Applied Evidence

A new paradigm for pain?

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

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.

15. Geuze E, Westenberg HGM, Jochims A, et al. Altered pain processing in veterans with posttraumatic stress disorder. Arch Gen Psychiatry. 2007;64:76-85.

16. Mickleborough MJ, Daniels JK, Coupland NJ. Effects of trauma-related cues on pain processing in posttraumatic stress disorder: an fMRI investigation. J Psychiatry Neurosci. 2011;36: 6-14.

17. Noll-Hussong M, Otti A, Laeer L, et al. Aftermath of sexual abuse history on adult patients suffering from chronic functional pain syndromes: an fMRI pilot study. J Psychoso Res. 2010; 68:483-487.

Pain in the absence of any pathophysiologic cause or injury

The clinician’s search for a pain diagnosis is typically predicated on the notion that there must be an underlying tissue injury of severity equal to the severity of the patient’s pain complaints. This approach to a pain evaluation rests on 2 assumptions that are not true for all patients:

Pain is simply a sensory experience that is always caused by tissue damage of some type.
The severity of the pain experienced by a patient should be tightly bound to the severity of the pain stimulus (ie, tissue damage).

These assumptions are true of acute nociceptive pain, they may or may not be true for NPP, but they do not apply to the third type of pain—pain for psychological reasons. While tissue pathology in humans and animals with nociceptive pain is usually visible, measurable, and correlates with observed pain behaviors, the damage to nerve tissue and the ensuing changes in nervous system function with NPP are not always visible or able to be imaged. These changes produce pain that can appear more severe than expected based on a brief exam. Some of the time, however, characteristic symptoms and physical signs of NPP will be present, and perhaps electrodiagnostic or other tests will be abnormal, thus providing some objective sense of changes in nervous system function.

In contrast, pain behavior due to the third type of pain usually appears very much out of proportion, and unbound to, tissue pathology. Furthermore, the patient’s pain behaviors often reflect heightened emotional pain processing (TABLE 2⁹). The resulting emotionally charged presentation can be alarming and suggestive of extreme tissue injury, but there may be absolutely no evidence of tissue injury or pathology.

Functional change in the CNS

There is evidence from experimental studies that psychologic factors change nervous system function. In one review, the authors concluded, “Pain…can vary widely between people and even within an individual depending on…the psychological state of the person.”¹⁰ In a second review, the authors concluded that our emotional state has an enormous influence on pain; a negative emotional state increases pain, whereas a positive state lowers pain.¹¹

But can psychological factors induce long-term changes in nervous system function analogous to the systems neuroplasticity responsible for irreversible changes in NPP? And can psychologically induced changes in nervous system sensory processing lead to pain without any tissue or nerve damage?

We theorize that a functional change in the CNS can occur in response to certain emotional states or traumatic experiences (eg, child abuse, assault, accidents). (More on this in a bit.) When such changes occur, mildly painful stimuli are amplified and processed through overly sensitized, dysregulated, ramped-up emotional and somatosensory pain circuits in the brain. This is analogous to the functional changes in the nervous system that occur with NPP; however, when the nervous system changes are due to psychological factors, there may be no tissue or nerve injury.