Relationship between Stress Exposure and a Neural Measure of Emotional Response in Combat Veterans

2014-10-28T00:00:00Z (GMT) by Jacklynn M. Fitzgerald
Prior research suggests that individuals exposed to severe trauma exhibit subsequent atypical emotional reactivity to trauma-related or fear-inducing stimuli, which may be referred to as hyper-reactivity. While the exact cause of hyper-reactivity is currently unknown, it is clear that individual differences in the trait do exist and that variability may relate to environmental circumstances connected either to the trauma itself or to the experience of additional stress exposure. Further, inter-individual differences in the initiation and/or regulation of arousal may also contribute to defining the symptom. In this study, twenty-eight military veterans were recruited and tested on an emotion regulation task (ERT) during electroencephalogram (EEG) recording in order to study hyper-reactivity following exposure to combat as a unique traumatic event. The Late Positive Potential (LPP) was extracted as a neurophysiological index of arousal during directed (1) maintenance and (2) voluntary regulation of reactivity to negative imagery. In order to test predictive associations between ability to sustain reactivity and regulate reactivity with current symptoms of posttraumatic stress disorder (PTSD), severity of combat experiences, combat-associated stress and non-combat associated stress, bivariate ordinary least squares (OLS) regressions were performed. Results demonstrated that both pre-deployment stress exposure and a lack of unit support during deployment increased the LPP amplitude in the condition that prompted individuals to voluntarily regulate reactivity, suggesting that these stressors selectively increased reactive response when individuals are instructed to regulate. These findings offer evidence that emotional hyper-reactivity in combat-exposed veterans may be influenced by both combat-related and non-combat-related stress exposure, specifically in contributing towards failure to regulate.