Multimodal structural neuroimaging markers of risk and recovery from posttrauma anhedonia: A prospective investigation

Abstract

Background: Anhedonic symptoms of posttraumatic stress disorder (PTSD) reflect deficits in reward processing that have significant functional consequences. Although recent evidence suggests that disrupted integrity of fronto-limbic circuitry is related to PTSD development, including anhedonic PTSD symptoms (posttrauma anhedonia [PTA]), little is known about potential structural biomarkers of long-term PTA as well as structural changes in fronto-limbic pathways associated with recovery from PTA over time. Methods: We investigated associations between white matter microstructure, gray matter volume, and PTA in 75 recently traumatized individuals, with a subset of participants (n = 35) completing follow-up assessment 12 months after trauma exposure. Deterministic tractography and voxel-based morphometry were used to assess changes in white and gray matter structure associated with changes in PTA. Results: Reduced fractional anisotropy (FA) of the uncinate fasciculus at around the time of trauma predicted greater PTA at 12-months posttrauma. Further, increased FA of the fornix over time was associated with lower PTA between 1 and 12-months posttrauma. Increased gray matter volume of the ventromedial prefrontal cortex and precuneus over time was also associated with reduced PTA. Conclusions: The microstructure of the uncinate fasciculus, an amygdala-prefrontal white matter connection, may represent a biomarker of vulnerability for later PTA. Conversely, development and recovery from PTA appear to be facilitated by white and gray matter structural changes in a major hippocampal pathway, the fornix. The present findings shed new light on neuroanatomical substrates of recovery from PTA and characterize white matter biomarkers of risk for posttraumatic dysfunction.

Prefrontal cortex, amygdala, and threat processing: implications for PTSD

“…Using DTI and structural imaging in the weeks following trauma exposure, research has shown that reduced fractional anisotropy of the uncinate fasciculus at around the time of trauma predicted greater PTSD symptoms (in particular posttraumatic anhedonia) at 12 months post-trauma. Furthermore, as the traumatized participants were followed over time, increased gray matter volume of the vmPFC was also associated with reduced trauma-related symptoms over the 12 months following trauma [157]. In another study recruiting patients after trauma exposure with mild traumatic brain injury, smaller cortical volumes of superior frontal cortex and rostral and caudal cingulate at 2 weeks after trauma exposure contributed to the prediction of increased likelihood of 3-month PTSD diagnosis in multivariable models incorporating other established risk factors [158].…”

Stress, PTSD, and COVID-19: the Utility of Disaster Mental Health Interventions During the COVID-19 Pandemic

“…The experts recommended longitudinal studies to ascertain the course of covid-related PTSD, to identify factors associated with PTSD, and to determine protective measures that can promote better outcomes [12] . These efforts might be supported when we are better able to utilize emerging biomarkers, multimodal early indicator assessment, and machine learning technology to increase the diagnostic accuracy of acute stress responses in order to prevent PTSD [13][14][15][16][17] .…”

An executive function subtype of PTSD with unique neural markers and clinical trajectories

“…These results also lend support to the idea that executive dysfunction contributes to the maintenance of PTSD [ 7 , 35 ] and above-average EF may be a protective factor. Previous work has also identified executive dysfunction as a risk factor for developing PTSD [ 63 , 64 ] and better EF as indicative of improved treatment outcomes and less dropout [ 12 , 15 , 16 ]. In addition, connectivity in regions associated with emotional regulation and EF predict PTSD symptoms post-trauma [ 64 ], consistent with the role of FPCN-LN in mediating the relationship between EF and PTSD chronicity.…”