Overview of Pain in the Lame Patient

Abstract

Pain is often the limiting factor associated with joint disease. Pain results from the stimulation of nociceptors by excessive mechanical stimulation, chemical stimulation associated with the inflammatory process, or a combination of both. Even though OA is considered to be a noninflammatory disease, the mild degree of inflammation frequently associated with this condition can result in peripheral sensitization. This results in increased spontaneous activity and decreased activation threshold of nociceptive fibers. Activity of the primary joint afferents also leads to changes within the dorsal spinal horn, resulting in central sensitization and changes in the neural structures of the dorsal horn that facilitate and amplify the nociceptive response. Changes in the periarticular tissues correspond to the neurobiologic changes, resulting in increased stimulation of nociceptors caused by mechanical and chemical alterations resulting from tissue damage. Similar pathophysiologic events occur regardless of whether the initiating event is an acute joint injury or a chronic condition such as OA. The combination of these events results in the complex dynamic of joint pain. Because of this complex interaction of the musculoskeletal and nervous systems, it is difficult to imagine a single treatment that is effective for the alleviation of pain, because that agent would require inhibition of a number of stimulatory pathways. Instead, restoration of mechanical integrity, relief of peripheral inflammation, and blockage of central neurotransmission are all likely to have a role in the relief of joint pain and resolution of lameness.