A 43-year-old woman presented to a rheumatologist for evaluation with a six-week history of arthralgias in the wrist, metacarpophalangeal (MCP), and proximal interphalangeal (PIP) joints. On examination, MCP joints were tender to palpation, and the left wrist and the right third and fourth PIPs were swollen. Because of a positive rheumatoid factor and anticyclic citrullinated peptide antibody test, the patient was diagnosed with rheumatoid arthritis (RA) and started on methotrexate and, subsequently, a tumor necrosis factor blocker. Although the inflammatory markers decreased and swelling subsided, the patient continued to have pain. In addition, she reported fatigue and inability to sleep. She also noted feeling sad and discouraged because pain limited the activities she could do. At this juncture, the rheumatologist was confronted with an important decision: to increase disease-modifying antirheumatic drug (DMARD) therapy or to develop an alternative plan to treat this patient’s pain. The key issue in the case focused on the origin of the pain. Was the pain from inflammation, or was it from something else?
You Might Also Like
Explore This IssueOctober 2011
Pain in Rheumatology
This scenario occurs almost every day in the offices of rheumatologists. Pain is the number one reason patients see a rheumatologist, and it is their highest priority when returning for follow-up. In a study of 2,795 patients who reported a physician diagnosis of RA, 86% stated that their disease was “somewhat to completely controlled,” but 64% were not satisfied with their pain levels. Although all of these patients were seeing a rheumatologist, 80% continued to rate their pain as “moderate to severe.”1
When faced with patients who have persistent pain despite seemingly adequate DMARD therapy, rheumatologists are often uncertain about the cause of pain and the best treatment strategy. According to the 2010 Report of the ACR Pain Management Task Force, rheumatologists “do not characterize themselves as ‘pain physicians’… Rheumatologists have traditionally approached pain from the perspective of the proximal causes of pain such as tissue injury and inflammation, and have concentrated therapy on reducing inflammation, either locally or systemically.”2
CNS Pain Mechanisms: Lessons from Fibromyalgia
This emphasis on inflammation as a therapeutic target to reduce pain is beginning to change, however, as neuroscience research reveals that, mechanistically, there are different types of pain. “Nociceptive” pain is generally considered adaptive and results from the appropriate detection of noxious stimuli (e.g., tissue injury or inflammation). “Pathological” pain is the product of damage to the central nervous system (CNS; e.g., neuropathic pain) or amplification of sensory signals in the CNS.3 Mounting evidence suggests that sensory amplification of pain and other stimuli may best explain the symptoms in syndromes like fibromyalgia.