Hyperalgesia: Versiyalar orasidagi farq

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„Hyperalgesia“ sahifasi tarjima qilib yaratildi
(Farq yoʻq)

28-Iyun 2022, 15:03 dagi koʻrinishi

Hyperalgesia ( /ˌhaɪpərælˈdʒiːziə/ yoki /-siə/ ; ‘giper’ yunoncha ὑπρr (huper, “o‘ta”)“, va "-algesia” yunoncha (algos, og'riq)) — bu nosiseptorlar yoki periferik nervlarning shikastlanishi natijasida yuzaga kelishi mumkin bo'lgan, biror bir qo'zg'atuvchiga yuqori sezuvchanlikni keltirib chiqarishi mumkin bo'lgan og'riqqa nisbatan g'ayritabiiy darajada yuqori sezuvchanlik hissidir. E va F prostaglandinlari asosan nosiseptorlar sezgirligi uchun javobgardir[1]. Og'riqqa nisbatan vaqtincha sezuvchanlikning oshishi kasallikning bir qismi sifatida paydo bo'ladi[2].

Turlari

Hyperalgesia fokal, diskret joylarda butun tanada yoki uning ko'proq qismida paydo bo'lishi mumkin. O'tkazuvchanlik (kondensatorlik) tadqiqotlari shuni ko'rsatdiki, oxirgi, diffuz shakldagi o'rganilgan hyperalgesiani boshdan kechirish mumkin.

Fokal shakl odatda shikastlanish bilan bog'liq va ikkita kichik tur mavjud:

  • Birlamchi hyperalgesia to'g'ridan-to'g'ri shikastlangan to'qimalarda paydo bo'ladigan og'riq sezuvchanlikni tavsiflaydi.
  • Ikkilamchi hyperalgesia esa atrofdagi shikastlanmagan to'qimalarda paydo bo'ladigan og'riq sezuvchanlikni tavsiflaydi.

Surunkali og'riqni davolashda opioidlarni uzoq muddatli qo'llash natijasida opioid tufayli kelib chiqqan hyperalgesia rivojlanishi mumkin[3]. Odamlar va hayvonlarda o'tkazilgan turli xil tadqiqotlar shuni ko'rsatdiki, birlamchi yoki ikkilamchi hyperalgesia opioidlarning surunkali va o'tkir ta'siriga javoban rivojlanishi mumkin. Ushbu nojo'ya ta'sir opioid bilan davolashni to'xtatishni talab qiladigan darajada jiddiy bo'lishi mumkin.

Sabablar

Giperalgeziya yallig'lanish yoki allergik reaktsiyada yuzaga keladigan trombotsitlarni faollashtiruvchi omil (PAF) tomonidan qo'zg'atiladi. Bu periferik asab tizimi bilan o'zaro ta'sir qiluvchi va og'riqni keltirib chiqaradigan kimyoviy moddalarni ( sitokinlar va kimokinlar) chiqaradigan immun hujayralari orqali sodir bo'ladi[4].

Fokal hyperalgesia g'ayrioddiy sabablaridan biri platypus zaharidir[5].

Uzoq muddatli opioid (masalan, geroin, morfin) foydalanuvchilari va surunkali og'riqni davolash uchun yuqori dozali opioid dori-darmonlarni qabul qilganlar hyperalgesiani hamda jismoniy ma'lumotlarga mutanosib ravishda og'riqni boshdan kechirishi mumkin. Bu ularning vaqt o'tishi bilan dorilar samaradorligini yo'qotishining keng tarqalgan sababidir[3][6][7] .Tolerantlikdan farqlash qiyin bo'lishi mumkinligi sababli, opioid tomonidan qo'zg'atilgan hyperalgesia ko'pincha opioid dozasini oshirish orqali davolanadi va og'riqqa sezgirlikni yanada oshirish orqali muammoni potentsial ravishda yomonlashtiradi. Opioid retseptorlarining surunkali giperstimulyatsiyasi tanadagi og'riq signalizatsiya yo'llarining gomeostazini bir necha ta'sir mexanizmlari orqali o'zgartiradi. Asosiy yo'llardan biri nositseptin retseptorini stimulyatsiya qilish[8][9][10] va bu retseptorni blokirovka qilish, shu asnoda, hyperalgesia rivojlanishining oldini olish vositasi bo'lishi mumkin[11].

Yallig'lanishdan kelib chiqqan holda, nosiseptiv tolalarni stimulyatsiya qilish orqa miyada kuchaytirish shakliga, uzoq muddatli kuchayishiga olib keladi[12]. Bu og'riq tolalari og'riq yo'liga, "periaqueduktal kulrang" sinaps qilingan joyda sodir bo'ladi. Orqa miyada sinaps holatini kuchaytirish hyperlgesiani keltirib chiqarishning yana bir usuli bo'lishi mumkin.

Lipopolisakkaridlar, endotoksinlar va infektsiyaning boshqa signallari tomonidan qo'zg'atilgan faollashtirilgan leykotsitlar tomonidan interleykin-1 kabi yallig'lanishga qarshi sitokinlarning chiqarilishi, shuningdek, kasallik xulq-atvorining bir qismi sifatida og'riq sezuvchanligini oshiradi[2][13][14].

Tashxis

Oddiy yotoqxona sinovlari paxta tayoqchasiga javob (og'riq intensivligi va xarakteri), barmoq bosimi, pinprick, sovuq va iliq ogohlantirishlarni, masalan, 20 ° C va 40 ° C haroratda metall termo roliklarni, shuningdek, anormallik maydonini xaritalashni o'z ichiga oladi.

Og'riq chegaralarini (og'riq chegarasining pasayishi allodiniyani ko'rsatadi) va ogohlantiruvchi / javob funksiyalarini (og'riq reaksiyasining kuchayishi giperaljeziyani ko'rsatadi) aniqlash uchun miqdoriy hissiy testdan foydalanish mumkin. Dinamik va mexanik allodiniya paxtadan tayyorlangan sumka yoki cho'tka yordamida baholanishi mumkin. Bosim algometri va standartlashtirilgan monofilamentlar yoki og'irlikdagi stimulyatorlar bosim va punktat allodiniya va hyperalgesiani baholash uchun va termal sinov uchun tester sifatida ishlatilinadi[15][16].

Davolash

Hyperalgesia nervlarning tirnalish xususiyati yoki shikastlanishi bilan bog'liq bo'lgan boshqa og'riqlarga o'xshab ketadi. Misol uchun: allodiniya va neyropatik og'riqlar. Ushbu kasallikka davo sifatida SSRI yoki trisiklik[17][18] yoki, steroid bo'lmagan antidepressantlar, yallig'lanishga qarshi dorilar (NSAID)[19], glyukokortikoidlar[20], gabapentin[21] yoki pregabalin[22], NMDA antagonistlari[23][24][25] yoki tramadol singari atipik opioidlar yordamida kasallikka yechim topish mumkin[26]. Agar opioidlarning surunkali yuqori dozalari tufayli hyperalgesia yuzaga kelgan bo'lsa, dozani kamaytirish og'riqni boshqarishni yaxshilashga olib kelishi mumkin[27]. Biroq, asab disfunksiyasi bilan bog'liq og'riqning boshqa shakllarida bo'lgani kabi, hyperalgesia davolash klinik jihatdan qiyin bo'lishi mumkin va ma'lum bir bemor uchun samarali bo'lgan mos dori yoki dorilar kombinatsiyasini topish sinov va xatoliklarni talab qilishi mumkin. Transkutan elektr nervlarni qo'zg'atuvchi vositadan foydalanish hyperalgesiani yengillashtirishi ko'rsatilgan[28][29].

Shuningdek qarang

  • Allodynia

Manbalar

  1. ↑ „Clinical Pharmacology“. www.clinicalpharmacology-ip.com. Qaraldi: 2017-yil 25-iyun.
  2. ↑ 2,0 2,1 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.  Manba xatosi: Invalid <ref> tag; name "Hart" defined multiple times with different content
  3. ↑ 3,0 3,1 "Opioid-induced hyperalgesia in humans: molecular mechanisms and clinical considerations". Clin J Pain 24 (6): 479–96. 2008. doi:10.1097/AJP.0b013e31816b2f43. PMID 18574358.  Manba xatosi: Invalid <ref> tag; name "Chu" defined multiple times with different content
  4. ↑ "Role of the immune system in chronic pain". Nat. Rev. Neurosci. 6 (7): 521–32. July 2005. doi:10.1038/nrn1700. PMID 15995723. 
  5. ↑ "Venom from the platypus, Ornithorhynchus anatinus, induces a calcium-dependent current in cultured dorsal root ganglion cells". J. Neurophysiol. 85 (3): 1340–45. March 2001. doi:10.1152/jn.2001.85.3.1340. PMID 11248005. https://semanticscholar.org/paper/02b43e593b132210bf7642fbe7e2af95dc634f53. 
  6. ↑ "Mechanisms of opioid-induced tolerance and hyperalgesia". Pain Manag Nurs 8 (3): 113–21. September 2007. doi:10.1016/j.pmn.2007.02.004. PMID 17723928. 
  7. ↑ Mitra S (2018). "Opioid-induced hyperalgesia: pathophysiology and clinical implications". J Opioid Manag 4 (3): 123–30. doi:10.5055/jom.2008.0017. PMID 18717507. 
  8. ↑ "The opioid peptide nociceptin/orphanin FQ mediates prostaglandin E2-induced allodynia, tactile pain associated with nerve injury". Eur. J. Neurosci. 23 (4): 995–1004. February 2006. doi:10.1111/j.1460-9568.2006.04623.x. PMID 16519664. 
  9. ↑ "Regulation of proinflammatory cytokines gene expression by nociceptin/orphanin FQ in the spinal cord and the cultured astrocytes". Neuroscience 144 (1): 275–85. January 2007. doi:10.1016/j.neuroscience.2006.09.016. PMID 17069983. 
  10. ↑ "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. May 2007. doi:10.1002/jnr.21272. PMID 17387690. https://dukespace.lib.duke.edu/dspace/bitstream/10161/13662/1/Chen_et_al-2007-Journal_of_Neuroscience_Research.pdf. 
  11. ↑ "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): 223–28. March 2005. doi:10.1016/j.ejphar.2005.01.033. PMID 15763246. 
  12. ↑ "Synaptic amplifier of inflammatory pain in the spinal dorsal horn". Science 312 (5780): 1659–62. June 2006. doi:10.1126/science.1127233. PMID 16778058. https://semanticscholar.org/paper/647289f4d21940e6db340c88d923a62674361817. 
  13. ↑ "Cytokine-induced sickness behavior". Brain Behav. 17 (Suppl 1): S112–18. February 2003. doi:10.1016/S0889-1591(02)00077-6. PMID 12615196. 
  14. ↑ "Interleukin-1 mediates the behavioral hyperalgesia produced by lithium chloride and endotoxin". Brain Res. 623 (2): 321–24. October 1993. doi:10.1016/0006-8993(93)91446-Y. PMID 8221116. 
  15. ↑ "NeuPSIG guidelines on neuropathic pain assessment". Pain 152 (1): 14–27. Jan 2001. doi:10.1016/j.pain.2010.07.031. PMID 20851519. 
  16. ↑ "Allodynia and hyperalgesia in neuropathic pain: clinical manifestations and mechanisms.". Lancet Neurol 13 (9): 924–35. Sep 2014. doi:10.1016/S1474-4422(14)70102-4. PMID 25142459. 
  17. ↑ "Antidepressants in the treatment of neuropathic pain". Basic Clinical Pharmacology Toxicology 96 (6): 399–409. June 2005. doi:10.1111/j.1742-7843.2005.pto_96696601.x. PMID 15910402. 
  18. ↑ "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. July 2008. doi:10.1038/sj.npp.1301590. PMID 17957217. 
  19. ↑ "The cyclooxygenase isozyme inhibitors parecoxib and paracetamol reduce central hyperalgesia in humans". Pain 108 (1–2): 148–53. March 2004. doi:10.1016/j.pain.2003.12.017. PMID 15109518. 
  20. ↑ "Methylprednisolone and Ketorolac rapidly reduce hyperalgesia around a skin burn injury and increase pressure pain thresholds". Acta Anaesthesiol Scand 51 (9): 1138–46. October 2007. doi:10.1111/j.1399-6576.2007.01415.x. PMID 17714578. 
  21. ↑ "Chronic oral Gabapentin reduces elements of central sensitization in human experimental Hyperalgesia.". Anesthesiology 101 (6): 1400–08. December 2004. doi:10.1097/00000542-200412000-00021. PMID 15564948. 
  22. ↑ "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. February 2007. doi:10.1093/bja/ael344. PMID 17251214. 
  23. ↑ "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. August 1997. doi:10.1016/S0304-3959(97)00006-7. PMID 9272793. 
  24. ↑ "The clinical role of NMDA receptor antagonists for the treatment of postoperative pain". Best Pract Res Clin Anaesthesiol 21 (1): 85–98. March 2007. doi:10.1016/j.bpa.2006.12.006. PMID 17489221. 
  25. ↑ "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. January 2008. doi:10.1016/j.ejpain.2007.02.002. PMID 17449306. 
  26. ↑ "Tramadol has a better potency ratio relative to morphine in neuropathic than in nociceptive pain models". Drugs in R&D 8 (1): 51–57. 2007. doi:10.2165/00126839-200708010-00005. PMID 17249849. 
  27. ↑ "Improved opioid analgesic effect following opioid dose reduction.". Pain Med 9 (6): 724–27. September 2008. doi:10.1111/j.1526-4637.2008.00501.x. PMID 18816332. 
  28. ↑ 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): 492–99. doi:10.1007/s11926-008-0080-z. PMID 19007541. PMC 2746624. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2746624. 
  29. ↑ Sluka, KA; Chandran, P (November 2002). "Enhanced reduction in hyperalgesia by combined administration of clonidine and TENS.". Pain 100 (1–2): 183–90. doi:10.1016/s0304-3959(02)00294-4. PMID 12435471.  
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