The current study examined biomarkers of stress in war-exposed young children and addressed maternal and child factors that may correlate with children's stress response. Participants were 232 Israeli children aged 1.5-5 years, including 148 children exposed to continuous war. Similarly, 56 were diagnosed with posttraumatic stress disorder (PTSD) and 92 were defined as exposed-no-PTSD. Child cortisol (CT) and salivary alpha amylase (sAA), biomarkers of the hypothalamic-pituitary-adrenal and sympathetic-adrenal-medullary arms of the stress response, were measured at baseline, following challenge, and at recovery. Maternal CT and sAA, PTSD symptoms, and reciprocal parenting, and child negative emotionality and regulatory strategies were assessed. Differences between war-exposed children and controls emerged, but these were related to child PTSD status. Children with PTSD exhibited consistently low CT and sAA, exposed-no-PTSD displayed consistently high CT and sAA, and controls showed increase in CT following challenge and decrease at recovery and low sAA. Exposed children showed higher negative emotionality; however, whereas exposed-no-PTSD children employed comfort-seeking strategies, children with PTSD used withdrawal. Predictors of child CT included maternal CT, PTSD symptoms, low reciprocity, and negative emotionality. Findings suggest that high physiological arousal combined with approach strategies may be associated with greater resilience in the context of early trauma.

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Exposure to combat-related trauma often leads to lifetime functional impairments. Previous research demonstrated the effects of oxytocin (OT) administration on brain regions implicated in post-traumatic stress disorder (PTSD); yet OT’s effects on brain patterns in trauma-exposed veterans have not been studied. In the current study the effects of OT on spontaneous brain oscillatory activity were measured in 43 veterans using magnetoencephalography (MEG): 28 veterans who were exposed to a combat-related trauma and 15 trauma-unexposed controls. Participants participated in two experimental sessions and were administered OT or placebo (PBO) in a double-blind, placebo-control, within-subject design. Following OT/PBO administration, participants underwent a whole-head MEG scan. Plasma and salivary OT levels were assessed each session. Spontaneous brain activity measured during a 2-min resting period was subjected to source-localization analysis. Trauma-exposed veterans showed higher resting-state alpha (8–13 Hz) activity compared to controls in the left dorsolateral prefrontal cortex (dlPFC), specifically in the superior frontal gyrus (SFG) and the middle frontal gyrus (MFG), indicating decreased neural activity in these regions. The higher alpha activity was “normalized” following OT administration and under OT, group differences were no longer found. Increased resting-state alpha was associated with lower baseline plasma OT, reduced salivary OT reactivity, and more re-experiencing symptoms. These findings demonstrate effects of OT on resting-state brain functioning in prefrontal regions subserving working memory and cognitive control, which are disrupted in PTSD. Results raise the possibility that OT, traditionally studied in social contexts, may also enhance performance in cognitive tasks associated with working memory and cognitive control following trauma exposure.

In the extant literature examining the brain mechanisms implicated in pain perception, researchers have theorized that the overlapping responses to pain in the self and in others mark the human capacity for empathy. Here we investigated how prior exposure to extreme pain affects pain perception, by assessing the dynamics of pain processing in veterans who were previously exposed to severe injury. Fortythree participants (28 pain-exposed and 15 controls) underwent whole-head magnetoencephalography (MEG) while viewing photographs of limbs in painful and nonpainful (neutral) conditions. Among controls, an early (0-220 ms) Bpain effect^in the posterior cingulate and sensorimotor cortices, and a later (760-900 ms) Bpain effect^in the posterior cingulate cortex, superior temporal gyrus/insula, and fusiform gyrus were found, indicated by enhanced alpha suppression to the pain versus nonpain conditions. Importantly, pain-exposed participants exhibited an atypical pain response in the posterior cingulate cortex, indicated by a normative response to pain, but no pain-to-no-pain differentiation. This may suggest that individuals exposed to extreme pain may perceive neutral stimuli as potentially threatening. Our findings demonstrate alterations in pain perception following extreme pain exposure, chart the sequence from automatic to evaluative pain processing, and emphasize the importance of considering past experiences in studying the neural response to others' states.