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. Author manuscript; available in PMC: 2024 Mar 8.
Published in final edited form as: J Affect Disord. 2020 Feb 13;267:203–210. doi: 10.1016/j.jad.2020.02.028

The role of emotion dysregulation in negative affect reactivity to a trauma cue: Differential associations through elicited posttraumatic stress disorder symptoms

Alexa M Raudales b, Nicole H Weiss b, Norman B Schmidt a,*, Nicole A Short b
PMCID: PMC10923236  NIHMSID: NIHMS1565566  PMID: 32217220

Abstract

Background:

Recent research has linked emotion dysregulation with increases in subjective ratings of negative affect (NA reactivity) to trauma reminders, a central symptom of posttraumatic stress disorder (PTSD). The current study adds to this burgeoning line of research by exploring elicited PTSD symptoms as a mechanism explicating the relation between emotion dysregulation and NA reactivity following trauma cue exposure.

Methods:

Participants were 60 treatment-seeking marijuana users with insomnia symptoms who reported exposure to a traumatic event. Participants were administered questionnaires assessing emotion dysregulation, PTSD symptoms, and NA prior to and/or after listening to a personalized trauma script, and subsequently completed a diagnostic interview.

Results:

Results demonstrated that greater emotion dysregulation was associated with heightened NA reactivity through re-experiencing symptoms, but not avoidance or dissociation symptoms, even after accounting for past 30-day PTSD symptom severity and pre-trauma script NA. These effects were driven by the dimensions of emotion dysregulation characterized by nonacceptance of negative emotions and limited access to effective emotion regulation strategies.

Limitations:

This study requires replication among other clinical samples, and is limited by use of self-report measures.

Conclusions:

Findings provide novel empirical support for one mechanism through which emotion dysregulation may confer vulnerability to PTSD symptomology, and offer implications for refining PTSD treatments.

Keywords: Posttraumatic stress disorder, PTSD, Emotion dysregulation, Reactivity, Re-experiencing

1. Introduction

Posttraumatic stress disorder (PTSD) is a serious mental disorder associated with functional impairment (Rodriguez et al., 2012), poor physical health outcomes (Pacella et al., 2013), and substantial economic costs (Kessler and Greenberg, 2002). PTSD is common, with an estimated lifetime prevalence rate of 8.3% in the U.S. (Kilpatrick et al., 2013). Symptoms of PTSD form clusters of intrusions, avoidance of trauma reminders, negative alterations in cognition and mood, and alterations in arousal and reactivity (American Psychiatric Association, 2013). One central symptom of PTSD entails heightened reactivity to internal (e.g., thoughts, feelings) or external (e.g., people, places) reminders of a trauma (American Psychiatric Association, 2013). Specifically, individuals with PTSD report greater ratings of negative affect (NA; McDonagh‐Coyle et al., 2001; Orsillo et al., 2004; Pineles et al., 2013; Wolf et al., 2009) and physiological (e.g., heart rate, skin conductance, and systolic blood pressure; Litz et al., 2000; Wolfe et al., 2000) responses to trauma cues compared to those without PTSD.

In addition to being a symptom of PTSD, increased reactivity to trauma cues is thought to be an etiological factor in the disorder. According to Foa and Kozak’s (1986) emotional processing theory, exposure to trauma cues is necessary to activate fear structures underlying PTSD and allow individuals to emotionally engage with trauma-related stimuli. Increased reactivity to trauma cues may motivate avoidance (Pineles et al., 2011), thereby hindering the information and opportunity for individuals to challenge feared stimuli and responses, ultimately leading to the development of PTSD. Neural markers of heightened NA reactivity in the laboratory have been found to significantly predict perpetuation of PTSD symptoms over the course of one year (Fitzgerald et al., 2018). Moreover, reductions in NA reactivity play a clinically relevant role in Prolonged Exposure (PE; Foa et al., 2007), an effective first-line treatment for PTSD that involves repeated exposures to trauma-related stimuli (Price et al., 2006; Rauch et al., 2012). Considering the role of NA reactivity in the development, maintenance, and treatment of PTSD, there is a need to better understand mechanisms underlying NA reactivity to trauma cues.

One key factor that may play a role in heightened NA reactivity to trauma cues is emotion dysregulation. Gratz and Roemer (2004) broadly define emotion dysregulation as (a) a lack of awareness, understanding, and acceptance of emotions; (b) the inability to control behaviors when experiencing emotional distress; (c) lack of access to situationally appropriate strategies for modulating the duration and/or intensity of emotional responses in order to meet individual goals and situational demands; and (d) an unwillingness to experience emotional distress as part of pursuing meaningful activities in life. Higher levels of self-reported emotion dysregulation are associated with PTSD diagnosis and symptom severity (McDermott et al., 2009; Tull et al., 2007; Weiss et al., 2013, 2019). Furthermore, Bardeen et al. (2013) found that emotion dysregulation prior to experiencing a trauma confers increased vulnerability to the development of PTSD symptoms eight months following a trauma (i.e., a mass shooting) among 691 undergraduates. Researchers posit that intense negative emotions – such as those experienced during a trauma and in response to trauma reminders – require additional coping resources (Flett et al., 1996). Individuals with greater emotion dysregulation might be less equipped to effectively manage trauma-related NA, which can perpetuate chronic PTSD. Specifically, non-acceptance of emotional responses may sustain distress by contributing to the development of secondary negative emotions (e.g., shame, fear; Gratz et al., 2007; Tull et al., 2007). Additionally, frequent use of maladaptive emotion regulation strategies such as emotional avoidance may prevent individuals from learning corrective information about their fear and ability to cope, ultimately leading to greater distress and impairment (Foa and Kozak, 1986; Plumb et al., 2004; Roemer et al., 2001).

Despite the robust link between emotion dysregulation and PTSD, little is known about how emotion dysregulation contributes to trauma cue reactivity. Among 21 women with a history of interpersonal assault, Badour and Feldner (2013) demonstrated a large positive association between PTSD symptoms and self-reported anxious reactivity to a trauma cue for those with high emotion dysregulation compared to low emotion dysregulation. However, without controlling for initial indices of anxious arousal, specificity to cue reactivity remains unknown. Extending these findings to a sample of 133 trauma-exposed substance use disorder inpatients, Tull et al. (2018) found that PTSD symptom severity was associated with NA reactivity through the state use of particular emotion regulation strategies (e.g., suppression, reappraisal) assessed by the Responses to Emotions Questionnaire (ERQ; Campbell Sills et al., 2006) in response to a trauma cue. Although this study adds to extant literature on emotion dysregulation strategies, further research may benefit from assessing emotion dysregulation abilities. The assessment of emotion regulation strategies in Tull and colleagues’ study is consistent with Gross’s (2015) framework of emotion regulation that focuses on the type and timing of emotion regulation strategies used to influence emotions. Alternatively, emotion regulation abilities may be thought of as a higher order process that reflects dispositional ways in which individuals respond to their emotions, including the nature and success of emotion regulation strategies (Tull and Aldao, 2015). Additional research in this area may indicate whether emotion dysregulation is an important target for exposure-based interventions.

In addition to addressing these critical gaps in the literature, further work is warranted to identify mechanisms underlying the relation between emotion dysregulation and NA reactivity to trauma cues. One potential mediator of the association between emotion dysregulation and trauma cue reactivity may be the type of PTSD symptoms elicited by trauma-related stimuli (i.e., state PTSD symptoms). Research has revealed three primary PTSD-related responses to trauma reminders: re-experiencing (e.g., upsetting intrusions or flashbacks), avoidance (e.g., avoidance of thoughts or sensations related to the trauma), and dissociation (e.g., depersonalization or derealization; for a review, see Lanius et al., 2006; Hopper et al., 2007). It is possible that emotion dysregulation may cause individuals to view emotional reactions to trauma reminders as threatening or overwhelming, and use maladaptive emotion regulation strategies (e.g., suppression) that paradoxically lead to more re-experiencing symptoms (Tull et al., 2018) or otherwise serve the purpose of avoiding trauma-related stimuli (Gratz et al., 2007). In turn, re-experiencing symptoms may prolong NA reactivity in response to trauma cues (Taft et al., 2007; Pinellas et al., 2011; Wolfe et al., 2000), while increased avoidance symptoms may perpetuate reactivity by amplifying the perceived danger of trauma-related stimuli (Pineles et al., 2011). Alternatively, greater emotion dysregulation may lead individuals to feel they are unable to tolerate emotional responses to trauma reminders, and consequently may dissociate (Powers et al., 2015). In contrast to the proposed effects of re-experiencing and avoidance symptoms leading to greater NA reactivity, dissociative symptoms might indicate a disengagement from trauma-related distress that results in dampened reactivity (Bryant et al., 2000; Giesbrecht et al., 2008).

The current study evaluated this potential model in which emotion dysregulation predicts NA reactivity following trauma cue exposure (i.e., script-driven imagery; Pitman et al., 1987) through evoked PTSD symptoms. Hypotheses were tested among treatment-seeking marijuana users with insomnia symptoms. This sample represents a vulnerable population as marijuana users frequently experience higher levels of PTSD symptoms (Bonn-Miller et al., 2007; Bremner et al., 1996) and worse treatment responses (Bonn-Miller et al., 2011; Wilkinson et al., 2015). Additionally, individuals experiencing sleep difficulties are more likely to experience emotion dysregulation and PTSD symptoms (Fairholme et al., 2013; Short et al., 2014). Building on prior research linking emotion dysregulation with PTSD symptoms (Badour and Feldner, 2013) and NA reactivity (Tull et al., 2018), we hypothesized that emotion dysregulation would be a significant predictor of elicited PTSD symptoms, and, in turn, NA reactivity. To demonstrate that emotion dysregulation affects reactivity above and beyond PTSD severity, we hypothesized these associations would remain significant after accounting for past 30-day PTSD symptom severity. We also hypothesized effects would be specific to this model and not an alternate mediation model in which the mediator (i.e., elicited PTSD symptoms) and dependent variable (i.e., NA reactivity) were reversed. Finally, we conducted exploratory analyses to ascertain whether these effects were specific to any particular emotion dysregulation subscales (i.e., non-acceptance of negative emotions, difficulties engaging in goal-directed behavior when distressed, difficulties controlling impulsive behaviors when distressed, limited access to effective emotion regulation strategies, and lack of emotional clarity).

2. Method

2.1. Participants

The sample consisted of 60 young adults from the community (n = 32) and the undergraduate research pool of a large university (n = 28). Participants were part of a randomized clinical trial testing the efficacy of a brief behavioral treatment for insomnia to reduce marijuana use disorder risk ( Short et al., 2021 ). Eligible participants were English speakers, at least 18 years of age, poor sleepers (i.e., scoring at least 10 on the Insomnia Severity Index [ISI]; Morin et al., 2011), trauma-exposed (assessed via the Posttraumatic Diagnostic Scale [PDS]; Foa, 1995), and regular marijuana users (i.e., at least once weekly for the past year). Exclusion criteria included high risk of obstructive sleep apnea (i.e., scoring greater than two on the STOP-BANG Questionnaire; Chung et al., 2012) and untreated psychotic or bipolar-spectrum disorder as assessed through a telephone screen.

Participants ranged in age from 18 to 41 (M = 20.52, SD = 3.69), and were 60.0% male. Most participants identified as White (73.3%), followed by Black (20.0%), Other (e.g., biracial; 5.0%), and Asian (1.7%), while 21.7% also identified as Hispanic. Regarding psychiatric diagnoses, most of the sample met for at least one diagnosis (93.3%), and 76.8% met for more than one diagnosis. Of particular relevance to the current study, 13.3% met diagnostic criteria for PTSD, 6.7% for other specified trauma disorder, 83.3% for a substance use disorder, 28.3% for a depressive disorder, and 35.0% for an anxiety and related disorder. Per the PDS, participants rated their most bothersome trauma to be a serious accident (18.3%), sexual assault by a known person (15.0%), non-sexual assault by a known person (15.0%), sexual assault by a stranger (11.7%), life-threatening illness (6.7%), combat (3.3%), childhood sexual assault (3.3%), natural disaster (3.3%), other (e.g., “almost drowning in a cave;” “emotional abuse – torture and imprisonment;” 18.3%), and three people did not select a most bothersome event (5.0%). These individuals who did not select a most bothersome trauma on the PDS reported this information during the clinical interview; specifically, these traumas were a serious accident, witnessing the unexpected death of a family member, and physical assault by a known person.

2.2. Procedure

Participants were recruited from the university’s undergraduate research pool or from the local community using flyers and online advertisements. Interested individuals completed a telephone screen, and if eligible (see Participants), were scheduled for a baseline appointment. To reduce the effects of substance use on PTSD symptom induction, participants were instructed to refrain from using marijuana or other drugs for at least four hours prior to the appointment, and were asked to verbally confirm adherence during the appointment. Upon arrival to the laboratory, written informed consent was obtained. Next, participants completed a series of self-report questionnaires (e.g., ISI, STOP-BANG Questionnaire; Chung et al., 2012; Morin et al., 2011) to confirm eligibility. Participants were then administered additional questionnaires. After completion of this battery of self-report measures, participants completed the personalized trauma script with a research assistant. Procedures for the trauma script are described in detail below. Immediately following the trauma script, participants completed additional questionnaires assessing state negative affect and PTSD symptoms. To avoid any reminders of the trauma prior to the trauma script, questionnaires that asked about the traumatic event were administered after the trauma script. Lastly, participants completed the Structured Clinical Interview for the DSM-5 (First et al., 2015). The current study uses baseline data from a larger clinical trial. Only baseline data prior to randomization and treatment onset were used for the present report. All procedures were approved by the university’s institutional review board.

2.2.1. Personalized trauma script

To induce PTSD symptoms, we adhered to the script-driven imagery procedure that was originally developed by Lang et al. (1980) and has since been adapted (e.g., Pitman et al., 1987). Participants were asked to describe in detail their most bothersome traumatic event using a written script preparation form. This form prompts for specific details such as date, time, location, presence of others, smells, sounds, feelings, and physical sensations during the traumatic event. A research assistant then wrote these details into a script format, and tape recorded a script in first person, present tense using the participant’s own verbiage. Recordings were approximately one minute. Participants were instructed to recall the experience as vividly as possible while listening to the script using headphones. This method has been widely used to reliably elicit trauma-related arousal such as self-reported NA in the laboratory (Norte et al., 2013; Pitman et al., 1987), and state PTSD symptoms (Hopper et al., 2007), including among marijuana users (Tull et al., 2016).

2.3. Measures

2.3.1. Structured clinical interview for DSM-5 Disorders-research version (SCID-5)

The SCID-5 (First et al., 2015) was used to determine psychiatric diagnoses and assess Criterion A traumatic event exposure. The SCID-5 is a semi-structured clinical interview that was administered by trained psychology graduate students and bachelor level research assistants. Training consisted of reviewing tapes, observing live administrations, and practicing interviews with trained therapists. All SCID-5s were reviewed by a licensed clinical psychologist. A random sample of 20 SCID-5s from our laboratory demonstrated high inter-rater agreement (i.e., kappa = 0.86; Schmidt et al., 2016).

2.3.2. Difficulties in emotion regulation scale––16 (DERS)

The DERS (Gratz and Roemer, 2004) is a widely-used measure of emotion dysregulation. This study utilized the brief 16-item version of the DERS (Bjureberg et al., 2016), which measures general emotion dysregulation and five domains: nonacceptance of negative emotions (e.g., “when I’m upset, I feel ashamed with myself for feeling that way”), difficulties engaging in goal-directed behavior when distressed (e.g., “when I’m upset, I have difficulty getting work done”), difficulties controlling impulsive behaviors when distressed (e.g., “when I’m upset, I have difficulty controlling my behaviors”), limited access to effective emotion regulation strategies (e.g., “when I’m upset, I believe that I will remain that way for a long time”), and lack of emotional clarity (e.g., “I am confused about how I feel”). Respondents rate the extent to which items apply to them using a five-point Likert scale, where higher scores indicate elevated emotion dysregulation. The DERS has demonstrated strong psychometric properties in prior research, including good test-retest reliability, convergent validity, and discriminant validity (Bjureberg et al., 2016). In the current study, the DERS demonstrated acceptable to excellent reliability for the total score (α = 0.94) and subscales: nonacceptance of negative emotions (α = 0.87), difficulties engaging in goal-directed behavior when distressed (α = 0.79), difficulties controlling impulsive behaviors when distressed (α = 0.89), limited access to effective emotion regulation strategies (α = 0.90), and lack of emotional clarity (α = 0.91). The DERS was used in the current study to assess emotion dysregulation as a predictor of NA and PTSD symptom reactivity to trauma cue exposure.

2.3.3. Responses to script-driven imagery scale (RSDI)

The RSDI (Hopper et al., 2007) is an 11-item measure of state PTSD symptoms evoked by script-driven imagery. Specifically, the RSDI assesses re-experiencing (e.g., “did you feel as though the event was reoccurring, like you were reliving it”), avoidance (e.g., “did you avoid thoughts about the event”), and dissociative (e.g., “did you feel disconnected from your body”) symptoms that were experienced during the trauma script and imagining periods. Items are rated on a seven-point Likert scale, where higher scores indicate greater state PTSD symptoms. Consistent with prior literature (Hopper et al., 2007), the RSDI was administered immediately following the trauma script. The RSDI has demonstrated high internal consistency and construct validity in prior research (Hopper et al., 2007), and has been shown to correlate with neural and physiological activity (e.g., heart-rate change; Hopper et al., 2007). The RSDI demonstrated acceptable to good reliability for re-experiencing (α = 0.87), avoidance (α = 0.78), and dissociation (α = 0.79) subscales. In the current study, the RSDI was used to assess state PTSD symptoms following trauma cue exposure.

2.3.4. Positive and negative affect schedule–state–negative affect subscale (PANAS-NA)

The PANAS-NA (Watson et al., 1988) is a 10-item measure of negative affect. Participants indicate the extent to which they were currently (i.e., “right now, that is, at this present moment”) experiencing 10 distinct negative mood states (e.g., guilty, afraid) using a five-point Likert scale, with higher scores indicating greater negative affect. The PANAS-NA was administered immediately prior to and following the trauma script as a measure of NA reactivity to trauma cues. Consistent with prior research (Watson et al., 1988), the PANAS-NA demonstrated good to excellent reliability in the current study before (α = 0.87) and after the trauma script (α = 0.91).

2.3.5. Posttraumatic stress disorder checklist––5 (PCL-5)

The PCL-5 (Weathers et al., 2013) is a 20-item measure that assesses PTSD symptoms according to the DSM-5. Participants use a five-point Likert scale to indicate the extent to which they have been bothered by each symptom in the past month, with higher scores reflecting greater PTSD symptom severity. The PCL-5 is a psychometrically sound measure (Wilkins et al., 2011) and demonstrated excellent reliability in the current study (α = 0.94). The PCL was used as a covariate in the current study.

2.4. Data analytic plan

Descriptive statistics and intercorrelations were first computed. Data were then examined for problematic skew and kurtosis values. All variables were within the acceptable range for normality (Tabachnick and Fidell, 2007). To explore the total effect of DERS total score on post-trauma script PANAS-NA, a linear regression analysis was performed while covarying for pre-trauma script PANAS-NA. Subsequently, separate mediation analyses were conducted to test the indirect effect of the DERS total score on post-trauma script PANAS-NA (i.e., NA reactivity) through RSDI re-experiencing, avoidance, and dissociation subscales. These models controlled for past 30-day PCL-5 and pre-trauma script state PANAS-NA. Next, to explore the specificity of direction for significant mediation effects, a separate mediational model was conducted in which the mediator and dependent variable were reversed. Any significant indirect effects for the DERS total score were further probed to test whether these effects were driven by specific subscales. Mediational models were conducted using the PROCESS macro (Model 4; Hayes, 2012) in SPSS Version 22.0, with 95% confidence intervals estimated using 5000 bias-corrected bootstrap resamples. Indirect effects are reported as standardized estimates.

3. Results

3.1. Preliminary analyses

Means, standard deviations, and zero-order correlations are presented in Table 1. As expected, we found significant positive associations among emotion dysregulation, NA, and PTSD state (RSDI) and trait (PCL-5) symptoms. While comparable to prior research among trauma-exposed community members (Price and van Stolk-Cooke, 2015), the mean PCL-5 score for this study (M = 22.49) is below the clinical cut off score of 33 (Wortmann et al., 2016), thus overall representing a subclinical sample. Moreover, the mean DERS total score for this study (M = 44.11) is higher compared to previous research among trauma-exposed community members (M = 21.00; Paulus et al., 2018). The mean RSDI scores (3.09, 2.32, 3.02) are comparable to prior work among individuals with PTSD (3.73, 2.18, 2.12; Hopper et al., 2007), suggesting that the trauma script effectively evoked state symptoms of PTSD. No significant differences were found between community members and undergraduate students across emotion dysregulation or PTSD symptoms (p’s > 0.05). Furthermore, there were no significant associations between emotion dysregulation or PTSD symptoms and demographic variables including age, race, and education.

Table 1.

Descriptive statistics and zero-order correlations for variables of interest.

M SD Possible range Actual range 1 2 3 4 5 6 7 8 9 10 11 12
1. DERS Total 44.11 14.95 16–80 18–79 –
2. DERS Accept 8.58 3.81 3–15 3–15 .83*** –
3. DERS Goals 9.82 2.98 3–15 3–15 .76*** 64** –
4. DERS Impulsivity 6.85 3.42 3–15 3–15 .79*** 48** .48*** –
5. DERS Strategies 13.25 5.80 5–25 5–25 .91*** 67** .55*** .72*** –
6. DERS Clarity 5.62 2.27 2–10 2–10 .68*** 53** .50*** .44*** .50*** –
7. Pre PANAS-NA 16.61 6.71 10–50 10–37 .56*** 45*** .44*** 43** .54*** 35** –
8. Post PANAS-NA 19.98 8.72 10–50 10–42 .64*** 53*** .45*** 40** .67*** .41** .74*** –
9. Post RSDI Re-experiencing 3.09 1.61 0–6 0–6 .51*** .46*** .32* 34** .55*** 26* 38** 64*** –
10. Post RSDI Avoidance 2.32 1.76 0–6 0–6 43** 33** .33* 34** 43** .20 .46*** .54*** .54*** –
11. Post RSDI Dissociation 3.02 1.66 0–6 0–6 .30* .30* .27* .20 .30* .09 .26* .33* .60*** .57*** –
12. PCL-5 Total 22.49 15.78 0–80 1–75 .61*** 38** .32* .57*** .65*** 41** .53*** .63*** .50*** .52*** .38** –
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Note. Pre = pre-trauma script; Post = post-trauma script; DERS = Difficulties in Emotion Regulation Scale, subscales: non-acceptance of emotional responses, difficulties engaging in goal-directed behavior when experiencing negative emotion, impulse control problems, limited access to emotion regulation strategies, and lack of emotional clarity; PANAS-NA = Positive and Negative Affect Schedule – State – Negative Affect subscale; RSDI = Responses to Script-Driven Imagery Scale

PCL-5 = Posttraumatic Stress Disorder Checklist – 5.

***

p < .001

**

p < .01

*

p < .05.

As a manipulation check, a t-test was performed to determine NA increased from before to after the trauma script driven imagery. Indeed, there was a significant difference between self-reported NA prior to (M = 16.48; SD = 6.61) and following (M = 19.98; SD = 8.72) the trauma script (t = 2.99, p = .004).

3.2. Mediational analyses

To explore the total effect of general emotion dysregulation on NA reactivity, we conducted an independent linear regression analysis while controlling for pre-trauma script NA. The overall model was significant (F [2, 57] = 47.46, p < 0.001), with an R2 of 0.63. Furthermore, higher levels of total emotion dysregulation were significantly associated with increased NA reactivity when accounting for pre-trauma script NA (β = 0.33, t = 3.35, p = .001).

Next, we conducted independent mediational models to examine the indirect effects of general emotion dysregulation on NA reactivity through evoked state symptoms, while controlling for past 30-day PTSD symptoms and pre-trauma script NA. These models are represented in Table 2 and Fig. 1. Regarding the a path of our first model exploring re-experiencing symptoms, overall emotion dysregulation was not significantly associated with re-experiencing symptoms in response to the trauma script (B = 0.03, SE = 0.02, t = 1.81, p = .08). In terms of the b path, greater re-experiencing symptoms were significantly associated with increased NA reactivity (B = 1.75, SE = 0.47, t = 3.71, p < .000). There was a significant indirect effect of elevated general emotion dysregulation on increased NA reactivity through re-experiencing symptoms (β = 0.09, SE = 0.06, 95% CI [0.002, 0.23]). The direct effect (c’ path) of overall emotion dysregulation on NA reactivity was not significant (B = 0.07, SE = 0.06, t = 1.13, p = .26).

Table 2.

Indirect effects of emotion dysregulation on negative affect reactivity through posttraumatic stress disorder symptoms.

Independent Variable Mediating Variable Dependent Variable Effect of IV on M Effect of M on DV Direct Effect Indirect Effect
(IV) (M) (DV) (a) (b) (c’) (a x b) 95% CI
DERS Total RSDI Re-experiencing NA Reactivity 0.03 (0.02) 1.75 (0.47) 0.07 (0.06) 0.09 (0.06) 0.002, 0.23
DERS Total RSDI Avoidance NA Reactivity 0.02 (0.02) 1.01 (0.49) 0.10 (0.06) 0.03 (0.04) −0.03, 0.14
DERS Total RSDI Dissociation NA Reactivity 0.01 (0.02) 0.37 (0.45) 0.01 (0.03) 0.01 (0.03) −0.03, 0.07
DERS Accept RSDI Re-experiencing NA Reactivity 0.12 (0.05) 1.71 (0.48) 0.22 (0.19) 0.09 (0.05) 0.01, 0.22
DERS Goals RSDI Re-experiencing NA Reactivity 0.07 (0.07) 1.81 (0.46) 0.21 (0.24) 0.05 (0.05) −0.03, 0.17
DERS Impulsivity RSDI Re-experiencing NA Reactivity 0.002 (0.07) 1.88 (0.46) −0.20 (0.23) 0.002 (0.05) −0.09, 0.11
DERS Strategies RSDI Re-experiencing NA Reactivity 0.09 (0.04) 1.64 (0.47) 0.27 (0.15) 0.10 (0.06) 0.02, 0.23
DERS Clarity RSDI Re-experiencing NA Reactivity 0.003 (0.09) 1.87 (0.46) 0.25 (0.31) 0.001 (0.05) −0.08, 0.11
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Note. NA = Negative affect; CI = Confidence interval; DERS = Difficulties in Emotion Regulation Scale, subscales: non-acceptance of emotional responses, difficulties engaging in goal-directed behavior when experiencing negative emotion, impulse control problems, limited access to emotion regulation strategies, and lack of emotional clarity. These models covary for Posttraumatic Stress Disorder Checklist – 5 and pre-trauma script Positive and Negative Affect Schedule – State – Negative Affect subscale. Bolded typeface indicates significance at the level of p < .05. Indirect effects are reported as standardized estimates.

Fig. 1.

Fig. 1.

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Independent mediational models examining the effects of overall emotion dysregulation on increases in negative affect in response to the trauma script through evoked posttraumatic stress disorder state symptoms: (A) re-experiencing, (B) avoidance, and (C) dissociation symptoms. These models covary for Posttraumatic Stress Disorder Checklist – 5 and pre-trauma script Positive and Negative Affect Schedule – State – Negative Affect subscale. *** p < .001; ** p < .01; * p < .05.

Overall emotion dysregulation did not significantly predict RSDI avoidance or dissociation in response to the trauma script. Furthermore, there were no significant indirect effects of overall emotion dysregulation on NA reactivity through avoidance (β = 0.03, SE = 0.04, 95% CI [−0.03, 0.14]) or dissociation (β = 0.01, SE = 0.03, 95% CI [−0.03, 0.07]) symptoms in response to the trauma script, after controlling for past 30-day PTSD symptoms and pre-trauma script NA.

3.3. Specificity analyses

To test any reverse direction effects, a separate mediational model was conducted in which overall NA reactivity was entered as the mediating variable and re-experiencing symptoms were entered as the dependent variable. This indirect effect was not significant (β = 0.13, SE = 0.07, 95% CI [−0.01, 0.28]).

3.4. Supplementary analyses

Utilizing five separate models, we probed for subscales that may be driving the total effect of emotion dysregulation on greater NA reactivity through re-experiencing symptoms when controlling for past 30-day PTSD symptoms and pre-trauma script NA. Significant indirect effects were detected for nonacceptance of negative emotions (β = 0.09, SE = 0.05, 95% CI [0.01, 0.22]) and limited access to effective emotion regulation strategies (β = 0.10, SE = 0.06, 95% CI [0.02, 0.23]), but not for difficulties engaging in goal-directed behavior when distressed (β = 0.05, SE = 0.05, 95% CI [−0.03, 0.17]), difficulties controlling impulsive behaviors when distressed (β = 0.002, SE = 0.05, 95% CI [−0.09, 0.11]), or lack of emotional clarity (β = 0.002, SE = 0.05, 95% CI [−0.08, 0.11]).

4. Discussion

The present study is the first to explore elicited PTSD symptoms as a mechanism explicating the relation between emotion dysregulation and NA reactivity following trauma cue exposure. Results offer empirical evidence that greater emotion dysregulation is associated with heightened NA reactivity through re-experiencing symptoms, but not avoidance or dissociation symptoms, even after adjusting for past 30-day PTSD symptom severity and pre-trauma script NA. These effects appear to be driven by the non-acceptance of negative emotions and limited access to effective emotion regulation strategies. These findings add to a growing body of literature implicating the role of emotion dysregulation in the etiology and maintenance of PTSD, and highlight the importance of considering differences in the type of responses to trauma reminders.

Consistent with our hypothesis, during trauma cue exposure, elevated levels of evoked re-experiencing symptoms mediated the association between emotion dysregulation and NA reactivity after accounting for past 30-day PTSD symptom severity and pre-trauma script NA. Individuals with greater difficulties regulating negative emotions might be more likely to perceive their emotional responses to trauma cues as threatening or overwhelming. In an attempt to modulate these emotions, such individuals may respond in ways that paradoxically heighten re-experiencing symptoms. In particular, results suggest an important role of the non-acceptance of emotions, which could perpetuate re-experiencing symptoms by leading to the development of secondary negative emotions such as guilt and fear associated with one’s initial response to the trauma reminder (Gratz et al., 2007; Tull et al., 2007). Increased distress to trauma-related stimuli might make it more difficult for these individuals to disengage from internal trauma reminders. Furthermore, findings imply a role of access to effective emotion regulation strategies in re-experiencing symptoms. One potential explanation for this finding is that individuals who rely on maladaptive emotion regulation strategies (e.g., suppression) are less likely to perceive themselves to be effective in modulating distress because these strategies often have paradoxical effects, increasing trauma-related symptoms and distress in the long-term (Campbell-Sills et al., 2006). This finding aligns with previous research demonstrating that greater use of maladaptive emotion regulation strategies mediated the relation between PTSD symptom severity and NA reactivity during trauma cue exposure (Tull et al., 2018). Results can also be interpreted within the context of Foa and Kozak’s (1986) emotional processing theory, whereby non-acceptance of emotions and maladaptive emotion regulation strategies may interfere with engagement with trauma-related stimuli, thereby preventing individuals from learning corrective information about their fear and coping abilities, ultimately exacerbating symptoms. Consistent with prior work, re-experiencing symptoms, in turn, were associated with increased reactivity to trauma cues (Pinellas et al., 2011; Taft et al., 2007; Wolfe et al., 2000). This finding may be useful for understanding risk for PTSD, considering that elevated levels of self-reported NA in response to intrusive memories are associated with greater PTSD symptom severity (Kleim et al., 2013; Michael et al., 2005). However, conclusions from the present study are unclear without replication among other samples (e.g., non-substance users without sleeping difficulties). Future studies should focus on emotion dysregulation as a potential causal factor for PTSD symptomology and target for interventions.

In contrast to re-experiencing symptoms, results of the current study did not lend support for evoked avoidance or dissociation symptoms of PTSD as mechanisms underlying the relation between emotion dysregulation and NA reactivity during trauma cue exposure. That is, individuals experiencing greater emotion dysregulation were not more likely to respond to trauma cues with increased avoidance or dissociation symptoms. This finding is inconsistent with theory suggesting that emotion dysregulation may cause individuals to avoid trauma reminders (Gratz et al., 2007) or dissociate (Powers et al., 2015) as means to cope, and is contrary to the limited research supporting the link between emotion dysregulation and experiential avoidance in the laboratory (Gratz et al., 2007). Additional empirical work is needed to better understand this finding. For instance, it is possible that a different pattern of findings may emerge if state levels of emotion dysregulation were assessed (e.g., S-DERS; Lavender et al., 2017) alongside state PTSD symptoms and NA. Regarding the b paths within these models, heightened avoidance symptoms contributed to more NA reactivity. This finding affirms research suggesting that experiential avoidance may increase reactivity by amplifying the perceived danger of trauma-related stimuli (Pineles et al., 2011). Interestingly, dissociation symptoms were not significantly related to NA reactivity. Dissociation symptoms could indicate a subjective detachment from trauma-related stimuli and thereby inhibit NA reactivity (Bryant et al., 2000; Giesbrecht et al., 2008).

In addition to providing further insight into the nature of PTSD symptomology, findings from the present study might help inform clinical practice. The current study emphasizes the need to investigate treatments targeting emotion dysregulation. In particular, PTSD treatments that enhance emotional acceptance and foster the use of adaptive emotion regulation strategies may demonstrate efficacy in reducing PTSD symptoms and related distress. Indeed, several PTSD treatments have been developed that target these aspects of emotion dysregulation, including Acceptance and Commitment Therapy for PTSD targetting primarily emotional acceptance (Orsillo and Batten, 2005), Skills Training in Affective and Interpersonal Regulation targetting primarily emotion regulation strategies (Cloitre et al., 2002), and Dialectal Behavior Therapy Prolonged Exposure targeting both emotional acceptance and emotion regulation strategies (Harned et al., 2012). Individuals with diminished emotion regulation abilities may also be more likely to experience elevated distress during Prolonged Exposure (PE; Foa et al., 2007) through heightened re-experiencing symptoms. Therefore, findings may be used to identify these at-risk individuals prior to initiating treatment who may benefit from additional intervention.

Results should be interpreted in the context of limitations. One strength of the current study is the sample of treatment-seeking marijuana users with insomnia symptoms, which comprises a vulnerable population characterized by heightened emotion dysregulation and PTSD symptoms (Bonn-Miller et al., 2007; Fairholme et al., 2013; Short et al., 2014). Results of this study need to be replicated among other clinical samples (e.g., treatment-seeking for PTSD) to better understand generalizability. Additionally, this study relied on self-report measures, which may be confounded by the willingness and ability to report accurately on one’s own emotionality. While subjective emotional responding and biological correlates of reactivity may capture unique factors (Tull et al., 2018), future research should incorporate multimodal assessments such as skin conductance or cortisol levels. Moreover, while the RSDI is a reliable measure of PTSD state symptoms and is associated with neural and physiological activity (Hopper et al., 2007), findings may be limited by accurate recall of symptoms evoked during the trauma script. Although in line with prior literature (Hopper et al., 2007) in which the RSDI is administered following the trauma script, future studies should assess changes in symptoms by measuring PTSD state symptoms prior to the trauma script. Subsquent studies are needed to assess emotion regulation abilities and responses to trauma reminders in real time (e.g., ecological momentary assessment; Short et al., 2020). Furthermore, although NA reactivity is associated with chronic PTSD (Fitzgerald et al., 2018), longitudinal research is warranted to determine the long-term effects of emotion dysregulation on trauma cue reactivity through elicted PTSD symptoms. Although we utilized previously validated clusters of responses to trauma script-driven imagery (Hopper et al., 2007), this study should also be replicated to examine responses to the trauma script as they correspond to the recent DSM-5 criteria of PTSD (American Psychiatric Association, 2013). Future work should consider various aspects of dissociation; results of this study may contribute to discussion on the addition of a dissociation subtype of PTSD (Lanius et al., 2012). The inter-rater reliability for diagnoses in the current study was also not assessed. Subsequent work should further assess the subjective experiences (e.g., vividness) of the trauma script. Finally, given that exposure to interpersonal trauma versus non-interpersonal trauma has been found to be associated with exacerbated PTSD symptoms (Ehring and Quack, 2010) and emotion dysregulation (Raudales et al., 2019), further work should assess the role of trauma type in the relation between emotion dysregulation and NA reactivity.

5. Conclusion

This study provides novel support for the distinct role of PTSD symptoms as a mechanism underlying emotion dysregulation and NA reactivity to a trauma script. Specifically, findings support the effects of greater emotion dysregulation on heightened NA reactivity through evoked re-experiencing symptoms. These results offer laboratory-based evidence that further clarify the role of emotion dysregulation in vulnerability to PTSD symptomology, and offer implications for optimizing PTSD treatment.

Funding source

This work was supported by the National Institute on Drug Abuse (NIDA; F31 DA044689-01, 2017).

Footnotes

CRediT authorship contribution statement

Alexa M. Raudales: Writing - review & editing. Nicole H. Weiss: Writing - original draft. Norman B. Schmidt: Writing - review & editing, Writing - original draft. Nicole A. Short: Writing - original draft.

Declaration of Competing Interest

There are no conflicts of interests.

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