Variations in response to pain have been reported in clinical settings (e.g., Bates et al. 1996; Cherkin et al. 1994; Jensen et al. 1986; Unruh, 1996; Wormslev et al. 1994). Patients with similar types and degrees of wounds vary from showing no pain to showing severe and disabling pain. Many chronic pain patients show disabling chronic pain despite showing no observable wound. Other patients show severe wounds but do not show pain. Why is it that two persons with identical lesions do not show the same pain or no pain at all? Why are all pain patients unique?

I propose that mind-brain identity theory may offer an answer to this difficult question. There are two main versions of identity theory: type and token identity. A sample type identical property is to identify “Being in pain” (X) with “Being the operation of the nervous-endocrine-immune mechanism” (Y) (i.e., X iff Y) (Chapman et al. 2008; van Rysewyk, 2013). For any person in pain the nervous-endocrine-immune mechanism (NEIM) must be active, and when NEIM is active in a person, he or she is in pain. Thus, type identity theory strongly limits the pattern of covariation across persons. According to token identity theory, for a person in mental state X at time t, X is identical to some neurophysiological state Y. However, in the same person at time t1, the same mental state X may be identical to a different neurophysiological state Y2. Token identity theory doesn’t limit the pattern of covariation across persons; it only claims that, at any given time, some mind-brain identity must be true.

In response to the topic question, I propose a hybrid version of identity theory – ‘type-token mind-brain identity theory’. Accordingly, for every person, there is a type identity between a mental state X and some neurophysiological state Y. So, when I am in pain, I am in NEIM state Y (and vice versa), but this NEIM state Y may be quite different across persons. Type-token identity theory therefore proposes a type identity model at the level of every person (i.e., it may vary across persons). A type-token identity theory implies that group-level type identities (i.e., type-type) cannot fully explain the pattern of covariation in pain responses across persons. Measuring changes of a pattern of psychological and neurophysiological indicators over time may then support a unidimensional model of chronic pain for each pain patient. Thus, being in chronic pain for me is identical with a specific pattern of NEIM activity (Chapman et al. 2008; van Rysewyk, 2013), but for a different patient, the same state of pain may be identical to a different pattern of NEIM activity. In preventing and alleviating chronic pain, it is therefore essential to best fit the intervention to the type-token pain identity profile of the patient.


Bates, M. S., Edwards, W. T., & Anderson, K. O. (1993). Ethnocultural influences on variation in chronic pain perception. Pain, 52(1), 101-112.

Chapman, C. R., Tuckett, R. P., & Song, C. W. (2008). Pain and stress in a systems perspective: reciprocal neural, endocrine, and immune interactions. Journal of Pain 9: 122-145.

Cherkin, D. C., Deyo, R. A., Wheeler, K., & Ciol, M. A. (1994). Physician variation in diagnostic testing for low back pain. Who you see is what you get. Arthritis & Rheumatism, 37(1), 15-22.

Jensen, M. P., Karoly, P., & Braver, S. (1986). The measurement of clinical pain intensity: a comparison of six methods. Pain, 27(1), 117-126.

Unruh, A. M. (1996). Gender variations in clinical pain experience. Pain, 65(2), 123-167.

van Rysewyk, S. (2013). Pain is Mechanism. Unpublished PhD Thesis. University of Tasmania.

Wormslev, M., Juul, A. M., Marques, B., Minck, H., Bentzen, L., & Hansen, T. M. (1994). Clinical examination of pelvic insufficiency during pregnancy: an evaluation of the interobserver variation, the relation between clinical signs and pain and the relation between clinical signs and physical disability. Scandinavian journal of rheumatology, 23(2), 96-102.