| 词条 | Hyperalgesia |
| 释义 |
| name = Hyperalgesia | synonyms = | image = | caption = | pronounce = | field = | symptoms = | complications = | onset = | duration = | types = | causes = | risks = | diagnosis = | differential = | prevention = | treatment = | medication = | prognosis = | frequency = | deaths = }} Hyperalgesia ({{IPAc-en|ˌ|h|aɪ|p|ər|æ|l|ˈ|dʒ|iː|z|i|ə}} or {{IPAc-en|-|s|i|ə}}; 'hyper' from Greek ὑπέρ (huper, “over”), '-algesia' from Greek algos, ἄλγος (pain)) is an abnormally increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves and can cause hypersensitivity to stimulus. Prostaglandins E and F are largely responsible for sensitizing the nociceptors.[1] Temporary increased sensitivity to pain also occurs as part of sickness behavior, the evolved response to infection.[2]TypesHyperalgesia can be experienced in focal, discrete areas, or as a more diffuse, body-wide form. Conditioning studies have established that it is possible to experience a learned hyperalgesia of the latter, diffuse form. The focal form is typically associated with injury, and is divided into two subtypes:
Opioid-induced hyperalgesia may develop as a result of long-term opioid use in the treatment of chronic pain.[3] Various studies of humans and animals have demonstrated that primary or secondary hyperalgesia can develop in response to both chronic and acute exposure to opioids. This side effect can be severe enough to warrant discontinuation of opioid treatment. CausesHyperalgesia 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).[4] One unusual cause of focal hyperalgesia is platypus venom.[5] 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.[3][6][7] 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,[8][9][10] and blocking this receptor may therefore be a means of preventing the development of hyperalgesia.[11] 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.[12] 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.[2][13][14] Diagnosis{{Empty section|date=March 2019}}TreatmentHyperalgesia is similar to other sorts of pain associated with nerve irritation or damage such as allodynia and neuropathic pain, and consequently may respond to standard treatment for these conditions, using various drugs such as SSRI or tricyclic antidepressants,[15][16] Nonsteroidal anti-inflammatory drugs (NSAIDs),[17] glucocorticoids,[18] gabapentin[19] or pregabalin,[20] NMDA antagonists,[21][22][23] or atypical opioids such as tramadol.[24] Where hyperalgesia has been produced by chronic high doses of opioids, reducing the dose may result in improved pain management.[25] However, as with other forms of nerve dysfunction associated pain, treatment of hyperalgesia can be clinically challenging, and finding a suitable drug or drug combination that is effective for a particular patient may require trial and error. The use of a transcutaneous electrical nerve stimulation device has been shown to alleviate hyperalgesia.[26][27] See also
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Neurosci. |volume=23 |issue=4 |pages=995–1004 |date=February 2006 |pmid=16519664 |doi=10.1111/j.1460-9568.2006.04623.x }} 9. ^{{cite journal |vauthors=Fu X, Zhu ZH, Wang YQ, Wu GC |title=Regulation of proinflammatory cytokines gene expression by nociceptin/orphanin FQ in the spinal cord and the cultured astrocytes |journal=Neuroscience |volume=144 |issue=1 |pages=275–85 |date=January 2007 |pmid=17069983 |doi=10.1016/j.neuroscience.2006.09.016 |url=http://linkinghub.elsevier.com/retrieve/pii/S0306-4522(06)01236-X}} 10. ^{{cite journal |vauthors=Chen Y, Sommer C |title=Activation of the nociceptin opioid system in rats. Sensory neurons produce antinociceptive effects in inflammatory pain: involvement of inflammatory mediators |journal=J. Neurosci. 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Pharmacol. Toxicol. |volume=96 |issue=6 |pages=399–409 |date=June 2005 |pmid=15910402 |doi=10.1111/j.1742-7843.2005.pto_96696601.x }} 16. ^{{cite journal |vauthors=Matsuzawa-Yanagida K, Narita M, Nakajima M, etal |title=Usefulness of antidepressants for improving the neuropathic pain-like state and pain-induced anxiety through actions at different brain sites |journal=Neuropsychopharmacology |volume=33 |issue=8 |pages=1952–65 |date=July 2008 |pmid=17957217 |doi=10.1038/sj.npp.1301590}} 17. ^{{cite journal |vauthors=Koppert W, Wehrfritz A, Körber N, etal |title=The cyclooxygenase isozyme inhibitors parecoxib and paracetamol reduce central hyperalgesia in humans |journal=Pain |volume=108 |issue=1–2 |pages=148–53 |date=March 2004 |pmid=15109518 |doi=10.1016/j.pain.2003.12.017 |url=http://linkinghub.elsevier.com/retrieve/pii/S0304395903004998}} 18. ^{{cite journal |vauthors=Stubhaug A, Romundstad L, Kaasa T, Breivik H |title=Methylprednisolone and Ketorolac rapidly reduce hyperalgesia around a skin burn injury and increase pressure pain thresholds |journal=Acta Anaesthesiol Scand |volume=51 |issue=9 |pages=1138–46 |date=October 2007 |pmid=17714578 |doi=10.1111/j.1399-6576.2007.01415.x}} 19. ^{{cite journal |vauthors=Gottrup H, Juhl G, Kristensen AD, etal |title=Chronic oral Gabapentin reduces elements of central sensitization in human experimental Hyperalgesia.|journal=Anesthesiology |volume=101 |issue=6 |pages=1400–8 |date=December 2004 |pmid=15564948 |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0003-3022&volume=101&issue=6&spage=1400 |doi=10.1097/00000542-200412000-00021}} 20. ^{{cite journal |vauthors=Chizh BA, Göhring M, Tröster A, Quartey GK, Schmelz M, Koppert W |title=Effects of oral pregabalin and aprepitant on pain and central sensitization in the electrical hyperalgesia model in human volunteers |journal=Br J Anaesth |volume=98 |issue=2 |pages=246–54 |date=February 2007 |pmid=17251214 |doi=10.1093/bja/ael344 |url=http://bja.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=17251214}} 21. ^{{cite journal |doi=10.1016/S0304-3959(97)00006-7 |vauthors=Warncke T, Stubhaug A, Jørum E |title=Ketamine, an NMDA receptor antagonist, suppresses spatial and temporal properties of burn-induced secondary Hyperalgesia in man: a double-blind, cross-over comparison with morphine and placebo.|journal=Pain |volume=72 |issue=1–2 |pages=99–106 |date=August 1997 |pmid=9272793 }} 22. ^{{cite journal |doi=10.1016/j.bpa.2006.12.006 |vauthors=De Kock MF, Lavand'homme PM |title=The clinical role of NMDA receptor antagonists for the treatment of postoperative pain |journal=Best Pract Res Clin Anaesthesiol |volume=21 |issue=1 |pages=85–98 |date=March 2007 |pmid=17489221 }} 23. ^{{cite journal |vauthors=Klein T, Magerl W, Hanschmann A, Althaus M, Treede RD |title=Antihyperalgesic and analgesic properties of the N-methyl-D-aspartate (NMDA) receptor antagonist neramexane in a human surrogate model of neurogenic Hyperalgesia. |journal=Eur J Pain |volume=12 |issue=1 |pages=17–29 |date=January 2008 |pmid=17449306 |doi=10.1016/j.ejpain.2007.02.002 |url=http://linkinghub.elsevier.com/retrieve/pii/S1090-3801(07)00029-8}} 24. ^{{cite journal |doi=10.2165/00126839-200708010-00005 |vauthors=Christoph T, Kögel B, Strassburger W, Schug SA |title=Tramadol has a better potency ratio relative to morphine in neuropathic than in nociceptive pain models |journal=Drugs in R&D |volume=8 |issue=1 |pages=51–7 |year=2007 |pmid=17249849 }} 25. ^{{cite journal |vauthors=Vorobeychik Y, Chen L, Bush MC, Mao J |title=Improved opioid analgesic effect following opioid dose reduction. |journal=Pain Med |volume=9 |issue=6 |pages=724–7 |date=September 2008 |pmid=18816332 |doi=10.1111/j.1526-4637.2008.00501.x |url=http://www3.interscience.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=1526-2375&date=2008&volume=9&issue=6&spage=724|archive-url=https://archive.today/20130105054105/http://www3.interscience.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=1526-2375&date=2008&volume=9&issue=6&spage=724|dead-url=yes|archive-date=2013-01-05}} 26. ^{{cite journal|last1=DeSantana|first1=JM|last2=Walsh|first2=DM|last3=Vance|first3=C|last4=Rakel|first4=BA|last5=Sluka|first5=KA|title=Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain.|journal=Current Rheumatology Reports|date=December 2008|volume=10|issue=6|pages=492–9|pmid=19007541|pmc=2746624|doi=10.1007/s11926-008-0080-z}} 27. ^{{cite journal|last1=Sluka|first1=KA|last2=Chandran|first2=P|title=Enhanced reduction in hyperalgesia by combined administration of clonidine and TENS.|journal=Pain|date=November 2002|volume=100|issue=1–2|pages=183–90|pmid=12435471|doi=10.1016/s0304-3959(02)00294-4}} External links{{Medical resources| DiseasesDB = 30788 | ICD10 = | ICD9 = {{ICD9|782.0}} | ICDO = | OMIM = | MedlinePlus = | eMedicineSubj = | eMedicineTopic = | MeshID = D006930 }}{{Pain}}{{Skin and subcutaneous tissue symptoms and signs}} 2 : Pain|Symptoms and signs: Skin and subcutaneous tissue |
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