Emerging evidence suggests that pain might be more effectively classified and treated according to the mechanisms underlying the onset and/or the maintenance of pain. Multiple mechanisms that can produce pain have been identified, including tissue injury and inflammation (inflammatory pain), damage to the nervous system (neuropathic pain), and abnormal responsiveness or function of the central nervous system (central sensitization, dysfunction of descending pain modulating systems). Central pain mechanisms may play an important role in rheumatic diseases, traditionally considered peripheral inflammatory entities. Inflammation sensitizes polymodal nociceptors. This peripheral sensitization induces hyperexcitability of nociceptive neurons in the central nervous system (central sensitization) and the two together generate the features of pathological pain, allodynia and hyperalgesia, confined to the inflamed tissues. Increased responsiveness of peripheral and central neurons (pain hypersensitivity) in the presence of tissue injury and inflammation is a normal response (neuroplasticity). As a rule, these sensitization phenomena extinguish themselves as the tissue heals and inflammation subsides. However, persistent pain is common in patients with inflammatory joint disorders and the key question is whether these neuroplastic changes persists in subsets of patients and leads to chronic pain states in which pain is no longer coupled to the presence of ongoing peripheral inflammation. If central pain mechanisms do play a significant role in pain processing and persistence of pain in subgroups of patients, strategies for managing pain in addition to inflammatory disease suppression may be required. Furthermore, in these patients, persistent pain hypersensitivity may lead to continuous high reports of tender joints and poor global health and pain leaving the physician with the clinical dilemma that patient reported outcomes and composite disease activity scores do not correspond to the objective level of inflammatory activity.
Simple methods assisting identification of underlying pain mechanisms in the clinical care of rheumatologic patients are therefore needed. The painDETECT Questionnaire (PDQ) is a patient administered screening questionnaire originally developed to determine the likelihood of a predominant neuropathic pain component being present. The questionnaire comprises 7 weighted somatosensory symptom and sign items and 2 items relating to the spatial (radiating) and temporal characteristics of the individual pain pattern. Although developed as a screening questionnaire for neuropathic pain, the PDQ has increasingly been used to assess neuropathic pain features as a proxy of central pain mechanisms in, for example, patients with osteoarthritis and fibromyalgia. Recently, the PDQ has also been introduced in studies assessing pain mechanisms in patients with rheumatoid arthritis (RA) and spondyloarthritis (SpA).
The clinical utility of the PDQ in patients with arthritis will be covered based on patient cases, registry data and clinical studies. The prevalence and description of PDQ-derived pain phenotypes and the prognostic value thereof will be discussed.
Disclosure of Interest None declared