Chronic pain disproportionately affects older adults and adversely impacts physical functioning and quality of life. Among adults age 65 and older living in the community, the prevalence has been estimated between 25% and 76%, with the wide variability reflecting differences in the surveyed population and study methodology. In long-term-care settings, the overwhelming majority (83%-93%) of older adults report chronic pain.¹ In a population-based survey in Sweden, the prevalence of pain lasting 3 or more months rose from 39% in the age group 65-74 to 48% among adults age 85 and older, with an estimated 5.4% annual increase in pain prevalence after age 65.² However, an increase in prevalence with advancing old age has not been found in all epidemiological studies.¹ Most studies have found a higher prevalence of chronic pain in older women compared to older men.^1,2 In the Swedish survey, the average severity of
chronic pain was moderate and caused moderate interference in daily activities, remaining fairly stable across old-age groups. Problems with mobility predicted the onset of chronic pain 12 months later. In women, but not men, pain duration, pain in more than 1 location, and pain severity predicted the persistence of chronic pain at 24 months of follow-up.² The most frequently reported sites for chronic pain include the back, the lower extremities (hip, knee), and other joints.¹

In older adults, chronic pain generally occurs in the context of multimorbidity. In the multicenter MultiCare Cohort study of 3189 older primary-care patients in Germany (mean age 74 years), men and women each had an average of 7 chronic conditions. Seventy percent of men and 85% of women reported chronic pain, which moderately or severely limited their functioning in 15% and 22%, respectively. Of importance, different combinations of comorbidities were associated with a significantly different prevalence of chronic pain. For example, in women with chronic low-back problems, the addition of gastroesophageal reflux disease (GERD) was associated with a 63% prevalence of chronic pain, compared to 47% in women without GERD. Men who had chronic low-back problems plus ischemic heart disease had a 38% prevalence of chronic pain, compared to 28% of men with back problems but no heart disease.³ The mechanism by which combinations of morbidities influence the perception of pain remains unknown.

Depression and anxiety: Significant depressive symptoms, which commonly co-occur with anxiety, are found in 10%-20% of adults age 65 and older, depending on the population surveyed and the screening instruments used.^4,5,6 The prevalence of depression rises to 27% among institutionalized older adults.⁷ Based on data from a continuing-care retirement community, it has been estimated that roughly 13% of older adults suffer from comorbid depression and chronic pain.⁸ Chronic pain and depression strongly influence each other. In patients with chronic pain, the odds ratio (OR) of having more severe and more disabling chronic pain increases in the presence of depression and anxiety. In the Netherlands Study of Depression and Anxiety, after adjusting for age, gender, chronic disease, antidepressant use, and other demographic factors, adults with depression and anxiety were 3 times more likely to experience mild, nondisabling pain than nondepressed, nonanxious adults, but they were 30 times more likely to have severe and disabling pain (95% CI 12.68-72.23). The association of depression or anxiety with pain is graded, with more severe depression and more severe anxiety more likely to be associated with higher pain grades. Compared to not being depressed, having moderate depressive symptoms increased the likelihood of having severely disabling and limiting pain 3-fold, but having severe depression increased the OR of severely disabling pain nearly 8-fold. Similarly, compared to no anxiety, moderate or severe anxiety increased the OR of severely disabling and limiting pain approximately 7 and 13 times, respectively.⁹ The physiological basis for the interrelationship between depression and the perception of pain remains unclear, but single nucleotide polymorphisms in the functional promoters of serotonin-receptor genes have been associated with chronic pain.¹⁰

Aging also appears to facilitate the dynamic interaction of depression and pain. It is generally accepted that abnormalities in serotonergic (5-hydroxytriptamine [5-HT]) neurotransmission play an important role in depression. In the rat brain, regional 5-HT levels change with aging and are accompanied by regional alterations in the brain density of 5-HT_1A children and young adults; older humans also show regional differences in 5-HT_1A and 5-HT_2A receptor density,¹² with significant increases in receptor density in brain regions (in the absence of known depression) that are qualitatively similar to the increased receptor density seen in depressed, middle-aged adults.¹³ The serotonergic system, along with the noradrenergic system, plays a role in pain modulation through a complex set of descending pathways that receive input from the cortex, thalamus, and amygdala and feed into the midbrain, brain stem, and spinal cord,¹⁴ which may help explain the efficacy of the serotonin-noradrenergic reuptake inhibitor, duloxetine, in neuropathic and osteoarthritic pain.¹⁵

With aging, there is a decline in both structure and function of peripheral sensory nerves, in particular, the Aδ fibers, corresponding to an unchanged or reduced sensitivity to pain-producing stimuli in older patients. However, once the pain is perceived, the perception of pain is often greater than that experienced by younger patients responding to an identical stimulus.¹⁶ To this aging phenomenon is added the pain amplification of nociceptive stimuli (pain hypersensitivity) that commonly accompanies chronic pain states. Among patients referred to a Swiss pain clinic, central pain hypersensitivity (determined by the threshold for a withdrawal reflex) was found in 80% (mean age = 50 years).¹⁷ In chronic joint pain, the poor association between radiologic abnormalities and perceived pain suggests an important role for central sensitization. Given the prevalence of musculoskeletal pain in older adults and the frequency of arthroplasties in this population, it is notable that chronic postoperative pain after knee replacement ranges from 10% to 24% and from 7% to 23% after total hip arthroplasty.¹⁸ In degenerative joint disease, patients commonly experience joint hyperalgesia that progresses to regional pain; this is believed to reflect central sensitization. Patients who experience general pain sensitization around (not just in) the knee after knee replacement tend to report higher levels of pain, greater disability, and worse quality of life.¹⁹

Aging predisposes to central sensitization through abnormalities in mast cell and glial function that amplifies and perpetuates the pain response through a state of neuroinflammation. Mast cells are strategically located near nerve endings and the vasculature, allowing mast
cell mediators such as bradykinin, histamine, and prostaglandins to stimulate a nociceptive response. In the central nervous system, mast cells are found in the spinal cord and are particularly concentrated in the thalamus. In older adults, mast cells are more likely to degranulate in response to inflammation, theoretically promoting an inflammatory response in peripheral tissues. Brain mast cells directly and indirectly (through somatosensory neurons) stimulate microglia and astrocytes to release proinflammatory cytokines. In old age, microglia exist primarily in a primed, rather than quiescent, state, resulting in more robust and prolonged production of proinflammatory cytokines.¹⁶ In this setting, dysfunctional modulation of chronic nociceptive stimuli can occur and offers a physiologic explanation for the prevalence of central sensitization and the burden of chronic pain in older patients.

Physicians commonly under-recognize pain in their older patients. On the patient’s side, it is not uncommon to under-report pain because of a belief that pain is normal in old age, culturally or socially mediated stoicism, language barriers, fear of becoming addicted to pain medications, or fear that admission of pain will result in a loss of independence.²⁰ Moderate to severe cognitive impairment impairs communication of pain. Despite the movement to include pain as the “fifth vital sign,” an absence of pain during the vital-sign check may result in the provider’s failure to inquire about pain experienced during daily activities or at night. Pressure to assess multiple chronic conditions and review medications during a short outpatient visit may limit the ability to assess chronic pain. The patient’s impaired hearing can lead to misleading answers and result in an inaccurate or incomplete assessment of symptoms. Family informants may have poor insight into the patient’s pain or pain-related changes in behavior. Disease-focused and time-pressured health care providers also may miss important visual clues that should elicit questions about pain, such as use of a cane, a severely kyphotic spine, or limited range of motion of the neck.

Clinicians’ fear of drug complications or causing addiction often results in the pharmacological undertreatment of older patients’ acute and chronic pain.^1,21,22 The misuse of opioids does occur in older patients and is more likely to occur in the presence of underlying comorbid psychiatric conditions, principally depression and a history of substance misuse.^23,24 Most misuse in the elderly involves opioids that are legitimately prescribed. However, prescribing too low a dose of opioid in moderate to severe pain may result in inadequately treated pain and repeated requests from the patient for more opioids, suggesting addictive behavior. When the physician does not increase the dose, the patient may resort to taking supplementary opioids from a friend or relative, reinforcing the appearance of addiction. Cessation of the opioid-seeking behavior when the physician increases the dose may reflect the phenomenon of “pseudoaddiction,” that is, opioid-seeking behavior for the purpose of pain relief, not opioid craving. Unfortunately, in clinical practice, pseudoaddiction can be difficult to differentiate from true addiction, worsening of the underlying condition and opioid-induced hyperalgesia.

Pain is commonly undertreated in older patients in institutional settings. Evaluation of 387 consecutive patients admitted to geriatric units in 8 acute-care Italian hospitals revealed that two-thirds of patients had at least moderate pain. Only one-third of patients reporting the severest level of pain received a strong opioid. Over 50% of all patients with moderate or more severe pain experienced no or only mild pain relief.²² In a study of 12 Austrian nursing homes, pain prevalence among cognitively impaired but verbally responsive patients was high (over two-thirds) but comparable to cognitively intact patients. However, approximately 80% of nonverbal, cognitively impaired patients were found to have pain using observational methods. Nearly 20% of nonverbal patients with pain did not receive analgesics, compared to 6% of cognitively intact patients.²⁵

Although this chapter focuses on chronic pain, a discussion of atypical presentations of acute pain conditions is necessitated by their frequency in older patients and their ability to delay diagnosis and adversely affect outcomes. Atypical presentation of abdominal pain and chest pain has the potential to cause the most serious consequences to the patient. Abdominal pain is the fourth most common complaint of older patients presenting to the emergency department (ED),²⁶ but the presenting symptoms may be vague and not include all components of the “classic” presentation and therefore may not point to the diagnosis. Among patients age 80 and older presenting with abdominal pain and requiring emergent surgery, only 30% have a fever >35.5°C and a white cell count >15,500/mm³.²⁷ The “typical” presentation of small-bowel obstruction includes diffuse abdominal pain, nausea, vomiting, distention, and constipation/obstipation. However, in older patients, the full constellation of symptoms may not be present early on, and diarrhea may be present. More than half of older patients with acute cholecystitis initially fail to exhibit the combination of nausea, vomiting, and fever, and leukocytosis is absent in up to 40%. With acute pancreatitis, older patients may present with vague upper abdominal pain without radiation to the back, with or without nausea and vomiting. Only 17% of older patients with acute appendicitis with perforation present with the “typical” triad of right lower quadrant pain, fever, and leukocytosis,²⁶ the pain often is vague and may begin as loss of appetite or diffuse abdominal pain. In an older patient, rebound tenderness may be absent in acute peritonitis. Reasons for the atypical presentations largely remain unknown. Age-related changes to peripheral nerves may change
the characteristics of the pain. Concomitant use of nonsteroidal anti-inflammatory drugs (NSAIDs) or opioids may blunt the pain and delay presentation.

Acute myocardial infarction without chest pain is more likely to occur in patients over the age of 70 (and particularly over the age of 80), as well as in women.²⁸ Older patients with urinary tract infection are more likely than younger patients to present atypically with loss of appetite, malaise, delirium, or falls rather than dysuria. Because of atypical presentations, any acute abdominal or chest pain in the older patient should be taken seriously.

Given the high prevalence of chronic pain, its assessment should be integrated into the routine review of systems (ROS) for older patients:

To facilitate pain assessment, a pain questionnaire, developed and validated for older patients, can be substituted for the pain ROS, such as the office-friendly 12-item version of the Geriatric Pain Measure,²⁹ whose use is not copyrighted (Table. 7-1).

Although self-report of pain loses its sensitivity and accuracy as cognitive impairment worsens, it can provide an important clue to the existence of pain and serves as a starting point for observing the patient and asking the caregiver questions that may help to localize the pain and determine its etiology. Table 7-2 summarizes clues to the presence of pain in patients with advanced dementia.

From the caregiver, ascertain whether there has been a change in activities or behavior. For example, does the patient now refuse to walk? Is there new agitated behavior or a change in sleep patterns? Does the patient resist being moved during routine caregiving? Severe pain in demented patients can present as withdrawal or involution, with reduced communication, reduced movement, clenched fists, grimacing, eyes tightly closed, and/or refusal to eat or open the mouth. On physical examination, does the patient exhibit any of these characteristics? Does he or she rub or hold any part of the body or guard a body part such as an arm or leg when he or she moves? Does he or she resist being touched generally or in a specific location? Does the patient grimace during a physical-exam maneuver such as sitting the patient up to auscultate the lungs? If the source of discomfort can be localized and appears musculoskeletal, the caregiver should be asked about recent trauma, and the patient should be inspected for signs of trauma such as ecchymoses or splinting during the lung examination, suggesting a broken rib. The physician should be mindful of the caregiver’s reaction to physical indicators of trauma; indifference or effusive denial of culpability should raise concern about elder mistreatment. A commonly overlooked source of pain in cognitively impaired patients is a dental abscess. The mouth should be inspected; if resistance is encountered, a panoramic dental roentgenogram or facial computerized tomography can be helpful to rule out dental abscesses.