Background It is now known that OA pain is a complex interaction between many different pain mechanisms. A subset of adults with chronic, symptomatic knee OA may therefore, have neuropathic mechanisms contributing to their pain experience. Objectives We evaluate pathogenetic mechanisms involved in the initiation of pain in OA, to measure the prevalence of neuropathic pain and NP(neuropathic) symptoms among adults with this condition and additionally to detect somatosensory deficit Methods Patients were 39 women aged from 45-65 years with chronic knee pain (the duration of painat least during the last 3 months) and OA severity II-III grade by Kellgren-Lawrence. Two main types of pain: nociceptive and neuropathic pain were revealed with the help of clinical (rheumatologic and neurological) examinations and neuropathic pain scales (Paindetect and DN4). The patients were asked about duration of knee symptoms and knee OA, knee OA severity (WOMAC), and pain intensity. We used the prevalence of anxiety and depressive disorders in population with OA, examined the interrelationships between severity of pain and emotional disturbances by Hospital Anxiety and Depression scale. The level of knee destruction was assessed with radiography using the Kellgren-Lawrence grading scale and US examination and rheumatologic examination. Results Patients were categorized into two groups according to the results of neuropathic questionnaire DN4: patients with DN4 score>4, having a neuropathic pain(NP) features and patients with DN4 score<4, who had no evident neuropathic pain. According to DN4 score patients, who used NP descriptors composed 28%(n=11). No significant differences between groups were seen in age, the character of pain, duration of knee OA, quantity of impacted knee joints, body index, quality of life, radiographic and US severity of knee OA. But the presence of NP features was correlated with higher pain intensity assessed, WOMAC and significantly correlated with higher level of anxiety. In clinical studies, compared to controls, patients with NP features had more diffuse hyperalgesia to mechanical stimuli, no other somatosensory defects were found. Conclusions The results indicated that people with chronic OA can experience pain due to both nociceptive and neuropathic mechanisms to varying degrees, so OA can be associated with a mixture of pain mechanisms. The likely neuropathic mechanism in OA is central sensitization, that may be the reason for the often observed discreapancy between joint damage (radiological joint changes) and clinical pain intensity. So treatment should also target central nervous system structures. Disclosure of Interest None Declared
Combination therapy using pregabalin in KOA patients having the signs of NP is more effective than monotherapy with nonsteroidal anti-inflammatory drugs (aceclofenac).
Background Chronic pain is the most typical clinical presentation of rheumatoid arthritis (RA) and osteoarthritis (OA). Suggest that the pain in RA and OA has mixed nature and includes nociceptive, neuropathic and psychogenic components (1,2). Objectives To study neuropathic pain (NP) in patients with RA and OA. Methods We recruited 183 patients with RA (male:female ratio 1:10) aged 18-60 years (average age 46±11.8) and 80 female patients with knee osteoarthritis (kOA) aged 45-65 years (average age 59±5) admitted to the Institute of Rheumatology. RA mean duration 9.03±7.6 years and mean duration of kOA was 9±6.5 years. Patients with chronic knee pain had OA Kellgren-Lawrence severity grade II-III. All patients underwent rheumatological and neurological examination. Patients were divided into two groups: patients with DN4 score>4 (with NP) and DN4 score<4 (no evident NP). Results 78 (43%) patients with active RA and 24 (30%) patients with kOA presented with NP. In the kOA group the presence of NP features was correlated with higher pain intensity, WOMAC index and significantly correlated with higher level of anxiety. Patients with NP had more diffuse hyperalgesia to mechanical stimuli compared to controls, no other somatosensory defects were found. Patients with NP and RA were older (50.1±9.4 vs. 44.4±12.8 years), had longer disease duration (10.7±8.2 years vs. 7.9±7.1 years) with a higher clinical stage (stage 3-4 92%, stage 2-3 68%) and R-stages (stage 3-4 73%, stage 2-3 84%) (p<0.05). We found no significant differences between the two groups in RA activity (DAS28 score) or quality of life. Neurologic findings in patients were characterized by the presence of polyneuropathy (distal senso-motor) - 62%, tunnel neuropathy - 9%, multiple mononeuropathy - 21%, cervical myelopathy – 3%, and their combinations - 3%. Conclusions This study has demonstrated the mixed nature of chronic pain, neuropathic pain detected in 43% patients with RA and 30% with OA. Identification of neuropathic mechanisms of pain has important practical implications and opens new therapeutic perspectives for comprehensive treatment of the painful syndrome in RA and kOA. References Rheumatology, 2 edition. Edited by Academician E.L. Nosonov, Moscow. 2010; 90-231. Schaible HG, Ebersberger A, Von Banchet GS. Mechanisms of pain in arthritis. Ann N Y Acad Sci 2002:966:343-354. Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.2954
BackgroundModern methods of treatment of osteoarthritis have mainly anti-inflammatory action. A few studies show the effectiveness of centrally acting drugs for chronic pain inosteoartritis (OA) of the knee.ObjectivesTo study the efficacy of Pregabalin in treatment of chronic pain in patients with knee OA.MethodsThe study involved 60 female patients with knee OA having neuropathic pain component (NPC; DN4 >4). Mean age 59.82±4.46 y (min 49, max 65 years). All patients were randomly divided into two groups to be treated with 2 therapeutic regimens: aceclofenac +pregabalin (Group I) or aceclofenac (Group II) for 5 weeks (3 visits). All patients were subjected to clinical and neurological examination, total WOMAC score assessment, verification of neuropathic pain (NP) (questionnaire DN4 and Pain DETECT), and VAS pain intensity assessment at rest.ResultsThe therapy was successful in both groups with respect to WOMAC score [figure 1] (Group I – 1385,30±365,83 vs 1034,70±402,37 vs 886,64±456,31; Group II – 1206,04±358,72 vs 1016,45±428,52 vs 976,55±408,02 respectively, p=0.01). Significant reduction of pain intensity at rest was documented in both groups [figure 2]. Group I 61,60±14.91 vs 45,34±16,14 vs 36,24±18,09; Group II 56,07±22,58 vs 44.86±18.68 and vs of 41.96±of 24.04, p=0.01, respectively). Therapeutic regimens in both groups had positive impact on NPC based on DN4 questionnaire and Pain DETECT scores. However, a combination of a NSAID with anticonvulsants agent (pregabalin) resulted in a more pronounced effect. Changes in DN4 values in Group I (visit1/visit3) were: 5.97±1,24/2,97±1,83 p=0.001; and in Pain DETECT values – 17,93±3,87/9,34±6,18, p=0.001; while in Group II DN4 scores were 5,35±0,93/3,79±2,29, p=0.001; and Pain DETECT – 15,03±5,26/12,24±6,29 p=0.02. [figures 3–4]ConclusionsComplex therapy with the use of Pregabalin in patients with OA of the knee, with signs of NPC, allows not only effectively reduce pain intensity and improve functional activity of patients and, consequently, the quality of life.Disclosure of InterestNone declared
BackgroundHistorically pain in OA considered to be nociceptive one. But recent studies has shown that in some cases mechanisms of chronic pain in knee osteoarthritis (OA) are likely to be complex. For characterizing knee pain 28-34% patients can use neuropathic descriptors such as burning, tingling, numbness. These sensor phenomena are caused by specific changes in the posterior horn – central sensitization and forms dysfunctional pain. This type of pain accompanies with dysfunction of biochemical process in CNS and does not characterize with organic changes of CNS. Dysfunctional pain is also typically characterized with hyperalgesia and pronounced affective disorders.ObjectivesTo reveal key features of dysfunctional pain in pt with knee OA and demonstrate its correlation with clinical picture and intensity of chronic pain.Methods89 women (middle age 58±5,4), II-III grade by Kellgren-Lawrence with chronic knee OA were neurologically tested. No neurological deficit was found. Examination of sensitive sphere revealed primary hyperalgesia (in the damaged knee) and also referred hyperalgesia in the intact region (shank and even hip). According to sensitive changes the pts were divided into two groups: pts with primary hyperalgesia and pts with referred hyperalgesia. In our trial we assed clinical rheumatological picture, X-ray and US of the knee. NP pain scales (Paindetect and DN4) were used. Duration of knee symptoms, knee OA severity (WOMAC) and pain intensity were taken into consideration. We used the prevalence of anxiety and depressive disorders in population with OA, examined the interrelationships between severity of pain and emotional disturbances by Hospital Anxiety and Depression scale.ResultsNeurologic examination revealed referred hyperalgesia not only knee localization but also hip and shank localization in 41,5%, (n=37) had and in 58,5% (n=52). No somatosensory defects were found. There was no association with age, body index, duration of knee OA, quality of life and level of structural changes. The presence of referred hyperalgesia accompanied with high levels of neuropathic pain scales, correlated with higher pain intensity (VAS), poor WOMAC and significantly associated with higher level of depression. The presence of referred hyperalgasia accompaned with more often observed neuropathic discriptors: numbness 60,5% vs 39,5%, current rush 51,9% vs 48,1% and tingling 55% vs 45%.ConclusionsChronic OA is a complex of mechanisms and includes nociceptive and dysfunctional pain. Dysfunctional pain in OA can be visualized clinically by the prevalence of referred pain, that was revealed in 41,5%. The degree of spreading sensitization is correlated with the level of clinical pain and does not correlate with structural changes. Additionally as screening test can be used neuropathic scales (DN4, PainDETECT), that include the most typical neuropathic transcriptorsDisclosure of InterestNone declared
Background In recent studies was shown that chronic pain in knee osteoarthritis (OA) has multicomponent mechanism. Besides degenerative changes of the knee, neuroplastic changes of CNS play a leading role in sustaining pain in chronic status. Objectives To evaluate the role of CNS in pathogenesis of chronic pain syndrome in knee osteoarthritis (OA). Methods 62 women (middle age 59±5) OA with chronic knee pain (duration more than 3 months)passed through WOMAC, X-ray and US of the knee. Duration of knee symptoms, and pain intensity were taken into consideration. Neurological examination with detailed analysis of pain sensitivity, as well as qualitative analysis of neuropathic transcripts with the help of neuropathic pain scales (Paindetect and DN4) were performed. We used the prevalence of anxiety and depressive disorders in population with OA, examined the interrelationships between severity of pain and emotional disturbances by Hospital Anxiety and Depression scale. Results According to the results of DN4 32% (n=20) pt with OA had DN4 score≥4 - neuropatic components of pain compared with 68% (n=42) who had only nociceptive mechanism of pain. Neurologic examination revealed 56%, (n=35) with referred hyperalgesia (not only knee localization (primary hyperalgesia) but also hip and shank localization) and 44%, (n=27) had primary hyperalgesia. No other somatosensory defects were found. The presence of referred hyperalgesia correlated with higher pain intensity (VAS), poor WOMAC and significantly associated with higher level of depression, poor quality of life.No significant differences between groups were seen in age, body index, duration of knee OA and level of structural changes. Conclusions Chronic OA is a mixture of pain mechanisms: nociceptive and dysfunctional pain. The presence of signs of NP and referred hyperalgesia, that spreads beyond impacted joint, may be qualified as clinical features of central sensitization.The degree of spreading sensitization is correlated with the level of clinical pain and does not correlate with structural changes. The central sensitization of pain neurons of spinal chord take place in sustaining chronic pain and demonstrates the important role of these dysfunctional changes of CNS of chronic pain mechanisms in knee osteoarthritis (OA). So rational treatment should also target structures of central nervous system. Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.3801
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