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Chronic pain is defined as a painful condition that lasts greater than 3 months, pain that persists beyond the reasonable time for an injury to heal, or pain that persists 1 month beyond the usual course of an acute disease. Whereas acute pain is a vital biologic signal to stop the individual from a potentially injurious activity or to pursue medical care, chronic pain serves no obvious biologic function. Complete pain relief is unrealistic in cases of chronic pain. Rather, the goal of therapy is pain reduction and return to functional status. Chronic pain syndromes discussed in this chapter are divided into neuropathic and nonneuropathic conditions, with a separate discussion of abdominal and pelvic pain syndromes. Aberrant drug-related behavior is also discussed.

Chronic pain is a common problem, affecting 20% to as much as 50% of the population in developed countries.1-3 Women (34%) are affected more than men (27%).1 The back is the most common site for chronic pain, followed by the knee and neck.1 The prevalence of neuropathic pain is 6.9% to 10% of the population.4 The prevalence of chronic abdominal pain in association with irritable bowel syndrome and functional dyspepsia is 23%.5 Risk factors for chronic pain include increasing age, female gender, higher body mass index, and chronic illness.2 An exacerbation of chronic pain is part of the presentation of 11% to 15% of ED visits.6 Compared to patients with acute pain, chronic pain patients are more likely to report their pain as severe and are more likely to be frequent visitors to the ED.7


Our understanding of the pathophysiology of chronic pain is incomplete. Many chronic pain syndromes follow nerve or tissue injury, producing nerve dysfunction secondary to the mechanical injury or in response to chemical mediators released from adjacent cell injury. Peripheral sensitization or central sensitization commonly follows, where peripheral nerves or the CNS become abnormally sensitive, exhibiting pathologic spontaneous activity through upregulation of sodium channels and receptors.8 Neuroplastic changes in the central descending pain modulatory systems, inhibitory or facilitatory, may lead to further hyperexcitability. These changes lead to hyperalgesia (exaggerated response to a normally painful stimulus) and allodynia (pain from a normally nonpainful stimulus). In several disorders, a history of injury may be lacking, such as for fibromyalgia, where central sensitization plays a key role.9 Psychological factors frequently precede or follow the onset of chronic pain and often predispose individuals to physiologic changes through the fear-avoidance model.10 The fear of pain may lead to disuse disability, which leads to nerve hyperexcitability and dysfunction, which may ultimately result in a chronic pain syndrome.11


The nonneuropathic syndromes share certain characteristics, with the most common feature being muscle-related pain (Table 38-1). A feature common to most ...

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