Presence Of Neuropathic Pain Component Research Articles

AB0135 A VERY EARLY CLINICAL RESPONSE TO TOFACITINIB IS ASSOCIATED WITH LOW RHEUMATOID ARTHRITIS ACTIVITY AFTER 3 AND 6 MONTHS

Background:JAK inhibitors block intracellular signaling pathways responsible for the synthesis of cytokines and mediators involved in the development of chronic pain and central sensitization (CS). This determines a very rapid clinical response to JAK inhibitors. However, it is not clear how the significant pain reduction in the first weeks of therapy is associated with the achievement of low rheumatoid arthritis (RA) activity.Objectives:to assess the relationship between the early clinical response to tofacitinib and the decrease in RA activity after 3 and 6 months.Methods:Study group included 88 patients with RA, their age was 53±11,5, 79.3% of women, 89.8% of RF “+”, DAS28 5.2±1.2, receiving DMARDs (methotrexate 59.5% and leflunomide 19.8%), who were administered with tofacitinib 5 mg 2 times a day due to inefficacy or intolerance of biological DMARDs. There were assessed the pain severity using Brief pain inventory (BPI) questionnaire, the presence of neuropathic pain component (NPC) using PainDETECT questionnaire and signs of CS using Central Sensitisation Inventory (CSI) questionnaire at early time after tofacitinib administration, RA activity using DAS28 after 3 and 6 months.Results:The mean pain severity at baseline was 5.3±2.0 according to the visual analogue scale (VAS 0-10), 51.1% of patients had signs of central sensitization (CSI ≥ 40), 15.9% had NPC (PainDETECT ≥18). 7 days after tofacitinib intake there was statistically reliable reduction of pain severity – up to 4.1±1.8 (р<0.05) and CS – CSI from 40.4±13.5 to 36.5±12.5 (р=0.01). After 28 days, the effect was higher: the pain level (VAS) was 2.8±1.6 (p=0.000), PainDETECT decreased from 11.8±5.6 to 6.8±3.1 (p=0.000), CSI – to 31.6±13.9 (p=0.000). DAS28 after 3 and 6 months was 3.7±1.3 and 3.6±1.2. The number of patients with pain decrease of ≥50% after 28 days of therapy was 59.9%. Low RA activity after 3 months. (DAS28 ≤3.2) was achieved in 64.4% of patients. There was a clear correlation between the number of patients with significant pain reduction at 28 days and the number of patients with low RA activity after 3 and 6 months (rS=0.548, p=0.000; rS=0.790, p=0.000). Six patients withdrew from the study due to inefficacy or social reasons. There were no serious adverse reactions.Conclusion:The application of JAK inhibitor tofacitinib allows to reach a fast analgesic effect and reduce CS signs. An early clinical response to tofacitinib (pain relief) predicts a decrease in RA activity after 3 and 6 months of the therapy.Limitation: Open-label observatory study.Disclosure of Interests:None declared

Are pain coping strategies and neuropathic pain associated with a worse outcome after conservative treatment for Achilles tendinopathy? A prospective cohort study

ObjectivesTo analyse whether (1) passive or active pain coping strategies and (2) presence of neuropathic pain component influences the change of Achilles tendinopathy (AT) symptoms over a course of 24 weeks in conservatively-treated patients. DesignProspective cohort study. MethodsPatients with clinically-diagnosed chronic midportion AT were conservatively treated. At baseline, the Pain Coping Inventory (PCI) was used to determine scores of coping, which consisted of two domains, active and passive (score ranging from 0 to 1; the higher, the more active or passive). Presence of neuropathic pain (PainDETECT questionnaire, −1 to 38 points) was categorized as (a) unlikely (≤12 points), (b) unclear (13–18 points) and (c) likely (≥19 points). The symptom severity was determined with the validated Victorian Institute of Sports Assessment-Achilles (VISA-A) questionnaire (0–100) at baseline, 6, 12 and 24 weeks. We analysed the correlation between (1) PCI and (2) PainDETECT baseline scores with change in VISA-A score using an adjusted Generalized Estimating Equations model. ResultsOf 80 included patients, 76 (95%) completed the 24-weeks follow-up. The mean VISA-A score (standard deviation) increased from 43 (16) points at baseline to 63 (23) points at 24 weeks. Patients had a mean (standard deviation) active coping score of 0.53 (0.13) and a passive score of 0.43 (0.10). Twelve patients (15%) had a likely neuropathic pain component. Active and passive coping mechanisms and presence of neuropathic pain did not influence the change in AT symptoms (p=0.459, p=0.478 and p=0.420, respectively). ConclusionsContrary to widespread belief, coping strategy and presence of neuropathic pain are not associated with a worse clinical outcome in this homogeneous group of patients with clinically diagnosed AT.

Somatosensory dysfunction related neuropathic pain component affects disease activity, functional status and quality of life in ankylosing spondylitis.

To investigate the neuropathic pain (NP) component in ankylosing spondylitis (AS) and to assess the relations between NP and disease characteristics. Eighty participants were included in this study. Demographic properties, duration of disease, laboratory values and clinical assessments (visual analog scale [VAS], Bath Ankylosing Spondylitis Disease Activity Index [BASDAI], Bath Ankylosing Spondylitis Functional Index [BASFI], Bath Ankylosing Spondylitis Metrology Index [BASMI], Short Form [SF]-36 questionnaire, Beck Depression Inventory [BDI]) were recorded. The NP component was assessed by both DN4 and PainDETECT questionnaires (PD-Q) and patients were classified into groups according to questionnaire scores. NP component was detected by the DN4 and PD-Q in 40% and 28.7% of our patients, respectively. Likely-NP group had significantly higher scores in VAS-pain, BASDAI, BASFI, BASMI and BDI compared with both uncertain-NP and unlikely-NP groups. There was no significant difference between the SF-36 scores of the likely-NP and uncertain-NP groups. Moreover, all SF-36 scores were significantly lower in the likely-NP group than in the unlikely-NP group. Based on DN4 scale, patients with NP had significantly higher erythrocyte sedimentation rate (ESR), VAS, BASDAI, BASFI, BASMI scores and significantly lower SF-36 (except social functioning) scores compared to patients without NP. Both painDETECT and DN4 scores of the patients were significantly positively correlated with ESR, VAS, BASDAI, BASFI, BASMI, BDI scores and negatively correlated with all SF-36 scores. Our results revealed that the presence of NP component in patients with AS is associated with various disease-related variables, including pain, high disease activity, reduced mobility of the axial skeleton, depression and poor quality of life.

Neuropathic Pain Component Insights in Patients with Knee Osteoarthritis: An Observational Study

Osteoarthritis (OA) is one of the most leading cause of chronic disability in musculoskeletal area with pain as the main manifestation. Chronic pain often leads to an abnormal excitability in pain pathway, resulting a central sensitization which corresponding to neuropathic pain (NP). To date, the existence of neuropathic component in osteoarthritis of the knee remains controversial.Methods:The cross-sectional study involved 74 patients of knee osteoarthritis who were diagnosed by using ACR classification criteria for osteoarthritis of the knee. The presence of NP component was assessed by DN4 and painDETECT questionnaire. All participant also completed the WOMAC score to evaluate their status of knee OA, and was divided into two groups, which were mild and severe OA. The prevalence of NP component within knee OA patients was evaluated and then compared between the mild and severe groups.Results:45,9% of the participants examined with DN4 score were likely to have the NP component, while the others were doubtful. On the other hand, painDETECT score revealed that 36,5% of the patients were likely to have NP component, 21,6% unclear, and 41,9% unlikely. Comparison between WOMAC score and DN4 showed that 67,6% of the severe population had NP component, significantly higher than the mild population, 24,3% (p<0,05). Alternatively, painDETECT score showed 13,5% likely to have NP component, 24,3% unclear, 62,2% doubtful in the mild population, while in the severe group 59,5% likely, 18,9% unclear, 21,6% unlikely (p<0,05).Conclusion:Knee osteoarthritis has a significantly high prevalence of neuropathic pain component. NP component prevalence appears higher in the severe OA population, whether it assessed by DN4 or painDETECT scoring.

Is There a Possible Neuropathic Pain Component in Knee Osteoarthritis?

This study aims to investigate the neuropathic pain (NP) component in patients with osteoarthritis (OA) of the knee and its association with physical function, risk factors, and stages of OA. One hundred and nine patients (16 males, 93 females; mean age 62.5±8.5 years; range 44 to 81 years) diagnosed with knee OA according to the American College of Rheumatology criteria were enrolled in this study between July 2014 and June 2015. Patients were evaluated with visual analog scale for pain severity, PainDETECT questionnaire for presence and severity of neuropathic pain, Western Ontario and McMaster Universities osteoarthritis index for physical function, and the Kellgren-Lawrence system for severity of OA. Presence of the associated risk factors were also questioned. A total of 12 patients (11%) were classified as having likely NP and 23 patients (21.1%) were classified as having possible NP. PainDETECT scores were significantly correlated with the visual analog scale scores and Western Ontario and McMaster Universities osteoarthritis index pain, physical function and total scores. Patients with neuropathic pain had significantly longer symptom duration than the patients without NP. However, we found no relationship between the other risk factors and NP. This study demonstrated that some of the knee OA patients had a NP component as the underlying cause of knee pain. Patients with NP had longer symptom duration, increased severity of pain, and disability. Therefore, the presence of NP component in these patients should be considered. Once it is determined, appropriate intervention strategies for NP should be incorporated in the routine treatment modalities of knee OA.