Pain syndrome in paraneoplastic and chemotherapy-induced polyneuropathy: ways of optimizing pathogenetic therapy

Many modern authors pay increased attention to the diagnostics of pain syndrome in patients with cancer. The greatest interest herein is the development of pain in these patients, not as a result of mechanical compression of the nervous structures by the tumor, but due to its systemic, distant effect leading to the development of paraneoplastic polyneuropathy (PNP) or as a result of complications of antitumor therapy (drug-toxic PNP). The main mechanisms contributing to the persistence of neuropathic pain is a complex cascade of processes involving peripheral and central sensitization. The leading role in the development of central sensitization is attributed to the formation of a vicious circle in which the excitatory mechanisms prevail over the inhibitory descending mechanisms, and the decrease in inhibitory influences contributes to the development of spinal hyperexcitability. Recently, the key role of a26-subunits of potential-dependent calcium channels in maintaining central sensitization and reducing the effect of inhibitory descending pathways has also been studied in detail. Meanwhile, the proven neurotoxicity of chemotherapy and the evidence of the development of chemotherapy-induced PNP led to the publication of attempts to prescribe preventive analgesic therapy, using antioxidants, neurotrophic drugs, etc., which turned out, however, to be insufficiently effective. Despite compliance with the WHO algorithm, including the use of co-analgesics, therapy for neuropathic pain in patients with malignant tumors remains inadequate. This provides a basis for the search of new drugs that could improve the quality of life of cancer patients and enable them to receive life-saving antitumor therapy with fewer side effects. One of these drugs could be Pregabalin, which has an analgesic and anti-anxiety effect, well-established for the treatment of neuropathic pain caused by other conditions.

neuropathic pain syndrome, paraneoplastic polyneuropathy, chemotherapy-induced polyneuropathy, pregabalin

1. Абузарова Г. Р., Прохоров Б. М. и др. Новые возможности таргетной терапии нейропатической боли в онкологии. // Современная онкология. - 2008.- Том 1.- № 1.- С. 2-6.

2. Алексеева О. П., Михайлова З.Д. Паранеопластические синдромы в клинике внутренних болезней. // Н. Новгород.НГМА.- 2008.- С. 112.

3. Беляков К. М. Дисметаболические полиневропатии: клинико-электронейромиографические критерии диагностики, патогенез, новые методы восстановительной терапии. //Автореферат докторской диссертации. - 2009.

4. Вершинина С. Ф., Струков А. Н. Противоболевая терапия в онкологии. // Психофармакология и биологическая наркология.- 2007.- Том 7.- С. 1471-1477.

5. ВОЗ. Рак. // Информационный бюллетень.-2017.- № 297.

6. Данилов А. Б. Диагностика и терапия нейропатической боли. // Лечение заболеваний нервной системы.- 2007.- № 1 (16).- С. 34-40.

7. Каприн А. Д. и др. Состояние онкологической помощи населению России в 2016 г. //М.: МНИОИ им. П. А. Герцена - филиал ФГБУ «НМИРЦ» Минздрава России.- 2017. С. 5.

8. Королева Е. С., Гольдберг В. Е. и др. Роль онконевральных антител паранеопластической полиневропатии в ранней диагностике рака. // Сибирский онкологический журнал. - 2013.- № 1 (55).- С. 28-31.

9. Крыжановский Г. Н. // Введение в общую патофизиологию.-М.: РГМУ, 2000.- C. 71.

10. Кукушкин М. Л. Этиопатогенетические принципы лечения хронической боли. // Р1МЖ.- 2007.- № 10.- С. 827-833.

11. Меркулов Ю. А., Калашников А. А. и др. Болевая полиневропатия на ранних стадиях развития злокачественных новообразований. // Российский журнал боли.- 2014.- № 1 (42).- С. 82-83.

12. Семенова А. И. Кардио- и нейротоксичность противоопухолевых препаратов (патогенез, клиника, профилактика, лечение). // Практическая онкология. - 2009.- Т. 10.- № 3 (6). С. 168-176.

13. Asbury A. K., Arnason B. G., Adams R. D. The inflammatory lesion in idiopathic polyneuritis. // Medicine.- 1969.-V. 48.- P. 173-215.

14. Baron R., Mechanisms of disease: neuropathic pain- a clinical perspective. // Nature Clinical Practice Neurology.-2006.-№ 2.-P. 95-106.

15. Bee L.A, Dickenson A. H. Neuropathic pain: multiple mechanisms at multiple sites. // Future Neurol.-2007.- № 6.- P. 661-671.

16. Bemeett M. I., Raymet C., Hjermstad M., et al. Prevalence and aetiology of neuropathic pain in cancer patients: a systematic review. // Pain.- 2012.- № 153.- P. 359-365.

17. Blumental D. T. Assessment of neuropathic pain in cancer patients. // Current pain & Headache reports.- 2009.- № 13.- P. 282-287.

18. Boehmerle W., Huenchen P., et al. Electrophysiological, behavioral and histological characterization of paclitaxel, cisplatin, vincristine and bortezomib-induced neuropathy in C57Bl/6 mice. // Sci-rep.- 2014. - 4.- P. 6370.

19. Camdessanche J-Ph., Antoine J-Ch., et al. Paraneoplastic peripheral neuropathy associated with anti-Hu antibodies. A clinical and electophysiological study of 20 patients. // Brain.-2002.- 125.- P. 166-175.

20. Caraceni A., Zecca E., et al. Gabapentin for neuropathic cancer pain; a randomized controlled trial from the Gabapentine. Cancer pain study group. // Journal of clinical oncology.- 2014.- V 22.- № 4.- P. 2909-2917.

21. Dropcho E. J. Remote neurologic manifestation of cancer. // Neurol. Clin. - 2002.- № 20 (1).- P. 85-122.

22. Fanous I., Dillon P. Paraneoplastic neurological complications of breast cancer. // Exp. Hematol. Oncol.-2016. - № 5 (29).-P. 2-13.

23. Giometto B., Grisold W., et al. Paraneoplastic neurologic syndrome in the PNS Euronetwork Database. A European study from 20 centers. // Arch. Neurol. - 2010.- № 67 (3).- P. 330-335.

24. Honnorat J. Antoine J-Ch., Paraneoplastic neurologic syndromes. // Orphanet Journal of rare diseases.- 2007.- № 2.- 22.- P. 1-8.

25. Mendell L. M. Computational functions of neurons and circuits signaling injury: Relantionship to pain behavior. // PNAS.- V.- 108.-sup. 3.- P. 15596-1601.

26. Ozdogan M., Samur M., et al. Venlafaxine for treatment of chemotherapy-induced neuropathic pain. // Turkish Journal of cancer pain. - 2004.- № 34 (3).- P. 110-113.

27. Paice J.A., B. Ferrell. The Management of Cancer Pain. // CA Cancer J Clin. - 2011.- № 61.- P. 157-182.

28. Perret D., Luo 1. D. Targeting voltage-gated calcium channels for neuropathic pain management. // Neurotherepeuthics.- 2009.- № 6 (4).- P. 679-692.

29. Ping Peng, Shu Xia. Pregabalin attenuates docetaxel-induced neuropathy in rats. // Journal of Huazhohg University of Science and Technology. - 2012.- V 32.- № 4.- P. 586-590.

30. Ripamonti C. I., Santini P., et al. Management of cancer pain: ESMO clinical practice guidelines. // Annals oncology.- 2012.- № 23 (7).- P. 139-154.

31. Sasu-Tenkorama J., Fudin J. Neuropathy in the Cancer Patient: Causes and Cures. // Practical Pain management.- 2013.- P. 1-14.

32. Serentny M., Currie G. L. et al. Incidence, prevalence, and predictor of chemotherapy-induced peripheral neuropathy. A systematic reviewant meta-analysis. // Pain.- 2014.- № 155.- P. 2461-2470.

33. Slatkin N. Cancer-related pain and its pharmacologic management in the patient with Bone metastasis. / / J Support Oncol.-2006.- № 4 (2).-sup. 1.- P. 15-21.

34. Shricant Atreya. Pregabalin in chemotherapy induced neuropathic pain. // Indian J Palliat Care.- 2016.- V. 22.- № 1.- P. 101-103.

35. Smith E. M. L. Pang H., et al. Effect of Duloxetine on pain: function, and quality-of-life among patients with chemotherapy-induced painful peripheral neuropathy: A randomized clinical trial. // JAMA.- 2013.- V. 309.- № 13.- P. 1359-1367.

36. Van den Beuken-van Everdingen MH, et al. Prevalence of pain in patients with cancer. A systematic review of the past40 years. // Ann. Oncol. - 2007.- 18 (9).- P. 1437-1449.

37. Vranken J. Y. Mechanisms and treatment of neuropathic pain. // Central nervous system agents in medicinal chemistry.- 2009.- № 9.- P. 71-78.

38. Wolf Sh., Barton D., et al. Chemotherapy-induced peripheral neuropathy: Prevention and treatment strategies. // European journal of cancer.-2008.- № 44.- P. 1507-1515.