Combat Exposure Severity Is Associated With Reduced Cortical Thickness in Combat Veterans: A Preliminary Report

Abstract

Background Chronic stress and related physiological responses are known to have deleterious effects on neural integrity. Combat exposure is a notoriously pathogenic stressor and with over 2 million U.S. troops deployed to active combat zones since 2001, there is an urgent need to advance our understanding of its potential neural impact. Previous evidence suggests structural alterations in PTSD and more recent studies have explored cortical thinning specifically. This preliminary study investigates the impact of combat exposure on cortical thickness, controlling for history of early life stress and age. Methods Twenty-one combat-exposed Veterans with PTSD and 20 non-PTSD combat-exposed controls (mean age 32.7) completed the Combat Exposure Scale, Childhood Trauma Questionnaire and structural magnetic resonance imaging in a Siemens 3T TIM trio system. GLM was used to examine the effect of combat exposure on cortical thickness, controlling for early life trauma exposure and age using cluster-wise correction (p<0.05). Results This preliminary study found a negative correlation between combat exposure severity (CES) and cortical thickness in the left superior temporal and left rostral middle frontal regions, as well as an interaction between PTSD diagnosis status and CES, in the superior temporal/insular region showing a stronger negative correlation between CES and cortical thickness in the non-PTSD group. Conclusions Though caution should be taken with interpretation given the preliminary nature of the findings, the results indicate combat exposure may affect cortical structure beyond possible alterations due to early life stress exposure or PTSD psychopathology. Though replication in larger samples is required, these results provide useful information regarding possible neural biomarkers and treatment targets for combat-related psychopathology as well as highlighting the pathogenic effects of combat.

Salience Network Disruption in U.S. Army Soldiers With Posttraumatic Stress Disorder

“… 1 , 27 Moreover, these cortical GBCr deficits have been reported in several psychiatric disorders with a considerable chronic stress component, including unipolar and bipolar depression, obsessive-compulsive disorder, and schizophrenia. 17 – 25 Intriguingly, despite extensive evidence suggesting stress- and PTSD-related cortical synaptic loss, 39 , 40 the current study and previous report 28 failed to demonstrate reduction in cortical GBCr in PTSD. Considering previous evidence correlating reduced cortical GBCr with avoidance and numbing symptoms, and increased cortical GBCr with arousal symptoms, 28 we interpret the increase of GBCr during trauma recollection as evidence that the functional dysconnectivity related to synaptic loss may have been masked by superimposed increased connectivity related to arousal and perhaps reexperiencing symptoms.…”

Salience Network Disruption in US Army Soldiers with PTSD

“…Moreover, these cortical GBCr deficits have been reported in several psychiatric disorders with a considerable chronic stress component, including unipolar and bipolar depression, obsessivecompulsive disorder, and schizophrenia (17)(18)(19)(20)(21)(22)(23)(24)(25). Intriguingly, despite extensive evidence suggesting stress-and PTSD-related cortical synaptic loss (39,40), the current study and previous report (28) failed to demonstrate reduction in cortical GBCr in PTSD. Considering previous evidence correlating reduced cortical GBCr with avoidance and numbing symptoms, and increased cortical GBCr with arousal symptoms (28), we interpret the increase of GBCr during trauma recollection as evidence that the functional dysconnectivity related to synaptic loss may have been masked by superimposed increased connectivity related to arousal and perhaps reexperiencing symptoms.…”

Blast-Exposed Veterans With Mild Traumatic Brain Injury Show Greater Frontal Cortical Thinning and Poorer Executive Functioning

“…Although we controlled for the total number of TBIs in our analyses, it is difficult to disentangle the unique contributions of subconcussive blast, mTBI, and repetitive mTBI on cortical thinning in the present study. Moreover, although PTSD has also been linked to cortical thinning ( 60 , 61 ) and cognition in Veteran mTBI samples ( 62 ), our mTBI+BE and mTBI-BE groups did not differ on this variable and we controlled for PTSD symptom severity in our analyses. Finally, additional work in this area should infuse other imaging metrics (e.g., arterial spin labeling) that may be more sensitive to blast-related brain changes, especially since mounting experimental animal evidence shows that blast-related head injury is associated with greater vascular pathology when compared to traditional blunt force TBI.…”