A new paradigm for pain?

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Applied Evidence

A new paradigm for pain?

J Fam Pract. 2016 September;65(9):598-600,602-605

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From The Journal of Family Practice | 2016;65(9):598-600,602-605.

References

1. Dubner R, Gold M. The neurobiology of pain. Proc Natl Acad Sci U S A. 1999;96:7627-7630.

2. Markenson JA. Mechanisms of chronic pain. Am J Med. 1996;101:S6-S18.

3. Rainville P, Duncan GH, Price DD, et al. Pain affect encoded in human anterior cingulate but not somatosensory cortex. Science. 1997;277:968-971.

4. Bushnell MC, Duncan GH. Sensory and affective aspects of pain perception: is medial thalamus restricted to emotional issues? Exp Brain Res. 1989;78:415-418.

5. Galer BS, Jensen MP. Development and preliminary validation of a pain measure specific to neuropathic pain: the Neuropathic Pain Scale. Neurology. 1997;48:332-338.

6. Fassoulaki A, Triga A, Melemeni A, et al. Multimodal analgesia with gabapentin and local anesthetics prevents acute and chronic pain after breast surgery for cancer. Anesth Analg. 2005;101:1427-1432.

7. Woolf CJ, Chong MS. Preemptive analgesia—treating postoperative pain by preventing the establishment of central sensitization. Anesth Analg. 1993;77:362-379.

8. International Association for the Study of Pain Web site. IASP Taxonomy. Available at: http://www.iasp-pain.org/Taxonomy. Accessed January 10, 2016.

9. Waddell G, McCulloch JA, Kummel E, et al. Nonorganic physical signs in low-back pain. Spine. 1980;5:117-125.

10. Bushnell MC, Ceko M, Low LA. Cognitive and emotional control of pain and its disruption in chronic pain. Nat Rev Neurosci. 2013;14:502-511.

11. Villemure C, Bushnell MC. Cognitive modulation of pain: how do attention and emotion influence pain processing? Pain. 2002;95:195-199.

12. Felitti VJ, Anda RF. The relationship of adverse childhood experiences to adult medical disease, psychiatric disorders, and sexual behavior: implications for healthcare. In: Lanius R, Vermetten E, eds. The Hidden Epidemic: The Impact of Early Life Trauma on Health and Disease. Cambridge University Press; 2010. Available at: http://www.unnaturalcauses.org/assets/uploads/file/ACE%20Study-Lanius.pdf. Accessed January 11, 2016.

13. Centers for Disease Control and Prevention. Injury prevention and control: Division of violence prevention. Adverse childhood experiences. Available at: http://www.cdc.gov/violenceprevention/acestudy/. Accessed January 11, 2016.

14. Kross E, Berman MG, Mischel W, et al. Social rejection shares somatosensory representations with physical pain. Proc Natl Acad Sci. 2011;108:6270-6275.

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Childhood trauma influences adult pain. One of the more compelling narratives emerging in health care has to do with the influence that childhood developmental trauma can have on health, including pain. In his chapter on the impact of early life trauma on health and disease, Lanius states:¹²

“Women were 50% more likely than men to have experienced 5 or more categories of adverse childhood experiences. We believe that here is a key to what in mainstream epidemiology appears as women’s natural proneness to ill-defined health problems like fibromyalgia, chronic fatigue syndrome, obesity, irritable bowel syndrome, and chronic non-malignant pain syndromes. In light of our findings, we now see these as medical constructs, artifacts resulting from medical blindness to social realities and ignorance of the impact of gender.”

Brain activity in response to emotional insult mimics physical pain, and it is difficult to tell from images of brain activity whether a person is experiencing one or the other.

Lanius¹² suggests that adverse childhood experiences¹³ (trauma such as abuse and sexual assault) can lead to long-term changes within the nervous system, including areas of pain processing. My coauthor and I describe these changes here in terms of nervous system sensitization or dysregulation, and we believe that these changes lead to a bias toward hyperactivation of emotional pain circuits, which leads to the emotionally laden pain behaviors that often seem out of proportion to tissue pathology.

SIDEBAR
Case study: Were psychological factors driving these symptoms?

Judith B, a 34-year-old single mother of 2, presents to the office after 2 years of fruitless medical, rheumatologic, and neurologic work-ups for diffuse muscle pain, headaches, fatigue, and difficulty falling asleep after a motor vehicle accident (MVA) in which her injuries were not severe. She reports that sleep is difficult “because I cannot shut my mind off.”

Before the accident, she was healthy and working full-time, but now she is thinking about applying for disability because she believes she cannot continue teaching grade school given the severity of her lingering post-accident symptoms. A previous physician prescribed immediate-release oxycodone 5 mg QID and carisoprodol 350 mg tid, which has provided little improvement in function. Her physical exam is relatively unremarkable although she is clearly distressed and moving slowly, with diffuse soft tissue tenderness. A brief psychosocial screening demonstrates an adverse childhood experience score of 3 with a “Yes” to question 3 (sexual abuse) and a high score on the Generalized Anxiety Disorder 7-Item Scale (14 out of 21), indicating significant anxiety.

Given our findings, we referred the patient to a psychologist for a complete psychologic evaluation, explaining that we were looking for answers to the question: “To what degree do psychosocial factors drive this patient’s physical complaints?” The psychologist reported that she believed that psychological factors were the main driver of her symptoms, with childhood trauma “reactivated” by the trauma of the MVA.

The patient was initially suspicious that we were simply going to tell her that her symptoms were "all in her head," but the following explanation helped her to understand where we were going with therapy: “Imagine that your muscles are trying to have a conversation with your brain, and your nervous system is the phone line. The phone line is full of static and is distorting the message, so we need to work on the communication system.”

Three months of a multi-pronged approach led to improvement in the patient's sleep and fatigue. This approach included cognitive behavioral therapy and somatic experiencing (a method designed to normalize the nervous system changes induced by adverse childhood or adult experiences without requiring patients to recall or think about those events). These efforts were supported by titration of sertraline to 150 mg/day (trials of duloxetine and venlafaxine caused too many adverse effects) and acupuncture. Ms. B returned to teaching and fulfilling relationships with her fiancé and children. She was able to stop the oxycodone and carisoprodol after 2 months of the sertraline and several sessions of somatic experiencing, and she remains pain-free.

Author’s note: This case exemplifies so many of the patients we, as clinicians, see in daily practice and highlights the necessity of vigorously pursuing research in the area of pain due to psychological reasons. This is particularly true when considered in the context of the magnitude of disability due to chronic pain and of pain treatment failures, which have contributed to the current prescription opioid crisis.