PTSD is associated with a variety of structural and functional brain abnormalities, but the molecular pathophysiological mechanisms are unknown. 25 pediatric PTSD and 24 matched healthy control subjects underwent single voxel 1H-MRS. Right amygdala NAA was significantly increased in pediatric PTSD subjects than in controls, and the other metabolites did not differ significantly between the groups. We hypothesis that long-term excessive activation in amygdala after traumatic events may lead to increase density and activity of the neurons in pediatric PTSD patients with increased NAA concentration, which may be an adaptive response to traumatic stimulation in the human brain. Our findings add the neurochemical abnormality evidence in pediatric PTSD.