Many people who suffer from chronic pain also endure anxiety, fear, frustration, and/or hopelessness. Bouncing from doctor to doctor, they try many forms of treatment, and nothing seems to provide them with lasting relief. What many of my patients don’t fully understand is the link between their emotional state and pain. Often, a vicious cycle is created whereby pain triggers stress and anxiety, making the pain worse, or stress and anxiety causes a flare-up in an old injury or recurring problem, such as neck pain. This, in turn, exacerbates stress and anxiety. Why are pain and emotions so closely related, and what can we do to start resolving chronic pain that is not responding to other treatments? Fortunately, a large amount of research has been devoted to understanding this relationship, so we can begin to answer this question and come up with a solution by understanding the vicious cycle.

Chronic pain is not just related to injury or other physical factors. Your emotions, particularly fear and anxiety, and other cognitive factors, play an active roll in the development, maintenance, severity, and duration of pain [1] [2][3, 4]. Anxiety, in particular, has a sensitizing effect and thus leads to increased reactivity to stimuli considered to be potentially harmful or unpleasant. As an example, a patient experiencing anxiety related to the anticipation of an unpredictable threatening event will experience enhanced pain [5]. But this response is not just psychological. Research has also shown that patients with chronic back pain have higher levels of the stress hormone cortisol than what is considered normal and healthy. In these patients, higher cortisol was associated with stronger pain-evoked activity in the part of the brain involved in anticipatory anxiety and associative learning. These findings support a stress model of chronic pain, suggesting that a sustained stress response may contribute to persistent pain states [6]. But how does this work, and what can you do about it?

During the initial stage of an acute stress response, the brain signals the release of fight or flight (stress) neurotransmitters and hormones (adrenalin and nor-adrenalin). These stress hormones increase heart rate, blood pressure and respiration, constrict the small arteries, stimulate sweat secretion, and dilate the pupils. This short-term response is called the sympathetic nervous system response. It is pro-inflammatory, and its function is to help the body put up a fight or run from danger, prepare the immune system to destroy invading organisms or foreign substances, and repair tissue damage.

After the initial stress perception and release of adrenaline and nor-adrenaline (fight or flight hormones), the brain signals the release of another hormone called cortisol. Cortisol mobilizes stored glucose for fuel (the fuel you would need to fight or flee), and it suppresses organ systems that are non-vital to immediate survival (such as the digestive system) so that all of your energy and physical resources can by used to survive the perceived threat to your safety. Cortisol not only helps to manage the stress response but, if the body is functioning correctly, it also decreases pain and inflammation [7]. The importance of the role cortisol plays in reducing inflammation can be emphasized by the common use of corticosteroids (cortisone) to treat inflammatory disorders [8]. However, in certain conditions, this anti-inflammatory function of cortisol is disrupted, and instead of helping to reduce inflammation and pain, it can lead to an increase in both.

Under normal conditions, cortisol binds to specific receptors and acts as an anti-inflammatory [9, 10]; however, chronic stress and anxiety, leading to prolonged or excessive cortisol secretion, can change the function of cortisol. When prolonged or persistently elevated cortisol levels flood special receptors, they become resistant, much like insulin receptors become resistant in type-2 diabetes and metabolic syndrome. This blocks the anti-inflammatory effects of cortisol [10, 11]. Further, research also suggests that extreme surges in cortisol can cause it to bind to different receptor types and take on a pro–inflammatory action [11]. Additionally, impaired binding of cortisol to the correct receptors disrupts the natural self-regulating mechanism that stops the release of other cortisol signaling neurotransmitters. This will activate inflammatory cells and continue to stimulate the release of even more pro-inflammatory sympathetic neurotransmitters (adrenalin and nor-adrenalin) [10]. (This could be why some people do not respond well to cortisone shots.) Continual anxiety, rumination or worry, feelings of helplessness, exaggerated or recurring negative thoughts, and magnification or general catastrophizing of pain or injuries can prolong cortisol secretion, and thus exacerbate pain and inflammation [12, 13]. A vicious cycle is created. Ultimately, a prolonged or exaggerated stress response may perpetuate cortisol dysfunction, resulting in widespread inflammation and chronic pain [2], which will not respond to conventional treatments.

Regulation of healthy cortisol levels is a vital and often overlooked aspect of treating chronic pain. Chinese medicine and Western functional medicine are holistic systems, so pain is never treated in isolation of the whole person. Acupuncture, herbal medicine, and the correct nutritional supplements can be used to provide physical support and help balance stress hormones. In addition to physiological support, utilizing stress management tools such as exercise and meditation, developing healthy coping mechanisms, engaging in cognitive reappraisal, or confronting stressors can help to minimize cortisol secretion and prevent chronic, recurrent pain and widespread inflammation [2].

Citations

1. Cannon, W.B., Bodily changes in pain, hunger, fear, and rage: an account of recent researches into the function of emotional excitement. 1915: D. Appleton and Company.

2. Hannibal, K.E. and M.D. Bishop, Chronic Stress, Cortisol Dysfunction, and Pain: A Psychoneuroendocrine Rationale for Stress Management in Pain Rehabilitation. Physical Therapy, 2014. 94(12): p. 1816-1825.

3. Gatchel, R.J., et al., The biopsychosocial approach to chronic pain: scientific advances and future directions. Psychol Bull, 2007. 133(4): p. 581-624.

4. Asmundson, G.J.G., J.W.S. Vlaeyen, and G. Crombez, Understanding and Treating Fear of Pain. 2004: Oxford University Press.

5. Rhudy, J.L. and M.W. Meagher, Fear and anxiety: divergent effects on human pain thresholds. Pain, 2000. 84(1): p. 65-75.

6. Vachon-Presseau, E., et al., The stress model of chronic pain: evidence from basal cortisol and hippocampal structure and function in humans. Brain, 2013. 136(Pt 3): p. 815-27.

7. Heim, C., U. Ehlert, and D.H. Hellhammer, The potential role of hypocortisolism in the pathophysiology of stress-related bodily disorders. Psychoneuroendocrinology, 2000. 25(1): p. 1-35.

8. Barnes, P.J., Mechanisms and resistance in glucocorticoid control of inflammation. The Journal of Steroid Biochemistry and Molecular Biology, 2010. 120(2–3): p. 76-85.

9. Tsigos, C. and G.P. Chrousos, Hypothalamic-pituitary-adrenal axis, neuroendocrine factors and stress. J Psychosom Res, 2002. 53(4): p. 865-71.

10. Fries, E., et al., A new view on hypocortisolism. Psychoneuroendocrinology, 2005. 30(10): p. 1010-6.

11. Norman, M. and S.D.Hearing, Glucocorticoid resistance – what is known? Curr Opin Pharmacol, 2002. 2(6): p. 723-9.

12. Müller, M.J., Helplessness and perceived pain intensity: relations to cortisol concentrations after electrocutaneous stimulation in healthy young men. Biopsychosocial Medicine, 2011. 5: p. 8-8.

13. Johansson, A.C., et al., Pain, disability and coping reflected in the diurnal cortisol variability in patients scheduled for lumbar disc surgery. Eur J Pain, 2008. 12(5): p. 633-40.