Defining Pain (Part 1/2)


Pain is complex. In its entirety, it is contextual and unique to each individual due to its multi-factorial nature. Instinctively, individuals view pain mechanically, or by means of structural damage. (i.e “wear and tear”, degeneration, etc). Through research development, it is now more evident that this belief is inaccurate. (Setchell 2017) Pain is modulated by a perception conglomerated from one’s experiences, learned behaviors, emotions and environmental exposures that drives their reality. A protective behavior to apprehend the recognized threat is the experience of pain. (Cohen 2018) Due to its complex inherent nature of subjectivity, pain cannot be observable by another individual, making it difficult to measure in a clinical setting.


The following definitions of common terms used in the context of pain are explained below.
The International Associate for the Study of Pain (IASP) defines pain as “An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” (Merskey, H et al 1994)
This definition has stood from 1979-2020, in which the 2020 extended version is added below:
  1. Pain is always a personal experience that is influenced to varying degrees by biological, psychological, and social factors.
  2. Pain and nociception are different phenomena. Pain cannot be inferred solely from activity in sensory neurons.
  3. Through their life experiences, individuals learn the concept of pain.
  4. A person’s report of an experience as pain should be respected.
  5. Although pain usually serves an adaptive role, it may have adverse effects on function and social and psychological well-being.
  6. Verbal description is only one of several behaviors to express pain; inability to communicate does not negate the possibility that a human or a nonhuman animal experiences pain.

(IASP 2020)

As mentioned by Stillwell and Harmon (2019), predictive processing is based on the idea that “perception is created by predictions informed by our past experiences and processing at a sub-conscious level based on predictions of what sensation, movement, or event will happen next.”

“Many patients experiencing back pain hope for the discovery of a clear organic cause of their pain and clinicians do their best to fulfill this expectation by providing a physical diagnosis (e.g., intervertebral disc bulge) to hang their hat on. (Slade et al. 2011; Stilwell et al. 2017; Stilwell and Harman 2017). This is misleading as most back pain cannot be tied to a specific biomedical cause (Maher et al. 2017) and this medicalization of a widespread phenomenon may backfire - resulting in increased pain, disability, fear, guilt, and poor adherence to evidence- based treatment recommendations, such as advice to return to daily movements/exercise. “ (Stilwell and Harman 2017a).” - (Stilwell, P and Harmon K 2019)

Acute pain: pain occurs through many different mechanisms and levels of intensities; however, most acute injuries tend to resolve through the inflammatory and healing process over the course of approximately six weeks. Nociceptors receive an input and transducers contribute most at this phase, followed by central sensitization, and an autonomic nervous system response.(Chen, JS et al 2019) (Basbaum, A. 2009)

Chronic pain: Chronic pain has been defined as pain lasting for greater than 3 to 6 months or persisting beyond the healing time of the initial injury or disease process. (Bosco, M et al 2013) This has estimated to affect more than 1.5 billion people globally, and 28% (91,896,000) of the 328.2 million Americans, making it one of the most common reasons why an individual seeks medical care. (Polaski 2019) Chronic pain can be an inconceivable encumbering condition due to its unrelenting longevity. For those who live with it on a daily basis, this condition can be so domineering that it affects multiple aspects of their lives. Neuroimaging studies suggest that the brain adapts with pain, thus increasing the risk for developing chronic pain. (Baliki MN, 2015) Adaptations can potentiate chronic tissue inflammation or changes within the properties of peripheral nerves. When dealing with chronic pain, particularly in the setting of external factors including emotional and social stressors, the brain undergoes a process of central sensitization. Structural and physiological changes result in a hypersensitized nervous system. This will cause the brain to perceive an amplification of pain that would normally cause minimal to no pain (hyperalgesia/allodynia). One’s hypervigilance to perceived pain in specific movements/positions due to past injury/experience will instill a memory of fear, a fear that turns into a hypersensitive nervous system. The brain is adaptive and learns behaviors, so much so that one will progressively learn to hurt with shorter ranges of motion, lowering their pain threshold to the point that it becomes difficult to perform daily tasks.

(Loeser, JD 1999) (McCarberg BH et al, 2008) (Chen JS et al, 2019) (Crofford, J 2015) (Wideman, TH 2019) (Bosco, M et al 2013)

“chronic pain negatively impacts the quality of life also because of the unmet needs of pain management… (Raffaeli, W et al, 2017)
“The resulting short-term reduction of pain and injury is positively reinforcing and therefore quickly learned. In the long-term, and in the absence of tissue damage, these safety behaviors are linked to threat avoidance, which strongly reinforces the behavior and paradoxically leads to persistent pain and disability.” (Stilwell P, Harman K 2019)
“The cycle of chronic pain is self-perpetuating and self-reinforcing, as painful sensations lead to a tendency to guard and/or avoid activity or therapy, which in turn leads to atrophied muscles, decreased range of motion or flexibility, and ultimately serves to maintain the pain cycle.” (Bosco, M et al 2013)

Allodynia: perceived pain resulting from a stimulus that normally wouldn’t cause pain. This mechanism isn’t fully understood, but it potentially appears to be due to a decreased threshold to nociceptors and/or damage to peripheral neurons leading to touch-sensitive fibers forming responses that a normal pain input would follow. (Chen, JS et al 2019) (Basbaum, A. 2009)

Hyperalgesia: an exaggerated pain response with a noxious stimulus, often seen in persistent pain. (Chen, JS et al 2019) (Basbaum, A. 2009) (International Associate for the Study of Pain (IASP)

Referred pain: the perceived location of pain is a different site from the actual painful stimulus. A common one we see is gallbladder dysfunction, with referral to right-sided inferior scapular pain. Another common referral site for visceral organs, is the heart. Myocardial infarction has a referral pain along the jaw, mid back, and down the left arm. The understanding behind this lies through the visceral sensory pain fibers that follow the dorsal root ganglia of the spinal cord, interrupting the CNS processing to a site different than the affected one. (Arendt-Nielsen, L et al 2001) (Chen, JS et al 2019) (Murray GM, 2009)

Visceral pain: pain arising from the viscera through activation of nociceptors of the thoracic, pelvis or abdominal regions. Visceral structures are highly sensitive to distention (stretch), ischemia and inflammation. It presents diffuse in nature, with subsequent development of symptoms characteristic of autonomic changes. (e.g. pallor, profuse sweating, nausea, GI disturbances, changes in BP, heart rate or body temperature.) (Sikander, S et al 2012)

Somatic pain: this form of pain is activated by the deep tissues from the musculoskeletal structures, limbs, spine, chest and abdominal walls, presenting in through different symptoms seen in both acute and chronic cases. This form of pain is used to distinguish pain that does not originate from the viscera. (Crofford LJ, 2015) (Murphy P, 2007)

Neuropathic pain: this is a pathology of the (somatosensory) nervous system, a consequence of nerve fiber damage, ensuing an altered firing to neurotransmitters. (Campbell, J 2006) (International Associate for the Study of Pain (IASP))

Dysesthesia: unpleasant abnormal experiences likely caused by sensorimotor incongruence between proprioception associated with motor intention and visual feedback. This does not meet the standard to which we understand of pain. (Katayama O et al, 2016)


Attempting to question why an individual became symptomatic or focusing on narrations of a ‘root cause’ may further perpetuate unnecessary hypervigilance (Karos, K et al 2018). This exemplifies apprehension to movement, whilst removing one’s autonomy and experience. A once benign experience ridiculed of intellect, becoming a resentment of one’s own capacity.

Pain in the absence of tissue damage or underlying pathophysiological cause also does not mean that one’s pain is not real. Tissue damage does not equal pain, and painful sensation does not require tissue damage. (Aydede, M 2019). All symptoms, including the ‘medically unexplained or explained’ ones are surfaced as a byproduct of inferential processing, with physiological dysfunctions being only loosely or unrelated to it. (Ongaro, G 2019). Assuming that ‘pain signals’ sent to the brain, causing pain is not only wrong, but also an oversimplification of such a complex concept. The idea in which tissue/structural damage (i.e.. degenerative disc) necessitates medical attention, with or without symptoms present stems from the biomedical model. The biomedical model remains supported by scientific findings that are designed for disease-based illnesses but lack adequate inclusivity of psychophysiological influences. Some of which include the experience of symptoms without pathophysiological disruption and the improvement or relief of said symptoms through placebo treatment. (Ongaro, G 2019).  Despite its success, it still has an incomplete definition, resulting in improper diagnosing and sub-optimal treatments. (DT wade, Halligan PW 2004) (Ongaro, G 2019). This narrative is built on hypothetical-generating models that are now used to rationalize invasive treatments and substantiate the falsehood means of anomalous sensations. These outdated biomedical models remain unsubstantiated and are continuously abandoning the presence of modern science with limitations easily overlooked. The progressive modification to newer models is pertinent to treatment.

The Biopsychosocial model has gained much traction by challenging a new perspective, where pain is a projection of the biological, psychological and social factors in the brain. (AJP. Engle, G 1980) This model has been constructed to take account for the dimensions lacking in the biomedical model. Though it is not a perfect framework, it is currently a relatively suitable model for scientific study and understanding of how human experience can be interpreted. (DT wade, Halligan PW 2004) (AJP. Engle, G 1980) (International Associate for the Study of Pain (IASP). As other models emerge, there is an increasing focus on an individual’s interpretations, allowing for greater personability, anatomic variations and adaptability. One in particular, is an article written by Peter Stilwell and Katherine Harman “An enactive approach to pain: beyond the biopsychosocial model”. This article encompasses a model to conceptualize pain as the 5 E’s: Embodied, Embedded, Enacted, Emotive, and Extended. This more advanced model removes the dualistic approach seen in previous models, including the biopsychosocial model. To briefly summarize; Embodiment is used to focus on how physiological dysfunction is experienced. Adding onto this, the interpretation and evaluation of one’s situation must be considered through physical body and subjectivity manners. Embedded approaches have been described as interpretations being based on our background and environment, both spatially and relationally. When environmental predictions fail to align with preemptive conclusions or predictions, error signals generate to forcefully resolve that error, at the expense of an altered behavior. Now going into the third ‘E’, enacted. This embraces the non-neural body, action, environment and sense-making. Enactive approach accepts the nociceptive process yet, deviates away from taking a reductionist thought process allowing it to overwhelm one’s cognitive attitude. This connection leads to the next ‘E’, Emotive. Emotions are inevitable through experiences; however, bodily action feedback theories work to manipulate emotive expressions to shape one’s experience. Conceptualizing feelings through internal process with experience, knowledge, and expectations reframe one’s perception. Lastly, we have Extended. This primarily extends to the mind to challenge boundaries, as well as to reinforce or reframe behaviors to change the experience.

(P Stillwell, K Harman 2019)

A major limitation in that we face is the lack of a definition agreed upon across all professionals. This conflicting matter comes from the attempt to conclusively establish a definition and/or sub-types to clarify what qualifies as pain, as opposed to the suffering, external stressors, minor discomforts and changes in sensation experienced by an individual. This is governed by individualistic approaches of social, cultural and environmental exposures linking to the linguistic ability to articulate that into a single word definition. Due to the lack of definitional unanimity, this renders another major limitation seen in specific specialty professional practices. Based on each clinician’s understanding of this information, they too will have a diagnosis particular to their bias’, experience, personal gain and scope of practice. This doctor-centered practice is enabling a pretentious falsehood practice, stigmatizing negative attachments to patients. Efforts to improve clinical assessments, education and treatment will influence the plight of patient/client interpretations, thus improving outcomes.

Given the extensive literature summarized above, it is apparent that pain has no single definition, but there is an understanding of contributing factors. The importance of understanding pain at a basic level is predicated on the prevalence of pain globally. The overarching goal is to collectively provide an insight on how pain is perceived to better assess and reduce the pervasive feelings of frailty.










  1. Loeser, J. D., & Melzack, R. (1999). Pain: an overview. The Lancet, 353(9164), 1607–1609.doi:10.1016/s0140-6736(99)01311-2 
  1. Raffaeli, W., & Arnaudo, E. (2017). Pain as a disease: an overview. Journal of pain research10, 2003–2008. doi:10.2147/JPR.S138864
  1. McCarberg BH, Nicholson BD, Todd KH, Palmer T, Penles L
  2. Am J Ther. 2008 Jul-Aug; 15(4):312-20.
  1. Chen JS, Sehdev JS. Physiology, Pain. [Updated 2019 Mar 16]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan-
  1. Basbaum, A. I., Bautista, D. M., Scherrer, G., & Julius, D. (2009). Cellular and molecular mechanisms of pain.Cell, 139(2), 267–284. doi:10.1016/j.cell.2009.09.028
  1. Arendt-Nielsen L, Svensson P. Referred muscle pain: basic and clinical findings.Clin J Pain. 2001 Mar;17(1):11-9.
  1. Murray G. M. (2009). Guest Editorial: referred pain.Journal of applied oral science : revista FOB, 17(6), i. doi:10.1590/s1678-77572009000600001
  1. Sikandar, S., & Dickenson, A. H. (2012). Visceral pain: the ins and outs, the ups and downs.Current opinion in supportive and palliative care, 6(1), 17–26. doi:10.1097/SPC.0b013e32834f6ec9
  1. Crofford L. J. (2015). Chronic Pain: Where the Body Meets the Brain.Transactions of the American Clinical and Climatological Association, 126, 167–183.
  1. Murphy P. (2007) Somatic Pain. In: Schmidt R., Willis W. (eds) Encyclopedia of Pain. Springer, Berlin, Heidelberg
  1. Merskey H, Bogduk N.Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes and Definitions of Pain Terms, 2nd Edition. Seattle, Washington: International Association for the Study of Pain (IASP) Press; 1994
  1. Slater, D., Korakakis, V., O’Sullivan, P., Nolan, D., & O’Sullivan, K. (2019).“Sit Up Straight”: Time to Re-evaluate. Journal of Orthopaedic & Sports Physical Therapy, 49(8), 562–564.doi:10.2519/jospt.2019.0610  
  1. Brumagne, S., Janssens, L., Janssens, E., and Goddyn, L. (2008). Altered postural control in anticipation of postural instability in persons with recurrent low back pain.Gait Posture 28, 657–662. doi: 10.1016/j.gaitpost.2008.04.015
  1. Koch C and Hänsel F(2018) Non-specific low back pain and postural control during quiet standing - A systematic review. Psychol. 10:586. doi:10.3389/fpsyg.2019.00586
  1. Wade, D. T., & Halligan, P. W. (2004). Do biomedical models of illness make for good healthcare systems?.BMJ (Clinical research ed.), 329(7479), 1398–1401. doi:10.1136/bmj.329.7479.1398
  1. The clinical application of the biopsychosocial model. (1980). American Journal of Psychiatry, 137(5), 535–544. doi:10.1176/ajp.137.5.535 
  1. Stilwell, P., Harman, K. An enactive approach to pain: beyond the biopsychosocial model.Phenom Cogn Sci 18, 637–665 (2019) doi:10.1007/s11097-019-09624-7
  1. Wideman, T. H., Edwards, R. R., Walton, D. M., Martel, M. O., Hudon, A., & Seminowicz, D. A. (2019). The Multimodal Assessment Model of Pain: A Novel Framework for Further Integrating the Subjective Pain Experience Within Research and Practice. The Clinical journal of pain35(3), 212–221. doi:10.1097/AJP.0000000000000670
  1. Louw, A., Nijs, J., & Puentedura, E. J. (2017). A clinical perspective on a pain neuroscience education approach to manual therapy.The Journal of manual & manipulative therapy, 25(3), 160–168. doi:10.1080/10669817.2017.1323699
  1. Karos, K., Williams, A. C. de C., Meulders, A., & Vlaeyen, J. W. S. (2018).Pain as a threat to the social self. PAIN, 1.doi:10.1097/j.pain.0000000000001257 
  1. Katayama, O., Osumi, M., Kodama, T., & Morioka, S. (2016). Dysesthesia symptoms produced by sensorimotor incongruence in healthy volunteers: an electroencephalogram study.Journal of pain research, 9, 1197–1204. doi:10.2147/JPR.S122564
  1. Cohen, Miltona,*; Quintner, Johnb; van Rysewyk, SimoncReconsidering the International Association for the Study of Pain definition of pain, PAIN Reports: March/April 2018 - Volume 3 - Issue 2 - p e634 doi: 10.1097/PR9.0000000000000634
  1. (International Associate for the Study of Pain (IASP)
  1. Aydede M. (2019). Does the IASP definition of pain need updating?. Pain reports4(5), e777.
  1. Wade, D. T., & Halligan, P. W. (2004). Do biomedical models of illness make for good healthcare systems?.BMJ (Clinical research ed.), 329(7479), 1398–1401. doi:10.1136/bmj.329.7479.1398
  1. The clinical application of the biopsychosocial model. (1980).American Journal of Psychiatry, 137(5), 535–544.doi:10.1176/ajp.137.5.535 
  2. Setchell J, Costa N, Ferreira M, Makovey J, Nielsen M, Hodges PW. Individuals' explanations for their persistent or recurrent low back pain: a cross-sectional survey.BMC Musculoskelet Disord. 2017;18(1):466. Published 2017 Nov 17. doi:10.1186/s12891-017-1831-
  3. Turk DC, Wilson HD. Fear of pain as a prognostic factor in chronic pain: conceptual models, assessment, and treatment implications.Curr Pain Headache Rep. 2010;14(2):88-95. doi:10.1007/s11916-010-0094
  4. Ng, S. K., Urquhart, D. M., Fitzgerald, P. B., Cicuttini, F. M., Hussain, S. M., & Fitzgibbon, B. M. (2017).The Relationship between Structural and Functional Brain Changes and Altered Emotion and Cognition in Chronic Low Back Pain. The Clinical Journal of Pain, 1.doi:10.1097/ajp.0000000000000534 
  1. Bosco, M. A., Gallinati, J. L., & Clark, M. E. (2013).Conceptualizing and Treating Comorbid Chronic Pain and PTSD. Pain Research and Treatment, 2013, 1–10.doi:10.1155/2013/174728 
  2. Polaski AM, Phelps AL, Kostek MC, Szucs KA, Kolber BJ. Exercise-induced hypoalgesia: A meta-analysis of exercise dosing for the treatment of chronic pain.PLoS One. 2019;14(1):e0210418. Published 2019 Jan 9. doi:10.1371/journal.pone.0210418 
  1. Baliki, M. N., & Apkarian, A. V. (2015). Nociception, Pain, Negative Moods, and Behavior Selection. Neuron87(3), 474–491.
  2. Ongaro, G., & Kaptchuk, T. J. (2019). Symptom perception, placebo effects, and the Bayesian brain. Pain160(1), 1–4.
  3. Boadas-Vaello P, Castany S, Homs J et al. Neuroplasticity of ascending and descending pathways after somatosensory system injury: reviewing knowledge to identify neuropathic pain therapeutic targets. Spinal Cord. 2016;54:330-340.
  4. Prediction of pain in patients with chronic low back pain: effects of inaccurate prediction and pain-related anxiety. McCracken LM, Gross RT, Sorg PJ, Edmands TABehav Res Ther. 1993 Sep; 31(7):647-52.
  5. Fear of movement/(re)injury in chronic low back pain and its relation to behavioral performance. Vlaeyen JW, Kole-Snijders AM, Boeren RG, van Eek H Pain. 1995 Sep; 62(3):363-72.
  6. Turk, D. C., & Wilson, H. D. (2010). Fear of pain as a prognostic factor in chronic pain: conceptual models, assessment, and treatment implications. Current pain and headache reports14(2), 88–95.
  7. Screening to identify patients at risk: profiles of psychological risk factors for early intervention. Boersma K, Linton SJ. Clin J Pain. 2005 Jan-Feb; 21(1):38-43; discussion 69-72.
  8. Woby SR, Urmston M, Watson PJ. Self-efficacy mediates the relation between pain-related fear and outcome in chronic low back pain patients. Eur J Pain. 2007;11(7):711-718. doi:10.1016/j.ejpain.2006.10.009



You may also like

View all