Figure 4.

Findings of significant difference from control in ¹H-MRS-visible brain metabolites for patients with post-traumatic stress disorder. General decreases in N-acetyl aspartate (NAA) in PTSD relative to trauma-exposed or -unmatched control groups have been observed predominantly in anterior cingulate cortex and hippocampus, while NAA increases in the amygdala have also been reported by one study. Differences from control in choline (Cho), when observed, have tended to be positive, also in anterior cingulate cortex and hippocampus, while decreases in choline have been observed in the medial temporal lobe. Regional effects of PTSD on common quantification reference metabolite creatine (Cr) have varied by region, with decreases reported in hippocampus and occipital cortex and increases in amygdala. Myoinositol (mIns) has been reported to increase in both anterior cingulate cortex and amygdala. Only a few studies have examined excitatory neurotransmitter glutamate to show increases in medial temporal lobe and hippocampus but decreases in both glutamate + glutamine (Glx) and glutamine (Gln) in anterior cingulate cortex. Reported alterations in GABA have similarly varied by region, with decreases reported in insula, medial temporal lobe, and parieto-occipital cortex; increases in dorsolateral prefrontal cortex; and mixed findings in anterior cingulate cortex. Only two published findings have been reported for glutathione (GSH), both increases, in dorsolateral prefrontal and anterior cingulate cortices. Studies of additional metabolites, such as sugars and lipids measurable by 2D J-resolved proton spectroscopy reported in Quadrelli et al,⁷⁹ have been limited. *PTSD versus control groups that included trauma-exposed and/or military veteran individuals. GABA: γ-aminobutyric acid; Glu: glutamate; IMI-1: imidazole from histamine, histidine, and homocarnosine.