ArticleJournal of anxiety disorders2022
Executive functioning deficits exacerbate posttraumatic stress symptoms: A longitudinal mediation model.
Article in Journal of anxiety disorders, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Pre-trauma cognitive traits predict fear generalization and associated prefrontal functioning in a longitudinal rodent model.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Cerebral small vessel disease moderates the association between executive dysfunction and spontaneous neural activity in adults who lost their only child.BMC medical imaging · 2026Article
- Relationships between executive function, mentalization and earthquake-related stress reactions in adults.BMC psychology · 2025Article
- The central executive network moderates the relationship between posttraumatic stress symptom severity and gastrointestinal related issues.Scientific reports · 2024Article
- The influence of aerobic exercise on model-based decision making in women with posttraumatic stress disorder.Journal of mood and anxiety disorders · 2023Article
- Executive Functioning Constructs in Anxiety, Obsessive-Compulsive, Post-Traumatic Stress, and Related Disorders.Current psychiatry reports · 2022Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Executive functioning (EF) consists of a set of related, but distinct, higher-level cognitive abilities that are used to organize and integrate lower-level processes in the service of engaging in goal-direct behavior. Evidence suggests that deficits in EF are a vulnerability factor for the development of posttraumatic stress (PTS) symptoms. Less understood, however, is the role that EF plays in symptom maintenance and exacerbation following trauma exposure. As such, the primary purpose of the present study was to determine whether EF deficits exacerbate PTS symptoms over the course of one year. A secondary aim of this study was to use a cross-lagged design to determine the directional relations among EF deficits and PTS. Trauma-exposed adults (N = 98) completed a clinical interview and self-report measures at an initial assessment session (Time 1 [T1]). Participants also completed self-report measures at 6- (Time 2 [T2]; n = 92) and 12-month (Time 3 [T3]; n = 91) follow-up sessions. As predicted, EF deficits at T2 mediated the relationship between PTS symptoms from T1 to T3, thus suggesting that EF deficits exacerbate PTS symptoms following trauma exposure. Results from a cross-lagged path analysis from T2 to T3 suggest that deficits in EF exert a stronger influence on the maintenance of PTS symptoms than vice versa. These results have implications for (a) identifying individuals that are at elevated risk for developing PTS symptoms, (b) developing precision medicine-based approaches for alleviating PTS symptoms, and (c) improving well-established PTSD treatments for those with relative deficits in EF.
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Registered trials
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