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== Referred Pain ==
== Introduction ==
 
[[File:Armin-lotfi-2WO8-ClYO9E-unsplash (1).jpg|right|frameless|200x200px]]
Referred pain is pain perceived at a location other than the site of the painful stimulus. It usually originates in one of the visceral organs but is felt in the skin or sometimes in another area deep inside the body. Its mechanism is likely due to the fact that pain signals from the viscera travel along the same neural pathways used by pain signals from the skin. The result is the perception of pain originating in the skin rather than in a deep-seated visceral organ or neural structure.  
When we think of pain behaviours, we tend to think of our behaviour to pain but the type of pain and how they present is also an important factor in understanding pain. Human Pain Behaviours is much more than a sensory perception of tissue injury. Pain is a complex and unpleasant multi-dimensional experience of the self associated with perceived tissue threat<ref>Visser EJ, Davies S. [https://www.notredame.edu.au/__data/assets/pdf_file/0013/3046/What-is-pain-part-II-philosophy-behaviours-ANZCA-Blue-Book.pdf What is pain? II: Pain expression and behaviour, evolutionary concepts, models and philosophies]. Australasian Anaesthesia. 2009(2009):35. Available from:https://www.notredame.edu.au/__data/assets/pdf_file/0013/3046/What-is-pain-part-II-philosophy-behaviours-ANZCA-Blue-Book.pdf (last accessed 20.5.2020)</ref>.
 
A different form of referred pain is radiating pain, which is pain located away from or adjacent to the organ involved. For example, the pain related to a myocardial infarction could either be referred or radiating pain from the chest. Referred pain would be when a person has pain only in their jaw or left arm, but not in the chest. Physicians and scientists have known about referred pain since the late 1880s. Despite an increasing amount of literature on the subject, the biological mechanism of referred pain is unknown, although there are several hypotheses.<ref name="Arendt">Arendt-Nielsen L, Svensson P (2001). "Referred muscle pain: basic and clinical findings". Clin J Pain 17 (1): 11–9.</ref><br>


'''Mechanism'''  
Pain behaviours can be adaptive or pathogenic, as when the pain behaviour is excessive in comparison to the objective pathology. It has been found that when pain behaviour exists in pain patients, a psychiatric disease may aggravate pain. <ref>Güleç, G., & Güleç, S. (2006). Pain and pain behavior. Agri: Agri (Algoloji) Dernegi’nin Yayin organidir [Agri: The journal of the Turkish Society of Algology], ''18''(4), 5–9. <nowiki>https://pubmed.ncbi.nlm.nih.gov/17457708/</nowiki></ref>


There are several proposed mechanisms for referred pain. Currently there is no definitive consensus regarding which is correct. The cardiac general visceral sensory pain fibers follow the sympathetic neurons back to the spinal cord and have their cell bodies located in thoracic dorsal root ganglia 1-4.<ref name="simons">Simons, D.G.; Travell, J.G.; Simons, L.S. (1999). Travell &amp;amp; Simons' Myofascial Pain and Dysfunction: Upper half of body. Williams &amp;amp; Wilkins. p. 750</ref>&nbsp;As a general rule, general visceral afferent (GVA) pain fibers follow sympathetic fibers back to the same spinal cord segments that gave rise to the preganglionic sympathetic fibers in the thorax and abdomen. The central nervous system (CNS) perceives pain from the heart as coming from the somatic portion of the body supplied by thoracic spinal cord segments 1-4.<ref name="simons" />&nbsp;Classically, the pain associated with a myocardial infarction is located in the mid or left side of the chest where the heart is physically located. The pain can radiate to the left side of the jaw and into the left arm. Also, the dermatomes of this region of the thoracic wall and upper limb have their neuronal cell bodies in the same dorsal root ganglia (T1-5) and synapse in the same second order neurons in the spinal cord segments (T1-5) as the general visceral sensory fibers from the heart. The CNS does not clearly discern whether the pain is coming from the body wall or from the viscera, but it perceives the pain as coming from somewhere on the body wall, i.e. substernal pain, left arm/hand pain, jaw pain.
Pain types differ. There are 4 widely accepted pain types relevant for musculoskeletal pain<ref>Painhealth [https://painhealth.csse.uwa.edu.au/pain-module/pain-types/ Pain Types] https://painhealth.csse.uwa.edu.au/pain-module/pain-types/ (last accessed 20.5.2020)</ref>:
* [[Nociception|Nociceptive pain]]
* [[Neurogenic inflammation in Musculoskeletal Condition|Nociceptive inflammatory pain]]
* [[Neuropathic Pain|Neuropathic pain]]
* [[Nociplastic Pain]]
Other types of pain are also described here:
* [[Referred Pain]]
* [[Hyperalgesia]]
* [[Allodynia]]
For more information also see:


'''Convergent Projection'''
* [[Pain Mechanisms]]
* [[Pain-Modulation|Pain Modulation]]


This represents one of the earliest theories on the subject of referred pain. It is based on the work of W.A. Sturge and J. Ross from 1888 and later TC Ruch in 1961. Convergent projection proposes that afferent nerve fibers from tissues converge onto the same spinal neuron, and explains why referred pain is believed to be segmented in much the same way as the spinal cord. Additionally, experimental evidence shows that when local pain (pain at the site of stimulation) is intensified the referred pain is intensified as well.<ref>Arendt-Nielsen L, Svensson P (2001). "Referred muscle pain: basic and clinical findings". Clin J Pain 17 (1): 11–9.</ref>
== Pain Behaviours ==
There are different types of behaviours that can be exhibited with the feeling of pain. These can include [[Phantom Limb Pain|phantom limb pain]] or pain catastrophising. There are many different types of pain related behaviours that can be experienced via the different types of pain presentations, as listed above (nociceptive and neuropathic pain).


Criticism of this model arises from its inability to explain why there is a delay between the onset of referred pain after local pain stimulation. Experimental evidence also shows that referred pain is often unidirectional. For example, stimulated local pain in the anterior tibial muscle causes referred pain in the ventral portion of the ankle; however referred pain moving in the opposite direction has not been shown experimentally. Lastly, the threshold for the local pain stimulation and the referred pain stimulation are different, but according to this model they should both be the same.<ref name="Arendt" />  
Different behaviours and characteristics can be exhibited between different types of groups. The points below outlines some of these different types of behaviours: <ref>Fillingim R.B. Individual Differences in Pain: Understanding the Mosaic that Makes Pain Personal. Pain. 2017:158(1):1-18.</ref>


'''Convergence Facilitation'''
==== Demographic factors  ====
* Demographic factors do not influence pain. However, they can influence differing individual factors which would account for a varied person's perception of pain


Convergence facilitation was conceived in 1893 by J MacKenzie based on the ideas of Sturge and Ross. He believed that the internal organs were insensitive to stimuli. Furthermore, he believed that non-nociceptive afferent inputs to the spinal cord created what he termed "an irritable focus". This focus caused some stimuli to be perceived as referred pain. However, his ideas did not gain widespread acceptance from critics due to its dismissal of visceral pain.<ref>Arendt-Nielsen L, Svensson P (2001). "Referred muscle pain: basic and clinical findings". Clin J Pain 17 (1): 11–9.</ref>
==== Sex differences ====
* Chronic pain is more prevalent among Women than Men
* Women were more likely to report persistent and bothersome pain - they are at a greater risk for more chronic type pain, like migraines and tension-type headaches, low back pain, fibromyalgia and widespread pain, temporomandibular disorders, irritable bowel syndrome, and osteoarthritis
* Women display greater sensitivity than men, including pain threshold, pain tolerance, and ratings of suprathreshold stimuli, females have shown greater adaptation than men, which indicates a stronger pain inhibitory response to thee stimuli
* Possible mechanisms can present as effects of sex hormones, differences in endogenous opioid function, cognitive/affective influences, and contributions of social factors such as stereotypic gender roles


Recently this idea has regained some credibility under a new term, central sensitization. Central sensitization occurs when neurons in the spinal cord's dorsal horn or brainstem become more responsive after repeated stimulation by peripheral neurons, so that weaker signals can trigger them. The delay in appearance of referred pain shown in laboratory experiments can be explained due to the time required to create the central sensitization.
==== Ethnic differences ====
* Pain prevalence was lowest among Asians compared to other race/ethnic groups in the US - the highest prevalence of persistent pain among whites, in comparison to other ethnic groups
* Among older adults some studies reported a higher pain prevalence among minorities compared to whites, while others reported no differences in pain prevalence
* While conflicting evidence exists regarding pain prevalence among minority versus majority ethnic groups, studies consistently suggest that the severity and impact of pain is greater among minorities who are experiencing chronic pain
* Differences in pain perception between racial/ethnic groups may contribute to variances in severity of clinical pain - it is interesting to note that African Americans display greater experimental pain sensitivity compared to non-Hispanic whites
* Mechanisms include factors related to socioeconomic standing and access to adequate health care  Increased pain prevalence and higher pain intensity in lower SES groups 
* Minority patients are at greater risk for undertreatment of their pain, which could obviously contribute to the greater clinical pain severity observed among members of minority groups 
* Pain coping also differs significantly across racial/ethnic groups
* Biological factors, such as genetic contributions, may play a role in racial/ethnic differences in pain responses


'''Axon -Reflex'''  
==== '''Age related differences''' ====


Axon reflex suggests that the afferent fiber is bifurcated before connecting to the dorsal horn. Bifurcated fibers do exist in muscle, skin, and intervertebral discs. Yet these particular neurons are rare and are not representative of the whole body. Axon-Reflex also does not explain the time delay before the appearance of referred pain, threshold differences for stimulating local and referred pain, and somatosensory sensibility changes in the area of referred pain.<ref>Arendt-Nielsen L, Svensson P (2001). "Referred muscle pain: basic and clinical findings". Clin J Pain 17 (1): 11–9.</ref>
* The prevalence of joint pain, lower extremity pain and neuropathic pains tend to increase monotonically with age.
* General chronic pain increases in prevalence until middle age, at which time the prevalence plateaus.
* Pain conditions such as headache, abdominal pain, back pain, and temporomandibular disorders show peak prevalence in the third to fifth decades of life, after which their frequency decreases.
* Older adults have reported lower acute pain intensity in some studies.
* Age-related differences in the intensity and impact of chronic pain have not been consistently demonstrated
* Older adults show less sensitivity to brief, cutaneous pains (e.g. heat pain threshold); however, sensitivity to more sustained pain stimuli that impact deeper tissues increases with age
* Several studies have demonstrated increased temporal summation of pain among older adults, while  conditioned pain modulation consistently has been found to decrease with age
* Aging is associated with a shift in pain modulatory balance, such that older adults show enhanced pain facilitation combined with decreased pain inhibition


'''Hyper-Excitability'''  
== Nociceptive Pain ==
Nociceptive pain can be thought of as pain associated with tissue injury or damage or even potential damage.
*'''Nociceptors:''' are sensory endings on nerves that can be excited or sensitized and signal potential tissue damage.
* Examples of nociceptive pain include jamming your finger in a car door, spraining your ankle or touching the hot plate on the stove.


Hyperexcitability hypothesizes that referred pain has no central mechanism. However, it does say that there is one central characteristic that predominates. Experiments involving noxious stimuli and recordings from the dorsal horn of animals revealed that referred pain sensations began minutes after muscle stimulation. Pain was felt in a receptive field that was some distance away from the original receptive field. According to hyperexcitability, new receptive fields are created as a result of the opening of latent convergent afferent fibers in the dorsal horn. This signal could then be perceived as referred pain.<ref>Arendt-Nielsen L, Svensson P (2001). "Referred muscle pain: basic and clinical findings". Clin J Pain 17 (1): 11–9.</ref>
[[File:Pain finger.jpg|right|frameless|200x200px]]
== Nociceptive Inflammatory Pain ==


Several characteristics are in line with this mechanism of referred pain, such as dependency on stimulus and the time delay in the appearance of referred pain as compared to local pain. However, the appearance of new receptive fields, which is interpreted to be referred pain, conflicts with the majority of experimental evidence from studies including studies of healthy individuals. Furthermore, referred pain generally appears within seconds in humans as opposed to minutes in animal models. Some scientists attribute this to a mechanism or influence downstream in the supraspinal pathways. Neuroimaging techniques such as PET scans or fMRI may visualize the underlying neural processing pathways responsible in future testing.  
* [[Neurogenic inflammation in Musculoskeletal Condition|Nociceptive inflammatory pain]] is associated with tissue damage and inflammatory response.
* '''Inflammation:''' is a coordinated body system response that is designed to help heal tissue damage.  
* The inflammatory response is well-coordinated and involves blood-borne chemicals, immune system chemicals and some chemicals released from specialised nerve fibres. These chemicals communicate with each other to help coordinate tissue repair.
* Examples of nociceptive pain include: jamming fingers in a car door, a sprained ankle, non-specific low back pain or neck pain, fractures.  
* There may be signs of tissue injury such as swelling, redness and later purple or yellowing of the skin, a limb that looks distorted, increased sensitivity to touch and movement. Such signs are part of tissue healing.


'''Thalamic-convergence'''
[[File:Sam-burriss-zHSX9o2 B7Y-unsplash.jpg|thumb|300x300px]]
== Neuropathic Pain ==


Thalamic convergence suggests that referred pain is perceived as such due to the summation of neural inputs in the brain, as opposed to the spinal cord, from the injured area and the referred area. Experimental evidence on thalamic convergence is lacking. However, pain studies performed on monkeys revealed several.<ref>Arendt-Nielsen L, Svensson P (2001). "Referred muscle pain: basic and clinical findings". Clin J Pain 17 (1): 11–9.</ref><br>
* [[Neuropathic Pain|Neuropathic pain]] is pain associated with injury or disease of nerve tissue.
* People often get this type of pain when they have shingles, sciatica, cervical or lumbar radiculopathy, trigeminal neuralgia, or diabetic neuropathy.
* Neuropathic pain is often described as burning, shooting, stabbing, prickling, electric shock-like pain, with hypersensitivity to touch, movement, hot and cold and pressure.  
* Neuropathic pain may cause even a very light touch or gentle movement to be very painful.


<br>  
== Nociplastic Pain ==
[[Nociplastic Pain|Nociplastic pain]] is mechanistically different from nociceptive pain and neuropathic pain.
The following is the definition recommended by the IASP:<blockquote>"Nociplastic Pain is a term used to describe persistent pain that arises from altered nociception, despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors, or evidence for disease or lesion of the somatosensory system causing the pain." </blockquote>Some facts about nociplastic pain:


[[Image:Derms2.jpg|frame|center|Dermatomal referral patterns]]  
* It is an umbrella term. <ref name=":0">International Association for the Study of Pain - What's in a Name for Chronic Pain? “Nociplastic pain” was officially adopted by IASP as the third mechanistic descriptor of chronic pain. Available from: <nowiki>https://www.iasp-pain.org/publications/pain-research-forum/prf-news/92059-whats-name-chronic-pain/</nowiki> (accessed 11 August 2023).</ref>
* It can be defined as [[Chronic Pain and the Brain|chronic pain]] leading towards an altered nociceptive function.
* It results in increased sensitivity from the altered function of pain-related sensory pathways in the periphery and central nervous system (CNS). <ref name=":1">Fitzcharles M-A, Cohen S.P, Clauw D.J, Littlejohn G, Usui C, Häuser W. Nociplastic pain: towards an understanding of prevalent pain conditions. The Lancet. 2021:397:2098–2110.</ref> <ref>Chimenti R.L, Frey-Law L.A, Sluka K.A. A Mechanism-Based Approach to Physical Therapist Management of Pain. Journal of the American Physical Therapy Association. 2018:98(5):302–314.</ref>
* It consists of multifactorial processes from different inputs, which could be either a bottom-up response to a peripheral nociceptive, a neuropathic stimulus (known as central sensitisation), or a top-down CNS-driven response. <ref name=":1" />
* It is not a diagnosis but a descriptor of the pain experienced. <ref name=":0" /><ref>Slater H, Hush J. Pain Terminology: Introduction Of a Third Clinical Descriptor. Pain Terminology. 2018:3:7-8.</ref>
* It encompasses pain from stereotypical terms such as dysfunctional pain or medically unexplained somatic syndromes. <ref name=":1" />
* Conditions that fall under the umbrella of Nociplastic Pain include [[fibromyalgia]], [[Complex Regional Pain Syndrome (CRPS)|complex regional pain syndrome]], other musculoskeletal pain such as [[Chronic Low Back Pain|chronic low back pain]], and visceral pain disorders such as [[Irritable Bowel Syndrome|irritable bowel syndrome]] and bladder pain syndrome. <ref name=":0" />


<br> {{#ev:youtube|wbpjEPRq6pA}}
== Referred Pain ==
* Referred pain is pain perceived at a location other than the site of the painful stimulus.
* It usually originates in one of the visceral organs but is felt in the skin or sometimes in another area deep inside the body.
* Its mechanism is likely due to the fact that pain signals from the viscera travel along the same neural pathways used by pain signals from the skin.
* The result is the perception of pain originating in the skin rather than in a deep-seated visceral organ or neural structure.
* Visceral nociceptors project into the spinal cord via small diameter myelinated and unmyelinated fibres from the autonomic nervous system. They go on to synapse close to the point of embryonic origin in the spine.
* When an organ develops pain, it can therefore be perceived as being at a different point in the body, on the surface, rather than in the organ itself.<ref name="Rog" />


<br> <br>  
[[File:Tumblr lb03ir2vgL1qzr2i2o1 500.png|frameless|500x500px|center]]
===== '''Mechanism''' =====
{{#ev:youtube|w_uSsFeA_lc}}<ref>UChicago Online. Visceral Pain. Available from: https://www.youtube.com/watch?v=w_uSsFeA_lc [last accessed 1/8/2021]</ref>  
== Hyperalgesia  ==


== Hyperalgesia<br> ==
* [[Hyperalgesia]] is defined as "An increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves".<ref name="hart">Hart BL. [https://www.sciencedirect.com/science/article/pii/S0149763488800046 Biological basis of the behavior of sick animals]. Neuroscience & Biobehavioral Reviews. 1988 Jun 1;12(2):123-37.</ref>
* It is divided into two types; primary and secondary.
#'''Primary hyperalgesia''' - pain and sensitivity in the damaged tissues.
#'''Secondary hyperalgesia''' - pain and sensitivity that occurs in area around the damaged tissues.


An increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves.<ref name="hart">Hart BL (1988). "Biological basis of the behavior of sick animals". Neurosci Biobehav Rev 12 (2): 123–37.</ref>
* Substance P appears to have a significant role in the sensitization of nociceptors, which may explain the heightened feeling of pain in injured tissue (primary hyperalgesia). Although, this does not account for the perception of non-painful stimuli as painful.  
 
* Secondary hyperalgesia is most likely accounted for by changes in the dorsal horn which affect the processing of sensory information. <ref name="Rog">Roger, Barker, Barasi, Neal. Neuroscience at a glance.1999 Blackwell science.</ref>
Hyperalgesia can be experienced in focal, discrete areas, or as a more diffuse, body-wide form.
* Normally silent nociceptors are likely recruited, and sprouting of large diameter sensory afferent occurs projecting into the dorsal horn laminae.
 
The focal form is typically associated with injury, and is divided into two subtypes:
 
<br>
 
*'''Primary hyperalgesia'''&nbsp;- pain sensitivity that occurs directly in the damaged tissues.
*'''Secondary hyperalgesia'''&nbsp;- &nbsp;pain sensitivity that occurs in surrounding undamaged tissues.
 
<br>
 
'''Causes'''
 
Hyperalgesia is induced by platelet-activating factor (PAF) which comes about in an inflammatory or an allergic response. This seems to occur via immune cells interacting with the peripheral nervous system and releasing pain-producing chemicals (cytokines and chemokines)<ref name="marchand">Marchand F, Perretti M, McMahon SB (July 2005). "Role of the immune system in chronic pain". Nat. Rev. Neurosci. 6 (7): 521–32</ref>
 
Long-term opioid (e.g. heroin, morphine) users and those on high-dose opioid medications for the treatment of chronic pain, may experience hyperalgesia and experience pain out of proportion to physical findings, which is a common cause for loss of efficacy of these medications over time.<ref name="dupen">DuPen A, Shen D, Ersek M (September 2007). "Mechanisms of opioid-induced tolerance and hyperalgesia". Pain Manag Nurs 8 (3): 113–21</ref><ref name="chu">Chu LF, Angst MS, Clark D (2008). "Opioid-induced hyperalgesia in humans: molecular mechanisms and clinical considerations". Clin J Pain 24 (6): 479–96.</ref> As it can be difficult to distinguish from tolerance, opioid-induced hyperalgesia is often compensated for by escalating the dose of opioid, potentially worsening the problem by further increasing sensitivity to pain. Chronic hyperstimulation of opioid receptors results in altered homeostasis of pain signalling pathways in the body with several mechanisms of action involved. One major pathway being through stimulation of the nociceptin receptor,<ref name="okuda">Okuda-Ashitaka E, Minami T, Matsumura S, et al. (February 2006). "The opioid peptide nociceptin/orphanin FQ mediates prostaglandin E2-induced allodynia, tactile pain associated with nerve injury". Eur. J. Neurosci. 23 (4): 995–1004.</ref> <ref name="ikeda">Ikeda H, Stark J, Fischer H, et al. (June 2006). "Synaptic amplifier of inflammatory pain in the spinal dorsal horn". Science 312 (5780): 1659–62</ref>and blocking this receptor may therefore be a means of preventing the development of hyperalgesia.<ref name="tamai">Tamai H, Sawamura S, Takeda K, Orii R, Hanaoka K (March 2005). "Anti-allodynic and anti-hyperalgesic effects of nociceptin receptor antagonist, JTC-801, in rats after spinal nerve injury and inflammation". Eur. J. Pharmacol. 510 (3): 223–8</ref>
 
Stimulation of nociceptive fibers in a pattern consistent with that from inflammation switches on a form of amplification in the spinal cord, long term potentiation.<ref name="kelley">Kelley KW, Bluthé RM, Dantzer R, et al. (February 2003). "Cytokine-induced sickness behavior". Brain Behav. 17 (Suppl 1): S112–8.</ref> This occurs where the pain fibres synapse to pain pathway, the periaqueductal grey. Amplification in the spinal cord may be another way of producing hyperalgesia.
 
The release of proinflammatory cytokines such as Interleukin-1 by activated leukocytes triggered by lipopolysaccharides, endotoxins and other signals of infection also increases pain sensitivity as part of sickness behavior, the evolved response to illness.<ref name="maier">Maier SF, Wiertelak EP, Martin D, Watkins LR (October 1993). "Interleukin-1 mediates the behavioral hyperalgesia produced by lithium chloride and endotoxin". Brain Res. 623 (2): 321–4.</ref>
 
<br>


[[Image:Hyperalgesia.jpg|frame|center|Primary and Secondary hyperalgesia Comparison]]  
[[Image:Hyperalgesia.jpg|frame|center|Primary and Secondary hyperalgesia Comparison]]  
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== Allodynia  ==
== Allodynia  ==


Central pain sensitization (increased response of neurons) following painful, often repetitive, stimulation. Allodynia can lead to the triggering of a pain response from stimuli which do not normally provoke pain.<ref name="merskey">Merskey &amp;amp;amp;amp;amp;amp;amp;amp; Bogduk (Eds.) Classification of Chronic Pain. Seattle: IASP Task Force on Taxonomy, 1994</ref><br>
* Central pain sensitization (increased response of neurons) following painful, often repetitive, stimulation.
 
<br>
 
'''Types of allodynia:'''
 
*Mechanical allodynia (also known as tactile allodynia)
*Static mechanical allodynia – pain in response to light touch/pressure<ref name="attal">Attal N, Brasseur L, Chauvin M, Bouhassira D (1999). "Effects of single and repeated applications of a eutectic mixture of local anaesthetics (EMLA) cream on spontaneous and evoked pain in post-herpetic neuralgia". Pain 81 (1–2): 203–9</ref>
*Dynamic mechanical allodynia – pain in response to stroking lightly<ref>LoPinto C, Young WB, Ashkenazi A (2006). "Comparison of dynamic (brush) and static (pressure) mechanical allodynia in migraine". Cephalalgia 26 (7): 852–6.</ref>
*Thermal (hot or cold) allodynia – pain from normally mild skin temperatures in the affected area
*Movement allodynia - pain triggered by normal movement of joints or muscles.
 
<br>
 
'''Pathophysiology'''
 
<u>Cellular level</u><br>The cell types involved in nociception and mechanical sensation are the cells responsible for allodynia. In healthy individuals, nociceptors sense information about cell stress or damage and temperature at the skin and transmit it to the spinal cord. The cell bodies of these neurons lie in dorsal root ganglia, important structures located on both sides of the spinal cord. The axons then pass through the dorsal horn to make connections with secondary neurons. The secondary neurons cross over to the other (contralateral) side of the spinal cord and reach nuclei of the thalamus. From there, the information is carried through one or more neurons to the somatosensory cortex of the brain. Mechanoreceptors follow the same general pathway. However, they do not cross over at the level of the spinal cord, but at the lower medulla instead. In addition, they are grouped in tracts that are spatially distinct from the nociceptive tracts.
 
Despite this anatomical separation, mechanoreceptors can influence the output of nociceptors by making connections with the same interneurons, the activation of which can reduce or completely eliminate the sensation of pain. Another way to modulate the transmission of pain information is via descending fibers from the brain. These fibers act through different interneurons to block the transmission of information from the nociceptors to secondary neurons.<ref name="fitzpatrick">Fitzpatrick, David; Purves, Dale; Augustine, George (2004). Neuroscience. Sunderland, Mass: Sinauer. pp. 231–250.</ref>
 
Both of these mechanisms for pain modulation have been implicated in the pathology of allodynia. Several studies suggest that injury to the spinal cord might lead to loss and re-organization of the nociceptors, mechanoreceptors and interneurons, leading to the transmission of pain information by mechanoreceptors<ref>Yezierski RP, Liu S, Ruenes GL, Kajander KJ, Brewer KL (1998). "Excitotoxic spinal cord injury: behavioral and morphological characteristics of a central pain model". Pain 75 (1): 141–55</ref><ref>Wasner G, Naleschinski D, Baron R (2007). "A role for peripheral afferents in the pathophysiology and treatment of at-level neuropathic pain in spinal cord injury? A case report". Pain 131 (1–2): 219–25</ref>A different study reports the appearance of descending fibers at the injury site.<ref>Kalous A, Osborne PB, Keast JR (2007). "Acute and chronic changes in dorsal horn innervation by primary afferents and descending supraspinal pathways after spinal cord injury". J. Comp. Neurol. 504 (3): 238–53</ref> All of these changes ultimately affect the circuitry inside the spinal cord, and the altered balance of signals probably leads to the intense sensation of pain associated with allodynia.
 
Different cell types have also been linked to allodynia. For example, there are reports that microglia in the thalamus might contribute to allodynia by changing the properties of the secondary nociceptors.<ref>Zhao P, Waxman SG, Hains BC (2007). "Modulation of thalamic nociceptive processing after spinal cord injury through remote activation of thalamic microglia by cysteine cysteine chemokine ligand 21". J. Neurosci. 27 (33): 8893–902.</ref> The same effect is achieved in the spinal cord by the recruitment of immune system cells such as monocytes/macrophages and T lymphocytes.<ref>Wei XH, Zang Y, Wu CY, Xu JT, Xin WJ, Liu XG (2007). "Peri-sciatic administration of recombinant rat TNF-alpha induces mechanical allodynia via upregulation of TNF-alpha in dorsal root ganglia and in spinal dorsal horn: the role of NF-kappa B pathway". Exp. Neurol. 205 (2): 471–84.</ref>


<u>Molecular level</u><br>There is a strong body of evidence that the so-called sensitization of the central nervous system contributes to the appearance of allodynia. Sensitization refers to the increased response of neurons following repetitive stimulation. In addition to repeated activity, the increased levels of certain compounds lead to sensitization, as well. The work of many researchers has led to the elucidation of pathways that can result in neuronal sensitization both in the thalamus and dorsal horns. Both pathways depend on the production of chemokines and other molecules important in the inflammatory response.  
[[Image:Allodynia.gif|right|frameless]]


A very important molecule in the thalamus appears to be cysteine-cysteine chemokine ligand 21 (CCL21). The concentration of this chemokine is increased in the ventral posterolateral nucleus of the thalamus where secondary nociceptive neurons make connections with other neurons. The source of CCL21 is not exactly known, but two possibilities exist. First, it might be made in primary nociceptive neurons and transported up to the thalamus. Most likely, neurons intrinsic to the ventral posterolateral nucleus make at least some of it. In any case, CCL21 binds to C-C chemokine receptor type 7 and chemokine receptor CXCR3 receptors on microglia in the thalamus.<ref>Dijkstra IM, de Haas AH, Brouwer N, Boddeke HW, Biber K (2006). "Challenge with innate and protein antigens induces CCR7 expression by microglia in vitro and in vivo". Glia 54 (8): 861–72</ref>The physiologic response to the binding is probably the production of prostaglandin E2 (PGE2) by cyclooxygenase 2 (COX-2).<ref>Alique M, Herrero JF, Lucio-Cazana FJ (2007). "All-trans retinoic acid induces COX-2 and prostaglandin E2 synthesis in SH-SY5Y human neuroblastoma cells: involvement of retinoic acid receptors and extracellular-regulated kinase 1/2". J Neuroinflammation 4: 1</ref>Activated microglia making PGE2 can then sensitize nociceptive neurons as manifested by their lowered threshold to pain.<ref>Rukwied R, Chizh BA, Lorenz U (2007). "Potentiation of nociceptive responses to low pH injections in humans by prostaglandin E2". J Pain 8 (5): 443–51.</ref>
* Allodynia can lead to the triggering of a pain response from stimuli which do not normally provoke pain.<ref name="merskey">Merskey &amp; Bogduk (Eds.) Classification of Chronic Pain. Seattle: IASP Task Force on Taxonomy, 1994</ref><br>'''Types of allodynia:'''
* '''Mechanical allodynia''' (also known as tactile allodynia)


The mechanism responsible for sensitization of the central nervous system at the level of the spinal cord is different from the one in the thalamus. Tumor necrosis factor-alpha (TNF-alpha) and its receptor are the molecules that seem to be responsible for the sensitization of neurons in the dorsal horns of the spinal cord. Macrophages and lymphocytes infiltrate the spinal cord, for example, because of injury, and release TNF-alpha and other pro-inflammatory molecules.<ref>Haskó G, Pacher P, Deitch EA, Vizi ES (2007). "Shaping of monocyte and macrophage function by adenosine receptors". Pharmacol. Ther. 113 (2): 264–75.</ref>TNF-alpha then binds to the TNF receptors expressed on nociceptors, activating the MAPK/NF-kappa B pathways. This leads to the production of more TNF-alpha, its release, and binding to the receptors on the cells that released it (autocrine signalling). This mechanism also explains the perpetuation of sensitization and thus allodynia. TNF-alpha might also increase the number of AMPA receptors, and decrease the numbers of GABA receptors on the membrane of nociceptors, both of which could change the nociceptors in a way that allows for their easier activation.<ref>Stellwagen D, Beattie EC, Seo JY, Malenka RC (2005). "Differential regulation of AMPA receptor and GABA receptor trafficking by tumor necrosis factor-alpha". J. Neurosci. 25 (12): 3219–28.</ref> Another outcome of the increased TNF-alpha is the release of PGE2, with a mechanism and effect similar to the ones in the thalamus.<ref>Coutaux A, Adam F, Willer JC, Le Bars D (2005). "Hyperalgesia and allodynia: peripheral mechanisms". Joint Bone Spine 72 (5): 359–71.</ref>.  
*'''Static mechanical allodynia''' – pain in response to light touch/pressure<ref name="attal">Attal N, Brasseur L, Chauvin M, Bouhassira D. [https://www.sciencedirect.com/science/article/pii/S0304395999000147 Effects of single and repeated applications of a eutectic mixture of local anaesthetics (EMLA®) cream on spontaneous and evoked pain in post-herpetic neuralgia]. Pain. 1999 May 1;81(1-2):203-9.</ref>
*'''Dynamic mechanical allodynia''' – pain in response to stroking lightly<ref>LoPinto C, Young WB, Ashkenazi A. [https://journals.sagepub.com/doi/abs/10.1111/j.1468-2982.2006.01121.x Comparison of dynamic (brush) and static (pressure) mechanical allodynia in migraine]. Cephalalgia. 2006 Jul;26(7):852-6.</ref>
*'''Thermal (hot or cold) allodynia''' – pain from normally mild skin temperatures in the affected area
*'''Movement allodynia''' - pain triggered by normal movement of joints or muscles.<br>


<br>
== Pain Behaviours ==
 
[[Image:Allodynia.gif|frame|center]]


== Inflammatory Pain  ==
== Inflammatory Pain  ==


One of the cardinal features of inflammatory states is that normally innocuous stimuli produce pain<ref>B. L. Kidd1 and L. A. Urban2. Mechanisms of inflammatory pain. Oxford JournalsMedicine &amp;amp;amp;amp;amp;amp;amp; Health BJA Volume 87, Issue 1Pp. 3-11</ref>  
One of the cardinal features of inflammatory states is that normally innocuous stimuli produce pain.<ref>Kidd BL, Urban LA. [https://bjanaesthesia.org/article/S0007-0912(17)36339-0/abstract Mechanisms of inflammatory pain.] British journal of anaesthesia. 2001 Jul 1;87(1):3-11.</ref>  


Please follow the link to this article for an overview of [http://bja.oxfordjournals.org/content/87/1/3.full Inflammatory pain]  
Please follow the link to this article for an overview of [http://bja.oxfordjournals.org/content/87/1/3.full Inflammatory pain]


<br> {{#ev:vimeo|88634321}}  
== Further Watching ==
Below is a 45 minutes video on Pain Mechanisms{{#ev:vimeo|88634321}}<ref>Tony Dickenson. Update on Pain Mechanisms. Available from: https://vimeo.com/88634321 [last accessed 1/8/2021]</ref>


== References  ==
== References  ==


References will automatically be added here, see [[Adding References|adding references tutorial]].
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[[Category:Pain]] [[Category:PPA_Project]]
[[Category:Pain]]  
[[Category:PPA_Project]]

Latest revision as of 15:07, 20 December 2023

Original Editor - Joanne Garvey

Top Contributors - Joanne Garvey, Kapil Narale, Jo Etherton, Aminat Abolade, Evan Thomas, Tarina van der Stockt, Kim Jackson, Lucinda hampton, Melissa Coetsee, Rachael Lowe, Lauren Lopez, Carina Therese Magtibay and Aya Alhindi

Introduction[edit | edit source]

Armin-lotfi-2WO8-ClYO9E-unsplash (1).jpg

When we think of pain behaviours, we tend to think of our behaviour to pain but the type of pain and how they present is also an important factor in understanding pain. Human Pain Behaviours is much more than a sensory perception of tissue injury. Pain is a complex and unpleasant multi-dimensional experience of the self associated with perceived tissue threat[1].

Pain behaviours can be adaptive or pathogenic, as when the pain behaviour is excessive in comparison to the objective pathology. It has been found that when pain behaviour exists in pain patients, a psychiatric disease may aggravate pain. [2]

Pain types differ. There are 4 widely accepted pain types relevant for musculoskeletal pain[3]:

Other types of pain are also described here:

For more information also see:

Pain Behaviours[edit | edit source]

There are different types of behaviours that can be exhibited with the feeling of pain. These can include phantom limb pain or pain catastrophising. There are many different types of pain related behaviours that can be experienced via the different types of pain presentations, as listed above (nociceptive and neuropathic pain).

Different behaviours and characteristics can be exhibited between different types of groups. The points below outlines some of these different types of behaviours: [4]

Demographic factors[edit | edit source]

  • Demographic factors do not influence pain. However, they can influence differing individual factors which would account for a varied person's perception of pain

Sex differences[edit | edit source]

  • Chronic pain is more prevalent among Women than Men
  • Women were more likely to report persistent and bothersome pain - they are at a greater risk for more chronic type pain, like migraines and tension-type headaches, low back pain, fibromyalgia and widespread pain, temporomandibular disorders, irritable bowel syndrome, and osteoarthritis
  • Women display greater sensitivity than men, including pain threshold, pain tolerance, and ratings of suprathreshold stimuli, females have shown greater adaptation than men, which indicates a stronger pain inhibitory response to thee stimuli
  • Possible mechanisms can present as effects of sex hormones, differences in endogenous opioid function, cognitive/affective influences, and contributions of social factors such as stereotypic gender roles

Ethnic differences[edit | edit source]

  • Pain prevalence was lowest among Asians compared to other race/ethnic groups in the US - the highest prevalence of persistent pain among whites, in comparison to other ethnic groups
  • Among older adults some studies reported a higher pain prevalence among minorities compared to whites, while others reported no differences in pain prevalence
  • While conflicting evidence exists regarding pain prevalence among minority versus majority ethnic groups, studies consistently suggest that the severity and impact of pain is greater among minorities who are experiencing chronic pain
  • Differences in pain perception between racial/ethnic groups may contribute to variances in severity of clinical pain - it is interesting to note that African Americans display greater experimental pain sensitivity compared to non-Hispanic whites
  • Mechanisms include factors related to socioeconomic standing and access to adequate health care Increased pain prevalence and higher pain intensity in lower SES groups
  • Minority patients are at greater risk for undertreatment of their pain, which could obviously contribute to the greater clinical pain severity observed among members of minority groups
  • Pain coping also differs significantly across racial/ethnic groups
  • Biological factors, such as genetic contributions, may play a role in racial/ethnic differences in pain responses

Age related differences[edit | edit source]

  • The prevalence of joint pain, lower extremity pain and neuropathic pains tend to increase monotonically with age.
  • General chronic pain increases in prevalence until middle age, at which time the prevalence plateaus.
  • Pain conditions such as headache, abdominal pain, back pain, and temporomandibular disorders show peak prevalence in the third to fifth decades of life, after which their frequency decreases.
  • Older adults have reported lower acute pain intensity in some studies.
  • Age-related differences in the intensity and impact of chronic pain have not been consistently demonstrated
  • Older adults show less sensitivity to brief, cutaneous pains (e.g. heat pain threshold); however, sensitivity to more sustained pain stimuli that impact deeper tissues increases with age
  • Several studies have demonstrated increased temporal summation of pain among older adults, while  conditioned pain modulation consistently has been found to decrease with age
  • Aging is associated with a shift in pain modulatory balance, such that older adults show enhanced pain facilitation combined with decreased pain inhibition

Nociceptive Pain[edit | edit source]

Nociceptive pain can be thought of as pain associated with tissue injury or damage or even potential damage.

  • Nociceptors: are sensory endings on nerves that can be excited or sensitized and signal potential tissue damage.
  • Examples of nociceptive pain include jamming your finger in a car door, spraining your ankle or touching the hot plate on the stove.
Pain finger.jpg

Nociceptive Inflammatory Pain[edit | edit source]

  • Nociceptive inflammatory pain is associated with tissue damage and inflammatory response.
  • Inflammation: is a coordinated body system response that is designed to help heal tissue damage.
  • The inflammatory response is well-coordinated and involves blood-borne chemicals, immune system chemicals and some chemicals released from specialised nerve fibres. These chemicals communicate with each other to help coordinate tissue repair.
  • Examples of nociceptive pain include: jamming fingers in a car door, a sprained ankle, non-specific low back pain or neck pain, fractures.
  • There may be signs of tissue injury such as swelling, redness and later purple or yellowing of the skin, a limb that looks distorted, increased sensitivity to touch and movement. Such signs are part of tissue healing.
Sam-burriss-zHSX9o2 B7Y-unsplash.jpg

Neuropathic Pain[edit | edit source]

  • Neuropathic pain is pain associated with injury or disease of nerve tissue.
  • People often get this type of pain when they have shingles, sciatica, cervical or lumbar radiculopathy, trigeminal neuralgia, or diabetic neuropathy.
  • Neuropathic pain is often described as burning, shooting, stabbing, prickling, electric shock-like pain, with hypersensitivity to touch, movement, hot and cold and pressure.
  • Neuropathic pain may cause even a very light touch or gentle movement to be very painful.

Nociplastic Pain[edit | edit source]

Nociplastic pain is mechanistically different from nociceptive pain and neuropathic pain.

The following is the definition recommended by the IASP:

"Nociplastic Pain is a term used to describe persistent pain that arises from altered nociception, despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors, or evidence for disease or lesion of the somatosensory system causing the pain."

Some facts about nociplastic pain:

  • It is an umbrella term. [5]
  • It can be defined as chronic pain leading towards an altered nociceptive function.
  • It results in increased sensitivity from the altered function of pain-related sensory pathways in the periphery and central nervous system (CNS). [6] [7]
  • It consists of multifactorial processes from different inputs, which could be either a bottom-up response to a peripheral nociceptive, a neuropathic stimulus (known as central sensitisation), or a top-down CNS-driven response. [6]
  • It is not a diagnosis but a descriptor of the pain experienced. [5][8]
  • It encompasses pain from stereotypical terms such as dysfunctional pain or medically unexplained somatic syndromes. [6]
  • Conditions that fall under the umbrella of Nociplastic Pain include fibromyalgia, complex regional pain syndrome, other musculoskeletal pain such as chronic low back pain, and visceral pain disorders such as irritable bowel syndrome and bladder pain syndrome. [5]

Referred Pain[edit | edit source]

  • Referred pain is pain perceived at a location other than the site of the painful stimulus.
  • It usually originates in one of the visceral organs but is felt in the skin or sometimes in another area deep inside the body.
  • Its mechanism is likely due to the fact that pain signals from the viscera travel along the same neural pathways used by pain signals from the skin.
  • The result is the perception of pain originating in the skin rather than in a deep-seated visceral organ or neural structure.
  • Visceral nociceptors project into the spinal cord via small diameter myelinated and unmyelinated fibres from the autonomic nervous system. They go on to synapse close to the point of embryonic origin in the spine.
  • When an organ develops pain, it can therefore be perceived as being at a different point in the body, on the surface, rather than in the organ itself.[9]
Tumblr lb03ir2vgL1qzr2i2o1 500.png
Mechanism[edit | edit source]

[10]

Hyperalgesia[edit | edit source]

  • Hyperalgesia is defined as "An increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves".[11]
  • It is divided into two types; primary and secondary.
  1. Primary hyperalgesia - pain and sensitivity in the damaged tissues.
  2. Secondary hyperalgesia - pain and sensitivity that occurs in area around the damaged tissues.
  • Substance P appears to have a significant role in the sensitization of nociceptors, which may explain the heightened feeling of pain in injured tissue (primary hyperalgesia). Although, this does not account for the perception of non-painful stimuli as painful.
  • Secondary hyperalgesia is most likely accounted for by changes in the dorsal horn which affect the processing of sensory information. [9]
  • Normally silent nociceptors are likely recruited, and sprouting of large diameter sensory afferent occurs projecting into the dorsal horn laminae.
Primary and Secondary hyperalgesia Comparison

Allodynia[edit | edit source]

  • Central pain sensitization (increased response of neurons) following painful, often repetitive, stimulation.
Allodynia.gif
  • Allodynia can lead to the triggering of a pain response from stimuli which do not normally provoke pain.[12]
    Types of allodynia:
  • Mechanical allodynia (also known as tactile allodynia)
  • Static mechanical allodynia – pain in response to light touch/pressure[13]
  • Dynamic mechanical allodynia – pain in response to stroking lightly[14]
  • Thermal (hot or cold) allodynia – pain from normally mild skin temperatures in the affected area
  • Movement allodynia - pain triggered by normal movement of joints or muscles.

Pain Behaviours[edit | edit source]

Inflammatory Pain[edit | edit source]

One of the cardinal features of inflammatory states is that normally innocuous stimuli produce pain.[15]

Please follow the link to this article for an overview of Inflammatory pain

Further Watching[edit | edit source]

Below is a 45 minutes video on Pain Mechanisms

[16]

References[edit | edit source]

  1. ↑ Visser EJ, Davies S. What is pain? II: Pain expression and behaviour, evolutionary concepts, models and philosophies. Australasian Anaesthesia. 2009(2009):35. Available from:https://www.notredame.edu.au/__data/assets/pdf_file/0013/3046/What-is-pain-part-II-philosophy-behaviours-ANZCA-Blue-Book.pdf (last accessed 20.5.2020)
  2. ↑ Güleç, G., & Güleç, S. (2006). Pain and pain behavior. Agri: Agri (Algoloji) Dernegi’nin Yayin organidir [Agri: The journal of the Turkish Society of Algology], 18(4), 5–9. https://pubmed.ncbi.nlm.nih.gov/17457708/
  3. ↑ Painhealth Pain Types https://painhealth.csse.uwa.edu.au/pain-module/pain-types/ (last accessed 20.5.2020)
  4. ↑ Fillingim R.B. Individual Differences in Pain: Understanding the Mosaic that Makes Pain Personal. Pain. 2017:158(1):1-18.
  5. ↑ 5.0 5.1 5.2 International Association for the Study of Pain - What's in a Name for Chronic Pain? “Nociplastic pain” was officially adopted by IASP as the third mechanistic descriptor of chronic pain. Available from: https://www.iasp-pain.org/publications/pain-research-forum/prf-news/92059-whats-name-chronic-pain/ (accessed 11 August 2023).
  6. ↑ 6.0 6.1 6.2 Fitzcharles M-A, Cohen S.P, Clauw D.J, Littlejohn G, Usui C, Häuser W. Nociplastic pain: towards an understanding of prevalent pain conditions. The Lancet. 2021:397:2098–2110.
  7. ↑ Chimenti R.L, Frey-Law L.A, Sluka K.A. A Mechanism-Based Approach to Physical Therapist Management of Pain. Journal of the American Physical Therapy Association. 2018:98(5):302–314.
  8. ↑ Slater H, Hush J. Pain Terminology: Introduction Of a Third Clinical Descriptor. Pain Terminology. 2018:3:7-8.
  9. ↑ 9.0 9.1 Roger, Barker, Barasi, Neal. Neuroscience at a glance.1999 Blackwell science.
  10. ↑ UChicago Online. Visceral Pain. Available from: https://www.youtube.com/watch?v=w_uSsFeA_lc [last accessed 1/8/2021]
  11. ↑ Hart BL. Biological basis of the behavior of sick animals. Neuroscience & Biobehavioral Reviews. 1988 Jun 1;12(2):123-37.
  12. ↑ Merskey & Bogduk (Eds.) Classification of Chronic Pain. Seattle: IASP Task Force on Taxonomy, 1994
  13. ↑ Attal N, Brasseur L, Chauvin M, Bouhassira D. Effects of single and repeated applications of a eutectic mixture of local anaesthetics (EMLA®) cream on spontaneous and evoked pain in post-herpetic neuralgia. Pain. 1999 May 1;81(1-2):203-9.
  14. ↑ LoPinto C, Young WB, Ashkenazi A. Comparison of dynamic (brush) and static (pressure) mechanical allodynia in migraine. Cephalalgia. 2006 Jul;26(7):852-6.
  15. ↑ Kidd BL, Urban LA. Mechanisms of inflammatory pain. British journal of anaesthesia. 2001 Jul 1;87(1):3-11.
  16. ↑ Tony Dickenson. Update on Pain Mechanisms. Available from: https://vimeo.com/88634321 [last accessed 1/8/2021]
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