Abstract
Substantial individual differences exist in how acute stress affects large-scale neurocognitive networks, including salience (SN), default mode (DMN), and central executive networks (CEN). Changes in the connectivity strength of these networks upon acute stress may predict vulnerability to long-term stress effects, which can only be tested in prospective longitudinal studies. Using such longitudinal design, we investigated whether the magnitude of acute-stress-induced functional connectivity changes (delta-FC) predicts the development of post-traumatic stress-disorder (PTSD) symptoms in a relatively resilient group of young police students that are known to be at high risk for trauma exposure. Using resting-state fMRI, we measured acute-stress-induced delta-FC in 190 police recruits before (baseline) and after trauma exposure during repeated emergency-aid services (16-month follow-up). Delta-FC was then linked to the changes in perceived stress levels (PSS) and post-traumatic stress symptoms (PCL and CAPS). Weakened connectivity between the SN and DMN core regions upon acute-stress induction at baseline predicted longitudinal increases in perceived-stress level but not of post-traumatic stress symptoms, whereas increased coupling between the overall SN and anterior cerebellum was observed in participants with higher clinician-rated PTSD symptoms, particularly intrusion levels. All the effects remained significant when controlling for trauma-exposure levels and cortisol-stress reactivity. Neither hormonal nor subjective measures exerted similar predictive or acquired effects. The reconfiguration of large-scale neural networks upon acute-stress induction is relevant for assessing and detecting risk and resilience factors for PTSD. This study highlights the SN connectivity-changes as a potential marker for trauma-related symptom development, which is sensitive even in a relatively resilient sample.
Highlights
Exposure to severely stressful events can lead to a wide range of mental health problems, including post-traumatic stress symptoms [1]
No significant effects were observed for delta-PCL, nor for delta-perceived stress levels (PSS) scores. In this prospective longitudinal study, we investigated whether acute-stress-induced neural network changes could function as a risk factor of or a resilience factor against the development of post-traumatic stress-disorder (PTSD) symptoms
A different pattern emerged for neural-network changes between assessments that followed symptom development and appear acquired rather than a pretrauma risk factor: individuals with higher levels of PTSD intrusions symptoms at follow-up showed increased coupling between the SN and anterior cerebellum after acute stress induction in the follow-up versus baseline assessment
Summary
Exposure to severely stressful events can lead to a wide range of mental health problems, including post-traumatic stress symptoms [1]. The vast majority of research studying the neural mechanisms underlying stress-related psychopathology has adopted cross-sectional designs. These studies have identified a number of critical brain regions that may be involved in resilience, but could potentially reflect the symptoms that have already arisen [4]. Converging evidence from these studies suggests hyperactive amygdala as a predisposing factor for PTSD [4,5,6] These studies have largely used task-based fMRI that is tailored to investigate targeted neural regions of interest, and generally leave open the question regarding the involvement of larger-scale neural networks, beyond the regional focus [5]
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