Pain pathophysiology: Difference between revisions
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#[[Visceral]] pain originates from body's viscera, or organs. Visceral nociceptors are located within body organs and internal cavities. The even greater scarcity of nociceptors in these areas produces pain that is usually more aching or cramping and of a longer duration than somatic pain. Visceral pain may be well-localized, but often it is extremely difficult to localize, and several injuries to visceral tissue exhibit "referred" pain, where the sensation is localized to an area completely unrelated to the site of injury. | #[[Visceral]] pain originates from body's viscera, or organs. Visceral nociceptors are located within body organs and internal cavities. The even greater scarcity of nociceptors in these areas produces pain that is usually more aching or cramping and of a longer duration than somatic pain. Visceral pain may be well-localized, but often it is extremely difficult to localize, and several injuries to visceral tissue exhibit "referred" pain, where the sensation is localized to an area completely unrelated to the site of injury. | ||
Nociception is the unconscious afferent activity produced in the peripheral and central nervous system by stimuli that have the potential to damage tissue. It should not be confused with pain, which is a conscious experience. | Nociception is the unconscious afferent activity produced in the peripheral and central nervous system by stimuli that have the potential to damage tissue. It should not be confused with pain, which is a conscious experience.It is initiated by [[nociceptors]]that can detect mechanical, thermal or chemical changes above a certain threshold. All nociceptors are free nerve endings of fast-conducting myelinated [[A delta fiber]]s or slow-conducting unmyelinated [[C fibers]], respectively responsible for fast, localized, sharp pain and slow, poorly-localized, dull pain. Once stimulated, they transmit signals that travel along the spinal cord and within the brain. Nociception, even in the absence of pain, may trigger withdrawal reflexes and a variety of autonomic responses such as [[pallor]], [[diaphoresis]],[[bradycardia]], [[hypotension]], [[lightheadedness]], [[nausea]] and [[fainting]].<ref>[http://www.ejbjs.org/cgi/reprint/36/5/981.pdfFeinstein B, J Langton, R Jameson, F Schiller. Experiments on pain referred from deep somatic tissues. J Bone Joint Surg 1954;36-A(5):981-97].</ref> | ||
Brain areas that are particularly studied in relation with pain include the [[somatosensory cortex]] which mostly accounts for the sensory discriminative dimension of pain, and the [[limbic system]], of which the [[thalamus]] and the [[anterior cingulate cortex]] are said to be especially involved in the affective dimension. | Brain areas that are particularly studied in relation with pain include the [[somatosensory cortex]] which mostly accounts for the sensory discriminative dimension of pain, and the [[limbic system]], of which the [[thalamus]] and the [[anterior cingulate cortex]] are said to be especially involved in the affective dimension. | ||
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The [[gate control theory of pain]] describes how the perception of pain is not a direct result of activation of nociceptors, but instead is modulated by interaction between different neurons, both pain-transmitting and non-pain-transmitting. In other words, the theory asserts that activation, at the spine level or even by higher cognitive brain processes, of nerves or neurons that do not transmit pain signals can interfere with signals from pain fibers and inhibit or modulate an individual's experience of pain. | The [[gate control theory of pain]] describes how the perception of pain is not a direct result of activation of nociceptors, but instead is modulated by interaction between different neurons, both pain-transmitting and non-pain-transmitting. In other words, the theory asserts that activation, at the spine level or even by higher cognitive brain processes, of nerves or neurons that do not transmit pain signals can interfere with signals from pain fibers and inhibit or modulate an individual's experience of pain. | ||
Pain may be experienced differently depending on [[genotype]]; as an example individuals with red hair may be more susceptible to pain caused by heat,<ref>{{cite journal |author=Liem EB, Joiner TV, Tsueda K, Sessler DI |title=Increased sensitivity to thermal pain and reduced subcutaneous lidocaine efficacy in redheads |journal=Anesthesiology |volume=102 |issue=3 |pages=509–14 |year=2005 |pmid=15731586 |doi=}}</ref>but redheads with a non-functional [[melanocortin 1 receptor|melanocortin 1 receptor (MC1R)]] gene are less sensitive to pain from electric shock.<ref>{{cite journal |author=Mogil JS, Ritchie J, Smith SB, ''et al'' |title=Melanocortin-1 receptor gene variants affect pain and mu-opioid analgesia in mice and humans |journal=J. Med. Genet. |volume=42 |issue=7 |pages=583–7 |year=2005 |pmid=15994880|doi=10.1136/jmg.2004.027698}}</ref> Gene [[Nav1.7]] has been identified as a major factor in the development of the pain-perception systems within the body. A rare genetic mutation in this area causes non-functional development of certain [[sodium channel]]s in the nervous system, which prevents the brain from receiving messages of physical damage, resulting in [[congenital insensitivity to pain]].<ref name="pmid17145499">{{cite journal |author=Fertleman CR, Baker MD, Parker KA, ''et al'' |title=SCN9A mutations in paroxysmal extreme pain disorder: allelic variants underlie distinct channel defects and phenotypes |journal=Neuron |volume=52 |issue=5 |pages=767–74 |year=2006|pmid=17145499 |doi=10.1016/j.neuron.2006.10.006}}</ref> The same gene also appears to mediate a form of pain hyper-sensitivity, while other mutations may be the root of [[paroxysmal extreme pain disorder]].<ref name="pmid17145499">{{cite journal |author=Fertleman CR, Baker MD, Parker KA, ''et al'' |title=SCN9A mutations in paroxysmal extreme pain disorder: allelic variants underlie distinct channel defects and phenotypes |journal=Neuron |volume=52 |issue=5 |pages=767–74 |year=2006 |pmid=17145499 |doi=10.1016/j.neuron.2006.10.006}}</ref><ref>{{cite news | url = http://www.nature.com/news/2006/061211/full/061211-11.html | title = The mutation that takes away pain | publisher = [[Nature (journal)|Nature]] News | doi = 10.1038/news061211-11 | date = 2006-12-13 | accessdate = 2008-03-29 | last = Hopkin | first = M }}</ref> | Pain may be experienced differently depending on [[genotype]]; as an example individuals with red hair may be more susceptible to pain caused by heat,<ref>{{cite journal |author=Liem EB, Joiner TV, Tsueda K, Sessler DI |title=Increased sensitivity to thermal pain and reduced subcutaneous lidocaine efficacy in redheads |journal=Anesthesiology |volume=102 |issue=3 |pages=509–14 |year=2005 |pmid=15731586 |doi=}}</ref>but redheads with a non-functional [[melanocortin 1 receptor|melanocortin 1 receptor (MC1R)]] gene are less sensitive to pain from electric shock.<ref>{{cite journal |author=Mogil JS, Ritchie J, Smith SB, ''et al'' |title=Melanocortin-1 receptor gene variants affect pain and mu-opioid analgesia in mice and humans |journal=J. Med. Genet. |volume=42 |issue=7 |pages=583–7 |year=2005 |pmid=15994880|doi=10.1136/jmg.2004.027698}}</ref> Gene [[Nav1.7]] has been identified as a major factor in the development of the pain-perception systems within the body. A rare genetic mutation in this area causes non-functional development of certain [[sodium channel]]s in the nervous system, which prevents the brain from receiving messages of physical damage, resulting in [[congenital insensitivity to pain]].<ref name="pmid17145499">{{cite journal |author=Fertleman CR, Baker MD, Parker KA, ''et al'' |title=SCN9A mutations in paroxysmal extreme pain disorder: allelic variants underlie distinct channel defects and phenotypes |journal=Neuron |volume=52 |issue=5 |pages=767–74 |year=2006|pmid=17145499 |doi=10.1016/j.neuron.2006.10.006}}</ref> The same gene also appears to mediate a form of pain hyper-sensitivity, while other mutations may be the root of [[paroxysmal extreme pain disorder]].<ref name="pmid17145499">{{cite journal |author=Fertleman CR, Baker MD, Parker KA, ''et al'' |title=SCN9A mutations in paroxysmal extreme pain disorder: allelic variants underlie distinct channel defects and phenotypes |journal=Neuron |volume=52 |issue=5 |pages=767–74 |year=2006 |pmid=17145499 |doi=10.1016/j.neuron.2006.10.006}}</ref><ref>{{cite news | url = http://www.nature.com/news/2006/061211/full/061211-11.html | title = The mutation that takes away pain | publisher = [[Nature (journal)|Nature]] News | doi = 10.1038/news061211-11 | date = 2006-12-13 | accessdate = 2008-03-29 | last = Hopkin | first = M }}</ref> | ||
==References== | ==References== | ||
Revision as of 05:44, 30 June 2012
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Pain pathophysiology On the Web |
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American Roentgen Ray Society Images of Pain pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Stimulation of a nociceptor, due to a chemical, thermal, or mechanical event that has the potential to damage body tissue, may cause nociceptive pain.
Mechanism
Damage to the nervous system itself, due to disease or trauma, may cause neuropathic (or neurogenic) pain.[1] Neuropathic pain may refer to peripheral neuropathic pain, which is caused by damage to nerves, or to central neuropathic pain, which is caused by damage to the brain, brainstem, or spinal cord.
Nociceptive pain and neuropathic pain are the two main kinds of pain when the primary mechanism of production is considered. A third kind may be mentioned: see below psychogenic pain.
Nociceptive pain may be classified further in three types that have distinct organic origins and felt qualities.[2]
- Superficial somatic pain (or cutaneous pain) is caused by injury to the skin or superficial tissues. Cutaneous nociceptors terminate just below the skin, and due to the high concentration of nerve endings, produce a sharp, well-defined, localized pain of short duration. Examples of injuries that produce cutaneous pain include minor wounds, and minor (first degree) burns.
- Deep somatic pain originates from ligaments, tendons, bones, blood vessels, fasciae, and muscles. It is detected with somatic nociceptors. The scarcity of pain receptors in these areas produces a dull, aching, poorly-localized pain of longer duration than cutaneous pain; examples include sprains, broken bones, and myofascial pain.
- Visceral pain originates from body's viscera, or organs. Visceral nociceptors are located within body organs and internal cavities. The even greater scarcity of nociceptors in these areas produces pain that is usually more aching or cramping and of a longer duration than somatic pain. Visceral pain may be well-localized, but often it is extremely difficult to localize, and several injuries to visceral tissue exhibit "referred" pain, where the sensation is localized to an area completely unrelated to the site of injury.
Nociception is the unconscious afferent activity produced in the peripheral and central nervous system by stimuli that have the potential to damage tissue. It should not be confused with pain, which is a conscious experience.It is initiated by nociceptorsthat can detect mechanical, thermal or chemical changes above a certain threshold. All nociceptors are free nerve endings of fast-conducting myelinated A delta fibers or slow-conducting unmyelinated C fibers, respectively responsible for fast, localized, sharp pain and slow, poorly-localized, dull pain. Once stimulated, they transmit signals that travel along the spinal cord and within the brain. Nociception, even in the absence of pain, may trigger withdrawal reflexes and a variety of autonomic responses such as pallor, diaphoresis,bradycardia, hypotension, lightheadedness, nausea and fainting.[3]
Brain areas that are particularly studied in relation with pain include the somatosensory cortex which mostly accounts for the sensory discriminative dimension of pain, and the limbic system, of which the thalamus and the anterior cingulate cortex are said to be especially involved in the affective dimension.
The gate control theory of pain describes how the perception of pain is not a direct result of activation of nociceptors, but instead is modulated by interaction between different neurons, both pain-transmitting and non-pain-transmitting. In other words, the theory asserts that activation, at the spine level or even by higher cognitive brain processes, of nerves or neurons that do not transmit pain signals can interfere with signals from pain fibers and inhibit or modulate an individual's experience of pain.
Pain may be experienced differently depending on genotype; as an example individuals with red hair may be more susceptible to pain caused by heat,[4]but redheads with a non-functional melanocortin 1 receptor (MC1R) gene are less sensitive to pain from electric shock.[5] Gene Nav1.7 has been identified as a major factor in the development of the pain-perception systems within the body. A rare genetic mutation in this area causes non-functional development of certain sodium channels in the nervous system, which prevents the brain from receiving messages of physical damage, resulting in congenital insensitivity to pain.[6] The same gene also appears to mediate a form of pain hyper-sensitivity, while other mutations may be the root of paroxysmal extreme pain disorder.[6][7]
References
- ↑ Compare definitions atIASP Pain Terminology: "Neurophathic pain —– Pain initiated or caused by a primary lesion or dysfunction in the nervous system." and "Neurogenic pain — Pain initiated or caused by a primary lesion, dysfunction, or transitory perturbation in the peripheral or central nervous system."
- ↑ Pain Physiology
- ↑ B, J Langton, R Jameson, F Schiller. Experiments on pain referred from deep somatic tissues. J Bone Joint Surg 1954;36-A(5):981-97.
- ↑ Liem EB, Joiner TV, Tsueda K, Sessler DI (2005). "Increased sensitivity to thermal pain and reduced subcutaneous lidocaine efficacy in redheads". Anesthesiology. 102 (3): 509–14. PMID 15731586.
- ↑ Mogil JS, Ritchie J, Smith SB; et al. (2005). "Melanocortin-1 receptor gene variants affect pain and mu-opioid analgesia in mice and humans". J. Med. Genet. 42 (7): 583–7. doi:10.1136/jmg.2004.027698. PMID 15994880.
- ↑ 6.0 6.1 Fertleman CR, Baker MD, Parker KA; et al. (2006). "SCN9A mutations in paroxysmal extreme pain disorder: allelic variants underlie distinct channel defects and phenotypes". Neuron. 52 (5): 767–74. doi:10.1016/j.neuron.2006.10.006. PMID 17145499.
- ↑ Hopkin, M (2006-12-13). "The mutation that takes away pain". Nature News. doi:10.1038/news061211-11. Retrieved 2008-03-29.