Post-traumatic stress disorder (PTSD) is a highly prevalent disorder and a highly debilitating condition. Although anhedonia is an important construct of the disorder, the relationship between PTSD and reward functioning is still under-researched. To date, the majority of research on PTSD has focused on fear: fear learning, maintenance, and extinction. Here we review the relevant literature—including clinical observations, self-report data, neuroimaging research, and animal studies—in order to examine the potential effects of post-traumatic stress disorder on the reward system. Our current lack of sufficient insight into how trauma affects the reward system is one possible hindrance to clinical progress. The current review highlights the need for further investigation into the complex relationship between exposure to trauma and the reward system to further our understandings of the ethology of PTSD.

Hyperactivation of amygdala is a neural marker for post-traumatic stress disorder (PTSD) and improvement in control over amygdala activity has been associated with treatment success in PTSD. In this randomized, double-blind clinical trial we evaluated the efficacy of a real-time fMRI neurofeedback intervention designed to train control over amygdala activity following trauma recall. Twenty-five patients with PTSD completed three sessions of neurofeedback training in which they attempted to downregulate the feedback signal after exposure to personalized trauma scripts. For subjects in the active experimental group (N = 14), the feedback signal was from a functionally localized region of their amygdala associated with trauma recall. For subjects in the control group (N = 11), yoked-sham feedback was provided. Changes in control over the amygdala and PTSD symptoms served as the primary and secondary outcome measurements, respectively. We found significantly greater improvements in control over amygdala activity in the active group than in the control group 30-days following the intervention. Both groups showed improvements in symptom scores, however the symptom reduction in the active group was not significantly greater than in the control group. Our finding of greater improvement in amygdala control suggests potential clinical application of neurofeedback in PTSD treatment. Thus, further development of amygdala neurofeedback training in PTSD treatment, including evaluation in larger samples, is warranted.

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