Central to the modern conceptualization of persistent clinical pain is the distinction between acute and chronic pain. Acute pain is caused by incomplete healing of tissue. It is primarily nociceptive. The first priority in treatment is to address the injury or disease causing nociception. Rest generally promotes healing and pain relief. It is increasingly recognized that adequate treatment of acute pain not only increases patient comfort but also speeds healing and functional recovery. Even brief periods of intense acute pain can induce neuronal remodeling and central sensitization of pain pathways. Guidelines for the appropriate management of acute pain have been published by the Agency for Health Care Policy and Research (Acute Pain Management Guideline Panel 1995). The panel recommended that both nonpharmacological interventions - including cognitive and behaviorally based interventions (e.g., relaxation, imagery, biofeedback, education) - and pharmacological interventions be used to manage postoperative and other acute pain. Because many of the nonpsychiatrically trained clinicians involved in the management of acute pain may lack the training and experience to provide these therapies, it is important that psychiatrists recognize this contribution they may be able to make to improving patient care.

Chronic pain is pain that persists beyond the completion of tissue healing. This time can vary according to the tissue damaged, but 6 months is a convenient marker for most types of clinical pain. Chronic pain is often not nociceptive. Treatment is generally directed to the pain and associated disability rather than the original disease or injury. Because psychiatrists are rarely involved in the management of acute pain, the remainder of this chapter focuses on the treatment of chronic pain.

The relation between acute and chronic pain is unclear. Only a relatively small percentage of patients with acute pain develop chronic pain. For example, the Quebec Task Force on Spinal Disorders (1987) reported that 74% of the individuals who had occupationally related back problems returned to work within 1 month and required no further medical treatment. Another 19% returned to work by the end of the fifth month. Multiple studies have reported that a small fraction of patients with acute back pain will develop chronic back pain. These individuals account for most of the medical and disability costs of back pain.

Much attention has been focused on the possible influence of psychological factors on the development of chronic pain. Among the most influential psychodynamic models is that of the “pain-prone patient” first proposed by Engel (1959). These patients were characterized by denial of emotional and interpersonal problems, an inability to deal with anger and hostility, craving for affection and dependency, and a family history of alcoholism and depression. This model was built on psychoanalytic formulations that understood pain as a conversion symptom. As a conversion symptom, pain is hypothesized to offer opportunity for intrapsychic benefit (“primary gain” such as anxiety reduction or diminished awareness of conflicting desires) or interpersonal benefit (“secondary gain” such as increased affection or time out from onerous responsibilities). The original formulations of these ideas were based on small uncontrolled case series. Subsequent controlled studies have not consistently supported affective inhibition as an important risk factor for the development of chronic pain. Nevertheless, being ill can clearly offer advantages and disadvantages to the ill individual. Assessing these intrapersonal and interpersonal advantages of the sick role for patients with chronic pain and helping patients find alternative ways to obtain these benefits is an important part of many multidisciplinary pain programs.

The currently favored model of chronic pain development is a vulnerability-diathesis-stress model. This model postulates both neurobiological and psychosocial predisposing factors. Neurobiological factors include genetic risks as well as neurological sequelae of previous disease or injury. Diverse psychosocial factors increase the risk for chronic pain, including patterns of somatization and somatic hypervigilance; mood, anxiety, and substance abuse disorders; childhood maltreatment; and pain attitudes and coping styles based on the experience of self and significant others. An illness or injury that produces acute pain interacts with this set of vulnerabilities and may produce a chronic pain problem.