Opioids: to use or not to use? That is the question.

Pain is the most common complaint of patients with rheumatic diseases. Almost all rheumatologic disorders, whether inflammatory or noninflammatory, can cause this symptom. Rheumatologists evaluate the character, duration, onset, and periodicity of the pain to make a diagnosis of musculoskeletal illnesses. Reduction of pain is an essential component of clinical improvement and frequently serves as the primary end point of clinical trials investigating the efficacy of pharmacologic therapies. Although rheumatologists diagnose and treat pain, they do not categorize themselves as algologists, or pain physicians. Rheumatologists are physicians who diagnose and treat musculoskeletal disorders associated with acute and chronic nonmalignant pain. A rheumatologist’s approach to pain control for inflammatory arthritis is the reduction of mediators responsible for inflammation and joint destruction. The use of biologic agents, disease-modifying drugs, corticosteroids, and nonsteroidal antiinflammatory drugs (NSAIDs) is the primary focus of therapy for the prevention or limitation of tissue damage and the relief of pain. In the noninflammatory disorders, where disease-modifying drugs are not available, the primary mode of therapy for controlling pain and improving function is NSAIDs. In both major categories of rheumatic illnesses, the focus of pain relief has been the control of inflammation, whether systemic or local. Opioids are not initial therapies prescribed for rheumatic disease patients by rheumatologists. The rheumatologist’s expectation is that NSAIDs are usually sufficiently effective in controlling musculoskeletal pain and additional analgesic therapy is not needed. This orientation puts our patients at risk of suffering that is preventable. In a recent pain survey of rheumatoid arthritis patients in Europe, two-thirds of the patients considered their pain control to be inadequate (1). Pain is frequently not specifically assessed or treated in arthritis patients (2). Understanding the neurologic basis and treatment of pain, of any source, has not been emphasized in rheumatologic training, clinical practice, or as a topic at the Annual Scientific Meetings of the American College of Rheumatology. Pain has been defined as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage” (3). This definition encompasses the complexities of the neurologic response to injury. A simple circuit composed of a single nerve transmitting impulses from the periphery to the brain is not the mechanism of pain transmission. Inducible receptors on the surface of multiple neurons, with intricate synapses within the spinal cord and cerebrum, are key elements in the transmission and perception of pain. Pain is not a homogeneous sensory entity but has distinct types: adaptive, for protection and survival to promote healing of injuries; and maladaptive, a disease unto itself, associated with primary disordering of nervous system function. Woolf has distinguished these types of pain into nociceptive, inflammatory, neuropathic, and functional (4). Nociceptive pain is an acute alarm elicited by a potential damaging stimulus. Inflammatory pain promotes healing of injured tissues. In this form of pain, sensitivity is increased so that stimuli to damaged tissues, which would not normally cause pain, are perceived as noxious. Inflammatory pain is reversible, in that increased sensitivity returns to a baseline state once healing has occurred. In the other forms of pain, increased sensitivity of the nervous system can lead to pain in the absence of peripheral noxious stimuli. Neuropathic pain is maladaptive, in that it is not associated with acute injury or healing and results from lesions in the peripheral or central nervous system that may occur spontaneously, without a specific peripheral stimulus (5). Functional pain is also maladaptive, resulting from David Borenstein, MD: The George Washington University Medical Center, and Arthritis and Rheumatism Associates, Washington, DC. Address correspondence and reprint requests to David Borenstein, MD, Arthritis and Rheumatism Associates, 2021 K Street, NW, Suite 300, Washington, DC 20006. E-mail: Dborenstein715@ aol.com. Submitted for publication September 10, 2004; accepted in revised form October 6, 2004.