The role of the central nervous system in the generation and maintenance of chronic pain in rheumatoid arthritis, osteoarthritis and fibromyalgia
1 Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, 75 Francis Street, PBB-B3, Boston, MA 02115, USA
2 Chronic Pain and Fatigue Center, University of Michigan Medical School, Domino's Farms, Lobby M, PO Box 385, 24 Frank Lloyd Wright Drive, Ann Arbor, MI 48106, USA
Arthritis Research & Therapy 2011, 13:211 doi:10.1186/ar3306Published: 28 April 2011
Pain is a key component of most rheumatologic diseases. In fibromyalgia, the importance of central nervous system pain mechanisms (for example, loss of descending analgesic activity and central sensitization) is well documented. A few studies have also noted alterations in central pain processing in osteoarthritis, and some data, including the observation of widespread pain sensitivity, suggest that central pain-processing defects may alter the pain response in rheumatoid arthritis patients. When central pain is identified, different classes of analgesics (for example, serotonin-norepinephrine reuptake inhibitors, α2δ ligands) may be more effective than drugs that treat peripheral or nociceptive pain (for example, nonsteroidal anti-inflammatory drugs and opioids).