The Research Domain Criteria (RDoC) initiative promoted by the National Institute of Mental Health emphasizes a dimensional approach to psychopathology that is agnostic to DSM diagnosis. The RDoC project offers exciting possibilities for advancing research aimed at preventing psychopathology. However, prevention has historically been defined using diagnostic status, requiring the field to redefine what constitutes prevention using an RDoC approach. This article outlines new criteria for prevention in the RDoC context and provides guidance for implementing these criteria. We also describe the role of prevention-mechanism trials that examine whether preventive interventions change proximal etiological mechanisms known to be associated with psychopathology. We hope that these modified criteria and recommendations will stimulate new possibilities for prevention research that will advance the field.

Introduction

Prolonged attentional bias to threat (AB) is associated with posttraumatic stress symptoms (PTSS). However, it is unclear whether this relationship extends to early threat detection (elicited by masked stimuli) and/or varies if AB is measured during an aversive context.

Methods

Two trauma-exposed samples of either intervention-seekers (N = 50) or community members (N = 98) completed a masked dot-probe task to measure early AB to angry faces in safe vs. aversive contexts (i.e., during threat of aversive noises).

Results

Linear mixed effects models showed that an aversive context increased the orienting responses in both samples; however, PTSS did not moderate these effects in either sample.

Limitations

Sample size and heterogeneity of trauma-type may have impacted effect of PTSS on AB.

Conclusion

These results highlight the importance of assessing AB in varying contexts and examining generalizability across populations. Given prior research, the results also suggest that increased AB in PTSS may only be present for later attentional processes rather than early threat detection, at least with behavioral methods.

Mechanisms and predictors for the successful treatment of anxiety and depression have been elusive, limiting the effectiveness of existing treatments and curtailing the development of new interventions. In this study, we evaluated the utility of three widely used neural probes of emotion (experience, regulation, and perception) in their ability to predict symptom improvement and correlate with symptom change following two first-line treatments-selective serotonin reuptake inhibitors (SSRIs) and cognitive-behavioral therapy (CBT). Fifty-five treatment-seeking adults with anxiety and/or depression were randomized to 12 weeks of SSRI or CBT treatment (ClinicalTrials.gov identifier: NCT01903447). Functional magnetic resonance imaging (fMRI) was used to examine frontolimbic brain function during emotion experience, regulation, and perception, as probed by the Emotion Regulation Task (ERT; emotion experience and regulation) and emotional face assessment task (EFAT; emotion perception). Brain function was then related to anxiety and depression symptom change. Results showed that both SSRI and CBT treatments similarly attenuated insula and amygdala activity during emotion perception, and greater treatment-related decrease in insula and amygdala activity was correlated with greater reduction in anxiety symptoms. Both treatments also reduced amygdala activity during emotion experience but brain change did not correlate with symptom change. Lastly, greater pre-treatment insula and amygdala activity during emotion perception predicted greater anxiety and depression symptom improvement. Thus, limbic activity during emotion perception is reduced by both SSRI and CBT treatments, and predicts anxiety and depression symptom improvement. Critically, neural reactivity during emotion perception may be a non-treatment-specific mechanism for symptom improvement.

Objective

Reward positivity (RewP), a neurophysiologic index of reward responsivity, is consistently reduced in participants with depression and, to a lesser extent, anxiety. It remains unknown, however, whether RewP can be altered as psychiatric symptoms change with treatment. The current study addressed this question by examining differences in RewP within patients before and after 12 weeks of treatment with a selective serotonin reuptake inhibitor (SSRI) or cognitive-behavioral therapy (CBT). We also examined the utility of RewP as a predictor of symptom change during CBT and SSRI treatment.

Methods

Participants were recruited between 2014 and 2017 and included adults with a primary DSM-5 anxiety or depressive disorder (n = 63) and healthy controls (n = 25). At baseline and 12 weeks, participants completed a monetary award task while electroencephalogram (EEG) was recorded. Between EEG sessions, patients completed CBT or SSRI treatment.

Results

At baseline, higher levels of depressive symptoms were associated with a more attenuated RewP. We found no significant differences between patients and healthy controls in the degree of RewP change across the 12 weeks; however, among patients, the extent of increase in RewP robustly correlated with the extent of decline in depressive (t = -2.21, P = .03) and anxiety (t = -2.57, P = .02) symptoms following CBT and SSRI treatment. Additionally, a more attenuated RewP at baseline predicted a greater reduction in depressive symptoms following treatment with SSRIs (t = -2.04, P < .05), but not after CBT.

Conclusions

These findings highlight neural responsiveness to reward as both a mechanism and a predictor of depressive symptom change that may be used serve as an objective index of symptom improvement.

Trial registration

ClinicalTrials.gov identifier: NCT01903447.