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→‎Causes: Opiod-induced hyperalegsia is relatively uncommon in long-term oxycodone use, it is much more common with morphine so I have amended the examples to reflect this
→‎Treatment: Refs, original seems to be referencing the second
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==Treatment==
==Treatment==
{{Wiktionary}}
{{Wiktionary}}
Hyperalgesia 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,<ref>{{cite journal |author=Sindrup SH, Otto M, Finnerup NB, Jensen TS |title=Antidepressants in the treatment of neuropathic pain |journal=Basic Clin. Pharmacol. Toxicol. |volume=96 |issue=6 |pages=399–409 |date=June 2005 |pmid=15910402 |doi=10.1111/j.1742-7843.2005.pto_96696601.x |url=http://www3.interscience.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=1742-7835&date=2005&volume=96&issue=6&spage=399}}</ref><ref>{{cite journal |author=Matsuzawa-Yanagida K, Narita M, Nakajima M, ''et al.'' |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}}</ref> [[Non-steroidal anti-inflammatory drugs]],<ref>{{cite journal |author=Koppert W, Wehrfritz A, Körber N, ''et al.'' |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}}</ref> [[glucocorticoids]],<ref>{{cite journal |author=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}}</ref> [[gabapentin]]<ref>{{cite journal |author=Gottrup H, Juhl G, Kristensen AD, ''et al.'' |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}}</ref> or [[pregabalin]],<ref>{{cite journal |author=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}}</ref> [[NMDA antagonist]]s,<ref>{{cite journal |doi=10.1016/S0304-3959(97)00006-7 |author=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 }}</ref><ref>{{cite journal |doi=10.1016/j.bpa.2006.12.006 |author=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 }}</ref><ref>{{cite journal |author=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}}</ref> or atypical opioids such as [[tramadol]].<ref>{{cite journal |doi=10.2165/00126839-200708010-00005 |author=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 R D |volume=8 |issue=1 |pages=51–7 |year=2007 |pmid=17249849 }}</ref> Where hyperalgesia has been produced by chronic high doses of opioids, reducing the dose may result in improved pain management.<ref>{{cite journal |author=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}}</ref> 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.
Hyperalgesia 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,<ref>{{cite journal |author=Sindrup SH, Otto M, Finnerup NB, Jensen TS |title=Antidepressants in the treatment of neuropathic pain |journal=Basic Clin. Pharmacol. Toxicol. |volume=96 |issue=6 |pages=399–409 |date=June 2005 |pmid=15910402 |doi=10.1111/j.1742-7843.2005.pto_96696601.x |url=http://www3.interscience.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=1742-7835&date=2005&volume=96&issue=6&spage=399}}</ref><ref>{{cite journal |author=Matsuzawa-Yanagida K, Narita M, Nakajima M, ''et al.'' |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}}</ref> [[Non-steroidal anti-inflammatory drugs]],<ref>{{cite journal |author=Koppert W, Wehrfritz A, Körber N, ''et al.'' |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}}</ref> [[glucocorticoids]],<ref>{{cite journal |author=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}}</ref> [[gabapentin]]<ref>{{cite journal |author=Gottrup H, Juhl G, Kristensen AD, ''et al.'' |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}}</ref> or [[pregabalin]],<ref>{{cite journal |author=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}}</ref> [[NMDA antagonist]]s,<ref>{{cite journal |doi=10.1016/S0304-3959(97)00006-7 |author=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 }}</ref><ref>{{cite journal |doi=10.1016/j.bpa.2006.12.006 |author=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 }}</ref><ref>{{cite journal |author=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}}</ref> or atypical opioids such as [[tramadol]].<ref>{{cite journal |doi=10.2165/00126839-200708010-00005 |author=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 R D |volume=8 |issue=1 |pages=51–7 |year=2007 |pmid=17249849 }}</ref> Where hyperalgesia has been produced by chronic high doses of opioids, reducing the dose may result in improved pain management.<ref>{{cite journal |author=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}}</ref> 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.<ref>{{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|url=http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2746624/#R4|pmc=2746624}}</ref><ref>{{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}}</ref>
<http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2746624/#R4>


==See also==
==See also==

Revision as of 21:25, 19 April 2015

Template:Distinguish2

Hyperalgesia
SpecialtyNeurology Edit this on Wikidata

Hyperalgesia (/ˌhaɪpərælˈdʒiziə/ or /-siə/; 'hyper' from Greek ὑπέρ (huper, “over”), '-algesia' from Greek algos, ἄλγος (pain)) is an increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves. Temporary increased sensitivity to pain also occurs as part of sickness behavior, the evolved response to infection.[1]

Types

Hyperalgesia 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:
  • Primary hyperalgesia describes pain sensitivity that occurs directly in the damaged tissues.
  • Secondary hyperalgesia describes pain sensitivity that occurs in surrounding undamaged tissues.

Opioid-induced hyperalgesia may develop as a result of long-term opioid use in the treatment of chronic pain.[2] 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.

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).[3]

One unusual cause of focal hyperalgesia is platypus venom.[4]

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.[2][5][6] 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,[7][8][9] and blocking this receptor may therefore be a means of preventing the development of hyperalgesia.[10]

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.[11] 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.[1][12][13]

Treatment

Look up hyperalgesia in Wiktionary, the free dictionary.

Hyperalgesia 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,[14][15] Non-steroidal anti-inflammatory drugs,[16] glucocorticoids,[17] gabapentin[18] or pregabalin,[19] NMDA antagonists,[20][21][22] or atypical opioids such as tramadol.[23] Where hyperalgesia has been produced by chronic high doses of opioids, reducing the dose may result in improved pain management.[24] 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.[25][26]

See also

References

  1. ^ a b Hart BL (1988). "Biological basis of the behavior of sick animals". Neurosci Biobehav Rev. 12 (2): 123–37. doi:10.1016/S0149-7634(88)80004-6. PMID 3050629.
  2. ^ a b Chu LF, Angst MS, Clark D (2008). "Opioid-induced hyperalgesia in humans: molecular mechanisms and clinical considerations". Clin J Pain. 24 (6): 479–96. doi:10.1097/AJP.0b013e31816b2f43. PMID 18574358.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  3. ^ Marchand F, Perretti M, McMahon SB (July 2005). "Role of the immune system in chronic pain". Nat. Rev. Neurosci. 6 (7): 521–32. doi:10.1038/nrn1700. PMID 15995723.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  4. ^ de Plater GM, Milburn PJ, Martin RL (March 2001). "Venom from the platypus, Ornithorhynchus anatinus, induces a calcium-dependent current in cultured dorsal root ganglion cells". J. Neurophysiol. 85 (3): 1340–5. PMID 11248005.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  5. ^ DuPen A, Shen D, Ersek M (September 2007). "Mechanisms of opioid-induced tolerance and hyperalgesia". Pain Manag Nurs. 8 (3): 113–21. doi:10.1016/j.pmn.2007.02.004. PMID 17723928.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  6. ^ Mitra S (2008). "Opioid-induced hyperalgesia: pathophysiology and clinical implications". J Opioid Manag. 4 (3): 123–30. PMID 18717507.
  7. ^ 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. doi:10.1111/j.1460-9568.2006.04623.x. PMID 16519664. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  8. ^ Fu X, Zhu ZH, Wang YQ, Wu GC (January 2007). "Regulation of proinflammatory cytokines gene expression by nociceptin/orphanin FQ in the spinal cord and the cultured astrocytes". Neuroscience. 144 (1): 275–85. doi:10.1016/j.neuroscience.2006.09.016. PMID 17069983.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  9. ^ Chen Y, Sommer C (May 2007). "Activation of the nociceptin opioid system in rats. Sensory neurons produce antinociceptive effects in inflammatory pain: involvement of inflammatory mediators". J. Neurosci. Res. 85 (7): 1478–88. doi:10.1002/jnr.21272. PMID 17387690.
  10. ^ 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. doi:10.1016/j.ejphar.2005.01.033. PMID 15763246.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  11. ^ 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. doi:10.1126/science.1127233. PMID 16778058. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  12. ^ Kelley KW, Bluthé RM, Dantzer R; et al. (February 2003). "Cytokine-induced sickness behavior". Brain Behav. 17 (Suppl 1): S112–8. doi:10.1016/S0889-1591(02)00077-6. PMID 12615196. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  13. ^ 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. doi:10.1016/0006-8993(93)91446-Y. PMID 8221116.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  14. ^ Sindrup SH, Otto M, Finnerup NB, Jensen TS (June 2005). "Antidepressants in the treatment of neuropathic pain". Basic Clin. Pharmacol. Toxicol. 96 (6): 399–409. doi:10.1111/j.1742-7843.2005.pto_96696601.x. PMID 15910402.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  15. ^ Matsuzawa-Yanagida K, Narita M, Nakajima M; et al. (July 2008). "Usefulness of antidepressants for improving the neuropathic pain-like state and pain-induced anxiety through actions at different brain sites". Neuropsychopharmacology. 33 (8): 1952–65. doi:10.1038/sj.npp.1301590. PMID 17957217. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  16. ^ Koppert W, Wehrfritz A, Körber N; et al. (March 2004). "The cyclooxygenase isozyme inhibitors parecoxib and paracetamol reduce central hyperalgesia in humans". Pain. 108 (1–2): 148–53. doi:10.1016/j.pain.2003.12.017. PMID 15109518. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  17. ^ Stubhaug A, Romundstad L, Kaasa T, Breivik H (October 2007). "Methylprednisolone and Ketorolac rapidly reduce hyperalgesia around a skin burn injury and increase pressure pain thresholds". Acta Anaesthesiol Scand. 51 (9): 1138–46. doi:10.1111/j.1399-6576.2007.01415.x. PMID 17714578.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  18. ^ Gottrup H, Juhl G, Kristensen AD; et al. (December 2004). "Chronic oral Gabapentin reduces elements of central sensitization in human experimental Hyperalgesia". Anesthesiology. 101 (6): 1400–8. doi:10.1097/00000542-200412000-00021. PMID 15564948. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  19. ^ Chizh BA, Göhring M, Tröster A, Quartey GK, Schmelz M, Koppert W (February 2007). "Effects of oral pregabalin and aprepitant on pain and central sensitization in the electrical hyperalgesia model in human volunteers". Br J Anaesth. 98 (2): 246–54. doi:10.1093/bja/ael344. PMID 17251214.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  20. ^ Warncke T, Stubhaug A, Jørum E (August 1997). "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". Pain. 72 (1–2): 99–106. doi:10.1016/S0304-3959(97)00006-7. PMID 9272793.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  21. ^ De Kock MF, Lavand'homme PM (March 2007). "The clinical role of NMDA receptor antagonists for the treatment of postoperative pain". Best Pract Res Clin Anaesthesiol. 21 (1): 85–98. doi:10.1016/j.bpa.2006.12.006. PMID 17489221.
  22. ^ Klein T, Magerl W, Hanschmann A, Althaus M, Treede RD (January 2008). "Antihyperalgesic and analgesic properties of the N-methyl-D-aspartate (NMDA) receptor antagonist neramexane in a human surrogate model of neurogenic Hyperalgesia". Eur J Pain. 12 (1): 17–29. doi:10.1016/j.ejpain.2007.02.002. PMID 17449306.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  23. ^ Christoph T, Kögel B, Strassburger W, Schug SA (2007). "Tramadol has a better potency ratio relative to morphine in neuropathic than in nociceptive pain models". Drugs R D. 8 (1): 51–7. doi:10.2165/00126839-200708010-00005. PMID 17249849.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  24. ^ Vorobeychik Y, Chen L, Bush MC, Mao J (September 2008). "Improved opioid analgesic effect following opioid dose reduction". Pain Med. 9 (6): 724–7. doi:10.1111/j.1526-4637.2008.00501.x. PMID 18816332.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  25. ^ DeSantana, JM; Walsh, DM; Vance, C; Rakel, BA; Sluka, KA (December 2008). "Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain". Current rheumatology reports. 10 (6): 492–9. PMC 2746624. PMID 19007541.
  26. ^ Sluka, KA; Chandran, P (November 2002). "Enhanced reduction in hyperalgesia by combined administration of clonidine and TENS". Pain. 100 (1–2): 183–90. PMID 12435471.
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