Chemotherapy-induced peripheral neuropathy (CIPN) is a toxic neuropathy, a syndrome consisting of highly distressing symptoms of various degrees of severity. It includes numbness of distal extremities, long-term touch, heat, and cold dysaesthesia and, in more severe cases, motor impairment affecting daily functioning. Each form of the syndrome may be accompanied by symptoms of neuropathic stinging, burning, and tingling pain. In the case of most chemotherapeutic agents, the incidence and severity of CIPN are dependent on the cumulative dose of the drug. The syndrome described is caused by damage to the axons and/or cells of the peripheral nervous system.Chemotherapeutic agents have distinct mechanisms of action in both neoplastic tissue and the peripheral nervous system; therefore, CIPN should not be regarded as a homogeneous disease entity. The present article is an attempt to systematize the knowledge about the toxic effects of chemotherapy on the peripheral nervous system.

The incidence of chemotherapy-induced peripheral neuropathy (CIPN) in the population of cancer patients is estimated at 3–7% in cytostatic monotherapy and as high as 38% in the case of polytherapy. While testing drugs that may reduce the damage to the peripheral nervous system, particular attention should be paid to their protective action against the severe and painful complication in the patient. Another aspect, perhaps a more important one, is the confidence that application of preventive drugs will not exert a significant impact on progression of the neoplastic disease or the effectiveness of the causal treatment.Many drugs have been tested for prevention of CIPN; however, none of them have thus far been irrefutably proven to possess preventive properties. No guidelines on chemotherapy-induced peripheral neuropathy preventive action have been established, either. This article is an attempt to present reports from the available literature about the possibilities of prevention of CIPN.

Częstość występowania obwodowej neuropatii wywołanej chemioterapią (chemotherapy-induced peripheral neuropathy -CIPN) w populacji pacjentów "onkologicznych" ocenia się na 3-7% w przypadku leczenia jednym cytostatykiem, a przy politerapii może ona sięgać nawet 38%. Badając leki, które miałyby wpłynąć na zmniejszenie uszkodzenia obwodowego układu nerwowego, należy zwrócić przede wszystkim uwagę na ich działanie zabezpieczające pacjenta przed wystąpie-niem uciążliwego i bolesnego powikłania. Drugim, być może nawet ważniejszym, aspektem jest zyskanie pewności, że stosowane w profilaktyce leki nie wpłyną w istotny sposób na rozwój choroby nowotworowej ani na skuteczność leczenia przyczynowego. Wiele leków zostało zbadanych pod kątem skuteczności w zapobieganiu CIPN, jednak dotąd nie wykazano niezbicie działania któregokolwiek z nich. Nie opracowano również wytycznych postępowania zapobiegawczego podczas chemioterapii. Niniejszy artykuł jest próbą przedstawienia doniesień z dostępnego piśmiennictwa dotyczą-cych możliwości profilaktyki CIPN. S Sł ło ow wa a k kl lu uc cz zo ow we e: : obwodowa neuropatia wywołana chemioterapią, ból neuropatyczny, efekty uboczne, patofizjologia. Dolegliwości bólowe odczuwane przez pacjentów w trakcie choroby nowotworowej najczęściej mają charakter mieszany, gdyż zespołom bólowym o charakterze nocyceptywnym i trzewnym towarzyszy komponent neuropatyczny, będący skutkiem uszkodzenia obwodowego układu nerwowego. Ból neuropatyczny jest wyjątkowo trudnym do leczenia zespołem, dlatego warunkiem osiągnięcia zmniejszenia dolegliwości jest m.in. trafna diagnoza i wdrożenie właściwego leczenia [1][2][3].Często przyczyną dolegliwości jest uszkodzenie nerwu jako struktury anatomicznej przez ucisk z zewnątrz (rozrost guza, materiał kostny przy złama-niach patologicznych, w rzadkich przypadkach przerzuty do nerwów). Z punktu widzenia neuropatologii w takim przypadku sekwencja zdarzeń jest dwuetapowa. W pierwszym etapie występuje ból neurogenny (spowodowany uciskiem nerwów), a następstwem przedłużającego się ucisku jest uszkodzenie włókien nerwowych i powstanie bólu neuropatycznego.Inną postacią bólu neuropatycznego jest obwodowa neuropatia wywołana chemioterapią (chemotherapy-induced peripheral neuropathy -CIPN). W tym przypadku dochodzi do uszkodzenia samego aksonu w wyniku działania cytostatyków, dlatego zespół ten zaliczany jest do neuropatii toksycznych [4].Częstość występowania CIPN w populacji pacjentów "onkologicznych" ocenia się na 1-12% [5], chociaż doniesienia ostatnich lat pozwalają przypuszczać, że mamy do czynienia z narastaniem tego zjawiska [6]. Nieco inne wnioski co do zachorowalności można wysnuć z pracy Cavalettiego i Zanny [7], którzy uważają, że w przypadku leczenia jednym cytostatykiem wynosi ona 3-7%, przy politerapii może zaś sięgać nawet 38%.Nie można mówić o CIPN jako o jednorodnym zespole chorobowym, choć -by z tego względu, że istnieje wiele grup cytostatyków, z których każda charakteryzuje się innym sposobem uszkodzenia obwodowego układu nerwowego. Jedynymi czynnikami wspól...

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

No abstract

The combination of long-acting opioids has not been sufficiently documented in the literature. Patient J.L., aged 67, with disseminated malignant process. Complaints of pelvic and visceral pain. Treatment: sustained release morphine 60 mg/daily. There occurred a need to increase the dose of the drug up to 120 mg/daily; the patient was referred to the Pain Management Outpatient Department. Nociceptive pain was diagnosed at the intensity of 7.5 on the VAS scale. Ketoprofen was included in the treatment at a dose of 200 mg/daily. After three days the morphine dose was increased to 180 mg/daily. Due to the lack of adequate pain control sustained release oxycodone was started, initially at a dose of 20 mg/ daily, and after three days 40 mg/daily. After two weeks, the dose of morphine was decreased to 140 mg/daily. Adequate pain control was obtained.K Ke ey y w wo or rd ds s: : opioid, morphine, oxycodone, opioid combination, pain management. Efficient management of pain in the course of cancer diseases often encounters serious difficulties [1,2]. A very frequent problem is, e.g. concomitant occurrence of many types of pain in the same patient. The course of the disease is often complicated by persistent post-surgical pain, pain related to bone metastases, neurogenic pain, or various types of neuropathic pain due to the infiltration of nerves, post-herpetic neuralgia, or chemotherapy-induced peripheral neuropathy. Unfortunately, very frequently there also occurs a lack of effectiveness of opioids, or a rapid increase in tolerance to the therapy applied.The principles of pain management, coded in the form of the WHO analgesic ladder, on assumption, introduce the principle of combining various drugs in order to increase their effectiveness, due to the use of combining and synergistic mechanisms [3]. Multimodal therapy in the form of opioids, non-steroid antiinflammatory drugs (NSAIDs) and co-analgesics, in the majority of cases allows efficient analgesia to be achieved, without the necessity for increasing the dosage of drugs, and often allows reduction of the amount of drugs applied.Simultaneous application of NSAIDs, opioids and co-analgesics, therefore, is the rule [4]; however, the administration of several drugs of the opioids group still evokes controversy. To date, few reports are available concerning the implementation of such a method of treatment [5]; therefore, it cannot be considered that there is scientific evidence which would justify such models of therapy [6]. At present, one can only rely on the opinion of experts that considering the variation in opioid receptors and varied susceptibility to exogenous ligands used, it is permissible to combine opioid drugs [5,6]. Case reportPatient J.L., aged 67, with endometrial cancer detected at the terminal stage. The patient was in a relatively good condition, in full possession of her faculties, running a household together with her daughter, totally independent. The complaints had started three months earlier, with intensifying pain in the pelvic bone radiating ...

Phantom pain (PhP)is reported by patients after limb amputation due to trauma or chronic diseases. We report the case of successful PhP treatment with pulsed radiofrequency (PRF) of the femoral and sciatic nerve. (PRF) reduced the intensity of pain for one year, improving the quality of life of the patient.

The aim of the study was to verify the effectiveness of two methods of introducing standard CIPN-treatment drugs into the therapy. Materials and Methods:Group A included patients attending weekly appointments, while group B monthly. Standard treatment with amitriptyline, gabapentin (GAB), and oxycodone (OXY) was administered. In group A, the drugs were gradually introduced, while in group B -within one week. After a month and six months of treatment, the therapy effectiveness was assessed by examination of pain intensity (VAS), symptoms of peripheral neuropathy (sNCI-CTC), occurrence of tactile and brush allodynia, and the daily dose of GAB and OXY.Results: Pain intensity during the study decreased from 5.59 to 2.9 and 2.76 in group A, and from 5.07 to 2.52 and 2.81 in group B. The sNCI-CTC values declined too and were, respectively. 1.9; 1.48; 1.34 in group A and 1.93; 1.52; 1.44 in group B. Tactile allodynia occurred in 15; 5; 5 group A patients and 18; 6; 5 group B patients. Brush allodynia decreased in group A (9; 5; 5) and B (11; 6; 5). The daily GAB dose was 0; 951.72; 927.41 in group A and 900.0; 900.0; 1000.0 in group B. The daily OXY dose was 0; 21.72; 22.07 in group A and 20.0; 20.0; 27.04 in group B; a statistically significant difference was found in the final stage.The results do not allow recommendation of non-schematic treatment and they should be regarded as a preliminary study. Randomized trials are indispensable for assessment of advantages and drawbacks such treatment.