Publications
APS Bulletin • Volume 7, Number 2, March/April 1997
Questions and Answers
Stephen W. Harkins, PhD, Department Editor
Sans Pain?
Stephen W. Harkins, PhD
Early Scenes
Shakespeare, in As You Like It, presented human aging negatively, noting that "All the world's a stage... and one man in his time plays many parts, his acts being seven ages." The seventh age ends in "second childishness... sans teeth, sans eyes, sans taste, sans everything." Swift, in Gulliver's Travels, satirized the desire to have a fountain of everlasting youth. In his travels, Gulliver encountered individuals known as Struldbrugs who, although destined to live forever, were not immune to senescence. Gulliver reports, "They were the most mortifying sight I ever beheld....Besides the usual deformities in extreme old age, they acquired an additional ghastliness in proportion to their number of years, which is not to be described." Both Shakespeare and Swift were aware of the folly of adding years to life without adding life to years.
Compression of Mortality
Over the past 100 years, the more developed countries have undergone a marked change in life expectancy from birth. A similar increase in life expectancy at the upper end of the life span has not occurred. This has resulted in a compression of mortality near the upper limit of the human life span (Fries, 1980; Fries, Green, & Levine, 1989). Combined with a decline in the birth rate, the increase in life expectancy has produced an increasingly older population, the fastest-growing segment of which consists of those 85 years of age and older. The estimated proportion of those who will be 65 years of age and older in 2030 is currently between 20% and 25% of the population of the United States.
Individuals 65 years of age and older do not represent an homogenous group. Increased variability in function, both physiological and psychological, characterizes the older population. Elderly people have been described as consisting of the "young-old" (those 65 to 74), the "old-old" (those 75 to 84) and the "oldest-old" (those over 84). This classification has merit, as functional ability decreases and risk of chronic health problems increases dramatically from the young-old to the oldest-old. The majority of the research on pain and aging has focused on the young-old.
Health and daily care costs increase with age owing to increasing frailty. The impact of poorly controlled pain on healthcare costs, limitations in activities of daily living, and deconditioning as well as psychological well-being in older adults has not been systematically evaluated. It is likely to be enormous.
Does Age Influence Report of Pain?
The expression of pain is mediated by birth cohort, life history, and expectations derived from social and cultural influences. One quite misleading stereotype is that pain sensitivity in general decreases with age in the later years of life. Paradoxically, another contrasting belief is that pain is a "natural" consequence of the aging process. Indeed, some recent findings suggest that chronic pain may be less emotionally evocative in the old, resulting in greater acceptance of chronic and recurrent pains as part of one's aging (Harkins, 1996; Harkins & Price, 1992). Other recent findings indicate that age may selectively de-crease responses to first and, under very controlled conditions, second pain (Chakour, Gibson, Bradbeer, & Helme, 1996; Harkins, Davis, Bush, & Kasberger, 1996). Nevertheless, under most conditions, the rating of the intensity of both experimental and clinical pain in young and older adults does not seem to differ (Harkins; Harkins & Warner, 1980; Harkins, Price, & Martelli, 1986; Harkins, Davis, et al.).
Several Scenarios
INCREASING LONGEVITY: There is no question that the more developed countries have undergone a compression of mortality into the later years of life. But this is due to demographic shifts in average survival from birth and not to changes in the maximum human life span. There is no evidence that maximum longevity (the maximum human life span) has increased. A fundamental question in gerontology is whether the emphasis of the field should focus on lengthening the maximum human life span or on quality of life while continuing to increase population life expectancy. The quest for adding years to life and thus increasing the maximum human life span beyond its current limit represents a research focus for some gerontologists.
The maximum human life span is about 120 years. Current research indicates that both life expectancy and maximum life span can be dramatically increased from birth. Caloric restriction increases life expectancy and maximum life span in a number of species (Masoro, 1987) and may do so for humans. Genetic interventions to increase the maximum life span are currently under investigation. A caution is that, as exciting as this prospect is, research focusing on increasing the "natural" life span to 130, 150, or 170 years may divert resources from a core mission of the National Institute on Aging, that of adding life to years. As Shakespeare and Swift recognized, there is a distinction between adding years to life and life to years.
What is the best marker of biological aging? Although chronological age is the best marker of senescence, it is a poor metric. No standardized biomarkers of senescence exist (Masoro, 1988), although candidates include levels of certain hormones (DHEA, melatonin, growth hormone), functional changes (near point vision), high frequency hearing, reaction time, and body system markers (blood pressure, density of slow wave [stage 4] sleep, vital capacity). The lack of physiological markers of biological senescence limits our ability to identify the onset of "old" age or its rate of progression. As Swift's Gulliver observed firsthand, the scenario of increasing the maximum (or upper limit) of the human life span without preventing or delaying painful degenerative conditions associated with very old age is a bleak one, particularly when we have such limited measurement tools for both rate of senescence and for pain in elderly people.
COMPRESSION OF MORBIDITY: A second scenario is that morbidity has decreased as life expectancy from birth has increased, with a resulting increase in quality of life in old age (Fries et al., 1989). Evidence that the population is healthier is seen in declining death rates due to cancer, stroke, and acute myocardial infarction. In contrast, incidence of ischemic heart disease, fractures, dementia (Alzheimer's-type cognitive disorders), and movement disorders (Parkinsonism) will increase in the coming decades.
Interestingly, those suggesting that morbidity is being compressed into the later years of life have not considered pain. No baselines are available to allow tracking prevalence and incidence of pain and its impact on morbidity and mortality in the older adult population.
IS PAIN AN IMPORTANT SOURCE OF MORBIDITY IN THE ELDERLY? A third scenario is that poorly controlled pain is an important but currently unrecognized source of both mortality and morbidity in the aged. As suggested by the data in Figures 1 and 2, elderly people are not a significant portion of patients treated at chronic pain clinical centers.
Figure 1. Percentage of Chronic Pain Patients as a Function of Age Evaluated at the Medical College of Virginia Chronic Pain Clinic (N = 174)*
*NOTE. Patients were consecutive.
Source: Harkins, Kwentus, & Price (1984). Reprinted with permission of Lippincott-Raven Publishers.
Figure 2. Age of Patients Attending an Orofacial Pain Clinic (N = 310)*
*NOTE. Patients were consecutive.
Source: Harkins (1996).
Does pain sensitivity decrease with age? Is the fact that few older adults are treated at chronic pain clinics because of decreased sensitivity to and perception of pain? Acute pain associated with ischemic conditions (acute myocardial infarction) is often absent in older adults. This confuses diagnosis, delays treatment, and increases mortality. It is, however, problematic to generalize that sensitivity to all forms of pain is reduced in elderly people. The experimental evidence does not support well-defined decrements in cutaneous and pressure pain sensitivity with age in the later years of life (Harkins & Warner, 1980; Harkins, Kwentus, & Price, 1990, Harkins et al., 1994). The prevalence and, more critically, the intensity of musculoskeletal pain in the general population increase with age and are responsible for considerable suffering in these elderly people (Harkins, Lagua, Price, & Small, 1995; Harkins, Price, Bush, & Small, 1994). The low number of older patients who attend pain diagnostic and treatment centers (Figures 1 and 2) does not represent systematic changes in pain sensitivity with aging, but rather self- and healthcare system referral biases. This is a sociocultural phenomenon and not biological senescence.
Pain occurs in approximately 50% of patients with idiopathic Parkinsonism (Tison et al., 1996). The quality, quantity, impact, and etiology of this type of pain have not been studied systematically. However, postsurgical pain is undertreated in older patients (Melzack, Abbott, Zackson, Mulder, & Davis, 1987), resulting in longer hospital stays and increased cost of hospitalization. The effects of pain on quality of life, alcohol and drug abuse, depression, and suicide in elderly individuals have not been systematically evaluated. The potential for drug-drug interactions and poor compliance with treatment regimens are particular challenges in pain management in the older adult. Factors influencing these deserve systematic attention.
Does Alzheimer's disease influence pain sensitivity? Dementia of the Alzheimer's type (DAT) is the major reason for long-term care placement of older adults and is the fourth leading cause of death in those 65 years of age and older. Pain sensitivity may be diminished in individuals with DAT (S.W. Harkins, clinical observation). Is this true? Or is it an artifact of the diminished cognitive, attention, and communication ability of these patients? R.D. Helme (personal communication, August 1996) advises considering DAT patients with apparent chronic pain as having recurrent acute pain. This position recognizes the critical nature of cognitive processes as determinants of pain-related suffering. Gibson, Voukelantos, Bradbeer, & Helme (1996) have demonstrated that psychophysiological responses to acute, experimental pain are not influenced by dementia of the Alzheimer's type, at least in the early-to-middle stages of these progressive brain disorders. Nevertheless, it is particularly difficult to recognize and treat pain in these patients, particularly those in the more advanced stages.
At any given time, approximately 5% of those 65 years of age or older reside in long-term care settings, more than 60% of whom suffer from DAT. Lifetime risk for residency in a nursing home is approximately 40%. Pain among residents in long-term care facilities is poorly recognized, assessed, monitored, and controlled (Stein & Ferrell, 1996). This results in significant unnecessary discomfort and suffering among the most vulnerable. Humanitarian care requires that we confront and address these issues.
A number of pressing questions about pain in nursing home settings remain unanswered. For example: Are agitation and other disruptive behavior in "problem" nursing home residents an expression of unrecognized and untreated pain? Is the high mortality following hip fracture in elderly people due, in part, to poor pain control?
POLICY: A fourth scenario is that of successful, healthful living. Many of the behaviors in which we engage and many of the environments in which we live influence our risk of chronic illnesses (Timiras, 1994). We tend to accept this in a context of "normal" aging--in contrast to "successful" aging, in which our own behaviors act to decrease risk of chronic impairment. Accepting pain as a natural consequence of normal aging is not consistent with successful, healthful living in later life.
Some years ago there was considerable controversy over the difference between presenile DAT and "senility." This controversy resulted in heated discussion and questions of assessment and diagnosis. Today the field has moved forward because of standardization of clinical assessment instruments and protocols (McKhann et al., 1984), with increasing insight into natural history (Mortimer, Ebbitt, Sung-Pyo, & Finch, 1992) and etiology of dementias in later life. The activities of the National Institutes of Health facilitated progress, particularly the National Institute of Aging's creation of collaborative research centers that specifically address epidemiology, diagnosis, treatment, and natural history of DAT. Such efforts, as well as those of the Alzheimer's Disease Association and the American Association of Retired Persons, focused attention on education of health delivery professionals, family members caring for older adults with dementing illnesses, and the general population about the nature of Alzheimer's disease and its psychological, social, and economic burden.
A Critical Question
Is it time to begin a collaborative research program to standardize assessment and diagnosis of recurrent and chronic pain as well as determine the epidemiology and etiology of pain in the frail elderly? Such a "scenario" would improve the quality of life of many older adults. Is the seventh age "... sans teeth, sans eyes, sans taste, sans everything" ...except pain?
References
Chakour, M.C., Gibson, S.J., Bradbeer, M., & Helme, R.D. (1996). The effect of age on A-delta and C-fiber thermal pain perception. Pain, 64,143-152.
Fries, J.F. (1980). Aging, natural death, and the compression of morbidity. New England Journal of Medicine, 300, 130-135.
Fries, J.F., Green, L.W., & Levine, S. (1989). Health promotion and the compression of morbidity. Lancet, 4, 481-483.
Gibson, S.J., Voukelantos, X., Bradbeer, M., & Helme, R.D. (1996). Pain perception in the cognitively impaired elderly. 8th World Congress on Pain. [Abstract 281], 521. Seattle: IASP Press.
Harkins, S. W. (1996). Geriatric pain: Pain perceptions in the old. Clinics in Geriatric Medicine, 12, 435-459.
Harkins, S. W., Davis, M., Bush, F., & Kasberger, J. (1996). Suppression of first pain and slow temporal summation of second pain in reaction to age. Journal of Gerontology: A. Biological Science and Medical Science, 51, M260-M265.
Harkins, S.W., Kwentus, J., & Proce, D.D. (1984). Pain in the elderly. Inc. Benedetti (Ed.), Advances in Pain Research and Therapy (Vol. 14, pp. 103-112). New York: Raven Press.
Harkins, S. W., Kwentus, J. , & Price, D.D. (1990). Pain and suffering in the elderly. In J.T. Bonica (Ed.), The clinical management of pain, (2nd ed., pp. 552-559) Philadelphia: Lea & Febiger.
Harkins, S.W., Lagua, B., Price, D.D., & Small, R. (1995). Geriatric pain. In R. Roy, (Ed.), Chronic pain in old age: An integrated biopsychosocial perspective (pp. 127-163). Toronto: University of Toronto Press.
Harkins, S. W., & Price, D.D. (1992). Assessment of pain in the elderly. In D.C. Turk & R. Melzack (Eds.), Handbook of pain assessment (pp. 315-331). New York: Guilford Press.
Harkins, S.W., Price, D.D., Bush, F.M., & Small, R. (1994). Geriatric pain. In P.D. Wall & R. Melzack, (Eds.), Textbook of pain (pp. 769-784). Edinburgh: Churchill Livingstone.
Harkins, S. W., & Warner, M. H. (1980). Age and pain. In C. Eisdorfer (Ed.), Annual review of gerontology and geriatrics (Vol. 1, pp. 315-331). New York: Springer.
Harkins, S.W., Price, D.D., & Martelli, M. (1986). Effects of age on pain perception: Thermonociception. Journal of Gerontology, 41, 58-63.
Masoro, E. J. (1987). Biology of aging: Current state of knowledge. Archives of Internal Medicine, 147, 166-169.
Masoro, E. J. (1988). Physiological system markers of aging. Experimental Gerontology, 23, 391-397.
McKhann, G., Drachman, D., Folstein, M., Katzman, R., Price, D., & Stadian, E. M. (1984). Clinical diagnosis of Alzheimer's disease: Report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease. Neurology, 34, 939-944.
Melzack, R., Abbott, F.V., Zackon, W., Mulder, D.S., & Davis, M.D. (1987). Pain on a post surgical ward. Pain, 29, 67-72.
Mortimer, J.A., Ebbitt, B., Sung-Pyo, J., and Finch, M.D. (1992). Predictors of cognitive and functional progression in patients with probable Alzheimer's disease. Neurology, 42, 1689-1696.
Stein, W., & Ferrell, B.A. (1996). Pain in the nursing home. Clinics in Geriatric Medicine, 12, 601-613.
Timiras, P.S. (1994). Physiological basis of aging and geriatrics (2nd ed.). Boca Raton, FL: CRC Press.
Tison, F., Wenning, G. K., Donte, M.A., Poewe, W.R., Henry, P., Quinn, N.P. (1996). Pain in multiple system atrophy. Journal of Neurology, 243, 153-156.
Stephen W. Harkins is professor of gerontology, psychiatry, and biomedical engineering and director of the Psychophysiology and Memory Laboratory at Virginia Commonwealth University in Richmond, VA.