Skip to main content
NCBI home page
NIHPA Author Manuscripts logoLink to NIHPA Author Manuscripts
. Author manuscript; available in PMC: 2023 Dec 1.
Published in final edited form as: J Trauma Stress. 2020 Jun 11;33(6):1007–1016. doi: 10.1002/jts.22551

Emotion Dysregulation Prospectively Predicts Posttraumatic Stress Disorder Symptom Severity 3 Months After Trauma Exposure

Courtney N Forbes 1, Matthew T Tull 1, Daniel Rapport 2, Hong Xie 3, Brian Kaminski 2, Xin Wang 2
PMCID: PMC10691918  NIHMSID: NIHMS1945767  PMID: 32529732

Abstract

Despite growing evidence in support of emotion dysregulation as a risk factor for the development of posttraumatic stress disorder (PTSD) following trauma exposure, few studies have examined temporal relations between emotion dysregulation and the onset and/or worsening of PTSD symptoms over time. The aim of the present study was to extend research on temporal associations between emotion dysregulation and PTSD in a sample of individuals recruited from hospital emergency departments soon after a traumatic event. Adult participants (N = 85; 62.4% female) completed self-report measures of emotion dysregulation and PTSD symptoms within 2 weeks of experiencing a traumatic event. Symptoms of PTSD were assessed approximately 3 months posttrauma. The results of a hierarchical linear regression analysis demonstrated that the inclusion of emotion dysregulation accounted for a significant amount of unique variance, β = .23, ΔR2 = .04, p = .042, in 3-month PTSD symptom severity over and above other risk factors and baseline PTSD symptoms. No specific facet of emotion dysregulation emerged as a significant predictor of 3-month PTSD symptoms when all facets were included on the same step of the model, βs = −.04–.33, ps = .133–.954. These results demonstrate that posttraumatic emotion dysregulation may predict PTSD symptoms 3 months after trauma exposure. These findings are consistent with a growing body of literature that speaks to the relevance of emotional processes to the onset and maintenance of PTSD following exposure to a traumatic event.

Although the vast majority of adults are exposed to potentially traumatic events in their lifetime, only a small proportion of trauma-exposed individuals go on to develop symptoms of posttraumatic stress disorder (PTSD), an often chronic and disabling psychiatric condition characterized by symptoms of reexperiencing, avoidance, negative alterations in cognition and mood, and hyperarousal (American Psychiatric Association [APA], 2013; Pietrzak, Goldstein, Southwick, & Grant, 2011). Given that PTSD is associated with high levels of functional impairment and healthcare utilization (Kartha et al., 2008; Thomas et al., 2010), there is a need to identify risk factors that can be targeted soon after trauma exposure to prevent the development of PTSD.

The findings from past studies have identified multiple risk factors for the development of PTSD following trauma exposure, including younger age at the time of the traumatic event, female gender, interpersonal versus noninterpersonal trauma exposure, and a history of other psychiatric disorders (Brewin, Andrews, & Valentine, 2000; Xue et al., 2016). Although these risk factors are informative in predicting which individuals may be more likely to develop PTSD following trauma exposure, they are not amenable to modification in the aftermath of a traumatic event. More recently, researchers have begun to explore a number of emotion-related risk factors, including anxiety sensitivity, emotional reactivity, and distress tolerance, which may be modifiable in the aftermath of a traumatic event and, thus, would be suitable targets for posttraumatic early interventions (Boffa et al., 2016; Fitzgerald et al., 2018; Overstreet et al., 2018). One factor that warrants additional attention as a modifiable risk factor for PTSD is emotion dysregulation.

Gratz and Roemer (2004) conceptualized emotion regulation as a multidimensional construct involving the (a) awareness, understanding, and acceptance of emotions; (b) ability to control impulsive behaviors and engage in goal-directed behavior when experiencing negative emotions; (c) flexible use of nonavoidant, situationally appropriate strategies to modulate the intensity and duration of emotional responses to meet individual goals and situational demands; and (d) willingness to experience negative emotions in the pursuit of meaningful activities in life. Emotion dysregulation would be characterized by deficits in one or more of these abilities. This model of emotion regulation broadly focuses on the ability to respond to emotions in a manner that promotes the functional use of emotions as information and the pursuit of valued actions and desired goals (Gratz & Roemer, 2004). As such, this model can be distinguished from other models of emotion regulation that emphasize the specific strategies individuals use in the moment to influence or modulate emotional arousal (Gross, 2015). However, it is important to note that these models are not expected to be mutually exclusive, as broad emotion regulation ability would be expected to impact which specific emotion regulation strategies are used in a given situation, and vice versa; for example, reliance on emotional avoidance as a specific emotion regulation strategy could negatively affect one’s ability to be aware of or differentiate between emotional states (Tull & Aldao, 2015).

Emotion dysregulation has been identified as a core component of PTSD (Ehring & Quack, 2010; Seligowski, Lee, Bardeen, & Orcutt, 2015; Tull, Barrett, McMillan, & Roemer, 2007) and is thought to influence the development of PTSD symptoms through multiple pathways (Hien, Lopez-Castro, Papini, Gorman, & Ruglass, 2017). An individual’s typical (i.e., trait) level of emotion dysregulation prior to a traumatic event has been identified as a risk factor for the development of PTSD in various diverse samples (see Seligowski et al., 2015, for a meta-analysis). In addition to trait-level vulnerabilities toward emotion dysregulation, recent findings have demonstrated that emotion dysregulation may vary over time and across situations, and that measures of state emotion dysregulation may only correlate moderately with trait measures at any given time (Boden et al., 2015; Lavender, Tull, DiLillo, Messman-Moore, & Gratz, 2017). The experience of a traumatic event can result in a wide range of intense emotional experiences, such as fear, shame, anger, and sadness (Rizvi, Kaysen, Gutner, Griffin, & Resick, 2008), which may exacerbate pretraumatic trait levels of emotion dysregulation. As the frequency of these intense emotions increases, they may become more difficult to regulate, resulting in more emotional nonacceptance, more difficulties distinguishing between different emotional states, and increased reliance on maladaptive emotion regulation strategies.

For example, the experience of distressing emotions in response to internal or external reminders of a traumatic event may lead to the development of maladaptive patterns of avoidance behaviors that are intended to reduce contact with those reminders. Frequent experiences of distressing emotions may also lead individuals to engage in risky and/or self-destructive behaviors in an effort to avoid and/or modulate unwanted emotional experiences. Although these strategies may bring about an immediate reduction in distress, they are likely to prevent exposure to corrective information in the long-term, ultimately interfering with emotional processing and increasing the risk for the development and exacerbation of PTSD symptoms (Foa & Kozak, 1986). Moreover, speaking to its clinical relevance, there is increasing evidence that baseline emotion dysregulation may influence outcomes in evidence-based treatments for PTSD (Hien et al., 2017; Jerud, Pruitt, Zoellner, & Feeny, 2016) and that change in emotion dysregulation over the course of PTSD treatment may predict posttreatment PTSD severity (Boden et al., 2013; McLean et al., 2019).

Several previous studies have provided evidence that specific putatively maladaptive emotion regulation strategies, such as dissociation, difficulties using cognitive reappraisal, experiential avoidance, and rumination, may predict PTSD symptom onset following trauma exposure (Fitzgerald et al., 2018; Jenness et al., 2016; Kampula, Orcutt, & Bardeen, & Varkovitzky, 2011; Murray, Ehlers, & Mayou, 2002). However, only one study of which we are aware has examined the predictive role of emotion dysregulation as defined by Gratz and Roemer (2004) in the development of PTSD symptoms (Bardeen, Kumpula, & Orcutt, 2013). In that study, emotion dysregulation and PTSD symptoms were assessed before and after a mass shooting on a college campus. Ratings of emotion dysregulation prior to the event predicted PTSD symptoms in the immediate aftermath of the shooting as well as PTSD symptoms approximately 8 months later. These preliminary data suggest that emotion dysregulation as defined by Gratz and Roemer (2004) before trauma exposure may influence the onset and maintenance of PTSD symptoms. However, the study by Bardeen and colleagues (2013) was conducted within an undergraduate sample and only assessed responses to one specific type of traumatic event (i.e., a mass shooting). Moreover, Bardeen et al. did not evaluate the influence of specific facets of emotion dysregulation, including nonacceptance of emotions, lack of emotional awareness and/or clarity, difficulties engaging in goal-directed behavior when distressed, difficulties controlling impulsive behaviors when distressed, and limited access to effective emotion regulation strategies, on the development of PTSD.

A small number of studies have examined specific facets of emotion dysregulation in relation to PTSD symptoms, with some results demonstrating associations between PTSD and all examined facets of emotion dysregulation (Ehring & Quack, 2010; Frewen, Dozois, Neufeld, & Lanius, 2012) and others showing associations with some facets of emotion dysregulation but not others. For example, the results of several studies have demonstrated associations between PTSD and all facets of emotion dysregulation apart from lack of emotional awareness and/or clarity (O’Brian, McLeish, Kramer, & Fleming, 2015; Weiss et al., 2012; Weiss, Tull, Anestis, & Gratz, 2013).

Specific facets of emotion dysregulation have also been examined concerning risky behaviors in the context of PTSD. In a study of male veterans, both difficulties controlling impulsive behaviors when distressed and lack of emotional awareness and/or clarity were found to mediate the relation between PTSD and alcohol misuse (Tripp & McDevitt-Murphy, 2015). In this example, a lack of awareness and/or clarity regarding one’s emotions may cause an individual to experience these emotions as overwhelming, unpredictable, and distressing, thus resulting in a reliance on alcohol to potentially escape that distress. Likewise, difficulty controlling impulsive behaviors when distressed may increase the likelihood of behaviors that function to provide immediate negative reinforcement, such as alcohol misuse. Similarly, in a large sample of women with alcohol dependence, difficulty engaging in goal-directed behavior when emotionally distressed fully mediated the relation between PTSD and alcohol use disorder (Goldstein, Bradley, Ressler, & Powers, 2017). It is possible that difficulty engaging in goal-directed behavior in the context of emotional distress may impair an individual’s ability to plan and enact adaptive coping behaviors to modulate emotional distress, resulting in a reliance on maladaptive coping strategies, such as alcohol use. However, given mixed findings on this topic, additional research using prospective designs is needed to understand how specific facets of emotion dysregulation may predict responses to different types of traumatic events across diverse populations of trauma-exposed individuals.

The present study aimed to extend research on the temporal relations between emotion dysregulation and PTSD. We examined the influence of both emotion dysregulation overall and specific facets of emotion dysregulation on later PTSD symptom severity in a diverse sample of individuals recruited from hospital emergency departments (EDs) shortly after a traumatic event. We hypothesized that higher levels of emotion dysregulation soon after a traumatic event would predict PTSD symptom severity 3 months after the traumatic event. We predicted that emotion dysregulation would continue to predict 3-month PTSD symptom severity even when accounting for other well-established PTSD risk factors and baseline PTSD symptom severity. We made no specific hypotheses regarding associations between different facets of emotion dysregulation and PTSD symptoms; thus, this aspect of the study was considered exploratory.

Method

Participants

Adult participants (N = 85, 62.4% female) were recruited from two hospital EDs within 48 hr after a traumatic event; recruitment was part of a larger, ongoing longitudinal study of neural and environmental predictors of PTSD development following trauma exposure. Participants were excluded from the larger study if they were pregnant, under the influence of alcohol or drugs at the time of the traumatic event, or had major injuries (i.e., Abbreviated Injury Scale score higher than 2; Petrucelli, States, & Hames, 1981), moderate to severe traumatic brain injury, major medical illness affecting general health, or conditions that precluded further assessment procedures. Concerning racial background, most participants were Black or African American (56.3%) or White (40.0%), with smaller percentages of participants identifying as Asian American (1.3%), multiracial (1.3%), and “other” (1.3%). A majority of participants were admitted to the ED for a motor vehicle accident (54.2%) or interpersonal traumatic event, including physical and sexual assault (41.9%). Data collection for the larger study is ongoing. At the time of data analysis, 85 participants had completed 3-month follow-up questionnaires.

Participants in the present study represented a subsample of a larger group (N = 149). The present study participants were included because they provided complete data for 3-month follow-up questionnaires. The response rate for 3-month follow-up questionnaires was 57.0%. There were no significant differences regarding gender, race, ethnicity, lifetime traumatic event exposure, and exposure to adverse and potentially traumatic childhood events in individuals who completed 3-month follow-up questionnaires and those who did not. There was a significant difference in baseline emotion dysregulation, t(147) = −2.34, p = .021. Individuals who returned 3-month questionnaires reported higher levels of baseline emotion dysregulation as measured using the Difficulties in Emotion Regulation Scale (DERS; Gratz & Roemer, 2004; MDERS = 101.95, SD = 28.33) compared to those who did not return 3-month questionnaires (MDERS = 91.47, SD = 25.26). There was also a significant difference in baseline PTSD symptoms, t(144) = −5.64, p < .001. Individuals who returned 3-month questionnaires reported higher levels of baseline PTSD symptom severity on the PTSD Checklist–Stressor-Specific version (PCL-5; Weathers et al., 2013; MPCL-5 = 49.77, SD = 16.48) compared to those who did not return 3-month questionnaires (MPCL-5 = 33.44, SD = 18.27).

Regarding trauma exposure before the index traumatic event, 8.7% of participants reported no prior exposure to traumatic events, 19.6% reported prior exposure to one traumatic event, 10.9% reported prior exposure to two traumatic events, 23.9% reported prior exposure to three traumatic events, and 36.9% reported prior exposure to four or more traumatic events. Concerning exposure to adverse and potentially traumatic experiences in childhood, 51.8% of participants reported exposure to a severe level of emotional abuse, 48.8% reported exposure to a severe level of physical abuse, 45.1% reported exposure to a severe level of sexual abuse, 34.1% reported exposure to a severe level of emotional neglect, and 48.81% reported exposure to a severe level of physical neglect (see Bernstein & Fink, 1998, for cutoff thresholds). At 3-month follow-up, 49 participants (57.6% of the sample) had PCL-5 scores above the clinical cutoff for probable PTSD. Additionally, 24.7% of participants reported that they had seen a psychologist, psychiatrist, or social worker in the time between the index traumatic event and 3-month follow-up.

Procedure

All study procedures were approved by the University of Toledo Institutional Review Board. Participants were contacted within 48 hours of their initial ED visit, and interested participants were scheduled for a brief informed consent session. Participants who provided informed consent were scheduled for a subsequent session within 2 weeks of the index traumatic event (M = 8.87 days, SD = 4.10). At this session, participants completed the Time 0 questionnaires, which included a survey of demographic information and the DERS, PCL-5, Brief Trauma Questionnaire, and Childhood Trauma Questionnaire.

Follow-up questionnaires, including the PCL-5, were mailed to participants’ homes approximately 3 months after the traumatic event. To encourage survey completion, participants were contacted by phone approximately 10 days after the questionnaires were mailed. Additionally, participants were asked to update their contact information if their home address changed over the course of the study. At both Time 0 and 3-month follow-up, participants were instructed to complete the PCL-5 using the event that brought them into the ED (i.e., the index traumatic event) as the reference. Participants were compensated $20 (USD) for the initial consent session, $10 for the Time 0 questionnaires, and $20 for the 3-month questionnaires, for total compensation of $50 if all sessions were completed.

Measures

Emotion regulation

The DERS (Gratz & Roemer, 2004) is a 36-item, self-report measure that assesses individuals’ typical level of emotion regulation difficulties. Participants rate each item on a 5-point Likert scale ranging from 1 (almost never [0%–10%]) to 5 (almost always [91%–100%]). Items were recoded and summed, with higher scores indicating a higher level of emotion dysregulation. The measure includes six domains: nonacceptance of negative emotions (six items; score range: 6–30), inability to engage in goal-directed behavior when distressed (five items; score range: 5–25), difficulties controlling impulsive behavior when distressed (six items; score range: 6–30), limited access to emotion regulation strategies perceived to be effective (eight items; score range: 8–40), lack of emotional awareness (six items; score range: 6–30), and lack of emotional clarity (five items; score range: 5–25). Scores for the total scale range from 36 to 180. The DERS has demonstrated adequate construct and predictive validity (Gratz & Roemer, 2004; Gratz & Tull, 2010). In the present sample, internal consistency was acceptable for the full scale, Cronbach’s α = .87, and for all subscales, Cronbach’s αs = .76–.92.

PTSD symptoms

Participants completed the PCL-5 (Weathers et al., 2013), a 20-item self-report measure that assesses the severity of PTSD symptoms as outlined in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), using the index traumatic event as a response reference. Respondents rate PCL-5 items on a scale of 0 (not at all) to 4 (extremely), with total scores ranging from 0 to 80. Item-level responses were summed to create a total score. The PCL-5 has been found to demonstrate strong test–retest validity as well as convergent and discriminant validity in a variety of samples (Blevins, Weathers, Davis, Witte, & Domino, 2015). A score of 33 has been recommended as a clinical cutoff for probable PTSD (Bovin et al., 2016; Weathers et al., 2013). In the present sample, internal consistency was acceptable, Cronbach’s α = .94.

Lifetime trauma history

The BTQ (Schnurr, Vielhauer, Weathers, & Findler, 1999) was used to assess lifetime traumatic event exposure prior to the index traumatic event. Participants are asked to indicate whether or not they have been exposed to a number of traumatic events (yes or no), and whether those events involved actual or threatened physical injury or fear of death. The BTQ was represented as a dichotomous variable (0 = no past traumatic event exposure; 1 = past traumatic event exposure).

Childhood trauma history

The CTQ (Bernstein et al., 2003) was used to assess exposure to adverse and potentially traumatic experiences in childhood. The measure assesses adverse childhood experiences in five domains: emotional abuse, physical abuse, sexual abuse, emotional neglect, and physical neglect. Each item is rated on a Likert scale ranging from 1 (never true) to 5 (very often true). Each domain-specific subscale contains five items, and scores for all subscales range from 5 to 25. Subscale scores were combined to create an overall score reflecting childhood adversity and exposure to traumatic events. In the present sample, internal consistency for the overall scale, Cronbach’s α = .75, and subscales, Cronbach’s αs = .78–.97, was acceptable, except for the Emotional Neglect subscale, α = .47.

Data Analysis

All participants provided complete data for the DERS at Time 0 and the PCL-5 at 3-month follow-up. Five participants (5.8%) had missing data for the Time 0 PCL-5, six participants (7.1%) had missing data for the CTQ, two participants (2.5%) had missing data for trauma type, and five participants (5.8%) had missing data regarding racial background. Given that these were not primary outcome variables and considering our desire to maximize statistical power for the primary analyses, these participants were included in analyses, with missing data excluded casewise. Data analyses were conducted using IBM SPSS Statistics for Windows (Version 25.0; IBM Corp., 2017). Pearson product–moment and point–biserial correlations were used to examine associations among the primary variables of interest. A hierarchical linear regression analysis was used to test whether emotion dysregulation after trauma exposure predicted 3-month PTSD symptom severity above and beyond baseline PTSD symptom severity and other PTSD risk factors. A second hierarchical linear regression analysis was used to test whether specific facets of emotion dysregulation (i.e., emotional nonacceptance, difficulties engaging in goal-directed behavior when distressed, difficulties controlling impulsive behaviors when distressed, lack of access to effective emotion regulation strategies, lack of emotional awareness, and lack of emotional clarity) predicted 3-month PTSD symptom severity above and beyond baseline PTSD symptoms and other risk factors. Our sample size (N = 85) provided adequate statistical power, 1-β = .94, to detect medium effect sizes in all regression analyses (G*Power 3.1; Faul, Erdfelder, Buchner & Lang, 2009).

Results

Descriptive statistics and intercorrelations for the variables of interest are presented in Table 1. Given acceptable ranges for normality (i.e., +/−2 for skewness; +/−7 for kurtosis; Field, 2009), no transformations were applied. To test whether emotion dysregulation after trauma exposure predicted 3-month PTSD symptom severity above and beyond baseline PTSD symptom severity and other PTSD risk factors, a hierarchical linear regression analysis was conducted. In the first step of the model, age, gender, race, ethnicity, type of traumatic event (represented as a dichotomous variable of interpersonal traumatic event [physical and sexual assault] vs. other types of events [motor vehicle accident, serious accident/fall, and other trauma exposure]), childhood adversity/trauma exposure (assessed via the CTQ), lifetime trauma exposure (assessed via the BTQ), and PTSD symptom severity at Time 0 were entered. Time 0 emotion dysregulation was entered in the second step of the model. The severity of PTSD symptoms at 3-month follow-up served as the dependent variable.

Table 1.

Pearson Product Moment and Point Biserial Correlations Between Variables of Interest

1 2 3 4 5 6 7 8 9 10 11 12 13 14
1. Age −.05 −.03 .05 .18 .12 −.18 −.02 −.03 .11 −.06 .06 −.10 −.10
2. Gender (% female) − −.16 −.19 −.24* −.36* −.13 −.16* −.21 −.02 −.13 −.20 −.004 −.16
3. Trauma (% IPTa) − .23* .11 .22 .17 .24* .25* .12 .34* .20 .02 .13
4. Time 0 PTSD symptoms - .58* .37* .09 .42* .53* .35* .30* .46* .06 .16
5. 3-month PTSD symptoms - .38* −.02 .45* .40* .40* .35* .55* .08 .23*
6. CTQ - .14 .42* .36* .28* .39* .48* .11 .19
7. BTQ (% with trauma history) - −.04 .05 .07 −.02 −.03 −.18 .004
8. Time 0 DERS - .75* .85* .83* .88* .48* .79*
9. Time 0 DERS ACCEPT - .59* .60* .73* .05 .42*
10. Time 0 DERS GOALS — .62* .79* .28* .62*
11. Time 0 DERS IMPULSE - .66* .26* .58*
12. Time 0 DERS STRATEGIES - .20 .59*
13. Time 0 DERS AWARE - .54*
14. Time 0 DERS CLARITY -
Range 18–59 27–78 2–77 29–121 48–160 6–30 5–25 6–30 8—40 6–30 5–23
% 62.4 42.2 91.7
M 34.12 50.96 37.51 60.09 101.95 16.47 16.24 15.91 23.41 16.40 13.51
SD 10.87 13.96 20.39 123.81 28.33 5.85 5.27 7.30 7.88 5.92 4.55
Open in a new tab

Note. Time 0 = baseline; IPT = interpersonal trauma; CTQ = Childhood Trauma Questionnaire; BTQ = Brief Trauma Questionnaire; DERS = Difficulties in Emotion Regulation Scale; ACCEPT = Emotional Non-Acceptance subscale; GOALS = Inability to Engage in Goal-Directed Behavior when Distressed subscale; IMPULSE = Difficulties Controlling Impulsive Behaviors when Distressed subscale; STRATEGIES = Lack of Access to Effective Emotion Regulation Strategies subscale; AWARE = Lack of Emotional Awareness subscale; CLARITY = Lack of Emotional Clarity subscale.

a

Includes physical and sexual assault.

*

p < .05.

The first step of the model was significant, accounting for 43% of the variance in 3-month PTSD symptom severity, R2 = .43, ΔF(8, 58) = 5.46, p < .001. Only Time 0 PTSD symptom severity emerged as a significant predictor of 3-month PTSD symptom severity in this step, β = .56, p < .001. The inclusion of Time 0 emotion dysregulation significantly improved the model, accounting for a significant amount of unique variance (4%) in 3-month PTSD symptom severity, ΔR2 = .04, ΔF(1,57) = 4.35, p = .042. Both Time 0 PTSD symptom severity and Time 0 emotion dysregulation emerged as significant predictors in the final model, βs = .23–.50, p < .001–p = .042. Notably, the association between Time 0 emotion dysregulation and 3-month PTSD symptom severity remained significant, β = .22, p = .049, when mental health treatment received between Time 0 and 3-month follow-up, assessed dichotomously as yes versus no, was included in the model.

A second hierarchical linear regression analysis was conducted to examine the associations between specific DERS subscale scores and 3-month PTSD symptoms. As in the regression model described previously, age, gender, race, ethnicity, type of traumatic event (represented as a dichotomous variable of interpersonal traumatic event versus other types of events), childhood adversity and/or trauma exposure, lifetime trauma exposure, and PTSD symptom severity at Time 0 were entered in the first step of the model. All DERS subscales were entered in the second step of the model. The inclusion of all DERS subscales on the second step did not result in significant improvement to the model, ΔR2 = .07, ΔF(6, 52) = 1.24, p = .302. No specific scales emerged as significant predictors of 3-month PTSD symptoms, βs = −.04–.33, ps = .133–.954. Variance inflation factor (VIF) statistics for DERS subscales in this model ranged from 1.72 to 4.89.

Discussion

The goal of the present study was to examine the impact of emotion dysregulation, relative to other risk factors, on PTSD symptom severity 3 months after trauma exposure. Our hypothesis was supported. Emotion dysregulation was significantly associated with PTSD symptom severity 3 months following exposure to a traumatic event. Of note, this finding was obtained even when taking into account other well-established risk factors for PTSD, including age, gender, race, ethnicity, trauma type, childhood adversity or trauma exposure, and lifetime trauma exposure, as well as baseline PTSD symptom severity; this finding speaks to the robust influence of emotion dysregulation on the risk for PTSD. These results are consistent with theoretical (Cloitre & Rosenberg 2006; van der Kolk, 1996) and empirical (Ehring & Quack, 2010; Tull et al., 2007) literature highlighting the relevance of emotion dysregulation to the onset and maintenance of PTSD symptoms. These results are also consistent with recent findings that have suggested emotion regulation abilities (Bardeen et al., 2013) and specific emotion regulation strategies (Fitzgerald et al., 2018; Jenness et al., 2016; Kampula et al., 2011; Murray et al., 2002) can be implicated in the development of PTSD symptoms after trauma exposure.

However, although the inclusion of emotion dysregulation in the regression model predicting 3-month PTSD symptoms resulted in significant improvement over the previous model, it is important to note that the inclusion of emotion dysregulation only resulted in a 4% increase in variance in 3-month PTSD symptoms, with 53% of the variance remaining unexplained. The pathogenesis of PTSD following trauma exposure is likely determined by multiple factors, and risk factor models will have more predictive ability when they consider variables across multiple levels or domains. For example, future research on this topic would benefit from the examination of other person-level factors, such as posttrauma alterations in beliefs about the self, others, and the world (Resick, Monson, & Chard, 2006), and environmental factors, such as social support (Brewin et al., 2000) that may account for additional variance in the onset and maintenance of PTSD symptoms following exposure to a traumatic event.

A number of individuals in the sample (n = 21; 24.7%) reported that they saw a psychologist, psychiatrist, or social worker in the time between the traumatic event and 3-month follow-up. It is somewhat surprising that the relation of baseline emotion dysregulation to 3-month PTSD symptoms remained significant when mental health treatment within the past 3 months, assessed dichotomously as yes or no, was included in the model. However, specific information, such as the type of mental health professional, treatment approach, or frequency and duration of treatment, was not collected in this study. Future research conducted in larger samples would benefit from examining these factors in greater detail to elucidate the mediating role of mental health treatment in the association between emotion dysregulation following trauma exposure and subsequent PTSD symptoms.

Despite zero-order correlations between all Time 0 DERS subscales (except the Lack of Emotional Awareness scale; see Table 1) and 3-month PTSD symptom severity, no specific facet of emotion dysregulation emerged as a significant predictor of 3-month PTSD symptoms when all subscales were included on the same step of the model. These results may have been influenced by the high degree of multicollinearity among DERS subscales, VIFs = 1.72–4.89. These results suggest that an overall score representing broad emotion dysregulation may be the most effective approach to examining risk for the development of PTSD symptoms. This is consistent with previous work supporting a unidimensional factor structure for the DERS (Bjureberg et al., 2015).

The strengths of the present study included the use of a recently traumatized sample recruited from hospital EDs and a longitudinal design that allowed for follow-up assessments of PTSD symptoms over a 3-month period. However, study limitations, which should be considered when interpreting the findings, must be discussed. An important limitation of the study is that we did not collect information regarding the presence of PTSD symptoms related to past traumatic events. We included lifetime traumatic event exposure and childhood exposure to stressful and potentially traumatic events as covariates in all analyses to account for the possible effects of experiences that could have given rise to PTSD symptoms, but it remains unclear to what extent PTSD symptoms related to past traumatic events may have influenced PTSD symptoms related to the index traumatic event as measured at 3-month follow-up.

Another key limitation of the study was the absence of information regarding participants’ levels of emotion dysregulation before the index traumatic event. Research suggests that emotion dysregulation has both trait and state components (Lavender et al., 2017), and, given the design of the present study, it was not possible to tease apart the relative contributions of participants’ typical levels of emotion dysregulation from emotion dysregulation precipitated by recent exposure to a traumatic event. Additionally, given high participant rates of exposure to both adverse childhood experiences and PTSD Criterion A traumatic events before the index traumatic event, participants’ exposure to previous traumatic experiences may have influenced their emotion regulation abilities both prior to and in the aftermath of the index traumatic event. Although there is little research on the influence of pretrauma emotion dysregulation on the development of PTSD after trauma exposure, preliminary findings suggest that pretraumatic emotion dysregulation may indeed be associated with the onset and maintenance of PTSD symptoms (Bardeen et al., 2013). In the future, prospective research designs could be used to further examine the associations among pretraumatic emotion dysregulation and PTSD-related outcomes following exposure to a traumatic event.

An additional limitation was that PTSD symptom severity was assessed using a self-report measure rather than clinical interviews. Similarly, the administration of 3-month follow-up questionnaires via mail may have contributed to a lower 3-month response rate (57.0%) than we would have gotten if participants had completed the 3-month questionnaires in person. This may have introduced bias into the study sample and results; for example, participants with less functional impairment as a result of PTSD symptoms may have been more likely to complete and return the questionnaires by mail. Were this the case, the present results may underestimate the relation between Time 0 emotion dysregulation and the severity of 3-month PTSD symptoms. It is also possible that participants who completed and returned the 3-month questionnaires differed from nonresponders on a relevant personality trait (e.g., conscientiousness) or clinical characteristic (e.g., lower levels of depression symptoms) that may have influenced the results.

As noted, participants in the present study were selected from a larger sample based on having provided 3-month follow-up data. There were significant differences in baseline emotion dysregulation and PTSD symptoms between individuals included in this study (i.e., individuals who provided data at the 3-month follow-up) and individuals from the larger subsample who were excluded from this study due to incomplete data, with those included in the present study reporting significantly higher levels of baseline emotion dysregulation and PTSD symptom severity. Although it is not clear why this is the case, these differences suggest that individuals included in the present sample may have experienced somewhat more severe emotion dysregulation and PTSD symptoms compared to a typical population of individuals seeking treatment in the ED after a traumatic event.

Participants for the present study were individuals who sought treatment from an ED following exposure to a traumatic event; as such, it is not clear whether these results would generalize to individuals who did not sustain physical injuries or did not seek treatment from an ED after a traumatic event. Moreover, most participants in the present sample experienced either a motor vehicle accident or physical assault, which may limit the generalizability of results to individuals who have been exposed to other types of traumatic events. Given prior research demonstrating that emotion dysregulation may be more prominent in individuals who have experienced early-onset chronic interpersonal trauma, versus single-event or late-onset trauma (Ehring and Quack, 2010), it will be especially important for future research in this area to examine the predictive role of emotion dysregulation in the development of PTSD symptoms in populations exposed to specific types of traumatic events. Further research is also needed to clarify the pathways through which emotion dysregulation may contribute to the development and maintenance of PTSD over extended periods, perhaps using longer follow-up periods. Ecological momentary assessment methods may also provide a window into the reciprocal relations between emotion dysregulation and PTSD symptoms in the context of individuals’ daily lives.

The present results demonstrate that in a sample of individuals initially assessed within 2 weeks of presentation to a hospital ED for treatment following exposure to a traumatic event, baseline emotion dysregulation predicted the severity of PTSD symptoms 3 months later over and above the influence of baseline PTSD symptoms and other established risk factors for the development of PTSD, including age, gender, race, ethnicity, trauma type, and lifetime traumatic event exposure. These findings are consistent with a growing body of literature that speaks to the relevance of emotional processes in the onset and maintenance of PTSD following trauma exposure and may lay the groundwork for future studies examining the pathways through which posttraumatic emotion dysregulation may influence the trajectory of PTSD symptoms over time.

Acknowledgments

This work was supported by R01 MH110483 awarded to Dr. Xin Wang.

References

  1. Adler AB, Castro CA, & McGurk D (2009). Time-driven battlemind psychological debriefing: A group-level early intervention in combat. Military Medicine, 174, 21–28. 10.7205/MILMED-D-00-2208 [DOI] [PubMed] [Google Scholar]
  2. American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Washington, DC: Author. [Google Scholar]
  3. Bardeen JR, Kumpula MJ, & Orcutt HK (2013). Emotion regulation difficulties as a prospective predictor of posttraumatic stress symptoms following a mass shooting. Journal of Anxiety Disorders, 27, 188–196. 10.1016/j.janxdis.2013.01.003 [DOI] [PMC free article] [PubMed] [Google Scholar]
  4. Bardeen JR, Tull MT, Stevens EN, & Gratz KL (2015). Further investigation of the association between anxiety sensitivity and posttraumatic stress disorder: Examining the influence of emotional avoidance. Journal of Contextual Behavioral Science, 4, 163–169. 10.1016/j.jcbs.2015.05.002 [DOI] [PMC free article] [PubMed] [Google Scholar]
  5. Bernstein DP, & Fink L (1998). Childhood Trauma Questionnaire: A retrospective self-report (CTQ). San Antonio, TX: NCS Pearson. [Google Scholar]
  6. Bernstein DP, Stein JA, Newcomb MD, Walker E, Pogge D, Ahluvalia T, . . . Zule W (2003). Development and validation of a brief screening version of the Childhood Trauma Questionnaire. Child Abuse & Neglect, 27, 169–190. 10.1016/S0145-2134(02)00541-0 [DOI] [PubMed] [Google Scholar]
  7. Bjureberg J, Ljόtsson B, Tull MT, Hedman E, Sahlin H, Lundh LG, . . . Gratz KL (2016). Development and validation of a brief version of the difficulties in emotion regulation scale: the DERS-16. Journal of Psychopathology and Behavioral Assessment, 38, 284–296. 10.1007/s10862-015-9514-x [DOI] [PMC free article] [PubMed] [Google Scholar]
  8. Blevins CA, Weathers FW, Davis MT, Witte TK, & Domino JL (2015). The Posttraumatic Stress Disorder Checklist for DSM-5 (PCL-5): Development and initial psychometric evaluation. Journal of Traumatic Stress, 28, 489–498. 10.1002/jts.22059 [DOI] [PubMed] [Google Scholar]
  9. Boden MT, Westermann S, McRae K, Kuo J, Alvarez J, Kulkarni MR, . . . Bonn-Miller MO (2013). Emotion regulation and posttraumatic stress disorder: A prospective investigation. Journal of Social and Clinical Psychology, 32, 296–314. 10.1521/jscp.2013.32.3.296 [DOI] [Google Scholar]
  10. Boffa JW, Norr AM, Raines AM, Albanese BJ, Short NA, & Schmidt NB (2016). Anxiety sensitivity prospectively predicts posttraumatic stress symptoms following a campus shooting. Behavior Therapy, 47, 367–376. 10.1016/j.beth.2016.02.006 [DOI] [PubMed] [Google Scholar]
  11. Bovin MJ, Marx BP, Weathers FW, Gallagher MW, Rodriguez P, Schnurr PP, & Keane TM (2016). Psychometric properties of the PTSD Checklist for Diagnostic and Statistical Manual of Mental Disorders ([fifth edition]; PCL-5) in veterans. Psychological Assessment, 28, 1379. 10.1037/pas0000254 [DOI] [PubMed] [Google Scholar]
  12. Goldstein B, Bradley B, Ressler KJ, & Powers A (2017). Associations between posttraumatic stress disorder, emotion dysregulation, and alcohol dependence symptoms among inner city females. Journal of Clinical Psychology, 73, 319–330. 10.1002/jclp.22332 [DOI] [PMC free article] [PubMed] [Google Scholar]
  13. Brewin CR, Andrews B, & Valentine JD (2000). Meta-analysis of risk factors for posttraumatic stress disorder in trauma-exposed adults. Journal of Consulting and Clinical Psychology, 68, 748. 10.1037/0022-006X.68.5.748 [DOI] [PubMed] [Google Scholar]
  14. Cloitre M, & Rosenberg A (2006). Sexual revictimization: Risk factors and prevention. In Follette VM & Ruzek JI (Eds.), Cognitive-behavioral therapies for trauma (pp. 321–361). New York: Guilford Press. [Google Scholar]
  15. Ehring T, & Quack D (2010). Emotion regulation difficulties in trauma survivors: The role of trauma type and PTSD symptom severity. Behavior Therapy, 41, 587–598. 10.1016/j.beth.2010.04.004 [DOI] [PubMed] [Google Scholar]
  16. Faul F, Erdfelder E, Buchner A, & Lang AG (2009). Statistical power analyses using G* Power 3.1: Tests for correlation and regression analyses. Behavior Research Methods, 41, 1149–1160. 10.3758/BRM.41.4.1149 [DOI] [PubMed] [Google Scholar]
  17. Field A (2009). Discovering statistics using SPSS. London, UK: Sage. [Google Scholar]
  18. Fitzgerald JM, Gorka SM, Kujawa A, DiGangi JA, Proescher E, Greenstein JE, . . . Hajcak G (2018). Neural indices of emotional reactivity and regulation predict course of PTSD symptoms in combat-exposed veterans. Progress in Neuropsychopharmacology and Biological Psychiatry, 82, 255–262. 10.1016/j.pnpbp.2017.11.005 [DOI] [PubMed] [Google Scholar]
  19. Foa EB, & Kozak MJ (1986). Emotional processing of fear: Exposure to corrective information. Psychological Bulletin, 99, 20–35. 10.1037/0033-2909.99.1.20 [DOI] [PubMed] [Google Scholar]
  20. Foa EB, Zoellner LA, & Feeny NC (2006). An evaluation of three brief programs for facilitating recovery after assault. Journal of Traumatic Stress, 19, 29–43. 10.1002/jts.20096 [DOI] [PubMed] [Google Scholar]
  21. Frewen PA, Dozois DJ, Neufeld RW, & Lanius RA (2012). Disturbances of emotional awareness and expression in posttraumatic stress disorder: Meta-mood, emotion regulation, mindfulness, and interference of emotional expressiveness. Psychological Trauma: Theory, Research, Practice, and Policy, 4, 152. 10.1037/a0023114 [DOI] [Google Scholar]
  22. Gratz KL, & Roemer L (2004). Multidimensional assessment of emotion regulation and dysregulation: Development, factor structure, and initial validation of the Difficulties in Emotion Regulation Scale. Journal of Psychopathology and Behavioral Assessment, 26, 41–54. 10.1023/B:JOBA.0000007455.08539.94 [DOI] [Google Scholar]
  23. Gratz KL, & Tull MT (2010). Emotion regulation as a mechanism of change in acceptance-and mindfulness-based treatments. In Baer R (Ed.), Assessing mindfulness and acceptance processes in clients: Illuminating the theory and practice of change (pp. 107–133). Oakland, CA: New Harbinger. [Google Scholar]
  24. Gross JJ (2015). The extended process model of emotion regulation: Elaborations, applications, and future directions. Psychological Inquiry, 26, 130–137. 10.1080/1047840X.2015.989751 [DOI] [Google Scholar]
  25. Hayes SC, & Wilson KG (1994). Acceptance and commitment therapy: Altering the verbal support for experiential avoidance. The Behavior Analyst, 17, 289–303. 10.1007/BF03392677 [DOI] [PMC free article] [PubMed] [Google Scholar]
  26. Hien DA, Lopez-Castro T, Papini S, Gorman B, & Ruglass LM (2017). Emotion dysregulation moderates the effect of cognitive behavior therapy with prolonged exposure for co-occurring PTSD and substance use disorders. Journal of Anxiety Disorders, 52, 53–61. 10.1016/j.janxdis.2017.10.003 [DOI] [PMC free article] [PubMed] [Google Scholar]
  27. Jenness JL, Jager-Hyman S, Heleniak C, Beck AT, Sheridan MA, & McLaughlin KA (2016). Catastrophizing, rumination, and reappraisal prospectively predict adolescent PTSD symptom onset following a terrorist attack. Depression and Anxiety, 33, 1039–1047. 10.1002/da.22548 [DOI] [PMC free article] [PubMed] [Google Scholar]
  28. Jerud AB, Pruitt LD, Zoellner LA, & Feeny NC (2016). The effects of prolonged exposure and sertraline on emotion regulation in individuals with posttraumatic stress disorder. Behaviour Research and Therapy, 77, 62–67. 10.1016/j.brat.2015.12.002 [DOI] [PMC free article] [PubMed] [Google Scholar]
  29. IBM Corp. (2017). IBM SPSS Statistics for Windows (Version 25.0). Armonk, NY: IBM Corp. [Google Scholar]
  30. Kartha A, Brower V, Saitz R, Samet JH, Keane TM, & Liebschutz J (2008). The impact of trauma exposure and post-traumatic stress disorder on healthcare utilization among primary care patients. Medical Care, 46, 388. 10.1097/MLR.0b013e31815dc5d2 [DOI] [PMC free article] [PubMed] [Google Scholar]
  31. Kearns MC, Ressler KJ, Zatzick D, & Rothbaum BO (2012). Early interventions for PTSD: A review. Depression and Anxiety, 29, 833–842. 10.1002/da.21997 [DOI] [PMC free article] [PubMed] [Google Scholar]
  32. Kumpula MJ, Orcutt HK, Bardeen JR, & Varkovitzky RL (2011). Peritraumatic dissociation and experiential avoidance as prospective predictors of posttraumatic stress symptoms. Journal of Abnormal Psychology, 120, 617. 10.1037/a0023927 [DOI] [PMC free article] [PubMed] [Google Scholar]
  33. Lavender JM, Tull MT, DiLillo D, Messman-Moore T, & Gratz KL (2017). Development and validation of a state-based measure of emotion dysregulation: The State Difficulties in Emotion Regulation Scale (S-DERS). Assessment, 24, 197–209. 10.1177/1073191115601218 [DOI] [PMC free article] [PubMed] [Google Scholar]
  34. Linehan MM (1993). Cognitive behavioural therapy of borderline personality disorder. New York, NY: Guilford Press. [Google Scholar]
  35. McLean CP, Zang Y, Gallagher T, Suzuki N, Yarvis JS, Litz BT, . . . STRONG STAR Consortium. (2019). Trauma-related cognitions and cognitive emotion regulation as mediators of PTSD change among treatment-seeking active-duty military personnel with PTSD. Behavior Therapy, 50, 1053–1062. 10.1016/j.beth.2019.03.006 [DOI] [PubMed] [Google Scholar]
  36. Murray J, Ehlers A, & Mayou RA (2002). Dissociation and posttraumatic stress disorder: Two prospective studies of road traffic accident survivors. The British Journal of Psychiatry, 180, 363–368. 10.1192/bjp.180.4.363 [DOI] [PubMed] [Google Scholar]
  37. O’Brian EM, McLeish AC, Kramer KM, & Fleming JB (2015). Emotion regulation difficulties and posttraumatic stress disorder symptom cluster severity among trauma-exposed college students. Psychological Trauma: Theory, Research, Practice, and Policy, 7, 131. 10.1037/a0037764 [DOI] [PubMed] [Google Scholar]
  38. Overstreet C, Brown E, Berenz EC, Brown RC, Hawn S, McDonald S, . . . Amstadter A (2018). Anxiety sensitivity and distress tolerance typologies and relations to posttraumatic stress disorder: A cluster analytic approach. Military Psychology, 30, 547–556. 10.1080/08995605.2018.1521682 [DOI] [PMC free article] [PubMed] [Google Scholar]
  39. Petrucelli E, States JD, & Hames LN (1981). The Abbreviated Injury Scale: Evolution, usage, and future adaptability. Accident Analysis & Prevention, 13, 29–35. 10.1016/0001-4575(81)90040-3 [DOI] [Google Scholar]
  40. Pietrzak RH, Goldstein RB, Southwick SM, & Grant BF (2011). Prevalence and Axis I comorbidity of full and partial posttraumatic stress disorder in the United States: Results from Wave 2 of the National Epidemiologic Survey on Alcohol and Related Conditions. Journal of Anxiety Disorders, 25, 456–465. 10.1016/j.janxdis.2010.11.010 [DOI] [PMC free article] [PubMed] [Google Scholar]
  41. Resnick H, Acierno R, Holmes M, Kilpatrick DG, & Jager N (1999). Prevention of post-rape psychopathology: Preliminary findings of a controlled acute rape treatment study. Journal of Anxiety Disorders, 13, 359–370. 10.1016/S0887-6185(99)00010-9 [DOI] [PubMed] [Google Scholar]
  42. Rizvi SL, Kaysen D, Gutner CA, Griffin MG, & Resick PA (2008). Beyond fear: The role of peritraumatic responses in posttraumatic stress and depressive symptoms among female crime victims. Journal of Interpersonal Violence, 23, 853–868. 10.1177/0886260508314851 [DOI] [PubMed] [Google Scholar]
  43. Resick PA, Monson CM, & Chard KM (2006). Cognitive processing therapy: Veteran and military version. Boston, MA: National Center for PTSD. [Google Scholar]
  44. Roemer L, Litz BT, Orsillo SM, & Wagner AW (2001). A preliminary investigation of the role of strategic withholding of emotions in PTSD. Journal of Traumatic Stress, 14, 149–156. 10.1023/A:1007895817502 [DOI] [Google Scholar]
  45. Rothbaum BO, Houry D, Heekin M, Leiner AS, Daugherty J, Smith LS, & Gerardi M (2008). A pilot study of an exposure-based intervention in the ED designed to prevent posttraumatic stress disorder. The American Journal of Emergency Medicine, 26, 326–330. 10.1016/j.ajem.2007.07.006 [DOI] [PubMed] [Google Scholar]
  46. Schnurr P, Vielhauer M, Weathers F, & Findler M (1999). The Brief Trauma Questionnaire. White River Junction, VT: National Center for PTSD. [Google Scholar]
  47. Seligowski AV, Lee DJ, Bardeen JR, & Orcutt HK (2015). Emotion regulation and posttraumatic stress symptoms: A meta-analysis. Cognitive Behaviour Therapy, 44, 87–102. 10.1080/16506073.2014.980753 [DOI] [PubMed] [Google Scholar]
  48. Thomas JL, Wilk JE, Riviere LA, McGurk D, Castro CA, & Hoge CW (2010). Prevalence of mental health problems and functional impairment among active component and National Guard soldiers 3- and 12-months following combat in Iraq. Archives of General Psychiatry, 67, 614–623. 10.1001/archgenpsychiatry.2010.54 [DOI] [PubMed] [Google Scholar]
  49. Tripp JC, & McDevitt-Murphy ME (2015). Emotion dysregulation facets as mediators of the relationship between PTSD and alcohol misuse. Addictive Behaviors, 47, 55–60. 10.1080/15504263.2015.1025013 [DOI] [PMC free article] [PubMed] [Google Scholar]
  50. Tull MT, & Aldao A (2015). Editorial overview: New directions in the science of emotion regulation. Current Opinion in Psychology, 3, iv–x. 10.1016/j.copsyc.2015.03.009 [DOI] [Google Scholar]
  51. Tull MT, Barrett HM, McMillan ES, & Roemer L (2007). A preliminary investigation of the relationship between emotion regulation difficulties and posttraumatic stress symptoms. Behavior Therapy, 38, 303–313. 10.1016/j.beth.2006.10.001 [DOI] [PubMed] [Google Scholar]
  52. Tull MT, Berghoff CR, Wheeless LE, Cohen RT, & Gratz KL (2018). PTSD symptom severity and emotion regulation strategy use during trauma cue exposure among patients with substance use disorders: Associations with negative affect, craving, and cortisol reactivity. Behavior Therapy, 49, 57–70. 10.1016/j.beth.2017.05.005 [DOI] [PMC free article] [PubMed] [Google Scholar]
  53. Turpin G, Downs M, & Mason S (2005). Effectiveness of providing self-help information following acute traumatic injury: Randomised controlled trial. The British Journal of Psychiatry, 187, 76–82. 10.1192/bjp.187.1.76 [DOI] [PubMed] [Google Scholar]
  54. van der Kolk BA (1996). The complexity of adaptation to trauma: Self-regulation, stimulus, discrimination, and characterological development. In van der Kolk BA, McFarlane AC, & Weisaeth L (Eds.), Traumatic stress: The effects of overwhelming experience on mind, body, and society (pp. 182–213). New York, NY: Guilford Press. [Google Scholar]
  55. Vujanovic AA, Hart AS, Potter CM, Berenz EC, Niles B, & Bernstein A (2013). Main and interactive effects of distress tolerance and negative affect intensity in relation to PTSD symptoms among trauma-exposed adults. Journal of Psychopathology and Behavioral Assessment, 35, 235–243. 10.1007/s10862-012-9325-2 [DOI] [PMC free article] [PubMed] [Google Scholar]
  56. Weathers FW, Litz BT, Keane TM, Palmieri PA, Marx BP, & Schnurr PP (2013). The PTSD Checklist for DSM-5 (PCL-5) [Measurement instrument]. Available from http://www.ptsd.va.gov
  57. Weiss NH, Tull MT, Anestis MD, & Gratz KL (2013). The relative and unique contributions of emotion dysregulation and impulsivity to posttraumatic stress disorder among substance-dependent inpatients. Drug and Alcohol Dependence, 128, 45–51. 10.1016/j.drugalcdep.2012.07.017 [DOI] [PMC free article] [PubMed] [Google Scholar]
  58. Weiss NH, Tull MT, Davis LT, Dehon EE, Fulton JJ, & Gratz KL (2012). Examining the association between emotion regulation difficulties and probable posttraumatic stress disorder within a sample of African Americans. Cognitive Behaviour Therapy, 41, 5–14. 10.1080/16506073.2011.621970 [DOI] [PubMed] [Google Scholar]
  59. Xue C, Ge Y, Tang B, Liu Y, Kang P, Wang M, & Zhang L (2015). A meta-analysis of risk factors for combat-related PTSD among military personnel and veterans. PloS One, 10, e01202. 10.1371/journal.pone.0120270 [DOI] [PMC free article] [PubMed] [Google Scholar]

RESOURCES