Evidence for central sensitization in patients with osteoarthritis pain: A systematic literature review

Abstract

Hyperexcitability of the central nervous system (CNS) has been suggested to play an important role in the chronic pain experienced by osteoarthritis (OA) patients. A systematic review following PRISMA guidelines was performed to evaluate the existing evidence from the literature related to the presence of central sensitization (CS) in patients with OA.Electronic databases PubMed and Web of Science were searched to identify relevant articles using pre-defined keywords regarding CS and OA. Full-text clinical reports addressing studies of CS in human adults with chronic complaints due to osteoarthritis were included and screened for methodological quality by two independent reviewers. From the 40 articles that were initially eligible for methodological quality assessment, 36 articles achieved sufficient scores and therefore were discussed. The majority of these studies were case-control studies and addressed OA of the knee joint. Different subjective and objective parameters considered manifestations of CS, which have been previously reported in other chronic pain conditions such as whiplash or rheumatoid arthritis, were established in subjects with OA pain. Overall results suggest that, although peripheral mechanisms are involved in OA pain, hypersensitivity of the CNS plays a significant role in a subgroup of subjects within this population. Although the majority of the literature provides evidence for the presence of CS in chronic OA pain, clinical identification and treatment of CS in OA is still in its infancy, and future studies with good methodological quality are necessary.

An Over-the-Counter Central Sensitization Therapy: A Chronic Back Pain Registry Study of Pain Relief, Medication Use and Their Adverse Effects

“…These results indicate that the mechanism of action is unlikely a masking phenomenon. It has previously been proposed that chronic pain resulting from osteoarthritis of the knee may involve central sensitization [42][43][44]. In the knee osteoarthritis pain study [26] discussed earlier, when subjects were tested for pain pressure thresholds future science group www.futuremedicine.com post-trial, the treatment group demonstrated a significantly higher pain tolerance than the placebo group, both locally and peripherally, indicating a decreased sensitivity to pain.…”

Dor articular: inflamatória ou neuropática? / Joint pain: inflammatory or neuropathic pain?

“…São igualmente identi icadas as abordagens terapeûticas comportamentais, motoras e farmacológicas para seu tratamento, e a componente de dor neuropática central, induzida pelas modiicações da persistencia de sinal nociceptivo no SNC. 18 Uma revisão sistemática explora a hiperexcitabilidade do SNC nas OA. O fenômeno de sensibilização central tambeḿ pode ser desencadeado pelo componente in lamatório das dores articulares reumáticas.…”

“…O fenômeno de sensibilização central tambeḿ pode ser desencadeado pelo componente in lamatório das dores articulares reumáticas. O excesso de informação nociceptiva in lamatória promove as alterações plásticas no sistema nervo, amplia o sinal nociceptivo no SNC, tanto pela somação temporal (repetição do estıḿ ulo no tempo) quanto pela somação espacial (estı-mulo nociceptivo proveniente de extensa superfıć ie somá- 5,18 tica) da dor. A sensibilização pode ocorrer ao nıv el espinhal, assim como nas vias de inibição descendente (tronco cerebral), pela precária ativação no mecanismo antinociceptivo, pela excitabilidade da neuromatriz da dor no córtex cerebral ou pela potencialização neuronal no cór-18 tex cingulado anterior.…”

The Short-Term Effects of a Single Lecture on Undergraduate Physiotherapy Students' Understanding Regarding Pain Neurophysiology: A Prospective Case Series

“…One reason why the financial burden of musculoskeletal pain is enormous is that there is no definitive treatment for chronic or persistent pain conditions [5]. In acute pain states, pain typically correlates with pathobiological changes in peripheral tissues, whilst recent studies demonstrated that central sensitisation in spinal cord and brain might have larger role in the production of pain in chronic pain states [6][7][8][9]. This evidence questions the validity of traditional biomedical model, in which symptoms are thought to be explained by pathobiological damage to local tissues [10].…”