Neuroimaging of posttraumatic stress disorder in adults and youth: progress over the last decade on three leading questions of the field

Abstract

Almost three decades have passed since the first posttraumatic stress disorder (PTSD) neuroimaging study was published. Since then, the field of clinical neuroscience has made advancements in understanding the neural correlates of PTSD to create more efficacious treatment strategies. While gold-standard psychotherapy options are available, many patients do not respond to them, prematurely drop out, or never initiate treatment. Therefore, elucidating the neurobiological mechanisms that define the disorder can help guide clinician decision-making and develop individualized mechanisms-based treatment options. To this end, this narrative review highlights progress made in the last decade in adult and youth samples on three outstanding questions in PTSD research: (1) Which neural alterations serve as predisposing (pre-exposure) risk factors for PTSD development, and which are acquired (post-exposure) alterations? (2) Which neural alterations can predict treatment outcomes and define clinical improvement? and (3) Can neuroimaging measures be used to define brain-based biotypes of PTSD? While the studies highlighted in this review have made progress in answering the three questions, the field still has much to do before implementing these findings into clinical practice. Overall, to better answer these questions, we suggest that future neuroimaging studies of PTSD should (A) utilize prospective longitudinal designs, collecting brain measures before experiencing trauma and at multiple follow-up time points post-trauma, taking advantage of multi-site collaborations/consortiums; (B) collect two scans to explore changes in brain alterations from pre-to-post treatment and compare changes in neural activation between treatment groups, including longitudinal follow up assessments; and (C) replicate brain-based biotypes of PTSD. By synthesizing recent findings, this narrative review will pave the way for personalized treatment approaches grounded in neurobiological evidence.

Fig. 1. A pictorial overview of findings from Question 1: which neural alterations serve as predisposing (pre-exposure) risk factors for PTSD development, and which are acquired (post-exposure) alterations?

Blue dots represent decreased activation. Red triangles represent increased activation. Solid blue represents decreased volume. Solid blue lines represent decreased structural integrity. Red lines represented increased structural integrity. Functional connectivity findings are depicted with arrows, with blue lines (–) that represent decreased functional connectivity and red lines (+) that represent increased functional connectivity. dACC dorsal anterior cingulate cortex, dmPFC dorsomedial prefrontal cortex, Hippo hippocampus, mPFC medial prefrontal cortex, OFC orbitofrontal cortex, rACC rostral anterior cingulate cortex, VS ventral striatum.

Fig. 2. A pictorial overview of findings from Question 2: Which neural alterations can predict treatment outcomes and define clinical improvement?

A Brain measures at baseline that predict a positive treatment response. B Brain measures associated with a positive response to treatment. Blue dots represent decreased activation. Red triangles represent increased activation. Solid blue represents decreased volume. Solid red represents greater volume. Solid blue lines represent decreased structural integrity. Functional connectivity findings are depicted with arrows, with blue lines (–) equating to decreased functional connectivity and red lines (+) equating to greater functional connectivity. dACC dorsal anterior cingulate cortex, dlPFC dorsolateral prefrontal cortex, Hippo hippocampus, OFC orbitofrontal cortex, PCC posterior cingulate cortex, rACC rostral anterior cingulate cortex, vmPFC ventromedial prefrontal cortex.