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. 2026 Aug 1;30(7):e70349. doi: 10.1002/ejp.70349

The Link Between Exposure to Traumatic Stress and Chronic Pain: The Mediation Effect of Hyperarousal Is Moderated by Sensitivity to Pain Traumatization

Noga Gur 1, Ruth Defrin 1,2, Yana Beitelman 3,4, Iftah Biran 3,4, Itay Goor‐Aryeh 4,5, Silviu Brill 4,6, Dorin Goldsmith 6, Eldad Katz 6, Nir Segev 6, Tali Ginsburg 1, Karni Ginzburg 7,✉
PMCID: PMC13428394  PMID: 42541396

ABSTRACT

Background

Posttraumatic stress disorder (PTSD) is highly comorbid with chronic pain. Yet, the effects of PTSD's seemingly opposing characteristics—hyperarousal and dissociation—on chronic pain are unclear. This study examined a moderated mediation model, accordingly (a) traumatic stress is associated with higher risk for chronic pain, through the mediation of hyperarousal, and (b) sensitivity to pain traumatization amplifies this association. Study 1 examined the moderated mediation model among a community sample, and Study 2 examined the moderation effect among PTSD outpatients.

Methods

This two‐part cross‐sectional study included a large community sample (N = 482; Study 1) and 47 PTSD outpatients (Study 2). Participants completed questionnaires assessing traumatic stress, hyperarousal, dissociation, sensitivity to pain traumatization, and chronic pain.

Results

Traumatic stress in the community sample was associated with chronic pain presence, through the mediation of hyperarousal, yet this effect was significant only among individuals with high levels of sensitivity to pain traumatization (p < 0.001; Study 1). Similarly, hyperarousal among PTSD outpatients was associated with chronic pain presence only among those with moderate (p = 0.009) or high levels of sensitivity to pain traumatization (p = 0.009; Study 2). In both studies, dissociation was not associated with chronic pain presence.

Conclusions

Posttraumatic hyperarousal is associated with a higher risk for chronic pain, and this association is enhanced by sensitivity to pain traumatization. Screening for these traits in trauma‐exposed individuals can help identify those at greater risk for chronic pain. Interventions for reducing hyperarousal may be valuable for mitigating chronic pain in high‐sensitivity to pain traumatization individuals.

Significance Statement

The findings of the current study suggest that the explanatory mechanism underlying the comorbidity of PTSD and chronic pain involves an interplay between hyperarousal and sensitivity to pain traumatization. Consequently, these factors may represent key targets for preventive or therapeutic interventions among survivors of traumatic events.

1. Introduction

Chronic pain is strongly associated with trauma. The prevalence of chronic pain among trauma survivors is 2–3 times higher than in the general population (Castillo‐Angeles et al. 2021; Herrera‐Escobar et al. 2018). Individuals with chronic pain are more likely than pain‐free individuals to report a history of traumatic events (Bussières et al. 2023), and the level of exposure to traumatic stress, indicated by the number of traumatic events, correlates with chronic pain severity (Siqveland et al. 2017).

Evidence suggests that posttraumatic symptoms following trauma, rather than exposure alone, underlie this link. For example, posttraumatic symptoms increase the likelihood of developing chronic pain following injury (Gruener et al. 2018). Moreover, among survivors of torture, chronic pain was more prevalent and intense in those with PTSD than in those without (Defrin et al. 2017). A systematic review concluded that PTSD contributed to chronic pain development and disability post‐musculoskeletal trauma (Jadhakhan et al. 2023).

Despite the frequent comorbidity of PTSD and chronic pain, not all individuals with PTSD develop chronic pain; one reason may be the diversity of PTSD manifestations, which can present with a dominance of hyperarousal or dissociation (Lanius et al. 2010; APA 2022). Evidence suggests that these distinct PTSD facets relate differently to the pain system: Hyperarousal is linked with increased experimental pain appraisal (Defrin et al. 2015), which is a pronociceptive factor (Yarnitsky 2015), whereas dissociation is associated with reduced pain sensitivity (Defrin et al. 2015), which is antinociceptive (Yarnitsky 2015). Thus, hyperarousal may increase chronic pain risk, whereas dissociation may not.

According to the stress‐diathesis model, individuals' orientation to pain predisposes them to chronic pain post‐trauma (Turk 2002). Katz and colleagues introduced the concept of Sensitivity to Pain Traumatization, defined as a predisposition to perceive pain as a potential stressor and to respond with somatic, cognitive, emotional, and behavioural reactions similar to those observed in traumatic stress (Katz et al. 2017; Kleiman et al. 2011). Although sensitivity to pain traumatization does not require prior exposure to a specific painful event, it has been shown to be a vulnerability factor which increases the risk for development of chronic pain (Kleiman et al. 2011; Clarke et al. 2019) and increases pain intensity among individuals with chronic pain (Maunder et al. 2022).

This two‐part study examined the link between level of exposure to traumatic stress and chronic pain, considering the roles of hyperarousal, dissociation, and sensitivity to pain traumatization. In line with the stress‐diathesis model, we hypothesized that: (a) Level of exposure to traumatic stress would be associated with higher risk for chronic pain, through the mediation of hyperarousal, and (b) Sensitivity to pain traumatization would amplify the association between hyperarousal and chronic pain. As dissociation is antinociceptive, it would not be associated with chronic pain, regardless of SPT levels (see Figure 1). Study 1, conducted among a large community sample, examined the complete moderated mediation model. Using a clinical sample of PTSD outpatients, Study 2 examined the moderation effect, namely whether SPT moderated the associations between hyperarousal/dissociation and chronic pain presence.

FIGURE 1.

FIGURE 1

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Illustration of the hypothesized research model.

2. Study 1 Methods

2.1. Participants and Procedure

A convenience sample of 482 participants was recruited through advertisements posted on social media, inviting them to participate in a study examining how people perceive and respond to various stimuli, including stress, noise, odours, or pain. The advertisements included a secure link that directed interested participants to Qualtrics Research Software. Those who met the inclusion criteria (being ≥ 20 years of age, fluent in Hebrew) received a detailed description of the study and a consent form. Upon consent, participants were redirected to the questionnaire; its completion took about 30 min. The study's protocol was approved by Tel Aviv University's institutional review board (protocol #0002453‐3). Power analysis using the G*Power (3.1.9.4) program indicated that the power for this sample size, for small to moderate effect size with six predictors, was 0.99.

2.2. Measures

2.2.1. Sociodemographic Information

Participants provided demographic information including age, gender, relational status, employment status, and years of education.

2.2.2. Chronic Pain

Chronic pain was defined as pain lasting more than 3 months (Raja et al. 2020). Participants with chronic pain rated their pain intensity in the past month on a scale from 0 (no pain) to 10 (worst imaginable pain). In addition, they provided information regarding the duration of their pain and any analgesic medications they were using.

2.2.3. Traumatic Stress

Level of traumatic stress was assessed by number of traumatic events as queried via the Stressful Life Events Inventory, a self‐report inventory which was designed by investigators familiar with life in Israel and has been used in studies of various Israeli populations (Ginzburg 2006). The scale lists 13 traumatic events (e.g., motor vehicle accident, war, assault, and an option to elaborate on another event), and participants indicated whether they had experienced each event and the year in which this event occurred. The total score is calculated by summing the number of reported events.

2.2.4. Hyperarousal

Hyperarousal was assessed by the hyperarousal subscale of the PTSD Checklist for Diagnostic and Statistical Manual of Mental Disorders (PCL‐5) (Blevins et al. 2015), consisting of six items. Participants rated the extent to which they experienced each symptom during the past month, on a 5‐point scale ranging from 1 (not at all) to 5 (extremely). To assess a provisional DSM‐5 PTSD diagnosis, we utilized the 20‐item PCL‐5. Symptoms were considered endorsed if items were rated 2 (“moderately”) or higher. Based on the DSM‐5 diagnostic rule, participants who met the criteria—that is, reporting at least one intrusion symptom, one avoidance symptom, two symptoms of negative alterations in cognition and mood, and two hyperarousal symptoms—were classified as meeting the threshold for provisional PTSD (see Blevins et al. 2015). The total hyperarousal score is calculated by averaging the responses. Reliability for the total PTSD and hyperarousal scores was high (α = 0.95, and α = 0.87, respectively).

2.2.5. Dissociation

Dissociation was assessed using the depersonalization/derealization subscale of the Dissociation Experiences Scale (DES) (Bernstein and Putnam 1986), consisting of six questions about different experiences. Participants rate the percentage of time they had each experience on an 11‐grade scale ranging from 0 (0%) to 10 (100% of the time). The total score is calculated by summing the responses. The DES has high validity and reliability, and the depersonalization/derealization subscale is used to assess dissociative tendencies among individuals with PTSD (see for example: Swart et al. 2020). Reliability was high (α = 0.84).

2.2.6. Sensitivity to Pain Traumatization

Sensitivity to pain traumatization was assessed by the Sensitivity to Pain Traumatization Scale (SPTS; Katz et al. 2017). This 12‐item scale presents cognitive and emotional responses to pain resembling traumatic stress reactions (e.g., “When I am in pain, everything I see or do reminds me of the pain”; “When I'm in pain, things don't feel real”). Participants rate the extent to which each item describes their response to pain on a 5‐grade scale ranging from 1 (not at all true) to 5 (entirely true). The total score is calculated by summing the responses. Examination of the convergent and discriminant validity of the SPTS demonstrated higher correlations with PTSD symptomatology and lower correlations with depressive symptomatology, among both pain‐reporting and pain‐free individuals (Katz et al. 2017). Reliability was high (α = 0.86).

2.3. Data Analysis

The statistical software package SPSS 31 was used to analyse the data. First, participants who reported persistent pain lasting more than 3 months were classified as the chronic pain group and the rest as the pain‐free group. A series of two‐tailed, corrected X 2 analyses and t‐tests examined group differences in demographic variables and in study variables. Pearson correlations were used to examine correlations between study variables.

To examine the moderated mediation hypothesis, we used Hayes' conditional indirect effect methodology (Hayes 2013), employing 5000 bias‐corrected bootstrapped confidence intervals for the indirect effects (Model 14). More specifically, we examined whether the association between number of potentially traumatic events and the presence of chronic pain was mediated through hyperarousal and dissociation (mediators) and conditioned on sensitivity to pain traumatization levels (moderator). Preliminary examination yielded that 1.18 < variance inflation factor (VIF) < 1.45; 0.69 < tolerance < 0.87, indicating that multicollinearity was unlikely (Thompson et al. 2017).

3. Study 1 Results

3.1. Missing Data

Little's Missing Completely at Random test (Little 1988) implied that the data were not missing completely at random, χ 2(251) = 311.54, p = 0.005. Missing data were replaced with maximum likelihood estimations based on all variables in the model, a procedure referred to as expectation maximization.

3.2. Group Comparisons

Of the entire sample, 137 (28.4%) participants had chronic pain, and 71.6% were pain‐free. Table 1 presents the two groups' demographics; they did not differ in age, gender, education level, or relationship/occupational status. Individuals with chronic pain had higher levels of traumatic stress, chronic hyperarousal, and sensitivity to pain traumatization than pain‐free individuals. More individuals in the chronic pain group were classified as having provisional PTSD than in the pain‐free group. The groups did not differ in their earliest traumatic events or in dissociation level.

TABLE 1.

Characteristics of the participants (Study 1).

Dichotomous variables Chronic pain (n = 137) Pain‐free group (n = 345) X 2 test
N % N %
Gender 0.83
Man 39 28.7 115 33.3
Woman 95 69.9 229 66.4
Other 2 1.5 1 0.3
In relationship (yes) 80 58.4 206 59.7 0.07
Employed (yes) 98 71.2 265 77.7 2.04
Pain medication (yes) 29 24 6 2 54.31***
Provisional PTSD (yes) 27 20.4 36 10.4 8.52**
Continuous variables M SD M SD t‐test
Age (years) 39.28 15.18 36.81 13.74 1.72
Chronic pain duration (years) 3.93 7.33 — — —
Pain intensity past month (0–10) 4.62 2.35 — — —
Traumatic stress (0–13) 3.70 2.36 2.73 1.86 4.76***
Earliest traumatic event (years) 16.13 12.88 15.46 13.11 0.44
Hyperarousal (1–5) 2.00 0.79 1.71 0.69 3.93***
Dissociation (0–60) 6.70 9.46 5.45 7.87 1.49
Sensitivity to pain traumatization (1–60) 28.33 9.01 26.45 7.44 2.34*
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Note: Dichotomous variables are described as numbers and percentages; continuous variables are described as means (M) and standard deviations (SD). The X 2 analysis testing for group differences in gender was restricted to participants who identified as either male or female. X 2 and t‐tests are two‐tailed (*p < 0.05, **p < 0.01, ***p < 0.001).

3.3. Moderated Mediation Model

A series of Pearson correlations indicated that sensitivity to pain traumatization was not associated with traumatic stress (r = 0.05, p = 0.25) and was weakly associated with hyperarousal (r = 0.29, p < 0.001) and dissociation (r = 0.25, p < 0.001).

Table 2 and Figure 2 present the results of the moderated‐mediation model examining whether the indirect effects of traumatic stress on presence of chronic pain, through hyperarousal and dissociation, were conditioned on sensitivity to pain traumatization levels, −2log‐likelihood = 531.76, df = 6, p < 0.001; Cox & Snell R 2 = 0.09; Nagelkerke R 2 = 0.12.

TABLE 2.

Moderated mediation model predicting chronic pain presence according to levels of traumatic stress, hyperarousal, dissociation, and sensitivity to pain traumatization (Study 1).

b SE t p
Outcome variable: hyperarousal
Traumatic stress 0.13 0.02 7.99 < 0.001
Outcome variable: dissociation
Traumatic stress 0.49 0.18 2.66 0.008
Outcome variable: chronic pain Z
Traumatic stress 0.21 0.05 3.88 < 0.001
Hyperarousal −1.23 0.56 −2.18 0.03
Dissociation −0.07 0.05 −1.28 0.20
Sensitivity to pain traumatization −0.10 0.04 −2.68 0.007
Hyperarousal × sensitivity to pain traumatization 0.05 0.02 2.81 0.005
Dissociation × sensitivity to pain traumatization 0.01 0.01 1.20 0.23
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Note: Chronic pain presence is a dichotomous variable (1 = yes, 0 = no). b = unstandardized coefficient.

Abbreviations: SE, standard error; t, statistic, Z, statistic.

FIGURE 2.

FIGURE 2

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Moderated mediation model (Study 1). Values are unstandardized coefficients (standard errors). Solid lines represent significant effects; dashed lines represent non‐significant effects. *p < 0.05, **p < 0.01, ***p < 0.001.

As can be seen, level of traumatic stress was positively associated with both hyperarousal and dissociation: The greater the traumatic stress, the higher the levels of both hyperarousal and dissociation. Additionally, levels of traumatic stress and sensitivity to pain traumatization were positively associated with the presence of chronic pain. Level of hyperarousal was negatively associated with the presence of chronic pain in this multivariate analysis, yet the higher levels of hyperarousal among the chronic pain group, as presented in Table 1, indicate that this negative effect was qualified by the significant interaction between hyperarousal and sensitivity to pain traumatization, and was thus irrelevant.

Probing the interaction between hyperarousal and sensitivity to pain traumatization revealed that among individuals with high sensitivity to pain traumatization levels (1 SD above the mean score), the higher the level of hyperarousal, the higher the probability of reporting chronic pain (p = 0.003). Among individuals with low (1 SD below the mean score) or moderate sensitivity to pain traumatization levels (mean scores), the hyperarousal level was not related to chronic pain presence (p = 0.39, p = 0.20, respectively; see Figure 3).

FIGURE 3.

FIGURE 3

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Presence of chronic pain according to levels of hyperarousal and sensitivity to pain traumatization (Study 1). SPT = Sensitivity to pain traumatization.

Finally, the indirect effect of traumatic stress on chronic pain presence through hyperarousal was conditioned by sensitivity to pain traumatization: Namely, the relation between level of traumatic stress and chronic pain presence through the mediation of hyperarousal was significant only among individuals with high sensitivity to pain traumatization levels (b = 0.08, SE = 0.01, 95% CI [0.03, 0.16]), but not among those with low or moderate sensitivity to pain traumatization levels (b = −0.03, SE = 0.03, 95% CI [−0.09, 0.03]; b = 0.03, SE = 0.02, 95% CI [−0.02, 0.08], respectively). The main effect of dissociation and the interaction of sensitivity to pain traumatization and dissociation on chronic pain presence were not significant.

4. Study 2 Methods

4.1. Participants and Procedure

Participants were 47 individuals with PTSD, recruited from the psychiatric outpatient clinic of Sourasky Medical Center. Eligible patients were approached by medical staff. Interested outpatients received additional details over the phone and afterwards could agree/decline to participate. PTSD was diagnosed by a senior psychiatrist (author YB) according to the DSM‐5.

Assuming a large effect size, with 0.80 power and 0.05 probability of a Type I error, and considering a model with six predictors, the minimum sample size was 46. Inclusion criteria were age ≥ 20 years and a PTSD diagnosis of at least 12 months. Exclusion criteria were pregnancy, any lesion in the forearms and arms (testing regions), diseases causing potential neural damage (e.g., diabetes), systemic/neurological illnesses, communication difficulties, or a current depressive or psychotic state.

Written informed consent was obtained after the procedures had been fully explained to the participants. The study was approved by both the Helsinki Committee of Sourasky Medical Center (protocol #TLV‐0701‐21) and the ethical review board of Tel Aviv University (protocol # 0005274‐9).

4.2. Measures

4.2.1. Chronic Pain

Consistent with Study 1, chronic pain was defined as pain lasting more than 3 months (Raja et al. 2020). Participants who met this criterion were asked to rate the intensity of their pain for the past month and provided information regarding its duration and usage of analgesic medications (see Study 1).

4.2.2. Hyperarousal, Dissociation, Sensitivity to Pain Traumatization

Consistent with Study 1, hyperarousal was assessed using the hyperarousal subscale of the PCL‐5 (see Study 1). Its reliability was high (α = 0.89). Dissociation was assessed using the depersonalization/derealization subscale of the DES (see Study 1). Its reliability was high (α = 0.84). Sensitivity to pain traumatization was assessed by the SPTS (see Study 1). Its reliability was high (α = 0.93).

4.2.3. Pain Sensitivity Evaluation

As previous studies have indicated that PTSD patients demonstrate low pain sensitivity (indicated in higher pain thresholds than healthy controls) and that sensitivity is associated with dissociation levels (Defrin et al. 2015, 2008), the associations between the study variables were examined while controlling for pain sensitivity, assessed both psychophysically and by self‐report questionnaire.

4.2.3.1. Heat‐Pain Threshold Measurement

Heat‐pain threshold was measured with a computerized thermal stimulator (Q Sense, Medoc, Ramat Ishay, Israel), using the method of limits. Participants received four successive stimuli of gradually increasing heat (baseline of 35°C, rate of 2°C/s) and were asked to press a switch the moment they perceived pain, thus freezing the temperature. Heat‐pain threshold was calculated as the average of four successive temperatures (Rivel et al. 2021) and was measured after the participants underwent a training session.

4.2.3.2. Pain Sensitivity Questionnaire (PSQ)

The Pain Sensitivity Questionnaire Short Form (PSQ) is a 10‐item scale which evaluates perceived pain sensitivity in daily life situations. Participants are asked to rank the items from 0 (not painful at all) to 10 (worst pain imaginable). The total score is calculated by summing the responses, and higher scores indicate greater pain sensitivity. The PSQ has shown high internal consistency (α = 0.92), and test–retest reliability (ICC = 0.83) over an interval (Melotti et al. 2018). Internal consistency for the current sample was high (α = 0.96).

4.3. Data Analysis

The statistical software package SPSS 31 was used to analyse the data. A series of X 2 analyses and t‐tests examined differences between PTSD patients with chronic pain and those who were pain‐free in demographics and study variables. Pearson correlations were used to examine correlations between study variables.

In this part, traumatic stress was not included, as all participants were exposed to traumatic events. To examine the moderation hypothesis, we used Hayes' conditional indirect effect methodology (Hayes 2013), employing 5000 bias‐corrected bootstrapped confidence intervals for the indirect effects (Model 1). More specifically, we examined whether the effects of hyperarousal and dissociation on the existence of chronic pain were conditioned on sensitivity to pain traumatization level. As preliminary analyses indicated that hyperarousal and dissociation were significantly correlated (r = 0.43, p < 0.001), the conditional effects for hyperarousal were conducted by controlling for dissociation, and those for dissociation were conducted while controlling for hyperarousal. The analyses were conducted while controlling pain sensitivity as assessed by both heat‐pain threshold and the PSQ. Finally, as participants with chronic pain were older than the pain‐free participants (see Table 3), participants' age was controlled. Preliminary examination yielded that 1.30 < VIF < 2.00; 0.50 < tolerance < 0.77, indicating that multicollinearity was unlikely (Defrin et al. 2008).

TABLE 3.

Characteristics of the participants (Study 2).

Dichotomous variables Chronic pain (n = 28) Pain‐free group (n = 19) X 2 test
N % N %
Gender 0.48
Man 23 82.1 14 73.7
Woman 5 17.9 5 26.3
In relationship (yes) 10 35.7 9 50.0 0.42
Employed (yes) 12 42.9 11 57.9 0.31
Pain medication (yes) 15 57 — — —
Trauma type 2.18
Combat 17 59 12 66.7
MVA 3 10.3 0 0
Terror 4 13.8 2 11.1
Abuse 5 17.2 4 22.2
Continuous variables M SD M SD t
Age (years) 54.64 15.42 40.41 16.94 2.99**
Chronic pain duration (years) 1.16 1.24 — — —
Pain intensity past month (0–10) 6.69 2.11 — — —
PTSD duration (years) 5.14 3.34 9.22 6.44 0.15
Hyperarousal (1–5) 3.88 0.85 3.70 0.56 0.81
Dissociation (0–60) 16.60 14.9 10.74 45.05 1.42
Sensitivity to pain traumatization (1–60) 37.18 9.07 33.26 8.63 1.48
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Note: Dichotomous variables are described as numbers and percentages; continuous variables are described as means (M) and standard deviations (SD). X 2 and t‐tests are two‐tailed (**p < 0.01).

5. Study 2 Results

5.1. Missing Data

Little's Missing Completely at Random test implied that the data were missing completely at random, χ 2(57) = 67.12, p = 0.17. Missing data were replaced using the expectation maximization procedure.

5.2. Sample Characteristics

Twenty‐eight participants (59.6%) reported chronic pain, and 19 (40.4%) were classified as pain‐free. The two groups did not differ in gender, relationship status, or employment status, yet participants with chronic pain were older than pain‐free participants (see Table 3). No significant differences were observed between groups in levels of hyperarousal, dissociation, sensitivity to pain traumatization, type of trauma experienced, or duration of PTSD diagnosis.

5.3. Moderation Effects

Pearson correlations indicated that sensitivity to pain traumatization was not associated with hyperarousal (r = 0.08, p = 0.58) but was associated with dissociation (r = 0.31, p = 0.03). Sensitivity to pain traumatization was negatively associated with heat‐pain threshold (r = −0.30, p = 0.04) and positively with PSQ (r = 0.41, p = 0.004).

To examine whether the associations between hyperarousal and presence of chronic pain were moderated by sensitivity to pain traumatization, controlling for age, dissociation, and pain sensitivity (pain threshold and PSQ), a conditional process model was conducted (−2log‐likelihood = 31.98, df = 7, p < 0.001; Cox & Snell R 2  = 0.19; Nagelkerke R 2 = 0.66).

The results indicated that the main effect of hyperarousal on presence of chronic pain was not significant (B = −3.04, SE = 2.24, p = 0.18), but the effect of sensitivity to pain traumatization on presence of chronic pain was significant (B = −0.70, SE = 0.34, p = 0.04). Additionally, the results yielded a significant interaction between hyperarousal and sensitivity to pain traumatization (B = 0.18, SE = 0.08, p = 0.03).

Probing the interaction between hyperarousal and sensitivity to pain traumatization revealed that among individuals with moderate (mean sensitivity to pain traumatization score) and high sensitivity to pain traumatization levels (1 SD above the mean score), the higher the hyperarousal level, the higher the probability of having chronic pain (for both p = 0.009). Among individuals with low sensitivity to pain traumatization levels (1 SD below the mean score), the hyperarousal level was not related to chronic pain presence (p = 0.15; see Figure 4).

FIGURE 4.

FIGURE 4

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Presence of chronic pain according to levels of hyperarousal and sensitivity to pain traumatization (Study 2). SPT = sensitivity to pain traumatization.

To examine whether the association between dissociation and chronic pain presence was moderated by sensitivity to pain traumatization, controlling for age, hyperarousal, and pain sensitivity (heat‐pain threshold and PSQ), a second conditional process model was conducted. Neither the main effects of dissociation (B = 0.23, SE = 0.1. p = 0.27) or sensitivity to pain traumatization (B = −0.02, SE = 0.08, p = 0.84), nor the interaction between them (B = 0.01, SE = 0.01, p = 0.47), were significant.

6. Discussion

Based on the large community sample (Study 1) and the clinical sample of individuals with diagnosed PTSD (Study 2), we found converging evidence that hyperarousal, but not dissociation, underlies the trauma‐chronic pain link, and that sensitivity to pain traumatization amplified this link. These findings point toward individual variability in trauma responses and chronic pain, and may offer insights for trauma‐informed pain prevention and management.

6.1. Trauma, PTSD, and Chronic Pain

About one‐third of the participants in the large community sample (Study 1) reported chronic pain, consistent with a large national internet‐based survey (Sharon et al. 2022). Previous surveys in Europe and the USA reported a prevalence rate of ~20% (Breivik et al. 2006; Yong et al. 2022), perhaps because more restrictive criteria for chronic pain than herein were employed (i.e., pain lasting 6 months or pain every day for the last 3 months, as opposed to pain lasting more than 3 months). The rate of chronic pain among PTSD patients (Study 2) was approximately 60%, resembling previous studies (Defrin et al. 2017; Langford et al. 2018).

Study 1 indicated that individuals with chronic pain experienced significantly more traumatic events and higher hyperarousal levels than pain‐free individuals. These findings align with previous studies showing elevated traumatic stress and PTSD symptoms among individuals with chronic pain (Bussières et al. 2023; Siqveland et al. 2017). However, among the PTSD outpatients who participated in Study 2, those with chronic pain did not differ from pain‐free participants in either hyperarousal or dissociation levels.

6.2. Hyperarousal vs. Dissociation

Hyperarousal reflects distress and heightened sympathetic activation (Blevins et al. 2015). Its relevance to chronic pain is reflected in studies showing that hyperarousal, not other PTSD symptoms, predicted pain‐related disability in trauma‐exposed individuals (Maujean et al. 2017). Several mechanisms may explain the hyperarousal‐pain link. First, hyperarousal relates to body vigilance (Vujanovic et al. 2007), the tendency to focus on internal bodily sensations (Vujanovic et al. 2007), and increased sensitivity to noxious stimuli (Defrin et al. 2015). Thus, hyper‐aroused individuals may be more attentive and vigilant to pain signals and interpret them as threatening, which may enhance and maintain pain severity and disability (McCracken 1997). Second, repeated sympathetic activation which occurs with hyperarousal can sensitize peripheral and central pain pathways (Lerman et al. 2016), enhance inflammatory‐ and adjuvant‐evoked hyperalgesia (Imbe and Kimura 2015), and increase activity in sensitized nociceptors (Baron 2000). Thus, peripheral and central sensitization may perpetuate pain hypersensitivity and hyperresponsiveness, and contribute to pain chronification. Third, activation of the noradrenergic locus coeruleus, a stress and hyperarousal modulator, has been implicated in enhanced pain facilitation and reduced diffuse noxious inhibitory control (Kucharczyk et al. 2022; Suárez‐Pereira et al. 2022), potentially underlying susceptibility to pain chronification. Hyperarousal also likely exacerbates chronic pain by increasing pain catastrophizing. Together, these mechanisms indicate hyperarousal as a significant pronociceptive factor.

In contrast, dissociation appears unrelated to chronic pain, neither mediating the trauma‐chronic pain relation nor interacting with sensitivity to pain traumatization to contribute to pain. Dissociation may even be antinociceptive, as shown by associations with reduced pain sensitivity, potentially reflecting an endogenous opioid‐like mechanism (Defrin et al. 2015). Induced dissociation reduces pain sensitivity, accompanied by activation of brain regions involved in descending pain inhibition (Ludäscher et al. 2010; Mickleborough et al. 2011).

The contrasting consequences of hyperarousal and dissociation align with conceptualizations of hyper‐aroused and dissociative PTSD subtypes, which are neurobiologically distinct (Lanius et al. 2010; Swart et al. 2020). Hyperarousal reflects emotional under‐modulation, mediated by prefrontal‐limbic inhibition failure, whereas dissociation involves emotional overmodulation, mediated by midline prefrontal inhibition of limbic regions (Lanius et al. 2010). Unlike dissociation, hyperarousal is a core mechanism linking trauma to chronic pain.

6.3. The Specific Role of Sensitivity to Pain Traumatization

In Study 1, sensitivity to pain traumatization was not associated with traumatic stress and was weakly associated with hyperarousal. This finding aligns with prior research demonstrating a moderate correlation between these constructs (Katz et al. 2017; Fashler et al. 2022), suggesting that sensitivity to pain traumatization and PTSD represent related yet distinct phenomena. PTSD requires traumatic stress, whereas sensitivity to pain traumatization may be independent of traumatic experience. High sensitivity to pain traumatization individuals perceive pain itself as a traumatic stressor, despite the lack of traumatic painful experiences. Furthermore, sensitivity to pain traumatization was associated with pain sensitivity, as evaluated through both psychophysical assessment and self‐report (Study 2). Although these variables are related, the data indicated that sensitivity to pain traumatization did not overlap with pain sensitivity itself. Cumulatively, these results suggest that sensitivity to pain traumatization reflects a unique cognitive orientation wherein pain experiences are perceived as a potential traumatic threat—an appraisal that, in turn, triggers intrusive, avoidant, and hyperarousal reactions.

Sensitivity to pain traumatization has been suggested as a diathesis predisposing individuals to develop chronic pain, once they are already experiencing painful events (Kleiman et al. 2011; Clarke et al. 2019). It may also be a shared vulnerability factor that underlies the comorbidity of PTSD and chronic pain following traumatic events (Katz et al. 2017). Our findings support this idea, yet indicate the role specifically for hyperarousal: High hyperarousal was associated with a greater likelihood of chronic pain only among individuals with moderate‐to‐high sensitivity to pain traumatization. Thus, individuals exhibiting strong hyperarousal responses and cognitive sensitization to pain seem particularly vulnerable to developing chronic pain post‐trauma.

Hyperarousal and sensitivity to pain traumatization likely share overlapping neurocognitive and physiological mechanisms that heighten chronic pain vulnerability. Hyperarousal is characterized by autonomic hyperactivity, hypervigilance, and exaggerated threat perception (Lanius et al. 2010; Blevins et al. 2015), mirroring sensitivity to pain traumatization features of catastrophic thinking, pain‐related fear, and trauma‐like reactions to noxious stimuli (Katz et al. 2017; Kleiman et al. 2011). Previous neuroimaging studies showed that both involve increased activity in the amygdala, insula, and anterior cingulate cortex, regions implicated in salience detection, interoception, and emotional appraisal of threat and pain (Baliki and Apkarian 2015; Etkin and Wager 2007). Moreover, reduced prefrontal regulation may impair modulation of pain and threat responses (Guerra et al. 2023), promoting hyperactivation and pain sensitization (Ong et al. 2019; Elman and Borsook 2018) Shared sensitivity to pain traumatization—and hyperarousal‐related activations may drive central sensitization promoting chronic pain.

This interpretation is further supported by the negative association between sensitivity to pain traumatization and pain thresholds (Study 2). A previous study demonstrated that pain thresholds measured early following spinal cord injury predicted central neuropathic pain 6 months post‐injury (Defrin et al. 2022). Posttraumatic hyperarousal has been shown to be related to high sensory responsiveness (Huberman et al. 2025). Thus, the interactive effect of sensitivity to pain traumatization and hyperarousal on chronic pain may suggest that individuals with high levels of sensitivity to pain traumatization and hyperarousal have a multisensory hypersensitivity, which characterizes central sensitization (Harte et al. 2018).

6.4. Summary and Clinical Implications

The studies had several limitations. First, the cross‐sectional design precludes causal inference. Indeed, participants' reports imply that the earliest reported traumatic event temporally preceded chronic pain (Study 1, see Table 1), and PTSD duration was longer than chronic pain duration (Study 2, see Table 3). Yet, the data remain insufficient to establish a causal link or conclude that chronic pain is an outcome of these variables. Second, Study 1 may have been affected by report biases due to convenience sampling and data collection method. Third, traumatic stress was calculated by the number of traumatic events, not taking into consideration each event's severity or impact. Fourth, examining other expressions of distress, such as anxiety or depression, would have substantiated the unique link between hyperarousal and chronic pain risk. Similarly, examining other potential moderators to examine competing models would have substantiated the unique role of sensitivity to pain traumatization. Finally, specific chronic pain diagnoses and detailed information regarding the nature of the pain and its frequency were not considered. To enhance the generalizability of our findings, future longitudinal studies should examine these mechanisms among wider clinical populations and diverse samples of individuals experiencing chronic pain.

The two studies herein investigated trauma‐to‐chronic pain pathways. Results indicate that hyperarousal, especially among high‐sensitivity to pain traumatization individuals, seems pronociceptive as it is associated with chronic pain. Conversely, dissociation appears unrelated to chronic pain and may even be antinociceptive. These findings emphasize the need for personalized, trauma‐informed interventions considering individual trauma symptoms and pain‐related cognitive vulnerabilities. Screening for sensitivity to pain traumatization and hyperarousal could identify individuals at highest risk for pain chronification. Integrated pre‐emptive interventions for reducing hyperarousal may be particularly valuable for mitigating chronic pain in high‐sensitivity to pain traumatization individuals.

Author Contributions

Noga Gur, Ruth Defrin, and Karni Ginzburg designed the study setting, planned the implementation of the study, ran the statistical analyses, critically examined the results, and took a primary role in preparing the manuscript. Yana Beitelman and Iftah Biran participated in study design and offered their expertise about posttraumatic stress disorder. Itay Goor‐Aryeh and Silviu Brill participated in study design and offered their expertise about chronic pain. Dorin Goldsmith, Eldad Katz, and Nir Segev offered their expertise about chronic pain and participated in study implementation. Tali Ginsburg participated in study implementation and critically examined the results. All authors edited the manuscript, revised and approved the final version, and agree to be accountable for all aspects of the work.

Funding

This work was supported by grants from the Israel Science Foundation (Grant number 2615/21) and Rosetrees Trust (Grant number PGS23/100079) awarded to Prof. Ruth Defrin and Prof. Karni Ginzburg.

Conflicts of Interest

The authors declare no conflicts of interest.

Acknowledgements

This study was performed in partial fulfilment of the requirements for a PhD degree in Physical Therapy by Noga Gur at the Faculty of Medicine and Health Sciences, Tel Aviv University, Tel Aviv, Israel. This work was supported by grants from the Israel Science Foundation (Grant number 2615/21) and Rosetrees Trust (Grant number PGS23/100079) awarded to Prof. Ruth Defrin and Prof. Karni Ginzburg.

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