Use of the painDETECT tool in rheumatoid arthritis suggests neuropathic and sensitization components in pain reporting

Abstract

Rheumatoid arthritis (RA) is an inflammatory autoimmune condition typified by systemic inflammation targeted toward synovial joints. Inhibition of proinflammatory networks by disease-modifying antirheumatic drugs, eg, methotrexate and biologic therapies, including tumor necrosis factor-α inhibitors, often leads to suppression of disease activity observed at the clinical level. However, despite the era of widespread use of disease-modifying treatments, there remain significant groups of patients who continue to experience pain. Our study formulated a pain assessment tool in the arthritis clinic to assess feasibility of measurements including the visual analog scale (VAS) and painDETECT to assess multimodal features of pain in people with established RA (n=100). Clinical measures of disease activity (Disease Activity Score in 28 Joints [DAS28]) were also recorded. Our data showed that despite the majority of subjects on at least one disease-modifying agent, the majority of patients reported severe pain (54%) by VAS, despite well-controlled clinical disease, with mean DAS28 2.07±0.9. Using the painDETECT questionnaire, 67% of patients had unlikely neuropathic pain. A significant proportion of subjects (28%) had possible neuropathic pain and 5% had features of likely neuropathic pain by painDETECT scoring. We found a positive correlation between VAS and painDETECT (R2=0.757). Of note, the group who had likely or probable neuropathic pain also showed significantly increased pain reporting by VAS (P<0.01). Subjects who were clinically obese (body mass index >30) also had statistically higher proportions of pain reporting (VAS 89.0±0.7 mm) compared with subjects who had a normal body mass index (VAS 45.2±21.8 mm), P<0.05. Our findings suggest that multimodal features of pain perception exist in RA, including neuropathic and sensitization elements, perhaps explaining why a subgroup of people with RA continue to experience ongoing pain, despite their apparent suppression of inflammation.

Neuropathic-like pain features and cross-sectional associations in rheumatoid arthritis

“…The 17 % proportion of RA patients with likely NP found in this study was very similar to the 19 % prevalence reported by Meirinhos et al [ 21 ]. Conversely, Ahmed et al [ 20 ] reported that 28 % of RA patients had possible NP symptoms and 5 % were likely to be experiencing NP symptoms according to the painDETECT. The relatively high proportion of patients (36 %) with NP in the study by Perrot et al [ 22 ] may have resulted from their use of the DN4 questionnaire, which tends to have a high sensitivity but low specificity in identifying NP [ 30 ].…”

“…To date, few studies have specifically examined the prevalence of NP features in RA. Only three studies in (subsamples of) RA patients estimated the prevalence of NP using screening tools such as the painDETECT [ 20 – 22 ]. However, prevalence rates of likely NP varied widely between 5 % and 36 %.…”

Comparison of Pain Characteristics in Patients with Rheumatoid Arthritis and Systemic Sclerosis with Particular Reference to the Neuropathic Pain Component: Cross-Sectional Study

“…These patients also had higher disease activity scores independently from inflammatory origins but related to the non-nociceptive pain [30]. On the other hand, higher levels of pain were reported to be unrelated to disease activity as assessed by Disease Activity Score 28 [31]. …”

Pain mechanisms and ultrasonic inflammatory activity as prognostic factors in patients with psoriatic arthritis: protocol for a prospective, exploratory cohort study

“… 46 Research of neuropathic pain features in other chronic pain and rheumatic conditions has expanded the applicability of PDQ. 23 24 53 54 The PDQ consists of nine items of which seven are somatosensory descriptor items, and two items relate to the spatial (radiating) and temporal pain characteristics. For screening purposes, PDQ cut-off scores ≤12 (a neuropathic component is unlikely) and ≥19 (a neuropathic component is likely) have been found to be appropriate.…”

“…These are also common pain qualities in patients with fibromyalgia 23 and frequently reported by rheumatic patients. 24–26 In some individuals, CS seems to develop into a state of chronic widespread pain (CWP) fully uncoupled from inflammatory activity. The mechanisms behind CWP is sparsely elucidated but may involve maladaptive neuroplasticity and cortical reorganisation of the somatosensory and motor systems, 26 27 aberrant peripheral inputs to central nervous system, 28 modulation of glia cell function, 29 and disruption of descending inhibitory and facilitating control.…”