Multidimensional Nature of Pain

This article or area is currently under construction and may only be partially complete. Please come back soon to see the finished work by 18 May 2019!

Original Editor - Alberto Bertaggia.

Top Contributors - Alberto Bertaggia, Nina Myburg, Admin, Kim Jackson, Michelle Lee, Vidya Acharya, 127.0.0.1, WikiSysop, Lauren Lopez, Jo Etherton and Jess Bell  

Introduction[edit | edit source]

A definition of pain is provided by the International association for the Study of Pain (IASP) as follows:[1]

"An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage"

Pain is always subjective and everyone learns the use of this word through experiences related to injury in early life.

Pain is a sensation in a part or parts of the body. It can vary in intensity, quality, duration and pain can refer to other parts of the body. Pain is usually an unpleasant sensation and therefore it also has an emotional aspect. It is strongly linked to suffering.[2]

Even in the absence of tissue damage or any likely pathophysiological cause, people still report pain. This could happen for psychological reasons. In these cases, it is challenging to distinguish whether someone's experience of pain arises from damaged tissue or not, as it can only be based upon the subjective report of such experience.[3]

In the following video Karen D. Davis tries to explain why some people react to the same painful stimulus in different ways.


The process of feeling pain[edit | edit source]

Pain is a physiological protective system. It is essential to warn, detect, and minimize contact with damaging stimuli.[4] Nerve endings and sensory receptors in the skin and tissues detect sensory stimuli. This can be thermal, mechanical or chemical stimuli (heat, cold, pressure etc.). Nociceptors (from the Latin word nocere that means "to hurt") are sensory receptors that respond to damaging or potentially damaging stimuli. With the stimulation of a nociceptor, a noxious stimulus is converted into electrical activity in the peripheral terminals of nociceptor sensory fibres. This is called transduction. This process is mediated by specific receptor ion channels. The stimulus is carried to the spinal cord (central nervous system) through a process called conduction. There the nociceptive nerve fibres terminate and the synaptic transfer and modulation of input from one neuron to another take place. This is called transmission. The neurons in the dorsal horn of the spinal cord transfer nociceptive input to the brainstem, hypothalamus, thalamus and brain cortex. In the brain is where perception of the experience occurs. This is a subjective process. The brain then creates pain as an output after processing the stimuli. It is important to underline that activity induced in the nociceptive pathways by a noxious stimulus does not always lead to pain. Nociceptors can be stimulated by potentially damaging stimuli as well as actual damaging stimuli. Only when the brain has processed the stimulus, will it lead to a response of pain or not. Pain is always the output of a widely distributed neural network in the brain rather than one coming directly by sensory input evoked by injury, inflammation or other pathology[5].

Nociception


Pain Classification[edit | edit source]

Based on the works of Woolf[4], this is a useful way of classifying pain:

  • Nociceptive pain. This kind of pain is concerned with the sensing of noxious stimuli. It is a signal of impending or actual tissue damage and is a high-threshold pain only activated in the presence of intense stimuli. It has a protective role requiring immediate attention and responses (i.e. withdrawal reflex). For example touching something too hot, cold or sharp
  • Inflammatory pain. This second kind of pain is important to promote healing and protection of injured tissues. It increases sensory sensitivity through pain hypersensitivity and tenderness. Thus normally innocuous stimuli now elicit pain. It creates an enviroment which suggests avoidance of movement, contact and stress of the injured body parts. This, in turn, assists in the healing of the injured body part. Inflammatory pain is caused by activation of the immune system that causes inflammation after tissue injury or infection. This type of pain can be seen as a protective mechanism, However, it still needs to be reduced in patients with ongoing inflammation, as with rheumatoid arthritis or in cases of severe or extensive injury.
  • Pathological pain. This type of pain is not protective, but rather maladaptive. It is not connected to tissue damage but results from abnormal functioning of the nervous system. To note, this is a low-threshold pain. Pathological pain can occur after damage to the nervous system or even when there is no damage or inflammation, It is largely the consequence of amplified sensory signals in the central nervous system. Conditions that cause this type of pain include fibromyalgia, irritable bowel syndrome, tension-type headache, temporomandibular joint disease etc. Usually, the pain is substantial without any noxious stimulus and minimal or even no peripheral inflammation.

Acute pain is caused by noxious stimuli and is mediated by nociception. It has an early onset and serves to prevent tissue damage. This is why this type of pain is defined as adaptive, it helps to survive and to heal[2]

Chronic pain is pain continuing beyond 3 months or after healing is complete[3]. It may arise as a consequence of tissue damage or inflammation or have no identified cause. Chronic pain is a complex condition embracing physical, social and psychological factors, consequently leading to disability, loss of independence and poor quality of life.[6]

Psychological factors in pain[edit | edit source]

Anxiety[edit | edit source]

Health anxious individuals form dysfunctional assumptions and beliefs about pain and other symptoms. This can be disease based and based on past experiences. They will have a tendency to misinterpret somatic information as catastrophic and personally threatening. Some studies report an increase in pain correlated with increased levels of anxiety.[7] Clinically, anxiety can compromise treatments as practitioners can expect to see catastrophization play a big role in these patients' report and they could report greater pain during activities. Thus, there is a need to target attentional focus and interpretation of sensations among health anxious clients.

Depression[edit | edit source]

There is strong evidence of an established comorbidity of pain and depression.[8] Furthermore, when patients with pain have comorbid depression, they could experience greater pain, have a worse prognosis, and more functional disability. Pain and depression are associated by neurobiological, cognitive, affective and behavioral factors, thus the optimal treatment approach for comorbid pain and depression should simultaneously address both physical and psychological symptoms.

Expectation[edit | edit source]

When an individual expects to experience pain, the perceived pain may vary based upon the types of cues received (i.e. a cue may indicate a more intense or damaging stimulus, then more intense pain is perceived and vice versa). Cues of an impending treatment could also decrease in pain, for example the process of taking an analgesic, usually decreases pain.[7] Thus, expectation is thought to play a big role in the placebo effect.

Attention and distraction[edit | edit source]

There is strong evidence that attention (and distraction) is highly effective in modulating the pain experience and demonstrate how cognitive processes can interfere with pain perception[9][10][11][12][13][14][15]. When a person is distracted with a cognitive task pain is perceived as less intense[9][12][16][17][18], even in chronic pain patients[19]. Conversely, pain increases when the pain is in the focus of attention[20]. Functional brain imaging and neurophysiological studies have shown that attention- and cognitive distraction-related modulations of nociceptive-driven activations take place in various pain-sensitive cortical und subcortical brain regions, accompanied by concordant changes in pain perception[9][12][13][14][16][18][21]. At present time, there are various hypothesis on the physiological bases of these phenomenons, although it is likely that a top-down modulation occur[22][23]. Previous studies on pain processing have demonstrated that key regions of the descending pain control system show enhanced responses during attentional distraction[9][12][16][15].

Fear[edit | edit source]

Pain-related fear is a general term to describe several forms of fear with respect to pain[24]. Fear of pain can be directed toward the occurrence or continuation of pain, toward physical activity, or toward the induction of (re)injury or physical harm[25].

Fear toward physical activity is also know as kinesiophobia, and is defined as “an excessive, irrational, and debilitating fear of physical movement and activity resulting from a feeling of vulnerability to painful injury or re-injury”[26][27].

Final Fear avoidance model.png

If pain, possibly caused by an injury, is interpreted as threatening (pain catastrophizing), pain-related fear evolves leading to avoidance behaviors, and hypervigilance to bodily sensations followed by disability, disuse and depression. This will maintain the pain experiences thereby fueling the vicious circle of increasing fear and avoidance[28].

In non-catastrophizing patients, no pain-related fear and rapid confrontation with daily activities is likely to occur, leading to fast recovery[28].

These concepts are explained by the Fear-Avoidance (FA) model, which was largely hypothetical in the beginning, but currently there is ample evidence to support the validity of the original FA model[29].

As of today, the FA model is considered to be a component in the development of disability in a variety of conditions, such as low back pain, chronic headache, whiplash disorder, osteoarthritis, knee injury pain, chronic-fatigue syndrome, fibromyalgia and neuropathic pain [30][31][32]

Social and cultural factors in pain[edit | edit source]

Culture is defined as "the beliefs, customs, arts, etc., of a particular society, group, place, or time" or "a particular society that has its own beliefs, ways of life, art, etc."[33].

Culturally-specific attitudes and beliefs about pain can influence the manner in which individuals view and respond both to their own pain and to the pain of others[34]. Cultural factors related to the pain experience include pain expression, pain language, lay remedies for pain, social roles, and expectations and perceptions of the medical care system[34].
Race/ethnicity, by virtue of their culturally-specific attitudes and beliefs, seems to have an impact on pain processing, including emotional and behavioural responses associated with chronic pain, larger in later stages[35][36].

Another psychosocial factor that may influence differences in pain sensitivity response is the gender role: individuals who considered themselves more masculine and less sensitive to pain have been shown to have higher pain thresholds and tolerances[37].

Socioeconomic factors (e.g. lower levels of education and income) seems to be correlated with a higher incidence of chronic pain diagnosis[38] and pain perception level[39].

The biopsychosocial model of pain[edit | edit source]

In the past, psychological and physiological (or patophysiological) factors were considered as separated components in a dualistic point of view. Later, the recognition that psychosocial factors, such as emotional stress, could impact the reporting of symptoms, medical disorders, and response to treatment lead to the development of the biopsychosocial model of pain[40].

The bio part is rapresented by the pathophysiology of the disease, or the mechanism of injury, and the relative nociception processes, considering the physiological aspects.

The psychosocial factors (as explaned above) involve both emotion (the more immediate reaction to nociception and is more midbrain based) and cognition (which attach meaning to the emotional experience)[40]. These could trigger additional emotional reactions and thereby amplify the experience of pain, thus perpetuating a vicious circle of nociception, pain, distress, and disability[40].

As of today there are evidencies of psychological factors, such as fear and anxiety, play an important role in the development of chronic pain[41].


Clinical implications[edit | edit source]

It has to be understood that there is an interaction among physiologic, psychological, and social factors[7], which perpetuates and may even worsen the clinical presentations[40].

  • There is the need to have sound knowledge of these interaction mechanism[7].
  • Targeting psychosocial factors should be a key component of physiotherapist-led intervention[42].
  • Treatment programs must be individually-tailored in order to specifically address the patients' attitudes and beliefs to improve treatment adherence and outcome[31].
  • The neurobiological mechanisms responsible for these different pains are beginning to be defined (1–3), providing insight into how distinct types of pain are generated by diverse etiologic factors, and in which patients (4). Moreover, we can now realistically expect to move from an empirical therapeutic approach to one that it is targeted specifically at the particular mechanisms of the type of pain experienced by an individual patient. Although current analgesic treatment is aimed at suppressing or controlling symptoms (5), interventions that can abort the development of pain mechanisms are beginning to be conceivable (1).[2] 
  • However, because the processes that drive each are quite different, treatments must be targeted at the distinct mechanisms responsible. [4]

Resources[edit | edit source]

Other Physiopedia Pages[edit | edit source]

External links[edit | edit source]

References[edit | edit source]

  1. ↑ International Association for the Study of Pain. IASP Terminology. Available from: https://www.iasp-pain.org/Education/Content.aspx?ItemNumber=1698. [Accessed 10 May 2019]
  2. ↑ 2.0 2.1 2.2 Woolf CJ. Pain: moving from symptom control toward mechanism-specific pharmacologic management. Ann Intern Med. 2004;140:441-51. Available from: http://www.smbs.buffalo.edu/acb/neuro/readings/SensitizMolecMech.pdf [Accessed 12 May 2019]
  3. ↑ 3.0 3.1 Merskey H (ed.), Bogduk N (ed.). Classification of chronic pain; Descriptions of chronic pain syndromes and definitions of pain terms. 2nd ed. Seattle: IASP Press; 1994 Available from: https://s3.amazonaws.com/rdcms-iasp/files/production/public/Content/ContentFolders/Publications2/FreeBooks/Classification-of-Chronic-Pain.pdf [Accessed on 10 May 2019]
  4. ↑ 4.0 4.1 4.2 Woolf CJ. What is this thing called pain?. The Journal of clinical investigation. 2010 Nov 1;120(11):3742-4. Available from: https://www.jci.org/articles/view/45178/pdf [Accessed on 10 May 2019]
  5. ↑ Dubin AE, Patapoutian A. Nociceptors: the sensors of the pain pathway. The Journal of clinical investigation. 2010 Nov 1;120(11):3760-72. Available from: https://www.jci.org/articles/view/42843/pdf [Accessed on 10 May 2019]
  6. ↑ Breivik H, Collett B, Ventafridda V, Cohen R, Gallacher D. Survey of chronic pain in Europe: prevalence, impact on daily life, and treatment. European journal of pain. 2006 May;10(4):287–333. Available from: http://www.nascholingnoord.nl/presentaties/2012_02_02_Breivik_et_al___Survey_of_chronic_pain_in_Europe.pdf [Accessed on 12 May 2019]
  7. ↑ 7.0 7.1 7.2 7.3 Moseley GL. Reconceptualising pain according to modern pain science. Physical therapy reviews. 2007 Sep 1;12(3):169-78. Available from: https://cdn.bodyinmind.org/wp-content/uploads/Moseley-2007-PTR-conceptualisation1.pdf [Accessed on 12 May 2019]
  8. ↑ Bair MJ, Robinson RL, Katon W, Kroenke K. Depression and pain comorbidity: a literature review. Archives of internal medicine. 2003 Nov 10;163(20):2433-45. Available from: https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/216320 [Accessed on 12 May 2019]
  9. ↑ 9.0 9.1 9.2 9.3 Bantick SJ, Wise RG, Ploghaus A, Clare S, Smith SM, Tracey I. Imaging how attention modulates pain in humans using functional MRI. Brain. 2002 Feb;125(Pt 2):310–9.
  10. ↑ Buhle J, Wager TD. Performance-dependent inhibition of pain by an executive working memory task. Pain. 2010 Apr;149(1):19–26.
  11. ↑ Eccleston C. Chronic pain and distraction: an experimental investigation into the role of sustained and shifting attention in the processing of chronic persistent pain. Behav Res Ther. 1995 May;33(4):391–405.
  12. ↑ 12.0 12.1 12.2 12.3 Valet M, Sprenger T, Boecker H, Willoch F, Rummeny E, Conrad B, et al. Distraction modulates connectivity of the cingulo-frontal cortex and the midbrain during pain--an fMRI analysis. Pain. 2004 Jun;109(3):399–408.
  13. ↑ 13.0 13.1 Villemure C, Bushnell MC. Cognitive modulation of pain: how do attention and emotion influence pain processing? Pain 95, 195-199. Pain. 2002;95(3):195–9.
  14. ↑ 14.0 14.1 Wiech K, Seymour B, Kalisch R, Stephan KE, Koltzenburg M, Driver J, et al. Modulation of pain processing in hyperalgesia by cognitive demand. Neuroimage. 2005 Aug 1;27(1):59–69.
  15. ↑ 15.0 15.1 Tracey I, Ploghaus A, Gati JS, Clare S, Smith S, Menon RS, et al. Imaging attentional modulation of pain in the periaqueductal gray in humans. J Neurosci. 2002 Apr 1;22(7):2748–52.
  16. ↑ 16.0 16.1 16.2 Petrovic P, Petersson KM, Ghatan PH, Stone-Elander S, Ingvar M. Pain-related cerebral activation is altered by a distracting cognitive task. Pain. 2000 Mar;85(1-2):19–30.
  17. ↑ Bingel U, Rose M, Gläscher J, Büchel C. fMRI reveals how pain modulates visual object processing in the ventral visual stream. Neuron. 2007 Jul 5;55(1):157–67.
  18. ↑ 18.0 18.1 Frankenstein UN, Richter W, McIntyre MC, Rémy F. Distraction modulates anterior cingulate gyrus activations during the cold pressor test. Neuroimage. 2001 Oct;14(4):827–36.
  19. ↑ McCracken LM, Turk DC. Behavioral and cognitive-behavioral treatment for chronic pain: outcome, predictors of outcome, and treatment process. Spine. 2002 Nov 15;27(22):2564–73.
  20. ↑ Quevedo AS, Coghill RC. Attentional modulation of spatial integration of pain: evidence for dynamic spatial tuning. J Neurosci. 2007 Oct 24;27(43):11635–40.
  21. ↑ Hauck M, Lorenz J, Engel AK. Attention to Painful Stimulation Enhances γ-Band Activity and Synchronization in Human Sensorimotor Cortex. J Neurosci. 2007 Aug 29;27(35):9270–7.
  22. ↑ Corbetta M, Shulman GL. Control of goal-directed and stimulus-driven attention in the brain. Nat Rev Neurosci. 2002 Mar;3(3):201–15.
  23. ↑ Gilbert CD, Sigman M. Brain states: top-down influences in sensory processing. Neuron. 2007 Jun 7;54(5):677–96.
  24. ↑ Gebhart GF, Schmidt RF, editors. Fear of Pain. In: Encyclopedia of Pain [Internet]. Springer Berlin Heidelberg; 2013 [cited 2016 Mar 29]. p. 1267–1267. Available from: http://link.springer.com/referenceworkentry/10.1007/978-3-642-28753-4_200800
  25. ↑ Helsen K, Leeuw M, Vlaeyen JWS. Fear and Pain. In: Gebhart GF, Schmidt RF, editors. Encyclopedia of Pain [Internet]. Springer Berlin Heidelberg; 2013 [cited 2016 Mar 29]. p. 1261–7. Available from: http://link.springer.com/referenceworkentry/10.1007/978-3-642-28753-4_1482
  26. ↑ Kori SH, Miller RP, Todd DD. Kinisophobia: A new view of chronic pain behavior. Pain manage. 1990 Jan 1;3(1):35–43.
  27. ↑ Lundberg M, Larsson M, Ostlund H, Styf J. Kinesiophobia among patients with musculoskeletal pain in primary healthcare. J Rehabil Med. 2006 Jan;38(1):37–43.
  28. ↑ 28.0 28.1 Vlaeyen JWS, Linton SJ. Fear-avoidance and its consequences in chronic musculoskeletal pain: a state of the art. Pain. 2000 Apr 1;85(3):317–32.
  29. ↑ Crombez G, Eccleston C, Van Damme S, Vlaeyen JWS, Karoly P. Fear-avoidance model of chronic pain: the next generation. Clin J Pain. 2012 Jul;28(6):475–83.
  30. ↑ Wertli MM, Rasmussen-Barr E, Weiser S, Bachmann LM, Brunner F. The role of fear avoidance beliefs as a prognostic factor for outcome in patients with nonspecific low back pain: a systematic review. The Spine Journal. 2014 May 1;14(5):816–36.e4.
  31. ↑ 31.0 31.1 Nijs J, Roussel N, Oosterwijck JV, Kooning MD, Ickmans K, Struyf F, et al. Fear of movement and avoidance behaviour toward physical activity in chronic-fatigue syndrome and fibromyalgia: state of the art and implications for clinical practice. Clin Rheumatol. 2013 May 3;32(8):1121–9.
  32. ↑ Leeuw M, Goossens MEJB, Linton SJ, Crombez G, Boersma K, Vlaeyen JWS. The fear-avoidance model of musculoskeletal pain: current state of scientific evidence. J Behav Med. 2007 Feb;30(1):77–94.
  33. ↑ Definition of CULTURE [Internet]. [cited 2016 Mar 31]. Available from: http://www.merriam-webster.com/dictionary/culture
  34. ↑ 34.0 34.1 Shavers VL, Bakos A, Sheppard VB. Race, ethnicity, and pain among the U.S. adult population. J Health Care Poor Underserved. 2010 Feb;21(1):177–220.
  35. ↑ Campbell CM, Edwards RR. Ethnic differences in pain and pain management. Pain Manag. 2012 May;2(3):219–30.
  36. ↑ Riley JL, Wade JB, Myers CD, Sheffield D, Papas RK, Price DD. Racial/ethnic differences in the experience of chronic pain. Pain. 2002 Dec;100(3):291–8.
  37. ↑ Alabas OA, Tashani OA, Tabasam G, Johnson MI. Gender role affects experimental pain responses: a systematic review with meta-analysis. Eur J Pain. 2012 Oct;16(9):1211–23.
  38. ↑ Jöud A, Petersson IF, Jordan KP, Löfvendahl S, Grahn B, Englund M. Socioeconomic status and the risk for being diagnosed with spondyloarthritis and chronic pain: a nested case-control study. Rheumatol Int. 2014 Sep;34(9):1291–8.
  39. ↑ Miljković A, Stipčić A, Braš M, Dorđević V, Brajković L, Hayward C, et al. Is experimentally induced pain associated with socioeconomic status? Do poor people hurt more? Med Sci Monit. 2014;20:1232–8.
  40. ↑ 40.0 40.1 40.2 40.3 Gatchel RJ, Peng YB, Peters ML, Fuchs PN, Turk DC. The biopsychosocial approach to chronic pain: scientific advances and future directions. Psychol Bull. 2007 Jul;133(4):581–624.
  41. ↑ Hasenbring MI, Chehadi O, Titze C, Kreddig N. Fear and anxiety in the transition from acute to chronic pain: there is evidence for endurance besides avoidance. Pain Management. 2014 Sep 1;4(5):363–74.
  42. ↑ Woby SR, Roach NK, Urmston M, Watson PJ. The relation between cognitive factors and levels of pain and disability in chronic low back pain patients presenting for physiotherapy. Eur J Pain. 2007 Nov;11(8):869–77.


Retrieved from "https://www.physio-pedia.com/index.php?title=Multidimensional_Nature_of_Pain&oldid=211477"