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While awareness of qualitative research of lived pain is slowly increasing in the field of pain, it is far from established and needs cultivating from within the field by pain researchers (Mitchell & MacDonald, 2009; Osborn & Rodham, 2010; Price & Barrell, 2012). Pain research has traditionally been dominated by quantitative research methods, which have their roots in physiology, physics, biology, and psychophysics, arising from mathematics, statistics, and psychometrics (Price et al. 2002; Price & Aydede, 2005; Price & Barrell, 2012). This trend continues unabated today, and perhaps explains why Osborn and Rodham (2010) found that many individual pain researchers have not yet accumulated a significant body of qualitative pain research. A body of qualitative pain research would enable researchers to develop their arguments in more depth concerning the nature and types of personal meanings apparent in pain experience, especially clinical pain experiences across the lifespan. The rationale for conducting qualitative pain research is likely not clear to many in the field of pain, and researchers are probably unaware of the potential richness of qualitative pain data to uniquely describe lived pain or the diverse tools available for analyzing qualitative data. In line with this, Osborn & Rodham (2010) found that many of the qualitative pain studies they reviewed used only one type of analysis (i.e., data analysis was not triangulated), description rather than interpretation prevailed in discussion of data meaning, and research methods were not thoroughly described.
A powerful reason to conduct more qualitative pain research is the common complaint from clinical pain patients that they feel they have never had an opportunity to fully explore their lived pain experiences with health care professionals, that no one has ever fully understood what is wrong with them and, most importantly, that no one appears to be listening (e.g., Melzack, 1990; Hoffmann & Tarzian, 2001; Hansson et al. 2011; McGee et al. 2011; Thacker & Moseley, 2012; De Ruddere et al. 2014). Clinical failure to sufficiently appreciate patient pain and its felt meanings can result in profound patient dissatisfaction, exacerbation of feelings of isolation and confusion, among other negative existential appreciations, and cause up-regulation of nociception (Butler et al. 2003). Despite this significant problem in the treatment and management of clinical pain, some pain researchers (e.g., Apkarian et al. 2011; Wortolowska, 2011) and government agencies (e.g., National Research Council of the National Academies, 2008; National Institutes of Health, 2011) have argued for replacing first-person patient experiential pain data with brain-imaging data.
Although qualitative research alone cannot solve these challenges, because of its exploratory nature, it can complement quantitative clinical pain research to describe lived pain and the psychosocial factors that improve or worsen the efficacy of pain interventions, as well as core intervention components that are associated with desired or undesired patient outcomes (Price et al. 2002; Price & Aydede, 2005; Price & Barrell, 2012; Thacker & Moseley, 2012).
Apkarian, A. V., Hashmi, J. A., & Baliki, M. N. (2011). Pain and the brain: specificity and plasticity of the brain in clinical chronic pain. Pain, 152(3 Suppl), S49–64.
De Ruddere, L., Goubert, L., Stevens, M. A. L., Deveugele, M., Craig, K. D., & Crombez, G. (2014). Health Care Professionals” Reactions to Patient Pain: Impact of Knowledge About Medical Evidence and Psychosocial Influences. The Journal of Pain, 15(3), 262–270.
Hoffmann, D. E., & Tarzian, A. J. (2001). The girl who cried pain: a bias against women in the treatment of pain. The Journal of Law, Medicine & Ethics, 28(s4), 13–27.
McGee, S. J., Kaylor, B. D., Emmott H., & Christopher, M. J. (2011). Defining chronic pain ethics. Pain Medicine, 12, 1376–1384.
Melzack, R. (1990). The tragedy of needless pain. Scientific American, 262(2), 27–33.
National Institutes of Health. (2011). Biomarkers for chronic pain using functional brain connectivity. Common Fund NIH Government.
National Research Council of the National Academies. Emerging cognitive neuroscience and related technologies. (2008). Washington, DC: National Academies Press.
Price, D. D., & Aydede, M. (2005). The experimental use of introspection in the scientific study of pain and its integration with third-person methodologies: The experiential-phenomenological approach. In M. Aydede (Ed.), Pain: New Essays on its Nature and the Methodology of its Study (pp. 243–273). Cambridge, Mass.: MIT Press.
Price, D. D., & Barrell, J. J. (2012). Inner Experiences and Neuroscience. Merging the two perspectives. Cambridge, Mass.: MIT Press.
Price, D. D., Barrell, J. J., & Rainville, P. (2002). Integrating experiential-phenomenological methods and neuroscience to study neural mechanisms of pain and consciousness.
Thacker, M. A., & Moseley, G. L. (2012). First-person neuroscience and the understanding of pain. The Medical Journal of Australia, 196(6), 410–411.
Wortolowska, K. (2011). How neuroimaging can help us to visualise and quantify pain? European Journal of Pain, 5, 323–327.
<span class=”Z3988″ title=”ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=http%3A%2F%2Fsimonvanrysewyk.wordpress.com&rft_id=info%3A%2F&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Towards+raising+awareness+of+qualitative+pain+research&rft.issn=&rft.date=2014&rft.volume=&rft.issue=&rft.spage=&rft.epage=&rft.artnum=http%3A%2F%2Fsimonvanrysewyk.wordpress.com%2F2014%2F10%2F29%2Fraising-awareness-of-qualitative-pain-research%2F&rft.au=Simon+van+Rysewyk&rfe_dat=bpr3.included=1;bpr3.tags=Health%2Cpain%2C+chronic+pain%2C+qualitative+research%2C+phenomenology%2C+philosophy%2C+psychology%2C+neuroscience%2C+pain+medicine”>Simon van Rysewyk (2014). Towards raising awareness of qualitative pain research <span style=”font-style: italic;”>https://simonvanrysewyk.wordpress.com</span></span>
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.