Pain is the most common reason patients seek medical care. Pain has sensory and emotional components and is often classified as acute or chronic. Acute pain is frequently associated with anxiety and hyperactivity of the sympathetic nervous system (eg, tachycardia, increased respiratory rate and BP, diaphoresis, dilated pupils). Chronic pain does not involve sympathetic hyperactivity but may be associated with vegetative signs (eg, fatigue, loss of libido, loss of appetite) and depressed mood. People vary considerably in their tolerance for pain.
Acute pain, which usually occurs in response to tissue injury, results from activation of peripheral pain receptors and their specific A delta and C sensory nerve fibers (nociceptors). Chronic pain (see Pain: Chronic Pain) related to ongoing tissue injury is presumably caused by persistent activation of these fibers. Chronic pain may also result from ongoing damage to or dysfunction of the peripheral or central nervous system (which causes neuropathic pain) (see Pain: Neuropathic Pain).
Nociceptive pain may be somatic or visceral. Somatic pain receptors are located in skin, subcutaneous tissues, fascia, other connective tissues, periosteum, endosteum, and joint capsules. Stimulation of these receptors usually produces sharp or dull localized pain, but burning is not uncommon if the skin or subcutaneous tissues are involved.Visceral pain receptors are located in most viscera and the surrounding connective tissue. Visceral pain due to obstruction of a hollow organ is poorly localized, deep, and cramping and may be referred to remote cutaneous sites. Visceral pain due to injury of organ capsules or other deep connective tissues may be more localized and sharp.
Although pain of predominantly psychologic origin is far less common than nociceptive or neuropathic pain, psychologic factors commonly contribute to chronic pain and may contribute to pain-related disability. Pain thought to be caused predominantly by psychologic factors is sometimes called psychogenic pain; however, psychophysiologic pain is a more accurate term because the pain results from interaction of physiologic and psychologic phenomena. This type of pain can be categorized in terms of defined somatoform disorders (eg, chronic pain disorders, somatization disorders, hypochondriasis—see Somatoform and Factitious Disorders) in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR).
Many pain syndromes are multifactorial. For example, chronic low back pain and most cancer pain syndromes have a prominent nociceptive component but may also involve neuropathic pain (due to nerve damage).
Pain transmission and modulation
Pain fibers enter the spinal cord at the dorsal root ganglia and synapse in the dorsal horn. From there, fibers cross to the other side and travel up the lateral columns to the thalamus and then to the cerebral cortex.
Repetitive stimulation (eg, from a prolonged painful condition) can sensitize neurons in the dorsal horn of the spinal cord so that a lesser peripheral stimulus causes pain (wind-up phenomenon). Peripheral nerves and nerves at other levels of the CNS may also be sensitized, producing long-term synaptic changes in cortical receptive fields (remodeling) that maintain exaggerated pain perception.
Substances released when tissue is injured, including those involved in the inflammatory cascade, can sensitize peripheral nociceptors. These substances include vasoactive peptides (eg, calcitonin gene-related protein, substance P, neurokinin A) and other mediators (eg, prostaglandin E2, serotonin, bradykinin, epinephrine).
The pain signal is modulated at multiple points in both segmental and descending pathways by many neurochemical mediators, including endorphins (eg, enkephalin) and monoamines (eg, serotonin, norepinephrine). These mediators interact in poorly understood ways to exaggerate or reduce the perception of and response to pain. They mediate the potential benefit of CNS-active drugs (eg, opioids, antidepressants, anticonvulsants, membrane stabilizers) that interact with specific receptors and neurochemicals in the treatment of chronic pain.
Psychologic factors are important modulators. They not only affect verbal expression of pain (ie, whether patients appear stoic or sensitive) but also generate neural output that modulates neurotransmission along pain pathways. Psychologic reaction to protracted pain interacts with other CNS factors to induce long-term changes in pain perception.
In the elderly, the most common causes of pain are musculoskeletal disorders. However, pain is often chronic and multifactorial, and the causes may not be clear.
NSAIDs: Risk of ulcers and GI bleeding due to NSAIDs for people > 65 is 3 to 4 times higher than that for middle-aged people. Risk depends on drug dose and duration of therapy. Elderly patients at high risk of GI adverse effects may benefit from concomitant use of cytoprotective drugs (usually, a proton pump inhibitor; occasionally, the prostaglandin misoprostol).
The newly recognized risk of cardiovascular toxicity, which presumably occurs with nonselective COX-1 and COX-2 inhibitors and with selective COX-2 inhibitors (coxibs), is particularly relevant to the elderly, who are more likely to have cardiovascular risk factors (eg, a history of MI or cerebrovascular or peripheral vascular disease). These drugs should be prescribed cautiously for such patients.
Both nonselective and selective NSAIDs can impair renal function and cause Na and water retention; they should be used cautiously in the elderly, particularly in those who have a renal or hepatic disorder, heart failure, or hypovolemia. Rarely, NSAIDs cause cognitive impairment and personality changes in the elderly. Indomethacin causes more confusion in the elderly than other NSAIDs and should be avoided.
Given the overall greater risk of serious toxicity in the elderly, low doses of NSAIDs should be used if possible, and using short-term therapy or interrupted therapy to confirm effectiveness should be considered.
Opioids: In the elderly, opioids have a longer half-life and possibly a greater analgesic effect than in younger patients. Opioid agonist-antagonists often have psychotomimetic effects (eg, delirium) in the elderly and should usually be avoided. Opioids can contribute to constipation and urinary retention in patients of any age, but the effects tend to be more problematic in the elderly.
Last full review/revision February 2007 by Russell K. Portenoy, MD