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 ((1)H 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 (1)H 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.