Blast-related traumatic brain injury (bTBI) is one of the most common injuries among Veterans who have served in recent wars in Iraq and Afghanistan. Despite representing a distinct mechanism of injury, long-term clinical and functional outcomes of bTBI are generally comparable with non-blast-related traumatic brain injury (TBI). However, controversy remains over whether bTBI etiology differentially impacts emotional regulation and neurocognition - particularly with respect to post-traumatic stress disorder (PTSD) and verbal and visual memory. Through diffusion tensor imaging (DTI), the present study investigates the microstructural pathophysiology of bTBI, compared to non-blast TBI, in neural pathways involved in emotional regulation and cognitive control.

Participants included 36 Veterans (25% female; age M = 36.33, SD = 10.11; years of education M = 15.67, SD = 2.34). Axial diffusivity (AD) in networks of emotional and cognitive control was acquired using magnetic resonance imaging (MRI) with a DTI protocol. Analyses of variance (ANOVA) were used to compare Veterans with self-reported bTBI (n = 23) to those with non-blast-related TBI (n = 13).

In the left hemisphere, Veterans with bTBI exhibited significantly smaller AD in axonal projections from the caudate nucleus (CN) to the orbitofrontal cortex (OFC), as well as in projections from the putamen to the OFC (p < 0.05). In the right hemisphere, Veterans with bTBI also exhibited significantly smaller AD in networks connecting the hippocampus to the amygdala (p < 0.05).

Compared to Veterans with non-blast-related TBI, Veterans with bTBI exhibited decreased AD in neural pathways from the CN to the OFC, the putamen to the OFC, and the hippocampus to the amygdala - indicative of increased axonal injury in these areas. Our results suggest that, on a microstructural level, emotional and cognitive networks are susceptible to longitudinal blast-related white matter damage. This is consistent with the literature in post-concussion syndrome (PCS) and provides a potential mechanism underlying results previously reported from this sample, describing subjective cognitive complaints in the absence of objective clinical deficits. As such, therapies that target networks of emotional and cognitive control may be particularly beneficial for Veterans with bTBI.