The continuous traumatic stress (type III trauma) model is an emerging paradigm ( Eagle & Kaminer, 2013 ; Kira et al., 2008, 2013 ; Kira, 2021, 2022 ) that may help us better understand the fundamental dynamics of traumatization in natural, ongoing phenomena, such as chronic pain. For instance, low back chronic pain that continues with the patient for long time is one of the most common contributors to disability ( Hoy et al., 2014 ). Chronic pain has been associated with anxiety and depression ( Gureje et al., 1998 ), dependence on opioids, and overdose ( Institute of Medicine, 2011 ).

Rates of overdose due to chronic pain are high ( Vowles et al., 2015 ; López-Martínez et al., 2019 ). Overdose is responsible for a significant number of deaths globally. Over the past decade, the rise of the opioid epidemic, especially in the United States, Europe, and worldwide, has led to a significant increase in mortality and disability (e.g. Martins et al., 2015 ). From 1999 to 2019 in the United States, opioid overdose from both regularly prescribed and illegally acquired drugs was the cause of death for nearly 500,000 people ( Centers for Disease Control and Prevention, 2024 ). The use of opioid-based treatments for pain management has been the traditional approach despite research showing their low effectiveness and potential long-term risks for addiction and suicide ( Busse et al., 2018 ; Chou et al., 2022 ). Furthermore, severe pain is linked to an increased risk of opioid abuse ( Novak et al., 2016 ) and dependence ( Blanco et al., 2016 ). The escalating misuse and dependence on opioids have been identified as a significant contributor to the high number of drug overdose deaths in the United States, leading to its classification as a public health crisis ( Rudd et al., 2016 ; Saloner et al., 2018 ). Chronic pain is one significant factor contributing to drug overdose, and its mortal consequences have been grossly misunderstood. The right understanding of CP dynamics and addressing it as continuous traumatic stress should help us find better ways to treat and deal with its negative health, mental health, and cognitive consequences and the overdose epidemic.

According to Kira et al. (2023b) , CP fall under the category of type III-e trauma (continuous life-threatening health conditions) despite not being immediately life-threatening. A significant percentage of individuals living with chronic pain contemplate or commit suicide due to various factors, including the severity or intolerability of the pain, which can lead to overdose (e.g. Calati et al., 2015 ). CP is considered a continuous stressor, which aligns with type III trauma, in contrast to types I (a single past acute stressor) and II (a sequence of past acute stressors).

Research in the pain literature proposed that PTSD affects chronic pain severity. For instance, some studies (e.g. Fishbain et al., 2017 ; Gasperi et al., 2021 ; Miró et al., 2008 ; Siqveland et al., 2017 ) indicated that PTSD symptoms can increase the perception of pain. As a result, PTSD may be a risk factor for increasing CP severity. Early research generally either did not explore the direction of the relationship between the two variables (CP and PTSD) or focused more on the effects of PTSD on CP severity. Research has observed a high co-occurrence of chronic pain and PTSD without implying a causal link between CP as continuous traumatic stressors and PTSD (e.g. Morasco et al., 2013 ; Otis et al., 2003 ; Outcalt et al., 2015 ). Research has demonstrated that this co-occurrence is associated with increased pain intensity and functional impairment ( Åkerblom et al., 2017 ; Outcalt et al., 2015 ; Ruiz-Párraga & López-Martínez, 2014 ). It was suggested that these concurrent and lagged associations may contribute to cyclical symptom exacerbation and may be mutually maintained via several shared pathways, including attentional biases to pain and threat, avoidant styles of emotional coping, and heightened anxiety sensitivity (i.e. fear of anxiety-related sensations; Brennstuhl et al., 2015 ; Sharp & Harvey, 2001 ). Post-traumatic stress and chronic pain conditions may influence each other in a way that exacerbates symptoms ( Sharp & Harvey, 2001 ), which may result in a vicious cycle or loop of perpetuating distress and an increased likelihood of abusing opioids to cope with the severity and chronicity of pain and distress ( Asmundson & Katz, 2009 ). Gasperi et al. (2021) noticed that people with chronic pain that does not have Criterion A’ trauma displayed PTSD symptoms.

The current literature has not fully acknowledged that chronic pain itself can be a persistent traumatic stressor that predicts not only PTSD but also other mental health conditions, such as depression and anxiety, which could ultimately lead to overdose and suicide. In addition, chronic pain, as a severe traumatic stressor, is not commonly assessed like other traumatic stressors in predicting pathological dissociation. Our current study aims to explore this potential outcome for chronic pain. By investigating the link between pathological dissociation and chronic pain, we aim to provide further evidence supporting the chronic pain model as a continuous traumatic stressor encompassing both ongoing acute and non-acute stressors.

Furthermore, the relationship between pain as a sensory phenomenon and somatization is strong. A meta-analytic study ( Burke et al., 2015 ) found that Individuals with CP were most likely to experience psychological problems in physically focused areas—namely, pain anxiety and somatization. CP is highly correlated with somatization and Somatic Symptom Disorder (SSD), which ranges between 0% - 53% ( Birket-Smith, 2001 ). There is a significant correlation between the two, and it may be related to pain level ( Fishbain et al., 2009 ). Somatization is “the tendency to experience and report somatic symptoms due to psychological distress” ( Lipowski, 1988 : p. 19). It is difficult to differentiate pain and clinical somatization. Similar etiologies have been proposed to underlie both somatization and pain. Neurobiological sensitivity, central sensitization, cognitive-affective mechanisms, social learning, and familial transmission are similar proposed etiologies or contributing pathways for both CP and somatization (e.g. Adams & Turk, 2018 ; Asmundson et al., 2012 ; Stone & Wilson, 2016 ). The co-occurrence of CP and somatization is associated with functional impairments (e.g. Eliasen et al., 2016 ).

Disability is an important potential outcome of CP from a clinical and public health perspective. Studies in different countries found that chronic pain intensity was the strongest predictor of pain-related disability (e.g. Raftery et al., 2011 ; Sirbu et al., 2023 ). Additionally, several meta-analyses have consistently found that people with chronic pain suffer from mild to moderate impairments in executive function ( Berryman et al., 2014 ; Rathbone et al., 2016 ). Additionally, research has shown a moderate decline in working and long-term memory performance among chronic pain patients ( Mazza et al., 2018 ). These findings suggest a potential two-way relationship: Pain may disrupt executive functioning, while poor executive functioning could also increase susceptibility to increased pain ( Bunk et al., 2019 ). Impairments in cognitive executive functioning can lead to inadequate regulation of stress, pain, and emotion-related information processing. Conversely, negative emotions, pain, and stress can impair executive functioning. The characteristics of the feedback and feedforward neural connections between the prefrontal cortex and the limbic system play a crucial role in determining adaptive behavior, stress response, and pain experience ( Feller et al., 2020 ).

The current study aims to explore the relationship between CP as a traumatic continuous stressor, PTSD, depression, anxiety, pathological dissociation, somatization, disability and executive functions. The conceptual model we want to test includes CP and predicts PTSD. Depression, anxiety, pathological dissociation, somatization, and executive functions after controlling for the impact of other cumulative stressors and traumas.

Hypothesis 1: Chronic pain as continuous traumatic stressors independently predicts PTSD, depression, and anxiety. It predicts somatization and pathological dissociation.

Hypothesis 2: Chronic pain as continuous traumatic stressors predicts executive function deficits.

Hypothesis 3: Chronic pain as continuous traumatic stressors predicts disability.

Descriptive Results: CP conditions, current treatment modalities, pain severity, somatization, disability, trauma exposure, dissociation, anxiety, depression and PTSD.

87.7% of the participants were treated with drugs, 9.5% underwent surgeries as the main treatment for their pain, and 2.8% used both surgical procedures and pain medication to control their pain. 34.6% reported that their pain was tolerable, 53.1% experienced moderate pain, and 12.3% had severe and unbearable pain. Furthermore, 39.8% had been in pain for three months to less than a year, 32.7% for 1 - 5 years, 27.5% for more than five years 18.5% of the sample suffered from headache syndromes, 32.2% experienced localized pain, 16.1% report rheumatoid-related pain, and 17.5% have pain related to medical conditions. 15.6% have multiple pain conditions. Pain severity (M = 17.37, SD = 11.03). 31% scored in the high severity of pain level (Physical pain (M = 14.27, SD = 8.73, Psychological pain, M = 3.10, SD = 2.72). Somatization (M = 15.94, SD = 6.70), 67.8% scored on the high levels of somatization. Disability (M = 12.70, SD = 14.07), about 10% scored at the high level of disability. Cumulative trauma frequency was (M = 16.42, SD = 13.98) and cumulative trauma occurrence was (M = 8.37, SD = 5.22). For anxiety (M = 8.71, SD = 5.68), 19.9% scored at or above the cut-off point of 15, which indicates severe anxiety. Depression (M = 11.40, SD = 7.32), 17.1% scored at or above the cut-off point of 20, which indicates severe depression. In pathological dissociation (M = 6.83, SD = 9.24),7.2% scored at or above the cut-off point 22, indicating severe pathological dissociation. PTSD (M = 22.89, SD = 15.36) 29.4% scored at or above the cut-off point of 31, which indicates probable PTSD diagnosis. All variables follow the normal distribution.

Correlation Results: Chronic pain has a large association with somatization, a medium to large association with disability, PTSD, pathological dissociation, depression, working memory deficits, anxiety, inhibition deficits, and a small to medium size association with cognitive flexibility deficits. Table 2 presents the zero-order correlations between these variables.

***Correlation is significant at the 0.01 level (2-tailed).

Hierarchical Multiple Regression Results:

To test if chronic pain predicts PTSD, depression, anxiety, pathological dissociation, working memory, inhibition, and cognitive flexibility deficits and disability, after controlling for basic demographics and cumulative stressors and traumas, we conducted a series of hierarchical multiple regressions.

For PTSD, in the first step (entering demographics) age was a negative predictive, while unemployment was a positive predictor of PTSD. The first step explained significant variance (R² = .211). In the second step adding cumulative traumas led to a significant increase in the explained variance (change in R² = .200; Beta = .40, p < .000). In the third step adding chronic pain led to a significant increase in variance predicting PTSD (change in R² = .061; Beta for chronic pain = .27, p < .000). VIF values indicated there is no multicollinearity. The model accounted for.422 of the variance in PTSD. Table 3 presents the details of these results. Similar results were found for depression ( Table A1 in Appendix), generalized anxiety ( Table A2 in Appendix), pathological dissociation ( Table A3 in Appendix), working memory deficits ( Table A4 in Appendix), inhibition deficits ( Table A5 in Appendix), and cognitive flexibility deficits ( Table A6 in Appendix). Chronic pain was a significant predictor of each after controlling for basic demographics and cumulative life stressors and traumas.

For disability, in the first step (entering demographics) income was a negative predictive, while gender was a positive predictor of disability. In the second step, after adding cumulative life stressors and traumas, gender lost its significance as a predictor (probably due to gender discrimination being one of the life traumatic stressors). Adding cumulative traumas led to a significant increase in explained variance (change in R² = .087; Beta = .30, p < .000). In the third step, adding chronic pain led to a significant increase in variance predicting disability (change in R² = .124; Beta for the effects of chronic pain = .38, p < .000); Beta for the effects of cumulative trauma = .21, p < .000). The effects of chronic pain on disability were much higher than cumulative stressors and traumas. VIF values indicated there is no multicollinearity. The model accounted for.276 of the variance in disability. Table 4 presents the details of these results.

Note: *p < .05, **p < .01, ***p < .001 (two-tailed).

SEM Results: The model fitted well (Chi-square = 23.108, d.f. = 16, p = .111, CFI = .993, RMSEA = .046). The observed variables loaded significantly on their latent variables (over .70). Chronic pain had direct medium-size effects on executive function deficits (as predicted by working memory deficits, inhibition deficits, and cognitive flexibility deficits), and direct and indirect effects on mental health (as predicted by PTSD, depression, anxiety) and disability. Its total effects on them are medium to high. Its direct effects on mental health accounted for 45% of its total effects. Its direct effects on disability accounted for 70% of its total effects.

Executive function deficits had direct large-size effects on mental health and indirect low to medium-size effects on disability. Mental ill-health had medium-sized direct effects on disability. Table 5 presents the direct, indirect, and total standardized effects and their 95% confidence intervals of each variable in the model. Figure 1 presents the direct standardized paths between variables.

Note: *p < .05, **p < .01, ***p < .001 (two-tailed).

Note: *p < .05, **p < .01, ***p < .001 (two-tailed). Notes: EFD = Executive Function Deficits, MHD = Mental Health Disorders, WMD = Working Memory Deficits, ID = Inhibition Deficits, CFD = Cognitive Flexibility Deficits, PTSD = Posttraumatic Stress Disorder.

The study validated chronic pain continuous traumatic stress model. CP independently predicted PTSD, pathological dissociation, depression, anxiety, somatization, disability and executive function deficits after controlling for demographics and all cumulative stressors and traumas and explained independent and significant variance in each. The study results shift the paradigm in our understanding of chronic pain and its dynamics as traumatic continuous stressors on their own that predict PTSD and other variables that may contribute to overdose epidemic.

Research suggests that chronic stress, such as in the case of Chronic Pain (CP), includes both acute and non-acute pain and can be just as stressful, or even more so, than a single acute stressor (trauma, e.g. Gold et al., 2005 ; Katz et al., 1981 ). The recurrence of chronic stressors, in this case, chronic pain, can have a cumulative impact. The prolonged sequence of repeated acute and non-acute pain can, over time, result in more complex post-trauma or complex peri-trauma symptoms. Exposure to continuous stressors may deplete a person’s resources, reducing their stress tolerance and causing severe traumatic reactions with adverse consequences (e.g. Monroe & Simons, 1991 ; Kira et al., 2020 ).

The study has important conceptual and clinical implications. Conceptually, the results proposed the existence of post or “peri chronic pain syndrome” that includes somatization, pathological dissociation, disability, PTSD, depression, generalized anxiety and executive function deficits. Such “peri-chronic pain syndrome” can lead to serious behavioral consequences such as suicide and overdose epidemic. Future research can explore further the existence and the structure of this syndrome and the differential impact of its components on behavior.

Clinically, research suggests new methods to address chronic pain and overdose through continuous trauma-focused interventions ( Kira, 2013 ; Kira et al., 2015a, 2015b ; Murray et al., 2013 ). Research found that treating PTSD in responsive active-duty veterans who suffer chronic pain using cognitive processing therapy, significantly reduced pain at the same time ( Hass et al., 2025 ). It is important to treat chronic pain as traumatic stress using current evidence-based interventions. Additionally, there is a need for new approaches to tailor current evidence-based interventions to better address the ongoing nature of chronic pain, such as traumatic stress. Urgently, we need to develop new, effective, evidence-based prevention and intervention strategies to prevent the proliferation and accumulation dynamics of chronic pain from reaching intolerable levels. Importantly, it is essential to develop strategies to prevent overdose and suicide resulting from intolerable CP.

The current dominant treatment approach for chronic pain is pharmacological treatment using opioid-based analgesics. Opioids pose a high risk of addiction and over-prescription. They contributed to the current opioid epidemic ( Nelson et al., 2015 ; Rose, 2018 )—the psych-social treatment approaches to treating chronic pain, as continuous traumatic stressors include individual and group psychotherapy. The study results call upon policymakers and clinicians to treat CP as they would any psychological trauma, focusing on mitigating its effects through psychotherapeutic interventions rather than through only relying on pharmacological treatments that focus on its physiological etiology. Addressing CP as a traumatic phenomenon may prevent medication addiction, deaths due to overdose, ultimately improving functioning, reducing suffering, suicide and overdose. Meta-analysis of chronic pain treatment ( Alldredge et al., 2024 ) found that group-based treatment produces significantly better outcomes than individual treatment. Group cognitive-behavioral therapy, group acceptance, and commitment therapy, self-management groups, and mindfulness-based stress reduction have shown good evidence. In contrast, group hypnotherapy and group music therapy were promising treatment modalities. There is a need for significant innovations in chronic pain treatment.

The current study has both strengths and limitations. SEM results cannot support causal claims without longitudinal data. The study uses cross-sectional data but implies that CP causes PCTSS symptoms. Given that depression/anxiety could exacerbate pain perception, you cannot rule out reverse causality or bidirectional relationships. Although the study used a random sample of chronic pain patients, it was mostly a convenience sample. The measures used in the study were self-reports, which can be biased by social desirability. For example, the Executive Function (EF) self-report may not represent the same cognitive structures as performance scales. Previous research has shown that self-report and performance scales of EF are related but distinct constructs of cognitive control ( Friedman & Gustavson, 2022 ). Future studies may consider using both performance and self-report measures.

Moreover, the study utilized a cross-sectional design, and future research may benefit from adopting a longitudinal approach. It’s essential to emphasize that in Structural Equation Modeling (SEM), direct and indirect effects are expressed as statistical probabilistic stochastic terms, which should not be conflated with causality in deterministic sciences. Additionally, we discussed in detail addiction without measuring it as a variable in the model. Notwithstanding these limitations, the study presented initial empirical evidence supporting the validity of the model of chronic pain as continuous traumatic stress and its severe consequences. Given the study’s relatively small size and substantial conceptual and clinical implications, there is a clear need for broader cross-cultural studies and future replications.

The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request.

All procedures performed in studies involving human participants followed the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.

The authors received no financial support for the research, authorship, and/or publication of this article.

Informed consent was obtained from all individual participants included in the study.

Note: *p < .05, **p < .01, ***p < .001 (two-tailed).

Note: *p < .05, **p < .01, ***p < .001 (two-tailed).

Note: *p < .05, **p < .01, ***p < .001 (two-tailed).

Note: *p < .05, **p < .01, ***p < .001 (two-tailed).

Note: *p < .05, **p < .01, ***p < .001 (two-tailed).

Note: *p < .05, **p < .01, ***p < .001 (two-tailed).