Pain is defined by the International Association for the Study of Pain as “an unpleasant sensory and emotional experience arising from actual or potential tissue damage.” Pain is an inherently subjective phenomenon, originating from a biologic source, but influenced by psychological factors. Unlike acute pain, chronic pain tends to be more multifactorial, less amenable to “cure,” and more influenced by both psychological and social factors. It typically requires continuous long-term and multidisciplinary management. These characteristics necessitate an appropriate adjustment of expectations and approach by both clinicians and patients to achieve a satisfactory outcome. The principal goal is improvement in quality of life and function, rather than complete elimination of the pain.
Biologic Components
Pain derives from afferent signals from nociceptive fibers in the periphery, triggered by tissue damage (nociceptive pain) or by direct neuronal injury (neuropathic pain). These primary afferent nociceptive fibers transduce pain signals to the central nervous system (CNS) via synapses in the dorsal horn of the spinal cord. From the dorsal horn, second-order nociceptors then carry the pain signals mainly via the spinothalamic tracts to the thalamus. Thalamic projections then transmit pain signals to both the somatosensory and frontal cortex. Modulation networks from the frontal cortex and limbic system create a final conscious perception. These networks are the medium by which psychological factors and the psychosocial context alter the sensation of pain.
The biologic component of chronic pain is less well understood than that of acute pain. On occasion, chronic pain can be triggered with a seemingly minor biologic stimulus or persist long after an injury has healed. Generation and maintenance of chronic pain is thought to occur via neuromodulation, primarily through the phenomena of peripheral and central sensitization. Furthermore, psychological and social factors may play a role in modulating the perception and perpetuation of pain.
In peripheral sensitization, primary nociceptors in the peripheral nervous system can be influenced by repetitive stimuli resulting in a decreased threshold for activating nociceptors and/or increased pain responses to suprathreshold stimuli. These changes can generate pain even when the stimulus is minimal. Clinically, these changes may manifest as allodynia (pain elicited from a nonpainful stimulus) or hyperalgesia (an increased responsiveness to noxious stimuli producing a heightened response to pain).
Central sensitization involves the dorsal horn, the site of neural transmission between primary and second-order nociceptors; it is the target of numerous analgesic agents. With chronic pain states, neuroplastic changes occur in the dorsal horn that lead to a decreased threshold for signal transmission between the peripheral and the CNSs. For example, up-regulation in N-methyl-D-aspartate (NMDA) receptor activity in the dorsal horn is thought to play a significant role in the development of chronic pain and neuropathic pain.
In addition to a lowered threshold for pain signaling, there are other changes in the CNS that may occur with chronic pain. In a normal state, there are descending pathways within the central nervous system that dampen pain transmission; with chronic pain, there is down-regulation of these inhibitory mechanisms leading to a heightened state of activity. It also is possible that immunomodulatory changes through microglial activation may play a role in maintaining chronic pain. The combination of these neural changes that occur with central sensitization is thought to potentiate chronic pain, even when the initial peripheral signal may have diminished.
Social Contributors
Social contributors to chronic pain include demographic variables that may influence the clinical course (
Table 236-1).
They may also emanate from home life or work (e.g., ongoing
litigation or a
work’s compensation claim), complicating a chronic pain state or persist due to a potential secondary gain. Injured workers respond less well to treatment than do individuals with similar medical conditions who do not have workers’ compensation claims. Chronic pain presentations may also result from
partner (
domestic)
violence, the presence of which greatly increases the risk of a chronic pain syndrome. Estimates of lifetime risk among women for partner violence range from 10% to 30%.
Partner (Domestic) Violence.
The vast majority of partner violence victims are women, outnumbering men by a ratio of 9:1. The condition occurs among people of all sociodemographic and age groups, including the elderly (sometimes referred to as elder abuse). Such violence greatly increases the risk of developing adverse physical and psychological consequences. Physical manifestations range from telltale “falls,” ecchymoses, and forearm injuries (from trying to protect oneself) to more subtle, otherwise unexplained chronic pain presentations such as headache, pelvic pain, back pain, abdominal pain, or dyspareunia. Severe premenstrual cramping and irritable bowel symptoms may ensue. Persons suffering from a preexisting chronic condition may experience a worsening of symptoms. Psychological presentations include anxiety, depression, and alcohol and substance abuse. Patients are at increased risk for somatization disorders, complications of pregnancy, sexually transmitted diseases, eating disorders, and noncompliance with medical regimens.