neurocognition, insomnia, PTSD symptoms, and drinking severity. In contrast to
PTSD, PAUD exhibited normal GABA and Glu concentrations in the parieto-occipital
and temporal cortices, respectively, but lower Glu and trends toward higher GABA
levels in the anterior cingulate cortex (ACC). Temporal NAA and Cho as well as
mI in the ACC were lower in PAUD than in both PTSD and CON. Within PAUD, more
cortical GABA and Glu correlated with better neurocognition. Heavy drinking in
PTSD is associated with partially neutralized neurotransmitter imbalance, but
also with neuronal injury commonly observed in AUD.