A stress model of chronic pain

The common elements making an event stressful to anybody are novelty, unpredictability, threat to the ego, and loss of sense of control. People suffering from chronic pain know how stressful spontaneous pain can be. The reciprocal influence of stress over the neural activity contributing to chronic pain has recently received growing interest from the pain community.  It has recently been suggested that repeated pain episodes induce a sustained stress response that contributes to the pain experienced by the patient, which further maintains the maladaptive stress response.[1] Little empirical evidence, however, has demonstrated how the endocrine response and brain structures and functions interact with chronic pain.

In our study, we tested the hypothesized maladaptive stress response and its impact on the hippocampal formation of patients suffering from idiopathic chronic low back pain.[2] We showed that basal levels of cortisol (i.e. stress hormone in humans) were higher in chronic back pain patients than in healthy individuals. In chronic pain patients, higher levels of cortisol were associated with smaller hippocampal volumes and stronger pain-related brain activity in the hippocampal system. Importantly, these anatomical and functional changes in the hippocampal formation mediated the relation between stress and clinical pain intensity reported by the patient immediately prior to entering the MRI. This is interesting because the hippocampal formation controls the hypothalamic pituitary adrenal response, sensitive to the deleterious effect of stress hormones, and part of a brain system that may be contributing to chronic pain. Further statistical modeling suggests that individuals with smaller hippocampii may be more vulnerable to develop a maladaptive stress response when trying to cope with chronic pain.

Together, these findings are in accordance with the emerging perspective that the limbic system involved in fear, learning, and motivation would be the neural networks mainly impacted by recurring pain.[3] It is further in accordance with the emerging concept that individuals could be more vulnerable, or resilient, in their ability to adjust to the physical instability[4] and to the evolution of the clinical pain[5]. Finally, although this study was conducted on a small sample of participants, it suggests that stress management could be a non-pharmacological interesting avenue for patients to better cope with their chronic pain.

Who I am

Etienne Vachon-PresseauMy name is Etienne Vachon-Presseau and I am completing my PhD in psychology at l’université de Montréal under the supervision of Pierre Rainville. I am interested in using neuroimaging to better understand how chronic pain impacts brain networks contributing to the clinical profile of the patients.


[1] Borsook D, Maleki N, Becerra L, & McEwen B (2012). Understanding migraine through the lens of maladaptive stress responses: a model disease of allostatic load. Neuron, 73 (2), 219-34 PMID: 22284178

[2] Vachon-Presseau, E., Roy, M., Martel, M., Caron, E., Marin, M., Chen, J., Albouy, G., Plante, I., Sullivan, M., Lupien, S., & Rainville, P. (2013). The stress model of chronic pain: evidence from basal cortisol and hippocampal structure and function in humans. Brain, 136 (3), 815-827 DOI: 10.1093/brain/aws371

[3] Apkarian, A., Baliki, M., & Geha, P. (2009). Towards a theory of chronic pain Prog Neurobiol, 87 (2), 81-97 DOI: 10.1016/j.pneurobio.2008.09.018

[4] Karatsoreos IN, & McEwen BS (2011). Psychobiological allostasis: resistance, resilience and vulnerability. Trends Cogn Sci, 15 (12), 576-84 PMID: 22078931

[5] Baliki MN, Petre B, Torbey S, Herrmann KM, Huang L, Schnitzer TJ, Fields HL, & Apkarian AV (2012). Corticostriatal functional connectivity predicts transition to chronic back pain. Nat Neurosci, 15 (8), 1117-9 PMID: 22751038


  1. Etienne Vachon-Presseau says

    @ John : In our study, we have adopted a perspective where increases in basal levels of stress hormones and hippocampal activity contributing to the clinical pain would be triggered by unpredictable pain episodes. The suggestion that undamped stress response would rather reflect physiological instability of the organism (allostatic load) that would be the origin of persistent pain is interesting. According to Borsook and McEwen’s theoretical model of stress and migraine, several effectors could contribute to the allostatic load. These effectors could be continuous (e.g. genetic), episodic (e.g. recurring pain episodes) and/or progressive (e.g. neurotoxic effect of stress on the brain). Although we feel that prediction errors in chronic pain episodes have to be considered as strong effectors of allostatic load, it is very plausible that other effectors, unrelated to pain, could trigger and maintain systemic modifications associated with chronic pain. This could be of particular interest regarding chronic widespread pain syndromes associated with altered diffuse pain inhibition.

    Lastly, we understand and share your concerns regarding the stigmatization patients. The terms “maladaptive stress response” and “vulnerability” might have to be rethink.


  2. Josph Sliwkowski MD says

    Your hypothesis has been clinically validated with over 10 years of research involving Somatic Functional Therapy developed by Ramon Nunez, PhD. SFT addresses psychoneuromuscular dysregulation through reconnecting limbic brain with reflexively hypercontracted muscles. Once limbic brain becomes aware it immediately releases muscle to neutral state. The spindle cell pain signal stops breaking pain stress cycle.

  3. John Quintner says

    @ Etienne. What if the pain you are discussing happens to be but one component of undamped stress response system activation? I do not like the term “maladaptive”. It is a short step away from the potentially stigmatising “maldynia” – proposed in all seriousness by the American Academy of Pain Medicine.