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Library of Congress Cataloging-in-Publication Data
Spar, James E.
Clinical manual of geriatric psychiatry / James E. Spar, Asenath La Rue.—1st ed.
p. ; cm.
Includes bibliographical references and index.
ISBN 1-58562-195-1 (pbk. : alk. paper)
1. Geriatric psychiatry—Handbooks, manuals, etc. 2. Older people—Mental
health—Handbooks, manuals, etc. 3. Older people—Psychology—Handbooks,
manuals, etc.
[DNLM: 1. Aged. 2. Mental Disorders—diagnosis. 3. Mental Disorders—therapy.
4. Age Factors. 5. Aging—psychology. WT 150 S736c 2006] I. La Rue, Asenath,
1948– II. Title.
RC451.4.A5S63 2006
618.97'689—dc22
2006005228
British Library Cataloguing in Publication Data
A CIP record is available from the British Library.
Contents
1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
An Aging World . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
Health and Functioning of Older Adults . . . . . . . . . . . . . . 3
Mental Disorders in Later Life . . . . . . . . . . . . . . . . . . . . . . 6
Barriers to Geriatric Mental Health Care. . . . . . . . . . . . . . 8
Diversity in Patterns of Health and Aging. . . . . . . . . . . .12
Working Effectively With Older Adults. . . . . . . . . . . . . . .15
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .16
2 Normal Aging . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21
Conceptual Issues. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .21
Cognitive Abilities in Later Life: A Processing
Resource Model . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .23
Personality and Emotional Changes . . . . . . . . . . . . . . . .38
Social Context of Aging . . . . . . . . . . . . . . . . . . . . . . . . . .43
Biological Aging. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .48
Aging and the Clinical Process. . . . . . . . . . . . . . . . . . . . .50
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .61
3 Mood Disorders—Diagnosis . . . . . . . . . . . . . . . . 67
“Normal” Grief (Bereavement) . . . . . . . . . . . . . . . . . . . .68
Complicated Grief . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .70
Depression Due to a General Medical Condition . . . . .70
Substance-Induced Mood Disorder . . . . . . . . . . . . . . . .76
Major Depression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .80
Dysthymic Disorder. . . . . . . . . . . . . . . . . . . . . . . . . . . . . .91
Minor Depression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .92
Depressive Personality Disorder . . . . . . . . . . . . . . . . . . .95
Laboratory Evaluation of Depression . . . . . . . . . . . . . . .95
Psychological Tests . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .96
Symptom Rating Scales and Depression Screening . . .97
Assessing Suicidality in the Elderly . . . . . . . . . . . . . . . .105
Theories of Depression . . . . . . . . . . . . . . . . . . . . . . . . .107
Hypomania and Mania . . . . . . . . . . . . . . . . . . . . . . . . . .110
Mixed Mood Disorder. . . . . . . . . . . . . . . . . . . . . . . . . . .117
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .117
5 Dementia and
Alzheimer’s Disease. . . . . . . . . . . . . . . . . . . . . . 173
Identifying the Dementia Syndrome. . . . . . . . . . . . . . .173
Common Etiologies of Dementia . . . . . . . . . . . . . . . . .186
Alzheimer’s Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . .192
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .221
Resources for Dementia Caregivers . . . . . . . . . . . . . . .228
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 389
1
Introduction
An Aging World
For the first time in history, most people in societies such as our own can plan
on growing old. Life expectancy from birth has increased dramatically in the
United States, from about 47 years in 1900 to 77.3 years in 2002 (Federal In-
teragency Forum on Aging-Related Statistics 2004). Even those people who
are currently “old” can expect to live for many years. For men at age 65, aver-
age life expectancy is more than 16 years, and for women at age 65, it is almost
20 years; at age 85, men can expect to live 6 more years and women 7 years
(Federal Interagency Forum on Aging-Related Statistics 2004).
More than 20% of the current U.S. population are older than age 55, and
more than 12% are 65 or older (Federal Interagency Forum on Aging-Related
Statistics 2004). The elderly population is the only age segment of the popu-
lation that is expected to grow substantially in the next quarter century, so
that by the year 2030, one in three Americans will be age 55 or older, and one
in five will be at least age 65. Very old people (85 years and older) constitute
one of the fastest-growing subgroups of the elderly population (Figure 1–1).
In 1900, a little more than 100,000 people were age 85 years or older in the
United States, compared with an estimated 4.2 million in 2000 (National
Center for Health Statistics 2004). By 2050, there will be 19 million to 24
million people in this 85 and older age group, or nearly 5% of the total pop-
ulation. In 2003, more than 50,000 U.S. residents were 100 years or older, an
increase of 36% since 1990 (Administration on Aging 2004).
1
2 Clinical Manual of Geriatric Psychiatry
100
80
60
Population
(millions)
65 and older
40
85 and older
20
0
1900 1930 1960 1990 2020 2050
Projected
Figure 1–1. Populations of older adults in the United States (in millions).
Source. Adapted from Federal Interagency Forum on Aging-Related Statis-
tics 2004.
100
80
Americans age ≥65 (%)
Men Women
60
40
20
0
Heart Hyper- Stroke Emphy- Asthma Chronic Cancer Diabetes Arthritic
disease tension sema bronchitis symptoms
Figure 1–2. Percentage of people age 65 and older with selected chronic
conditions, 2001–2002.
Source. Adapted from Federal Interagency Forum on Aging-Related Statis-
tics 2004.
agency Forum on Aging-Related Statistics 2004). Of disabled older people
living in the community, 66% received informal care only, generally from rel-
atives; 26% received a combination of formal and informal services; and 9%
had formal care only (Federal Interagency Forum on Aging-Related Statistics
2004). The proportion receiving paid care has increased since the early 1980s,
reflecting improved financial resources of older persons as well as liberaliza-
tion in coverage rules under Medicare and Medicaid. Figure 1–3 shows age
trends in independent and assisted living within the United States.
Those with chronic needs that cannot be met at home generally receive care
in nursing homes. Although fewer than 5% of elderly Americans are in nursing
homes at a given time, the proportion of older persons requiring such care in-
creases quite sharply with age (see Figure 1–3). Among persons who reached
their 60th birthday in 1990, more than one-half of the women and one-third
of the men are expected to enter a nursing home at some point in the future.
However, older black Americans and elders from other minority groups use
Introduction 5
1
100 5
1
5 Long-term-
2 3
19 care facility
Medicare enrollees (%)
80 7
Community housing
with services
60 93
98
92
Traditional
74
40 community
20
0
≥65 65–74 75–84 ≥85
Age (years)
shared by other developed nations. In 2001, the average annual cost for el-
derly residents of long-term-care facilities in the United States was $46,810,
compared with $8,466 for community residents of comparable age (Federal
Interagency Forum on Aging-Related Statistics 2004). Total Medicare spend-
ing increased from $33.9 billion in 1980 to $252.2 billion in 2002 and is pro-
jected to grow to twice that amount by 2012 (Centers for Disease Control
and Prevention 2004).
These trends present a significant challenge to the health care community.
The need to learn about aging and older people extends throughout the med-
ical and mental health professions. Creative approaches are required to stem
rising costs while maintaining quality assessment and intervention. Alliances
with families and other natural supports must be formed to ensure continuity
of care, and the strengths of older patients themselves must be marshaled to
cope with illness and to interact effectively within the health care system.
costs for patients in primary care (Simon et al. 1995), and over time, depres-
sion is associated with decrements in function and well-being that are similar
to, or greater than, those associated with chronic medical disease (Hays et al.
1995). Geriatric depression can be treated effectively with standard therapies
in 60%–80% of cases (U.S. Public Health Service 1999), but it is unlikely to
resolve spontaneously. Depression, anxiety, and alcohol and drug abuse in the
elderly today are only about one-quarter to one-third as common as among
middle-aged persons, and as the 55 million baby boomers grow old, their
mental health needs may prompt a crisis in geriatric care (Jeste et al. 1999).
Many older people without major mental disorders experience adjust-
ment reactions to personal stresses, bereavement, pain syndromes, and sleep
disturbance. Education and interventions directed at these problems may pre-
vent more serious psychiatric or medical problems from developing. The im-
portance of increasing prevention efforts for older adults as well as other age
groups was underscored in the U.S. surgeon general’s report on mental health
(U.S. Public Health Service 1999).
For psychiatrists, therefore, it is important not only to identify and treat
specific psychiatric disorders but also to provide education, support, and pre-
ventive interventions to strengthen older people and their families in manag-
ing common stresses of aging.
living and community-based programs for senior care, mental health services
are patchy and largely unregulated (Moak and Borson 2000).
Contemporary older Americans report less past use of mental health ser-
vices than do younger adults, and older Americans are less likely to express a
need for such services (Klap et al. 2003; Wetherell et al. 2004). Older adults
most often turn to primary care providers for help with mental health problems
(Kaplan et al. 1999), and typically, only one-half or fewer follow through with
referrals to specialty mental health providers. In a recent multisite randomized
trial, elderly primary care patients who screened positive for depression, anxiety,
or increased risk of alcohol use problems were offered collaborative mental
health services within primary care or enhanced referral assistance (e.g., sched-
uling, transportation, and payment assistance to outside mental health special-
ists) (Bartels et al. 2004). A significantly higher percentage of the patients
followed through on pursuing mental health treatment when it was available
within primary care (71% vs. 49%), and they completed more mental health
visits overall, than did those referred to mental health clinics or specialists, even
with enhanced assistance aimed at increasing the odds of compliance with the
referral. As the baby boom generation edges into the geriatric age range, the
“stiff upper lip” approach to managing emotional distress (Wetherell et al.
2004) may change, but the desire for proximal, integrated medical and mental
health services is likely to continue. Without more effective collaborative care,
underrecognition of mental health problems, especially among older patients
(Young et al. 2001), is likely to continue for several reasons:
chiatrist are half or less of the typical fee expected for this service). The elderly,
who generally have many health care needs, often have trouble coordinating
their own care, but there is usually no reimbursement for mental health pro-
viders to help with coordination.
The need for psychiatrists who are capable and willing to work with el-
derly patients, both in primary care and in specialty roles, is clear. Effective
models for collaborative medical and mental health services recently have
been developed for primary care (see Chapter 4, “Mood Disorders—Treat-
ment”), but this approach needs to be extended beyond clinical research, and
additional models need to be developed for geropsychiatric services within
community mental health settings and the full spectrum of long-term-care
services (Moak and Borson 2000). Older adults with medical comorbidity,
the oldest old, and those with significant chronic mental illness present par-
ticular challenges to existing service models (Borson et al. 2001).
100
2003
80
2050–projected
Americans age ≥65 (%)
60
40
20
0
Non-Hispanic Black alone Asian alone All other races alone Hispanic
white alone or in combination of any race
Figure 1–4. Percentage of population age 65 and older, by race and His-
panic origin.
Source. Adapted from Federal Interagency Forum on Aging-Related Statis-
tics 2004.
comparable to non-Hispanic white Americans in rates of hypertension but
were more likely to have diabetes. By contrast, older white people were more
likely to have some form of cancer than were older Hispanic or black people
(National Center for Health Statistics 2004). Black and Hispanic elders are
less well educated than non-Hispanic white and Asian elders (see Figure 2–1
in Chapter 2, “Normal Aging”), and older black and non-Hispanic white per-
sons are more likely to find themselves living alone in old age than are their
Hispanic or Asian peers (see Figure 2–2 in Chapter 2).
Reports of prevalence of mental disorders for minority groups must be
viewed with caution because language and cultural differences can affect re-
sults on tests and interviews assessing depression, dementia, and other psychi-
atric disorders. However, data are emerging on the relative prevalence of
mental health–related problems in various groups and on availability and use
of mental health services. A recent supplement (U.S. Public Health Service
14 Clinical Manual of Geriatric Psychiatry
2005) to Mental Health: A Report of the Surgeon General (U.S. Public Health
Service 1999) concluded that the prevalence of mental disorders within the
most populous racial and ethnic minority groups in the United States (blacks,
Hispanics, and Asian Americans and Pacific Islanders) is similar to that of
white Americans. Among older adults, however, some important differences
in prevalence of mental health–related conditions have been documented for
racial/ethnic and gender subgroups. For example, the suicide rate is much
higher among non-Hispanic white men than in any other elderly subgroup
(National Center for Health Statistics 2004), and rates of alcohol abuse and
dependence are higher among elderly black men and women compared with
elderly white and Hispanic persons (U.S. Public Health Service 1999).
The surgeon general’s recent supplement underscored the pivotal role of
culture in maintaining mental health and the continuing, often striking, dis-
parities in availability of and access to mental health services among Ameri-
cans from minority backgrounds. Although not specific to older adults, the
recommendations for reducing barriers are as important for diverse geriatric
populations as they are for younger groups. The recommendations include
the following:
Women constitute the majority of older persons in the United States, out-
numbering men by a ratio of nearly 3 to 1 by age 85 and older. Important
gender differences have been reported for longevity, prevalence of specific
Introduction 15
The psychiatrist also must have patience and skill in explaining diagnoses
and treatments and in assisting older people in medical decision making. El-
derly patients often defer to physicians without truly comprehending benefits
and risks. This deference may increase efficiency of care in the short run, but
it may place the older person at risk for iatrogenic illness (e.g., delirium sec-
ondary to drug interactions). Finally, it is helpful to have a willingness to ex-
plore one’s own feelings about aging, as well as to be open to discussing older
patients’ reservations about the wisdom of youth. Elderly patients may be in-
clined to view younger therapists as similar to their children, and the thera-
pist, in response, may experience the reactivation of unresolved conflicts with
parents or grandparents or unresolved issues related to his or her own personal
aging (Meador and David 1994).
References
Administration on Aging: A Profile of Older Americans: 2004. Washington, DC, Ad-
ministration on Aging, 2004. Available at: http://www.aoa.gov/prof/Statistics/
profile/2004/profiles2004.asp. Accessed March 9, 2006.
Areán PA, Unützer J: Inequities in depression management in low-income, minority,
and old-old adults: a matter of access to preferred treatments? J Am Geriatr Soc
51:1808–1809, 2003
Introduction 17
Bartels SJ, Coakley EH, Zubritsky C, et al: Improving access to geriatric mental health
services: a randomized trial comparing treatment engagement with integrated
versus enhanced referral care for depression, anxiety, and at-risk alcohol use. Am
J Psychiatry 161:1455–1462, 2004
Boise L, Camicioli R, Morgan DL, et al: Diagnosing dementia: perspectives of primary
care physicians. Gerontologist 39:457–464, 1999
Borson S, Unützer J: Psychiatric problems in the medically ill, in Comprehensive Text-
book of Psychiatry/VII. Edited by Kaplan HI, Sadock BJ. Philadelphia, PA, Lip-
pincott Williams & Wilkins, 2000, pp 3045–3053
Borson S, Bartels SJ, Colenda CC, et al: Geriatric mental health services research:
strategic plan for an aging population. Am J Geriatr Psychiatry 9:191–204, 2001
Centers for Disease Control and Prevention and Merck Institute of Aging and Health:
The State of Aging and Health in America 2004. Available at: http://www.cdc.gov/
aging/pdf/State_of_Aging_and_Health_in_America_2004.pdf or http://
www.miahonline.org/press/content/11.22.04_SOA_Report.pdf. Accessed Au-
gust 26, 2005.
Charney DS, Reynolds CF III, Lewis L, et al: Depression and bipolar support alliance
consensus statement on the unmet needs in diagnosis and treatment of mood
disorders in late life. Arch Gen Psychiatry 60:664–672, 2003
Chodosh J, Petitti DB, Elliott M, et al: Physician recognition of cognitive impairment:
evaluating the need for improvement. J Am Geriatr Soc 52:1051–1059, 2004
Cohen JE: Human population: the next half century. Science 302:1172–1175, 2003
Cole SA, Christensen JF, Raju M, et al: Depression, in Behavioral Medicine in Primary
Care: A Practical Guide. Edited by Feldman MD, Christensen JF. Stamford, CT,
Appleton & Lange, 1997, pp 177–192
Crystal S, Sambamoorthi U, Walkup JT, et al: Diagnosis and treatment of depression
in the elderly Medicare population: predictors, disparities, and trends. J Am Geri-
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Evans DA, Funkenstein HH, Albert MS, et al: Prevalence of Alzheimer’s disease in a
community population of older persons. JAMA 262:2551–2556, 1989
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Key Indicators of Well-Being. Washington, DC, U.S. Government Printing
Office, 2004. Available at: http://www.aoa.gov/prof/Statistics/profile/2004/
profiles2004.asp. Accessed March 9, 2006.
Ganguli M, Rodriguez E, Mulsant B, et al: Detection and management of cognitive
impairment in primary care: the Steel Valley Seniors Survey. J Am Geriatr Soc
52:1668–1675, 2004
Gatz M, Pearson CG: Ageism revisited and the provision of psychological services. Am
Psychol 43:184–194, 1988
18 Clinical Manual of Geriatric Psychiatry
Hays RD, Wells KB, Sherbourne CD, et al: Functioning and well-being outcomes of
patients with depression compared with chronic general medical illness. Arch Gen
Psychiatry 52:11–19, 1995
Hybels CF, Blazer DG: Epidemiology of late-life mental disorders. Clin Geriatr Med
19:663–696, 2003
Jeste DV, Alexopoulos GS, Bartels SJ, et al: Consensus statement on the upcoming
crisis in geriatric mental health: research agenda for the next two decades. Arch
Gen Psychiatry 56:848–853, 1999
Kaplan MS, Adamek ME, Calderon A: Managing depressed and suicidal geriatric pa-
tients: differences among primary care physicians. Gerontologist 39:417–425,
1999
Klap R, Unroe KT, Unützer J: Caring for mental illness in the United States: a focus
on older adults. Am J Geriatr Psychiatry 11:517–524, 2003
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the United States. Arch Gen Psychiatry 45:977–986, 1988
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to Mental Health: A Report of the Surgeon General. Rockville, MD, Office of
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mentalhealth. Accessed March 9, 2006.
Introduction 19
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older and younger primary care patients. Int J Psychiatry Med 34:219–233, 2004
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2
Normal Aging
Conceptual Issues
Who Is Old?
Biological and psychological aging changes usually occur gradually, over years or
decades, and as a result, there is no single age at which people in general can be
said to be old. The common practice of designating people older than 65 as “old”
began in Germany in the 1880s, when Otto von Bismarck selected 65 as the start-
ing age for certain social welfare benefits. In the United States, the age at which
full Social Security benefits can be received has now been raised to 67 years for
persons born in 1960 and later. Although this change is primarily a response to
fiscal concerns, the upward shift is also indicative of the increasing vitality and
productivity of the aging population. According to a recent national survey, 63
years is the average age at which Americans perceive individuals as becoming old,
but there was much variation in perceptions (Abramson and Silverstein 2004).
More than one-third of the sample named an age greater than 70 as the start of
old age, whereas another one-fourth cited ages less than 60 years.
Gerontologists often draw finer chronological demarcations within the
general group of aging persons. Comparisons may be made between the young-
old and the old-old (generally, those younger than and older than age 75, respec-
tively) or between these groups and the oldest old (generally 85 years and older).
Although these distinctions are also arbitrary, they can be useful in identifying
important differences in levels of functioning and can help to limit overgener-
alization about characteristics of older adults. It is also important to keep in
21
22 Clinical Manual of Geriatric Psychiatry
mind that individuals may age faster in some dimensions than others (e.g.,
being “old” physically but more youthful psychologically or socially).
ing trajectories may exist, with varying trends for different genetic and socio-
cultural subgroups. Intraindividual variability (i.e., fluctuating performance
within and across assessments) is also increased in old age, especially for cog-
nitive and physical performance measures. Heightened variability within the
individual has been linked to an accelerated rate of cognitive decline over time
and may be a marker for neurobiological aging (MacDonald et al. 2003).
Processing Speed
Perhaps the most predictable of all cognitive changes is the reduced speed of
information processing and response. Slowed execution of component per-
ceptual and mental operations can affect attention, memory, and decision
making and can influence performance even on tasks that have no obvious
speed requirements (Salthouse 1996).
Working Memory
Working memory refers to short-term retention and manipulation of informa-
tion held in conscious memory, a type of “online” cognitive processing (Bad-
deley 1986). Examples include consciously recalling a telephone number long
enough to write it down, mentally calculating the sale price of an item that is
reduced by 15%, and mentally traversing a route that one intends to walk or
drive. Information fades from working memory within about 2 seconds, so to
keep details “alive” for a longer time requires active rehearsal or continuing re-
focusing of attention.
Aging is associated with a decline in working memory skills, especially
when active manipulation of information is required (e.g., repeating numbers
24 Clinical Manual of Geriatric Psychiatry
ing changes in the hippocampus and entorhinal cortex, with some studies
noting minimal cell loss with normal aging in these regions and others show-
ing decremental changes. Areas in which there is relative sparing with age in-
clude the globus pallidus, the paleocerebellum, the sensory cortices, and the
pons (Raz 2000).
Some of the behavioral changes in aging, such as slowed information pro-
cessing and response, may be related to generalized changes such as decreased
brain volume and white matter density. Other changes appear to mirror the se-
lective pattern of differential change in prefrontal cortical structures and striatal
dopaminergic nuclei. Decreased working memory, problems with effortful
learning and recall, and changes in efficiency of executive functions are some of
the findings that suggest a mild degree of frontal or subcortical brain dysfunc-
tion in normal aging (Prull et al. 2000). The “frontal lobe hypothesis” is perhaps
the most popular neuropsychological model of normal aging at this time. How-
ever, hippocampal changes also may play a role in normal aging memory. Hip-
pocampal volume, as measured by magnetic resonance imaging, correlates with
memory performance in older adults, and those with smaller hippocampal vol-
umes are at greater risk for developing dementia. What remains to be resolved,
however, is whether reduced hippocampal volume is truly within the normal
aging spectrum or instead is a preclinical phase of dementia.
Functional neuroimaging studies have shown less regional specificity in
older adults’ patterns of brain activation to various cognitive tasks compared
with the regional specificity in young adults (Prull et al. 2000; Raz 2000). One
interpretation of this finding has been that older persons must recruit more
neural systems to perform even relatively simple mental operations. This inter-
pretation coincides in a general way with the behavioral model of reduced pro-
cessing resources and increased susceptibility to overload on complex tasks.
Intelligence
Vocabulary, fund of Stable or increasing May decline slightly in very old age; most pronounced on novel
knowledge tasks
Perceptual-motor skills Declining Decline begins by ages 50–60
Attention
Attention span Stable to mild decline
Complex attention Mild decline Problems with dividing attention, filtering out noise, shifting
attention
Language
Communication Stable In absence of sensory impairment
Syntax, word knowledge Stable Varies with education
Fluency, naming Mild decline Occasional word-finding lapses
Comprehension Stable to mild decline Some erosion in processing complex messages
Discourse Variable May be more imprecise, repetitive
Memory
Short-term (immediate) Stable to mild decline Forward digit span intact (7±2 items), but easily disrupted by
interference
Working Mild to moderate decline Reduced ability to manipulate information in short-term
memory
Secondary (recent) Moderate decline Encoding and retrieval deficits; storage intact
Table 2–1. Aging effects on cognitive performance (continued)
Ability Direction of aging change Comment
Memory (continued)
Implicit Stable to mild decline May recall incidental features more easily than consciously
processed information
Remote Variable Intact for major aspects of personal history
Prospective Variable Mild to moderate decline on laboratory tasks, but older adults
often outperform younger people on naturalistic prospective
memory tasks
Visuospatial
Design copying Variable Intact for simple but not complex figures
Topographic orientation Declining Most noticeable in unfamiliar terrain
Executive functions
Cognitive flexibility Mild to moderate decline Slower and less accurate in shifting from one thought or action
to another
Logical problem solving Declining Some redundancy and disorganization
Practical reasoning Mild to moderate decline Qualitatively intact, but reduced efficiency on complex or novel
Normal Aging
tasks
Speed Declining Slowing of thought and action is the most reliable aging change
27
28 Clinical Manual of Geriatric Psychiatry
of abilities shown in Table 2–1 is less apparent among the oldest-old (e.g., 85 or
older), for whom some studies report a generalized pattern of gradual decline. An-
other important qualification concerns secular trends in levels of performance. In-
tellectual performance scores have been increasing over the past few decades, and
the rate of increase is higher among older, as opposed to younger, adults. For ex-
ample, vocabulary scores on the commonly used Wechsler Adult Intelligence
Scale (Wechsler 1997) have increased nearly 5 IQ points per decade for 65- to 74-
year-olds, compared with 1.5 points for 18- to 24-year-olds (Uttl and Van Alstine
2003). Higher absolute levels of intellectual ability may benefit contemporary
older adults in learning new information and acquiring new skills (see the subsec-
tion “Effect of Cognitive Change on Everyday Function” later in this section).
Normal Aging
than women.
Racial and ethnic differences Performance differences favoring elderly white persons have been reported on some cognitive tests,
but when education is equated across groups, these differences are reduced or eliminated.
29
30 Clinical Manual of Geriatric Psychiatry
younger adults. For example, elderly people report less spontaneous use of mne-
monic strategies than do younger people and do not appear to capitalize as readily
on the organization inherent in words or actions as a basis for learning and recall.
The shallower memory traces that result are subsequently harder to retrieve, espe-
cially without the aid of reminders or cues. If older individuals are explicitly in-
structed to use mnemonics or organizational strategies, their learning and recall
often improve dramatically, at least in the short term.
Active encoding and retrieval may require greater expenditure of effort and
energy than most older people can afford. Declines in effortful processing may be
caused by altered neurotransmitter functions (especially catecholamines). Alterna-
tively, such processing changes may be seen as an adaptive response to the dimin-
ished demands of older adults’ everyday lifestyles. Also, it is important to note that
some healthy and active elderly people do as well on demanding recent memory
tasks as do more average young adults.
Older adults (and younger persons, too) often ask about ways to improve
their recall of everyday information. Mnemonic training can produce notable
gains in troublesome areas, such as recall of names, locations of objects, and lists
of things to be purchased or done, for old as well as young adults. Training is most
likely to be effective for young-old persons as opposed to the oldest-old and for
individuals with no decline on mental status examination (Verhaeghen et al.
1992). Training also works best in an individual or a small-group format and with
relatively short (e.g., half-hour) sessions as opposed to longer workshops or lec-
tures. Follow-up studies often show that people discontinue memory techniques
they have learned within a few weeks. In some cases, this may simply mean that
the training served its intended purpose (i.e., to prove that one can remember
more if need be), but it is also likely that the use of mnemonics may be too effort-
demanding in the long run. A greater drawback of mnemonic training ap-
proaches is that benefits often fail to generalize to everyday tasks not specifically
included in training (Ball et al. 2002). Education and counseling about memory
improvement is best approached from a broad perspective, in which improving
memory is seen as part of an overall wellness plan.
Of the many self-help books providing advice on how to maintain memory
function into old age, Keep Your Brain Young (McKhann and Albert 2002) is
among the best in terms of readability, breadth, and linkage to research. Learning
Throughout Life (National Retired Teachers Association et al. 2004) is another
good guide for the general reader. In The Memory Prescription, Small (2004) out-
32 Clinical Manual of Geriatric Psychiatry
lines a 2-week program of diet, exercise, stress reduction, and mental exercise de-
signed to boost brain function. The program is derived from an ongoing program
of research, but independent studies are needed to assess benefits of this approach.
Executive Function
The term executive function refers to cognitive abilities necessary for complex goal-
directed behavior and adaptation to change. Some of the skills included in this
category are reasoning, planning, anticipating outcomes of behavior, directing at-
tentional resources in a flexible manner, monitoring one’s own behavior, and self-
awareness. Performance of such skills requires the coordinated activity of multiple
regions of the brain and can be affected by injury to several different areas. How-
ever, the prefrontal cortex and frontal-subcortical brain circuits have been shown
to play a central role in executive functions. As noted earlier, normal aging has a
greater decremental effect on these brain regions than on many other areas, and
predictably, age differences are relatively large on executive function tasks (see
Table 5–5 in Chapter 5, “Dementia and Alzheimer’s Disease,” for examples of
neuropsychological tests of executive function). Performance on executive func-
tion tests correlates more closely than scores on many other cognitive tasks with
activities of daily living, and changes in executive function may play a role in de-
termining which older people come to clinical attention for mild cognitive
changes (Royall et al. 2005).
Although research generally shows that older adults do worse than young or
middle-aged persons on both laboratory-based and practical reasoning tasks
(Thompson and Dumke 2005), not all studies show this trend. For example, one
recent investigation found that cognitively healthy 65- to 74-year-olds provided
more relevant solutions to problem situations—such as trying to improve the
acrimonious tone of a meeting, dealing with excessive demands by one’s sons to
babysit their children, or having blood drawn by a physician who is having diffi-
culty with the procedure—than did a comparison group of 20- to 29-year-olds
(Artistico et al. 2003). In general, interpersonal problem solving is an area of
strength for older people (Thompson and Dumke 2005).
Several factors help to maintain daily function in the face of mild cognitive
decline (Park 1999). The very gradual nature of age-related change allows time to
adjust to diminished speed and efficiency in cognitive function. The fact that gen-
eral knowledge is well preserved in later life allows older adults to access a broad
base of information that is useful in solving problems and addressing everyday
needs. With practice, many tasks become automatic and require little cognitive
processing or effort to perform, and maintaining a familiar environment and rou-
tine further reduces cognitive load. Also, many older adults make frequent and ef-
fective use of external cognitive aids such as writing reminder notes.
Some areas, such as driving and monitoring medications, pose particular
risks (Park 1999). Older adults are more likely to be involved in accidents while
driving than are younger persons, particularly in certain situations (e.g., left
turns in intersections). Cognitive research has identified a measure of peripheral
vision (so-called useful field of vision) that is more predictive of driving success
than are standard visual acuity measures, and this research also has found that
older adults can improve driving skill through a combination of perceptual
training and traditional drivers’ education classes (see Chapter 9, “Competency
and Related Forensic Issues,” for additional information on driving). Regarding
medications, it is important to note that some studies show better compliance
with medication regimens among older adults than among younger or middle-
aged persons, particularly if the older adults are taking only a single medication
for a long-standing condition (e.g., hypertension or arthritis). When they are
taking multiple medications that require dosing several times a day, the risk of
errors is increased, and it has been estimated that about 1% of acute hospital
admissions for older persons are precipitated by medical errors or medication
reactions.
In industrialized nations, an overabundance of new information and rapidly
changing technologies place a heavy demand on learning skills. Older adults
bring to this situation a wealth of accumulated knowledge and experience, which
can facilitate learning of new information in areas of prior knowledge. One re-
cent study found, for example, that older age proved to be an advantage in learn-
ing new information about cardiovascular disease, presumably because of older
adults’ greater baseline knowledge of health-related subjects (Beier and Acker-
man 2005). By contrast, younger adults were more adept at learning about a new
technology. Research on training methods has shown that older adults learn best
with self-paced training or other training environments that allow ample time to
34 Clinical Manual of Geriatric Psychiatry
assimilate the information presented (Callahan et al. 2003). These modes of ed-
ucating most effectively remediate, or compensate for, reduced speed of process-
ing and working memory or sensory limitations.
tions are formed early in life and remain fairly constant in their relative promi-
nence in an individual’s makeup, despite variations in life experiences over the
years (Roberts and DelVecchio 2000).
To the extent that ordered transitions exist, they may differ for women and
men. Among middle-class women in the United States, increasing assertiveness
and feelings of efficacy are evident, combined with declining dependency, as
they approach their 50s. Among men of similar socioeconomic background, an
increase in interpersonal orientation and nurturance in later years is seen.
Most contemporary developmental theorists do not propose stage theo-
ries but instead emphasize the creative effect on personality of assuming and
relinquishing adult roles—most importantly, parenting (Gutmann 1987)—
or the dynamic interplay of cognitive processing resources and particular so-
cial contexts in shaping expressed personality (Staudinger and Pasupathi
2000).
60
40
20
0
Total Non-Hispanic Black alone Asian alone Hispanic
white alone of any race
changes in Social Security policies regarding delayed retirement credits and earned
income. Good health, a strong psychological commitment to work, and an active
distaste for retirement are among the strongest predictors of continuing to work
past traditional retirement ages. Employment trends for women have moved in
the opposite direction. Labor force participation rates have increased for older
women since the early 1960s, as new cohorts with a history of working outside
the home have begun to age. In 2003, 64% of women ages 55–61 years, and 23%
of those ages 65–69, were employed.
Although people who retire report that they miss the money and opportu-
nities for social contact provided by their everyday work, most take retirement
in stride, adopting new routines and activities to take the place of their work.
This type of adjustment is particularly likely when retirement is predictable or
self-imposed and when postretirement income is adequate. Health problems,
Normal Aging 45
either physical or mental, usually do not increase in the weeks or months after
retirement, and some studies show that retirees have lower stress levels and en-
gage in more healthful behaviors than do similar-age peers who are still em-
ployed (Midanik et al. 1995).
Because of Social Security and other pension programs, a majority of
older people in the United States are financially independent. Persons with
medium income now constitute the largest group of older Americans (35%),
and 26% have been rated as having high income (Federal Interagency Forum
on Aging-Related Statistics 2004). In 2003, Social Security provided 39% of
the total income for Americans age 65 and older, with an additional 25% pro-
vided by personal earnings, 19% by pensions, and 14% by asset income. The
poorest older adults are heavily dependent on Social Security. In 2003, for ex-
ample, Social Security provided more than 80% of the funds of older Amer-
icans in the lowest two-fifths of the income distribution.
About 10% of Americans age 65 and older were considered poor by federal
guidelines in 2002, compared with 35% in 1959 (Federal Interagency Forum
on Aging-Related Statistics 2004). However, elderly women and members of
minority groups have more severe financial strain than do older white men. In
2002, 12% of older women lived in poverty, compared with 8% of older men.
Twenty-four percent of older black Americans and 21% of older Hispanics had
incomes below the poverty line, compared with 8% of older non-Hispanic
white Americans.
gradually declining, but this trend is being offset by increasing numbers of di-
vorced and single older persons. Rates of widowhood are similar for Hispanic
and non-Hispanic white women but are higher for black women.
M W M W M W M W M W
100
80
Americans age ≥65 (%)
60
40
20
0
Total Non-Hispanic Black alone Asian alone Hispanic
white alone of any race
Biological Aging
What Is Aging?
A useful definition of aging was proposed by Birren and Zarit (1985): “Bio-
logical aging, senescing, is the process of change in the organism, which over
time lowers the probability of survival and reduces the physiological capacity
for self-regulation, repair and adaptation to environmental demands” (p. 9).
Modern gerontologists distinguish primary aging, which is postulated to re-
Normal Aging 49
defined (DSM-IV-TR) diagnostic categories, and the older the patient, the
more this tends to be the case. The ability to initiate treatment on the basis
of only provisional diagnostic impressions, to continue to gather information
and modify the treatment plan as a clearer picture emerges, and to take age-
related changes in clinical circumstances into account throughout the process
is the hallmark of the well-adapted and successful geriatrician.
The following case report is typical:
Mr. A, an 85-year-old married, retired businessman presenting for an outpa-
tient assessment, tells the clinician, “There’s nothing wrong with me, and
I don’t need to be here.” Gentle probing induces Mr. A to admit to mild
memory impairment, some loss of appetite and energy, and multiple somatic
symptoms, including dry mouth, intermittent urinary retention, chronic
pain in several body parts, occasional episodes of dizziness, and occasional
constipation. Mr. A’s spouse adds that she has noticed his irritability, chronic
worrying, and social withdrawal and an increasing tendency to stay in bed.
She goes on to say that he had been working part-time at a company that he
started 40 years ago, which is now being run by their son, but was “invited”
to stop coming to the office about 6 months ago and has not been back since.
Late in the session, she mentions that Mr. A’s brother died a month prior to
the clinic visit. Mr. A discounts the importance of both of these events.
Mental status examination finds mildly depressed mood, anxiety, short-
term memory impairment that is partially ameliorated by cues, and inconsis-
tent results on assessment of frontal executive functions. Mr. A has chronic
moderate hypertension and coronary artery and peptic ulcer disease; he takes
daily doses of a statin, two antihypertensive medications (including a β-
blocker), a proton pump inhibitor, and intermittent hydrocodone bitartrate–
acetaminophen preparations, in addition to stool softeners, ginkgo biloba,
low-dose aspirin, and vitamin E.
By the end of the interaction, it is clear that Mr. A is suffering and that
his physical and social functioning have declined, but the clinician’s persistent
effort has failed to establish a clear timetable of the onset and progression of
any of the symptoms or their temporal relation to losses, other social stressors,
or his other illnesses and their treatments. The patient has no history of men-
tal or emotional problems and does not qualify for any DSM-IV-TR diagno-
sis (outside the not-otherwise-specified categories), and he says, “Doc, if you
had my medical problems, if you’d been through what I’ve been through, you
wouldn’t be so chipper, either. I don’t need a psychiatrist, and I don’t need
treatment for any ‘mental illness.’”
With this “typical” patient in mind, then, a few general principles of di-
agnosis and treatment are important to keep in mind.
Table 2–4. Primary aging: changes in anatomy and function of major organ systems
Cardiovascular
Heart Decreased size, flexibility of collagen matrix; Impaired left ventricular diastolic filling, reduced
lipofuscin and fat deposition in β-adrenergic (i.e., chronotropic and inotropic)
myocardium; fatty infiltration and response to catecholamines, leading to decreased peak
calcification of aortic and mitral valves exercise cardiac index and ejection fraction (Schulman
1999)
Arteries Redistribution and molecular rearrangement Increased systolic blood pressure
(cross-linking) of elastin and collagen in
arterial walls; calcification
Respiratory
Lungs Enlarged alveolar ducts and alveoli; loss of Reduced ventilatory capacity, especially during exercise
elasticity
Musculoskeletal Increased chest wall and joint rigidity; Same as above
increased kyphosis; degeneration and
calcification of cartilage
Gastrointestinal Some loss of smooth muscle cells of intestine; Reduced eliminatory efficiency: constipation; reduced
atrophy of gastric mucosa; increase in metabolism of drugs
gastric pH; some loss of hepatocytes;
reduction in hepatic blood flow
Table 2–4. Primary aging: changes in anatomy and function of major organ systems (continued)
System Anatomical changes with age Functional changes with age
Genitourinary Loss of renal mass, loss of glomeruli, Reduced glomerular filtration rate and renal plasma
thickening of basement membrane of flow; loss of bladder-emptying capacity
glomeruli and tubules, development of
tubular diverticula, intimal thickening of
arteries, development of afferent-efferent
shunts in juxtamedullary glomeruli,
obliteration of arterioles in cortical
glomeruli (Davison 1998); reduced bladder
elasticity, especially in women; prostate
enlargement in men
Endocrinological Atrophy and fibrosis; loss of vascularity; General decline in secretory rate, but resting hormone
changes may be very minimal blood levels may remain constant as clearance also
declines
Nervous Loss of brain weight and volume in most Inconsistent evidence of reduced blood flow; reduced
studies; loss of neurons, depending on metabolism of glucose and oxygen; intellectual
brain area studied; loss of dendritic arbor, changes as described in text (see “Cognitive Abilities
with reduced interneuronal connectivity; in Later Life: A Processing Resource Model”)
Normal Aging
interneuronal accumulation of lipofuscin
and loss of organelles; neurofibrillary
degeneration of neurons; accumulation
of senile plaques, especially in
hippocampus, amygdala, and frontal cortex
53
Table 2–4. Primary aging: changes in anatomy and function of major organ systems (continued)
Musculoskeletal Reduced muscle and bone mass; Loss of muscular strength and stamina
demineralization of bone; increased fat
in muscles and calcium in cartilage;
degeneration of cartilage; loss of elasticity
in joints
Immunological Involution of thymus; reduced proportion Increased susceptibility to cancer
of naïve T cells; increased proportion of
activated/memory T cells; decreased
expression of interleukin-2 receptors;
decreased cellular proliferative response to
T-cell receptor stimulation (Ginaldi et al.
1999)
Special senses Yellowing of lens in eye Loss of auditory and visual acuity, especially night
vision
Normal Aging 55
Diagnostic Process
• Identify “secondary syndromes” first. A growing list of general medical con-
ditions and medications appear to be risk factors for clinically significant
depression, and in some cases, appropriate treatment of the general med-
ical condition and/or modification of the medication regimen may be suf-
ficient to ameliorate depressive symptoms.
• Do not accept bland denial of symptoms. Sometimes the clinician must use
several different approaches, with terms that the patient can understand
and is comfortable with, before the true picture emerges. Some elderly pa-
tients who vehemently deny being depressed will admit to “the dwindles”
or will acknowledge loss of interest in usual activities or irritability.
• Seek information from ancillary sources when possible. Ancillary sources in-
clude the spouse, caregiver, board and care home or nursing home spon-
sor or head nurse, and other physicians. Lack of insight exacerbated by a
widespread cultural bias against acknowledging emotional or mental in-
firmity may render the patient the least reliable informant.
• Maintain a healthy index of skepticism. If the history does not fit the cur-
rent clinical picture, the clinician should probe more deeply. Some bipolar
patients and their family members “forget” hypomanic episodes, only to
“remember” when the patient switches into one: “Oh yes, he was just like
this back in 1984!” “Abrupt onset” of significant cognitive impairment
sometimes turns out to be merely “abrupt discovery” of a long-developing
condition that has been acutely exacerbated by the patient’s anxious re-
sponse to a relatively minor change in living circumstances.
Therapeutic Process
• First, undo harm. Some presenting signs and symptoms may be due to side
effects and adverse reactions to over-the-counter and prescription medi-
cations used for physical conditions. Replacement with an alternative
agent, or dosage adjustment of medications that can provoke, mimic, or
exacerbate depressive or anxiety symptoms, may render specific psycho-
pharmacological treatment unnecessary. See Table 2–5 for a list of com-
mon offenders.
• Do not hesitate to treat just because a full syndrome is not present. There is
growing recognition of the clinical significance of subsyndromal condi-
56 Clinical Manual of Geriatric Psychiatry
Age effects on renal excretion of drugs have been much more clearly delin-
eated. Reduction in glomerular filtration rate (which generally corresponds to
rate of excretion of drugs) of approximately 1% per year between ages 30 and
80 has been documented, as has comparable reduction in renal plasma flow and
renal tubular function, including absorption and secretion (Rowe et al. 1976).
For drugs that are excreted by the kidney unchanged, such as lithium salts, or
that have active water-soluble metabolites, such as desipramine (i.e., 2-OH-
desipramine), this reduction may have great clinical significance. For other
agents with inactive water-soluble metabolites, this change is less important.
When pharmacokinetic factors are constant, increased or decreased effec-
tiveness of drugs can be assumed to reflect pharmacodynamic changes (the ac-
tual physiological response produced by a drug at its site of action). Only a few
such pharmacodynamic changes have been documented in healthy elderly per-
sons: increased sensitivity to the depressant effects of benzodiazepine anxiolyt-
ics and hypnotics on the central nervous system (Greenblatt et al. 1977),
increased sensitivity to the effects of warfarin, and decreased sensitivity to the
chronotropic effects of isoproterenol. The emerging field of pharmacogenetics,
which attempts to understand and predict genetically determined interindi-
vidual differences in pharmacokinetic and pharmacodynamic responses to
drugs, is likely to produce clinically applicable findings in the near future
(Malhotra et al. 2004). The age-related changes in pharmacokinetics and phar-
macodynamics cited above are reflected in the following bullet points:
doses—for example, one-third to one-half of the usual adult dose. The cli-
nician should proceed slowly when dosage increase is indicated and re-
main alert for the development of adverse reactions, side effects, and drug
interactions.
• Choose appropriate target symptoms. Failure to identify appropriate target
symptoms is a common cause of unsuccessful treatment. Target symp-
toms may be absolutely inappropriate (e.g., social withdrawal in a de-
pressed patient who is characterologically antisocial, or unhappiness and
dissatisfaction in a patient who feels stuck in a bad marriage) or tempo-
rally inappropriate (e.g., adjusting antipsychotic therapy to eliminate
delusional content while failing to appreciate improved behavior and re-
duced agitation; the latter are appropriate early indicators of adequate
treatment, whereas the former may require months of therapy). Similarly,
typical early indicators of response to antidepressants are improvement in
sleep, appetite, and anxiety; subjective improvement in mood usually ap-
pears later in the course of therapy. In general, global improvement is a
suboptimal target of therapy because it is relatively more sensitive to the
vicissitudes of daily life, is subject to more interrater variability, and is
more influenced by the mood and expectations of a single rater than are
more concrete targets such as appetite, sleep, and specific psychological
states such as hopelessness, helplessness, and anhedonia.
• Keep it simple. The apparently widespread practice of “mixing and match-
ing” antidepressants, antipsychotics, and anticonvulsants to achieve just
the “right balance” of neurotransmitter activation and inhibition is inad-
visable on several counts. First, because these combinations have had es-
sentially no systematic study, every instance of their use is an “n of 1”
clinical trial in which the patient is an unwitting subject; and second, such
polypharmacy renders the clinical picture unnecessarily complex, making
the task of sorting out which symptoms are “primary” and which are side
effects or adverse reactions a matter of guesswork.
• When possible, change one thing at a time. One goal of psychopharmaco-
therapy is to identify ineffective approaches. Only if treatment is con-
ducted systematically, adequate dosages are prescribed, adequate amounts
of time are allowed, and changes are made one at a time is it possible to
determine which treatments are ineffective or unnecessary and need no
further exploration. For example, in a patient whose symptoms are unre-
60 Clinical Manual of Geriatric Psychiatry
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3
Mood Disorders—Diagnosis
Depression is the most common mood disorder in later life. It can have
serious consequences, including “disability, functional decline, diminished
quality of life, mortality from comorbid medical conditions or suicide, de-
mands on caregivers, and increased service utilization” (Charney et al. 2003,
p. 664). Because of the seriousness of these consequences, geriatric depression
has been identified as a major public health problem, yet it is undiagnosed in
about 50% of cases (Mulsant and Ganguli 1999). Even when it is recognized,
depression in the elderly tends to be undertreated: Steffens and colleagues
(2000) found that only 35.7% of elderly patients with major depression were
taking an antidepressant; of these, it is likely that a substantial minority were
less than optimally compliant with treatment (Katon et al. 1999). Several
factors contribute to this suboptimal response by the medical profession,
including 1) the “normative fallacy”—that is, the belief that symptoms of
depression are “normal” or “expectable” given the patient’s age, social circum-
stances (including recent losses), and medical condition; 2) the tendency of
clinicians to attribute neurovegetative symptoms and signs (such as loss of
energy, poor appetite, and disturbed sleep) to concomitant medical problems;
3) the reluctance of many older patients to acknowledge “mental” problems,
67
68 Clinical Manual of Geriatric Psychiatry
and other dysphoric moods are common but generally less severe than in major
depression. Depressed patients are more prone to focus on themselves and their
role in the loss and, consequently, are more likely to feel guilt and reduced self-
esteem than are nondepressed mourners, who tend to think more of the lost ob-
ject (Gallagher et al. 1982). One series of studies found that 35% of a group of
109 bereaved widows (average age=61 years) were depressed 1 month after the
death of their spouse, but only 17% remained depressed after 13 months.
Moreover, the best predictor was depression itself: 75% of those depressed at 13
months were depressed at 1 month (Bornstein et al. 1973; Clayton et al. 1972).
In a sample of 133 widows and widowers (average age=70.6 years), only 10%
had symptoms that met DSM-III-R (American Psychiatric Association 1987)
criteria for major depression 13 months after the death of a spouse, but 14%
had symptoms that met criteria at 25 months. In this study, the authors also ob-
served “clinically significant” depressive symptoms in the 86% whose condi-
tions did not meet formal diagnostic criteria (Zisook et al. 1994). In another
series of studies, Glick et al. (1974) and Parkes (1965, 1972) discerned the fol-
lowing approximate stages of normal bereavement:
1. The first few weeks after the death of a loved one: During this initial period,
numbness, shock, disbelief, and emptiness are often accompanied by in-
tense anxiety, sleep disturbance, and somatic complaints.
2. The first year after the death of a loved one: This is a period of adjustment, dur-
ing which cognitive and affective “working through” occurs via a process of
recollection, fantasy, and rationalization. This phase is completed when ac-
ceptance occurs.
3. After the first year postloss: A recovery phase ensues, during which “redef-
inition” of self without the lost loved one occurs.
Although the studies cited earlier did not address the specific circum-
stances surrounding the onset and course of bereavement, they do suggest
that the time course of normal grief in the individual patient is fairly variable
and that most patients should be at, or clearly moving toward, baseline status
by the end of the first year. But specific circumstances also appear to be im-
portant. A study of 217 caregivers of family members with dementia (Schulz
et al. 2003) found that 72% of the caregivers reported feeling relief after the
death of their loved one. Their scores on the Center for Epidemiologic Stud-
70 Clinical Manual of Geriatric Psychiatry
ies Depression Scale increased about 50% over prebereavement scores imme-
diately after the death but returned to prebereavement levels within 15 weeks;
within 1 year, scores were below the levels reported when these persons had
been active caregivers.
Complicated Grief
A syndrome of complicated grief, which occurs in 10%–20% of bereaved in-
dividuals, has been differentiated from both normal grief (bereavement) and
clinical depression or anxiety. Proposed diagnostic criteria for this syndrome
are shown in Table 3–1. Complicated grief symptoms are clearly distinct from
normal bereavement–related depressive and anxiety symptoms and may en-
dure for several years in some cases. These symptoms predict
substantial morbidity and adverse health behaviors over and above depressive
symptoms (e.g., cardiac events, high blood pressure, cancer, ulcerative colitis,
suicidality, social dysfunction, anergia, changes in food, alcohol, and tobacco
intake, and global dysfunction) and, unlike depressive symptoms, are not ef-
fectively reduced by interpersonal psychotherapy and/or tricyclic antidepres-
sants. These findings revealed a need to identify and treat complicated grief
as a psychiatric disorder distinct from major depressive disorder (MDD).
(Prigerson and Jacobs 2001, p. 1370)
Source. Prigerson HG, Jacobs SC: “Caring for Bereaved Patients: ‘All the doctors just suddenly
go.’” Journal of the American Medical Association 286:1369–1376, 2001. Copyright © 2001,
American Medical Association. All rights reserved.
Chronic Illness
Major depression is a common accompaniment of many chronic medical ill-
nesses. Dunlop and colleagues (2004) studied 7,825 subjects ages 54–65 in a
national probability sample and found a strong association between chronic
72 Clinical Manual of Geriatric Psychiatry
illness and depression: only 3.6% of the subjects without chronic illness had
major depression, but 9.9%–18.5% of the subjects with chronic illness had
major depression. Of the conditions studied, which included arthritis, cancer,
diabetes, heart disease, hypertension, lung disease, stroke, and obesity, heart
disease and arthritis were most often associated with major depression, and
the combination of heart disease and arthritis had the strongest association of
any combination of two conditions. In the Longitudinal Aging Study Am-
sterdam (N= 2,288), Bisschop et al. (2004) also found heart disease and ar-
thritis to be most frequently associated with major depression, but the two
studies disagreed on the role of functional disability. In the former study, the
risk of major depression in both conditions (as well as in all the other condi-
tions studied) was strongly mediated by functional disability, whereas the lat-
ter study found no mediating role for functional disability in the association
between either cardiac disease or arthritis and depression.
Heart Disease
The relation between depression and ischemic heart disease is particularly
complex. Depression is a risk factor for myocardial infarction (Ariyo et al.
2000), and major depression occurring in the weeks after a myocardial infarc-
tion significantly increases 6- and 18-month mortality (Frasure-Smith et al.
1995). Moreover, patients with ischemic heart disease who are taking seroto-
nin reuptake inhibitors (but not other classes of antidepressants) have a re-
duced risk of myocardial infarction (Sauer et al. 2001). The mechanism of
this protective effect has been hypothesized to be related to the inhibiting ef-
fects of selective serotonin reuptake inhibitors on platelet aggregation, which
tends to be abnormally increased in patients with ischemic heart disease or de-
pression and even higher in patients with both diseases. This protective effect
is robust enough that some authors have proposed that selective serotonin re-
uptake inhibitors be prescribed for all patients with ischemic heart disease
(Jiang and Krishnan 2004).
Congestive heart failure is also associated with a high prevalence of de-
pression. Gottlieb et al. (2004) examined 155 patients of average age (64
[±12]) who had a mean left ventricular ejection fraction of 24. Of these pa-
tients, 46% had ischemic heart disease, and 38% were diabetic; 48% met
study criteria for depression (Beck Depression Inventory [BDI; Beck et al.
1961] score of 10 or higher). Interestingly, the depressed patients were slightly
Mood Disorders—Diagnosis 73
younger than the nondepressed patients (average age= 62 vs. 65). The authors
concluded that “pharmacologic or non-pharmacologic treatment of depres-
sion could conceivably reduce morbidity and, perhaps, mortality” (p. 1548)
from congestive heart failure.
Stroke
Between 20% and 50% of stroke patients have poststroke depression, with
women about twice as likely to be affected as men (Paradiso and Robinson
1998). Of stroke patients have poststroke depression, about half have a major
depression–like syndrome that is clinically indistinguishable from primary
major depression, and the other half meet criteria for dysthymia (if the dura-
tion requirement is waived). Poststroke depression is mediated by functional
impairment (Bisschop et al. 2004), and patients with major depression fol-
lowing dominant-hemisphere stroke have more severe cognitive impairment
(Robinson et al. 1986) than is seen in stroke without depression. The effect
of poststroke depression on long-term prognosis is also negative. House and
colleagues (2001) found that major depression within 1 month poststroke
was not statistically associated with mortality at 12 and 24 months poststroke,
but the presence of depressive symptoms was associated, even after adjusting
for other confounding variables such as age and cognitive impairment. L.S.
Williams et al. (2004) analyzed a Veterans Affairs database of more than
50,000 stroke patients and found that those who received a diagnosis of de-
pression within 3 years of the stroke were 13% more likely to die during the
study period than were those who had no diagnosis of mental illness. Inter-
estingly, this study found a comparable risk of death if mental conditions
other than depression, including substance abuse, anxiety disorders, schizo-
phrenia, and personality disorder, were diagnosed within 3 years of the stroke.
Despite the well-documented clear association between stroke and depres-
sion, a systematic literature review (Hackett et al. 2004) found “no evidence
to support the routine use of pharmacotherapeutic or psychotherapeutic
treatment for depression after stroke” (p. 1).
“Vascular Depression”
Alexopoulos and colleagues (1997) have argued for the recognition of a dis-
tinct category of depression due to a general medical condition called vascular
depression; they have cited the
impaired and more disabled, had more psychomotor retardation and less in-
sight, and had less depressed mood than those with nonvascular depression.
They hypothesized that disruption by vascular lesions of striato-pallido-
thalamo-cortical pathways may constitute the pathogenesis of depression in
such patients, and they suggested that further research may define a distinctive
pharmacological approach to the prevention and treatment of this syndrome.
This pathogenetic hypothesis was only partially supported by Thomas et
al. (2001), who studied postmortem tissue from 20 elderly patients with a his-
tory of depression and 20 with no such history. They found a significant in-
crease in atheroma overall in the depressed group (this increase was mainly a
result of the difference in the cerebral arteries and aorta) but found no evidence
for increased microvascular disease in the four neocortical lobes or within the
deep white matter of the frontal lobe.
Other studies have cast doubt on the strength of association between vas-
cular disease and late-onset depression. Stewart and colleagues (2001) exam-
ined the association between stroke, vascular risk factors, and depression in a
community-based Caribbean-born population ages 55–75 years living in the
United Kingdom. In the 287 subjects who were studied, depression (diag-
nosed with a cutoff score of 3/4 on the 10-item Geriatric Depression Scale
[GDS]) was positively associated with a history of stroke but not with other
indicators of vascular disease or risk factors for vascular disease. Kim and col-
leagues (2004) found a similar association between depression (diagnosed
with a community version of the Geriatric Mental State Schedule) and previ-
ous stroke but not other vascular risk factors (except an atherogenic lipid pro-
file) in 732 Korean subjects whose average age was 72.8. These findings did
not change when the small number of subjects who reported onset of depres-
sive episodes before age 60 were eliminated from the analysis. Cervilla and
colleagues (2004) studied genetic material from 370 subjects to determine
whether polymorphic variation at three genes (APOE, encoding for apolipo-
protein E; VLDLR, encoding for the very low-density lipoprotein cholesterol
receptor; and DCP1, encoding for angiotensin-converting enzyme) that are
related to vascular disease, and other vascular disease risk factors, determined
late-life depression. These authors found “no association between late-life de-
pression and three polymorphisms related to vascular disease. Depression was
found to be independently associated with smoking, female gender, poorer
cognitive functioning, and higher diastolic blood pressure” (p. 202). The
76 Clinical Manual of Geriatric Psychiatry
authors concluded that “this study does not seem to support the notion of a
specific link between the studied vascular risk factors or these vascular-related
loci and late-life depression” (p. 202), but they did not limit their sample to
subjects with late-onset depression. Finally, Devanand and colleagues (2004)
found no higher prevalence of cardiovascular disease in elderly patients with
late-onset (after age 60) as compared with early-onset major depression (but
the prevalence of vascular disease was increased in patients with late-onset
dysthymic disorder). In light of these conflicting data, “vascular depression”
remains a hypothetical entity at present.
Parkinson’s Disease
A similar prevalence of depression (i.e., about 40%) has been observed in pa-
tients with Parkinson’s disease, in a similar 50:50 ratio of major depression to
dysthymia (Nuti et al. 2004). As in stroke, depression in Parkinson’s disease
patients increases the risk for and severity of dementia and exacerbates disabil-
ity, and so is an important focus of diagnostic and therapeutic attention for
geriatric psychiatrists (Tröster et al. 2000). Treatment generally follows guide-
lines for primary mood disorder as detailed in Chapter 4 (“Mood Disorders—
Treatment”).
depressive symptoms. However, the studies analyzed had few elderly subjects,
and in almost every study the method of assessing depressive symptoms was
not specified. As the preceding case illustrates, merely asking elderly patients
about “depression” may elicit misleading responses.
Major Depression
Epidemiology
Major depression, as defined in DSM-IV-TR, is the most serious presentation
of primary mood disorder in the elderly. The prevalence of major depression
in the elderly has varied in large-scale studies from 1%–2% (Heithoff 1995)
to 3.7% (Steffens et al. 2000), and the prevalence appears to increase with age;
one study of subjects (average age=85) found a community prevalence of 4%
(Forsell and Winblad 1999). Depression accounts for more than 60% of
admissions to geriatric psychiatry units and is present in about 30% of elderly
patients with acute and chronic medical illnesses (Okimoto et al. 1982) and
in about 15% of nursing home residents (Falck et al. 1999).
Risk Factors
As discussed in earlier sections, chronic illness in general, a few specific illnesses,
and exposure to certain substances are clear risk factors for the onset of major
depression in the elderly. The role of stressful life events as precipitants of major
depression has been studied by several groups, although none has focused on
elderly patients per se. Kendler et al. (2003) studied 98,592 person-months in
7,322 male and female twin pairs and found that the baseline risk per month
for the onset of an episode of major depression was 0.6%. Of the stressful life
events studied (which were categorized as loss, humiliation, entrapment, and
danger), only loss and humiliation events were statistically significantly associ-
ated with onset of major depression in the month of occurrence. Loss included
death, respondent-initiated separation, and other key losses, whereas humilia-
tion included only other-initiated separation. Because old age is a time of loss,
less so of other-initiated separation, loss events likely play an increasingly signif-
icant role in the provocation of major depression in the elderly.
Mood Disorders—Diagnosis 81
Diagnostic Criteria
The diagnosis of major depression in an elderly person begins with a detailed
history of the present illness, focusing on relatively abrupt changes in one or
more neurovegetative functions. For example, the patient may report that his
or her usual pattern of unsatisfactory sleep became noticeably worse around
the time that feelings of hopelessness and apathy were first experienced. Sim-
ilarly, the gradual decline in activity and appetite that had been occurring for
quite a while also may have been abruptly accelerated around the same time.
Informants such as a spouse or a child, a board and care home operator, or the
family physician can be invaluable in establishing the timing of these changes
(Wiener et al. 1997). DSM-IV-TR criteria for major depressive episode are
summarized in Table 3–3.
Major depression affects the elderly in many of the same ways that it af-
fects young adults. Nelson et al. (2005) analyzed data from 728 elderly sub-
jects with nonpsychotic major depression and found that depressed mood,
loss of interest in work and activities, psychic anxiety, somatic anxiety, lack of
energy, guilt, middle and late insomnia, and suicidal ideation best described
the presentation of depression in their subjects and were the symptoms most
sensitive to change during treatment with either sertraline or placebo. Bro-
daty et al. (1997) reported that diminished self-esteem and guilt were less
common in older depressed patients (i.e., 60 or older), but these patients had
more severe depression (higher Hamilton Rating Scale for Depression [Ham-
D] scores), more appetite loss and weight loss, and higher rates of psychotic
and melancholic depression. Caine et al. (1994) reviewed the literature and
concluded that “medical illness emerges consistently as the most common
clinical feature associated with depressive symptoms and diagnoses in com-
munity, outpatient, and inpatient samples” (p. 38). Still, accurate detection
of major depression in old age can be challenging because several features of
normal aging overlap with complaints of depression. Table 3–4 lists the most
troublesome of these normal aging changes. Signs and symptoms associated
with normal and complicated bereavement can also complicate diagnosis.
Finally, recognition and diagnosis of major depression may be complicated by
variable presentation of illness, as discussed in the following subsection.
82 Clinical Manual of Geriatric Psychiatry
Source. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of
Mental Disorders, 4th Edition, Text Revision. Washington, DC, American Psychiatric Associa-
tion, 2000, p. 356. Copyright © 2000, American Psychiatric Association. Used with permission.
Mood Disorders—Diagnosis 83
A 72-year-old woman was an ongoing problem for neighbors and police be-
cause she was convinced that men were following her and wanted to put her
in a “car with a large dog that would attack and kill” her. Although neurolep-
tics partially controlled her fear and her bizarre behavior, her symptoms were
not completely ameliorated until antidepressant treatment was initiated, at
which time her mood also greatly improved.
Accurate diagnosis is also impeded when patients cannot or will not re-
port hallucinations or express the content of delusions and when the presence
of hallucinations or delusions must be inferred from bizarre behavior or severe
thought disorder. Near-catatonic behavioral withdrawal is one such particu-
Mood Disorders—Diagnosis 85
A 90-year-old woman complained of her “arms and legs twisting,” along with
a feeling of “buzzing” from the top of her head radiating into her chest, ab-
domen, arms, and hands. She insisted that the symptoms reflected a “heart
86 Clinical Manual of Geriatric Psychiatry
attack” and made frequent unproductive visits to her local emergency depart-
ment. Careful interviewing found that the onset of these symptoms was asso-
ciated with marital conflict, and exacerbation tended to occur when marital
tensions escalated. Over the long run, she responded well to psychotherapy
but refused antidepressants. She eventually gained a modest degree of insight
into the functional nature of her complaints.
The variant of major depression depicted in this case differs from soma-
tization disorder with depressed mood in 1) the number of physical symp-
toms, which is typically as high as 20 or more in somatization disorder; 2) the
history, which is typically much more chronic and unremitting in somatiza-
tion disorder; and 3) the presence of neurovegetative features of depression,
which are typically not present in somatization disorder. Elderly patients with
masked depression may vary considerably in their hypochondriacal preoccu-
pation with physical symptoms. At one extreme, they may be simultaneously
disabled by but relatively indifferent to their symptoms, whereas at the other
extreme, they may have a near-delusional conviction that symptoms reflect
life-threatening illness, along with appropriate levels of psychic distress, and
may make a lifestyle of doctor and diagnostic procedure shopping. Unfortu-
nately, available data do not support precise criteria for establishing the diag-
nosis of masked depression. Indeed, Bschor (2002) has argued that the
concept of masked depression has been “abandoned” and replaced with “so-
matization disorder, somatoform disorder, psychosomatic disorder, conver-
sion disorder, neurasthenia or hypochondriasis” (p. 207). He cites
the expansion of that diagnosis onto a vast number of disorders, the continuing
lack of clarity of the concept (disorder of recognition vs. disorder of communi-
cation; the positive proof of psychic symptoms as a prerequisite vs. the positive
proof of psychic symptoms as an exclusion criterion for that diagnosis)…and
the introduction of DSM-III and ICD-10 as operationalized, purely descriptive
and rather theory-free systems of diagnostic classification (p. 207)
Five (or more) of the following symptoms have been present during the same
2-week period and represent a change from previous functioning; at least one
of the symptoms is either (1) depressed mood; (2) loss of interest or pleasure
(p. 356); or (3) persistent physical symptoms that do not meet DSM-IV-TR cri-
teria for any somatoform or other disorder, cannot be explained by structural or
functional pathology, or have a distinctly bizarre or unusual quality that is not
consistent with any known medical diagnosis. (italicized text added by authors)
Clinical behavior
Detailed complaints of cognitive loss Few complaints of cognitive loss
Distress caused by cognitive problems Varied reaction to cognitive loss
Behavior does not reflect cognitive loss Behavior compatible with cognitive loss
Persistent mood disorder Mood apathetic or environmentally
responsive
Nocturnal exacerbation rare Nocturnal exacerbation common
Mood-congruent delusions Mood-incongruent delusions
Examination findings
Patients expend little effort during Patients commonly struggle to perform
examination cognitive tasks
Patients frequently answer, “I don’t know” Patients usually make an effort to answer
questions
Memory loss is inconsistent for recent and Memory impairments are greater for
remote events recent than for remote events
Patients may have specific memory gaps Patients do not have specific memory
gaps
Inconsistent performance across similar Consistently impaired performance on
types of tasks tasks of a particular ability
Prompting and semantic organization are Prompting and semantic organization
helpful in improving recall have limited benefit
Recognition memory is relatively intact Recognition memory is impaired; there
may be false-positive errors
Source. Adapted from Strub and Black 1988; Kaszniak and Christenson 1994.
90 Clinical Manual of Geriatric Psychiatry
Center for Epidemiologic Studies Depression Scale were associated with both
the risk of developing Alzheimer’s disease and the rate of cognitive decline.
For each depressive symptom, the risk of developing Alzheimer’s disease in-
creased by an average of 19%, and annual decline on a global cognitive mea-
sure increased by an average of 24%.
Anorexia
A less common presentation of depression in the elderly is profound anorexia,
which may occur in the absence of any other neurovegetative features of de-
pression and in the presence of what otherwise appear to be normal mood and
affect. This form of depression seems to occur mainly in the old-old and is
often accompanied by multiple chronic, often “end-stage,” medical illnesses.
It can be thought of as the “anorexia of aging” (Morley 2001), severely exac-
erbated by concomitant mood disorder, and is classified here as a form of ma-
jor depression mainly because of its severity.
The typical clinical picture is of a visibly aged, deteriorated, dysphoric pa-
tient who has “given up” and, by refusing to eat, appears to be committing
passive suicide. Hospitalization of such patients may be complicated by pas-
sive refusal of treatment and family discord around the issue of the patient’s
“right to quit”; similar ambivalence is not uncommon among treatment staff,
who may be prone to engage in prolonged discussion of the appropriateness
of hospitalization, the quality of life required to warrant aggressive treatment,
and so forth. In some patients, particularly those from non-Western cultures,
this clinical picture is interpreted by friends and family as an indication of the
patient’s wish to die, and the rendering of treatment aimed at restoring appe-
tite is regarded as an insult to the elderly patient. These and similar consider-
ations notwithstanding, a reasonable proportion of patients in this category
respond to antidepressant treatment with restoration of normal appetite,
weight gain, and the emergence of a new will to live.
Behavioral Regression
Major depression in the elderly occasionally presents with a picture of behav-
ioral regression. The patient gradually becomes less physically and socially ac-
tive, neglects personal hygiene and necessary medical treatment, loses contact
with friends and family, allows the home environment to become disordered
and filthy, and discontinues shopping and begins living off canned or other-
Mood Disorders—Diagnosis 91
Dysthymic Disorder
Dysthymic disorder in adults as described in DSM-IV-TR is a chronic depres-
sion of mood (for at least 2 years) that is variably accompanied by associated
symptoms of appetite disturbance, sleep disturbance, low energy or fatigue,
low self-esteem, poor concentration or difficulty making decisions, and feel-
ings of hopelessness. It occurs in about 1.8% of elderly individuals during any
given month. Dysthymic disorder is similar to but less severe and more
chronic than major depression and has a somewhat earlier onset in elderly in-
dividuals. The average age of onset of dysthymic disorder in 68 subjects over
age 55 was 31, while the average age of onset of major depression in 61 sub-
jects over age 55 was 53 (Beekman et al. 2004). Dysthymic disorder may be
preceded by an Axis I (nonmood) or Axis III disorder (“secondary dys-
thymia”), may occur as an isolated syndrome (“primary dysthymia”), or may
present as “double depression” (i.e., with major depressive disorder superim-
posed on dysthymic disorder). Kirby and colleagues (1999) studied 40 dys-
thymic individuals (average age= 74.4) and found a relatively low rate (15%)
of comorbid Axis I disorder (3 with generalized anxiety, 3 with agoraphobia
without panic) and a high prevalence of hopelessness: 47.5% felt that life was
not worth living, 17.5% expressed a death wish, and 7.5% had suicidal ide-
ation. Overall, the prevalence of dysthymic disorder, like major depressive
disorder, appears to decline with age (Beekman et al. 2004); it is more com-
mon in women, although the difference declines with age, and almost half of
elderly patients with dysthymic disorder have a history of major depressive
disorder. This figure increases to 80% if the presenting illness is “double de-
pression.” The risk of developing dysthymic disorder appears to be related to
environmental factors (e.g., relative lack of social and emotional support, his-
tory of traumatic events) and personal vulnerability factors (e.g., female sex,
92 Clinical Manual of Geriatric Psychiatry
family history). Age at onset also may be important; Devanand et al. (2004)
found that elderly patients with late-onset (i.e., after age 60) dysthymic dis-
order were more likely to have cardiovascular disease and less likely to have
comorbid anxiety disorder than were those with early-onset dysthymia, but
the two groups were similar otherwise.
One potential cause of a dysthymia-like syndrome is partial treatment of
major depression, either with anxiolytics alone or with inadequate doses of
antidepressants, resulting in amelioration of enough signs and symptoms as
to no longer qualify as major depression. This condition is properly termed
major depressive disorder, in partial remission (American Psychiatric Associ-
ation 2000), and is usually identifiable with an accurate treatment history.
Minor Depression
The importance of minor or “subthreshold” depression (i.e., depression that
causes clinically significant distress or impairment in social, occupational, or
other functioning but does not meet criteria for major depression or dys-
thymia) has been recognized at least since 1980, when Blazer and Williams
found that 14.7% of a community sample of subjects age 65 or older had
“substantial depressive symptoms” but only 3.7% met DSM-III (American
Psychiatric Association 1980) criteria for major depression (Blazer and Wil-
liams 1980). Interest in subthreshold depression was further stimulated by
the Epidemiologic Catchment Area studies (Regier et al. 1988), which con-
firmed Blazer and Williams’s findings of low prevalence of major depression
in this age group. These findings challenged geriatric psychiatrists to reconcile
their clinical impressions of a relatively high prevalence of mood disturbance
among the elderly with the scientific fact that major depression and dys-
thymia were actually less prevalent among the elderly than among young and
middle-aged persons.
The relatively high prevalence of what has come to be known by many
investigators as minor depression, based on criteria presented in Appendix B to
DSM-IV-TR (“Criteria Sets and Axes Provided for Further Study”), seems to
resolve this apparent contradiction. These criteria are presented in Table 3–6.
Beekman and colleagues (1997) found that minor depression, unlike major
depression, was closely associated with physical illness in elderly subjects.
Mood Disorders—Diagnosis 93
However, it also was associated with as much disability (e.g., affecting general
functioning as well as specific functions such as housekeeping, socializing,
and exercising) as major depression was, even after controlling for the effects
of chronic physical illness. Minor depression also was associated with a signif-
icant (but less than in major depression) reduction in the subjective sense of
well-being, which was independent of general health status and, in a later
study, was associated with an increased risk of dying (1.80 times the risk to
nondepressed control subjects) (Penninx et al. 1999). A 10-year longitudinal
study of 131 elderly individuals with minor depression (defined by Center for
Epidemiologic Studies Depression Scale scores) found chronic illness to be a
significant risk factor for minor depression: the co-occurrence of just two dis-
eases doubled the risk for minor depression, when compared with persons
with no diseases or just one chronic disease. Functional decline also appeared
as a highly significant risk factor, especially deteriorating eyesight: people with
poorer than average visual acuity had more than twice as high a risk for minor
depression as did those with better than average eyesight. This study (Heik-
kinen and Kauppinen 2004) also found that people who had difficulties in
the use of public transport had three times the risk of minor depression com-
pared with those with no such difficulties. The authors concluded that “mi-
nor depression among the elderly is most typically a dynamic and episodic
phenomenon. Adverse life-events such as the loss of a spouse or some other
close person had predictive value for depressive symptoms in our study. We
also found the same impact from deteriorating health, deteriorating financial
situation and increased loneliness” (p. 248).
Psychotic features also have been reported in subsyndromal depression.
Ohayon and Schatzberg (2002) investigated the associations between depres-
sive symptoms and psychotic features in a sample of 18,980 subjects in five
European countries and found that as many as 10% of the subjects with just
two depressive symptoms (with or without a diagnosis of major depressive ep-
isode) had psychotic features. Other studies have generally confirmed these
findings, and in a review of this topic, Pincus and colleagues (1999) proposed
that “subthreshold” categories for all of the major phenomenological groups
of DSM-IV-TR might serve as more precise and more useful categories than
the current “adjustment disorder.”
94 Clinical Manual of Geriatric Psychiatry
Source. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of
Mental Disorders, 4th Edition, Text Revision. Washington, DC, American Psychiatric Associa-
tion, 2000. Copyright © 2000, American Psychiatric Association. Used with permission.
Psychological Tests
Table 3–8 lists some of the psychological assessment procedures that may be
useful in older patients whose depressive symptoms are complicated or unclear.
Psychodiagnostic tests document current mood, thought patterns, and social
tendencies and can suggest personality features that may affect the presentation
of major depression or response to treatment. For example, a Minnesota Mul-
tiphasic Personality Inventory–2 profile in which elevated scores on the hysteria
or hypochondriasis scales are combined with depressive symptoms is often ob-
served in individuals with masked depression. More generally, personality dis-
orders amplify the effect of depression and have been associated with long-term
reductions in function and quality of life.
In older patients with a combination of depressive and cognitive symptoms,
a referral for neuropsychological testing may be appropriate. Such testing provides
a detailed survey of cognitive functions, which is compared with normative values
for healthy older people and patient populations with depression or dementia (see
Chapter 5, “Dementia and Alzheimer’s Disease”). If an individual’s scores closely
Mood Disorders—Diagnosis 97
Complete blood count with differential Folate deficiency anemia, viral infection
white blood cell count
Serum thyroid-stimulating hormone, Hypothyroidism and hyperthyroidism;
thyroxine, serum cortisol hypoadrenocorticism and
(A.M. and P.M.) hyperadrenocorticism
Sequential multiple analysis of 18 Hypercalcemia, hypokalemia,
chemical constituents of blood hyperglycemia
(SMA-18)
Urinalysis, serum urea nitrogen Uremia
Computed tomography or magnetic Brain tumor, stroke
resonance imaging of head
(as indicated by results of above tests,
physical examination)
Objective Minnesota Self-rated Helps establish differential Personality profile, Anchored to DSM
personality Multiphasic questionnaire diagnosis, severity of estimate of response categoriesb
Personality depression bias, diagnosis,
Inventory–2 presence of suicidality;
(MMPI-2)a may detect masked
depression,
uncooperative or
confused patient
Millon Clinical Self-rated Same as for MMPI-2 Same as for MMPI-2 Anchored to DSM
Multiaxial questionnaire Axis II categoriesb;
Inventory–III fewer data available
(MCMI-III)c for older adults
than with MMPI-2
Revised NEO Self-rated Five-dimension taxonomy Ratings on dimensions Traits (e.g.,
Personality questionnaire of personality of personality relevant neuroticism) may
Inventory to everyday coping predict use of
(NEO-PI-R) medical services,
and NEO adjustment to
Five-Factor stresses
Inventory
(NEO-FFI)d
Table 3–8. Psychological tests useful in assessing geriatric depression (continued)
Projective Rorschach Patient describes Same as for MMPI-2; also Description of Many older adults
personality Inkblot Teste complex useful for assessment of prominent concerns, reluctant to
unfamiliar thought disorder and in thought patterns, and respond, see test as
patterns patients unaware of or pathological too ambiguous;
unwilling to admit tendencies may give too few
psychiatric problems answers to score b
Thematic Patient creates Same as for MMPI-2 and Same as for Rorschach Geriatric version also
Apperception stories about Rorschach test, but also test availableg
Test (TAT)f pictures of identifies interpersonal
people in concerns and habits
Mood Disorders—Diagnosis
different
situations
a
Butcher JN, Dahlstrom WB, Graham JR, et al: Manual for the Restandardized Minnesota Multiphasic Personality Inventory: MMPI-2. Minneapolis,
University of Minnesota Press, 1989.
bComputerized scoring and interpretation available.
cMillon T: Millon Clinical Multiaxial Inventory Manual, 3rd Edition. Minneapolis, MN, National Computer Systems, 1983.
d
Costa PT, McCrae RR: Revised NEO Personality Inventory (NEO-PI-R) and NEO Five-Factor Inventory (NEO-FFI): Professional Manual. Odessa,
FL, Psychological Assessment Resources, 1992.
eRorschach H: Psychodiagnostics: A Diagnostic Test Based on Perception. Translated by Lemkau P, Kronenburg B. Berne, Switzerland, Huber, 1942.
f
Murray HA: The Thematic Apperception Test. Cambridge, MA, Harvard University Press, 1943.
gWolk RL, Wolk RB: The Gerontological Apperception Test. New York, Behavioral Publications, 1971.
99
100 Clinical Manual of Geriatric Psychiatry
ment-related change. Table 3–9 lists some of the self-rated and observer-rated
scales that have proved useful in assessing severity of depression in older adults.
The GDS (Yesavage et al. 1982) is a self-rated measure developed specif-
ically for older adults (see the Appendix for GDS items and scoring instruc-
tions). Mood is extensively examined in this 30-item scale, and the questions
assess cognitive complaints and social behavior; in contrast, most somatic
items have been omitted from the GDS to prevent inflation of scores due to
normal aging changes. A simple yes-no answer format is another attractive
feature. The GDS has been shown to be reliable and valid in clinical research
with elderly medical and psychiatric patients, and it is often the standard
against which other rating scales are compared in clinical research with older
patients. A cutoff score of 11 or higher is useful in identifying persons who
may be experiencing clinically significant levels of depression and who may
benefit from more thorough diagnostic assessment. A 15-item short form of
this scale has been developed that includes most of the key items for assessing
dysphoria and hopelessness; however, it includes only a single cognitive item
that does not correlate strongly with the other cognitive items on the full
GDS (Adams et al. 2004). For most mental health assessment settings, the
full 30-item GDS is recommended. The full form typically takes 10 minutes
or less to complete, and most older adults can complete it independently or
with only brief task orientation.
The BDI (Beck et al. 1961) is another self-rated scale that has been widely
used with older adults. The BDI is particularly useful for assessing psycholog-
ical features of depression, including dysphoric mood, pessimism, self-criti-
cism, and guilt. This instrument is recommended for tracking symptom
severity in older persons with relatively clear-cut depression that is not com-
plicated by psychosis or prominent somatization. It also may help to distin-
guish normal or complicated bereavement from major depression because
bereaved individuals would not be expected to obtain high scores on items
evaluating guilt, self-criticism, or risk of suicide.
The most recent version of the BDI, the BDI-II (Beck et al. 1996), is a
21-item questionnaire that has been modified from the original to coincide
more closely with DSM-IV-TR diagnostic criteria for depression. Most items
are still rated on a 4-point scale, but rating options on the sleep and appetite
items have been expanded to allow for both increases and decreases in those
areas. Items on the initial version that pertained to body image, weight loss,
Table 3–9. Depression rating scales and screening procedures for older adults
Approximate time
Scale or procedure Type Number of items to complete (min) Recommended uses
Mood Disorders—Diagnosis
treatment
Hamilton Rating Scale Observer-rated, by 17–28 20–25 Screening in mental
for Depression trained professional, 17- and 21-item versions health or medical
(Ham-D) based on interview of most commonly used settings; tracking
patient symptom changes with
treatment
Cornell Scale for Observer-rated, by 19 30 Screening cognitively
Depression in trained professional; impaired patients;
Dementia both patient and tracking symptom
caregiver interviewed changes with treatment
101
Table 3–9. Depression rating scales and screening procedures for older adults (continued)
and somatic preoccupation were replaced in the BDI-II with questions per-
taining to agitation, concentration, and energy loss. The BDI-II and original
BDI correlate highly, but the BDI-II averages nearly 3 points higher than the
original version. Scores of 14 or higher suggest clinically significant elevations
in depression. In a study of 130 psychiatric inpatients age 55 years and older
(Steer et al. 2000), internal consistency of the BDI-II was found to be accept-
ably high, and factor analysis identified the same cognitive and noncognitive
dimensions of depression that had been previously identified in younger adult
psychiatric outpatients; scores on the BDI-II did not vary significantly with
age, sex, or ethnicity. (The BDI-II is a copyrighted instrument and is available
for purchase through the Psychological Corporation.)
Because both the GDS and the BDI-II minimize items assessing somatic
symptoms, they may underestimate the severity of depression in patients in
whom depression is expressed primarily through physical complaints or in
whom the subjective effect of the medical disorder is amplified by depression.
In general, a high score on the BDI or the GDS is useful in suggesting the
presence of depression, but somatic symptoms also must be considered before
a low score is interpreted to mean the absence of depression.
Most depression rating scales were initially studied with predominantly
white populations, so it has been unclear whether these measures are as appli-
cable to persons of different racial, ethnic, or language backgrounds. However,
translations of commonly used scales are now available, and validity studies
with diverse populations are becoming more frequent. A public access Web site
(http://www.stanford.edu/~yesavage/GDS.html) created by the authors of the
GDS provides links to translations of the scale in 24 languages, but published
information on the various translated versions varies, and users are strongly en-
couraged to contact persons responsible for translations before using translated
instruments. One small-scale study found comparable GDS scores for English-
and Spanish-speaking elderly people with and without dementia (Taussig et al.
1992). However, another study found that the GDS was ineffective in detecting
depression in elderly black persons with psychiatric disorder, perhaps because of
the paucity of somatic symptoms included in this scale (Baker et al. 1995). A
Spanish version of the BDI-II is available from the Psychological Corporation,
and translations into other languages also have been reported. In a study com-
paring white and Mexican American older adults, no differences were found in
BDI scores or reliability indices (Gatewood-Colwell et al. 1989).
104 Clinical Manual of Geriatric Psychiatry
Self-rated scales may not be appropriate for some elderly patients, espe-
cially those who have visual deficits, limited education, poor language profi-
ciency, psychosis, or masked depression. An observer-rated instrument, such
as the Ham-D (Hamilton 1980), is recommended for these situations. Ob-
server ratings also may be used in conjunction with patient ratings to obtain
a more complete view of symptom presentation or change. The Ham-D is
weighted toward the types of symptoms that antidepressant medications
would be expected to alter early in the course of treatment (e.g., sleep, weight
change, psychomotor speed), although it also taps depressive mood, anxiety,
and other psychological features. It has been widely used as an outcome mea-
sure in studies of efficacy of pharmacotherapies with both elderly and younger
adults. Several different cutoff scores have been used in the literature, but we
have found that scores of 16 or higher are best for detecting significant de-
pression when the 21-item scale is used. A structured interview guide that
may help to increase interrater reliability of the Ham-D has been published
(J.B. Williams 1988). The following is a sample item from this scale:
Depressed Mood (rate)
0=Absent
1=These feeling states indicated only on questioning
2=These feeling states spontaneously reported verbally
3=Communicates feeling states nonverbally, i.e., through facial expres-
sion, posture, voice and tendency to weep
4=Patient reports VIRTUALLY ONLY these feeling states in his sponta-
neous verbal and nonverbal communication. (p. 744)
Concerns have been raised about interrater reliability of the Ham-D, even
for the structured form. However, a recent study reported significantly higher
item- and total-score reliabilities for the structured interview version com-
pared with the original Ham-D, with intraclass correlations ranging from
0.78 to 1.0 for individual items (Moberg et al. 2001). Nonetheless, consider-
able training and experience are needed for this scale to yield reliable results.
Although self-rated depression scales can be used effectively by persons with
mild levels of cognitive impairment, observer-rated measures are needed for as-
sessing depression in older adults with moderate to severe cognitive impairment.
The Ham-D can be useful in some cases, but scales developed specifically for
cognitively impaired populations should be considered. The Cornell Scale for
Depression in Dementia (Alexopoulos et al. 1988) includes content similar to
Mood Disorders—Diagnosis 105
that in the Ham-D, but ratings are assigned on the basis of semistructured inter-
views with both the person with dementia and his or her caregiver. Although in-
tended as a severity rating instrument once a diagnosis of depression has been
established, the Cornell scale has been shown to be effective in identifying de-
pression in nursing home patients with dementia. Internal consistency and in-
terrater reliability are acceptable when the scale is used by trained examiners.
Procedures for identifying depression in medically ill populations have re-
ceived increased attention in recent years, especially since the U.S. Preventive
Services Task Force (2002) endorsed depression screening in primary care.
Although the scales described earlier have been shown to be useful for case
finding in medically ill populations, these measures have been criticized for
including nondiscriminating items or, in the case of observer-rated scales such
as the Ham-D, for being too lengthy and impractical for most medical situa-
tions. Existing scales have been revised for medical applications, and several
new scales have been developed.
The Beck Depression Inventory for Primary Care, a seven-item version of the
BDI, has been used to screen for major depression in both primary and secondary
care settings (Beck et al. 1996). New scales include a nine-item depression module
(Kroenke et al. 2001) from the Patient Health Questionnaire (PHQ-9), and a
self-report questionnaire for medically ill persons that establishes DSM-IV psy-
chiatric diagnoses (Spitzer et al. 1999). A recent study with more than 900 elderly
patients in the multisite Improving Mood: Promoting Access to Collaborative
Treatment (IMPACT) intervention trial reported that the PHQ-9 was sensitive
and reliable in detecting depression in primary care patients and responsive to
treatment-related improvements in depressive symptoms (Löwe et al. 2004).
Other studies have shown that systematically asking even one or two questions
about mood (“Do you often feel sad or depressed?” [Mahoney et al. 1994] or
“Over the past two weeks, have you felt down, depressed, or hopeless?” and “Over
the past two weeks, have you had little interest or pleasure in doing things?”
[Whooley et al. 1997]) substantially improves identification of depressed individ-
uals in busy medical settings where time is at a premium.
port by the surgeon general specifically targeting older adults for prevention
efforts (U.S. Public Health Service 1999). White, male, older adults are at the
greatest risk for suicide, followed by black males; white, female, older adults
have the third highest suicide rate. Other risk factors include physical illness,
especially cancer, and loss of a significant other. Older adults often use more
lethal methods than do younger adults and are less likely to directly express
suicidal ideation or to have a history of suicide attempts. Despite the obvious
importance of assessing suicidality in older persons, few interview or rating
scales have been developed to help with detection of increased suicide risk in
the elderly. The Beck Hopelessness Scale (Beck et al. 1974), a short true-false
inventory, may be helpful in this regard, and norms are available that include
some older adults; a new scale for suicidal ideation has been developed by
Beck and colleagues but has not yet been studied adequately with older
adults.
Studies have found that most older people who commit suicide consult
their primary health care providers within days or months of their deaths, so
all health care personnel must be alert to the possibility of suicide in older
adults. Screening for suicidal ideation is best accomplished as part of a general
diagnostic interview conducted by a health professional with whom the indi-
vidual has ongoing close rapport. Areas to cover include current sources of
stress, such as recent losses; signs and symptoms of depression; vague somatic
complaints or complaints of severe, unremitting pain; family and personal
history of mental health problems, including depression, alcoholism, or sub-
stance abuse; and past suicide attempts. If answers to these questions raise
concern about suicidality, direct questions should be asked to assess the sever-
ity of suicidal thoughts and any possible plan that may involve injury to self
or others. Whenever possible, family members should be interviewed for sui-
cide clues that they may have observed, such as the elder purchasing a gun,
stockpiling medications, or abruptly changing a will. Table 3–10 lists some of
the factors that have been associated with increased risk of suicide in older
adults, as well as protective factors associated with lower risk of suicide.
Holkup (2003) has provided a protocol for assessing suicidality in older
adults; although designed primarily for nurses, the concrete suggestions pro-
vided could be useful to a wide range of health professionals. Other thorough
discussions of geriatric suicide can be found in Gallagher-Thompson and Os-
good (1997) and McIntosh and colleagues (1994).
Mood Disorders—Diagnosis 107
Theories of Depression
The causes of clinically significant depression in the elderly are not known. A
genetic vulnerability is strongly suggested by the increased prevalence of de-
pression in the families (particularly first-degree relatives) of affected individ-
uals and is supported by evidence from twin studies (Jansson et al. 2004).
Genetic influences tend to be stronger in bipolar disorder than in unipolar
mood disorder and in early-onset cases than in late-onset cases. As discussed
earlier in this chapter (in the section “Substance-Induced Mood Disorder”
and in Table 3–2), some cases of depression in the elderly appear to be at least
partially caused or provoked by medications or other chemical agents and by
general medical conditions, such as hypothyroidism; and several other
chronic medical conditions appear to be “risk factors” for the development of
108 Clinical Manual of Geriatric Psychiatry
depression in old age. Three schools of thought have weighed in on the etiol-
ogy and pathogenesis of depression, and they are summarized in the following
subsections.
Psychodynamic Theories
Psychodynamic theories of depression were among the earliest published, be-
ginning with Freud’s elaborations on the theories of Karl Abraham regarding
psychopathological developments in the process of mourning. In Freud’s con-
ception, the image of the lost object (which may be an abstract object, such
as professional status) is eventually introjected and becomes part of the self.
Subsequent rage at the object—for leaving and for past hurts and disappoint-
ments—thereby becomes directed at the self. The resultant guilt, loss of self-
esteem, and need for punishment form the core of the symptom complex of
pathological grief (not to be confused with complicated grief, a clinically de-
fined condition discussed earlier in this chapter). More recently, Blatt and
Zuroff (1992) proposed that certain personality configurations are predis-
posed to depression. These configurations derive from distinct developmental
lines: the anaclitic (or dependent) line, which concerns the establishment of
satisfying interpersonal relationships, and the introjective (self-critical) line,
which focuses on the achievement of a positive and cohesive sense of self.
These configurations seem to fit well with analytical conceptualizations of ge-
riatric depression, which focus on helplessness experienced by the ego in light
of failed attempts to live up to one’s ideals, and the narcissistic injuries inevi-
tably associated with the functional declines of aging.
Loss or threatened loss during childhood also has been a focus of psycho-
dynamic formulations of depression. Although psychoanalytical theories of
depression have not emphasized late life, the relatively high frequency of
losses confronting many older individuals lends a measure of pertinence to
each of these dynamic approaches to geriatric depression. The interested
reader is directed to useful reviews by Blau (1983) and Bemporad (1988).
often expressed by elderly depressed patients (Seligman and Maier 1967). Sim-
ilarly, cognitive theorists point to the interaction between these losses and sub-
sequent activation of deeply ingrained, stable thought schemas as resulting in
negative self-perceptions, negative interpretations of life events, and pessimism
about the future, which lead to depressed mood (Sadavoy 1994). Contem-
porary research on cognitive-behavioral therapy in late-life depression (e.g.,
Thompson et al. 2001) accepts (with little critical analysis) “negative cogni-
tions” as the proper focus of therapeutic attention, and the reported effective-
ness of cognitive-behavioral therapy indirectly supports the claim that these
cognitions play a role in the psychogenesis of depressive mood.
Neurobiological Theories
A consensus conference held by the National Institutes of Health concluded
that “the hallmark of depression in the elderly is its association with medical
comorbidity” (National Institutes of Health Consensus Conference 1992,
p. 1023). This conclusion was based on data associating late-life depression,
particularly the late-onset variant, with a broad spectrum of medical disor-
ders, including cardiovascular, cerebrovascular, musculoskeletal, metabolic,
and pulmonary illnesses and malignancies. Possible mediating mechanisms to
account for these associations have focused on cerebrovascular pathology (the
“vascular depression” hypothesis discussed earlier in the subsection “Vascular
Depression”) and on decreases in brain volume, which have been reported in
the prefrontal lobe, caudate nucleus, and hippocampus of elderly depressed
subjects. Several authors (Duman 2004; Jacobs et al. 2000) have proposed
that decreased neurogenesis contributes to hippocampal atrophy and thereby
underlies the pathophysiology of depression, and they cite several lines of in-
direct evidence in support of this theory. Other authors have challenged this
theory, however (Henn and Vollmayr 2004), and it remains provocative but
essentially untested at this time. A path analysis conducted by Kumar and col-
leagues (2000) found two distinct pathways to late-life major depression: One
path proceeded via vascular and nonvascular medical comorbidity—which
contributed equally to high-intensity lesions, which led to major depressive
disorder. The second path proceeded from frontal lobe atrophy (apparently
not consequent to medical morbidity) to late-life major depressive disorder.
Other neurobiological theories of late-life depression are similar in their
focus on central neurotransmitter function to the theories of middle-age
110 Clinical Manual of Geriatric Psychiatry
Substance-Induced Mania
Substances known to induce mania include sympathomimetic agents (iproni-
azid, procarbazine), psychostimulants (e.g., amphetamines, methylphenidate,
cocaine, phencyclidine), tricyclic antidepressants, monoamine oxidase inhib-
itors, levodopa, yohimbine, bromide, alprazolam, corticosteroids, and many
other substances (Table 3–11). In this regard, hypomania or mania that be-
gins during or within 1 month of treatment with one or more of the medica-
tions listed here should be considered substance induced.
Bipolar Disorder
Epidemiology
The Epidemiologic Catchment Area study found a 1-year prevalence of 0.1% of
bipolar disorder among adults older than 65 living in the community. In light of
the 1%–2% prevalence of major depression, this finding suggests that about
112 Clinical Manual of Geriatric Psychiatry
Metabolic Hemodialysis
disturbances Postoperative state
Uremia, hyperthyroidism, pellagra, carcinoid syndrome,
hyperbaric chamber use, cyanocobalamin deficiency
Source. Chen ST, Altshuler LL, Spar JE: “Bipolar Disorder in Late Life: A Review.” Journal of
Geriatric Psychiatry and Neurology 11:29–35, 1998. Reprinted by permission of Sage Publica-
tions, Inc.
5%–10% of elderly patients with major mood disorder have bipolar disorder.
Relatively little research has been published on bipolar disorder in the elderly.
Depp and Jeste (2004), in a review, stated, “To date, there have been no pub-
lished large-scale multi-center studies of prevalence, etiology, or clinical features
of bipolar disorder in late life, nor have there been any double-blind randomized
controlled trials of pharmacologic treatments in this population” (p. 343).
Diagnostic Criteria
DSM-IV-TR criteria for manic episode and hypomanic episode are listed in
Table 3–12 (please refer to DSM-IV-TR for criteria for the various forms of
bipolar disorder).
Clinical Presentation
Bipolar disorder typically is first diagnosed in young adulthood, but cases in
which the first episode of mania occurs after age 50 are not rare. Depp and
Jeste (2004) reviewed 13 studies of older bipolar disorder patients (sample-
weighted mean age=68.2) in which age at onset of any psychiatric illness and
of mania were reported and 8 studies in which age at onset of mania was re-
ported. The average age at onset of any mood disorder was 48, and the aver-
age age at onset of mania was 56. These ages are significantly later than the
reported age at onset of mixed-age patients with bipolar disorder, which tends
to be in the 20s. Few other consistent findings distinguish bipolar disorder in
the elderly from bipolar disorder in young and middle-aged adults, but Depp
and Jeste did conclude that older bipolar patients are less likely to have co-
morbid substance abuse than are younger patients and that late-onset mania
is associated with more neurological impairment.
114 Clinical Manual of Geriatric Psychiatry
Hypomanic episode
A. The same as criterion A for manic episode above, but only 4 days’ duration is
required, and the mood must be clearly different from the usual nondepressed
mood.
B. The same as criterion B for manic episode above.
C. The episode is associated with an unequivocal change in functioning that is
uncharacteristic of the person when not symptomatic.
D. The disturbance in mood and the change in functioning are observable by others.
Mood Disorders—Diagnosis 115
Source. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of
Mental Disorders, 4th Edition, Text Revision. Washington, DC, American Psychiatric Associa-
tion, 2000. Copyright © 2000, American Psychiatric Association. Used with permission.
Pathogenesis—Psychodynamic Theories
Relatively little has been written about the psychodynamics of hypomania
and mania in elderly patients per se. Early psychodynamic considerations
about mania compared the relative importance of predisposing personality
characteristics with that of precipitating events. Investigators such as Emil
Kraepelin were influenced by what seemed to be an inconsistent relationship
between manic episodes and external life events. Although the question re-
mains open, the psychodynamic literature from that point has generally
agreed on the primary importance of constitutional factors in the develop-
ment of the illness. Analytical theorists beginning with Abraham attempted
to understand these constitutional factors in terms of predisposing personal-
ity characteristics and the interplay of classic psychodynamic mechanisms. In
this regard, Abraham saw mania as a psychic regression to a state of intense
ambivalence directed toward love objects, reflected in behavior by primitive
impulsiveness. Later theorists conceptualized mania as a defense and tended
to see the manic personality as immature, egocentric, chronically depressed,
dependent on others for self-esteem, and dominated by feelings of interper-
sonal competitiveness and envy. Generally, psychodynamic theories of mania
have come to be seen as more relevant to shifts in mood in nonmanic individ-
uals and have largely been supplanted by neurobiological theories in attempts
to understand frank hypomania and mania.
116 Clinical Manual of Geriatric Psychiatry
Blood studies
Thyroid-stimulating hormone, Hyperthyroidism
thyroxine
Cortisol (A.M. and P.M.) Hyperadrenocorticism
Sedimentation rate Collagen vascular disease, especially lupus
Lumbar puncture Encephalitis
Computed tomography or magnetic Brain tumor, stroke, multiple sclerosis
resonance imaging of head
Pathogenesis—Neurobiological Theories
A postmortem study of brain tissue (Young et al. 1994) found decreases in se-
rotonin turnover in the frontal, parietal, and temporal cortices from subjects
with bipolar disorder, as well as decreased dopamine turnover in the parietal
and occipital cortices and increased norepinephrine turnover in the thalamus
and frontal, temporal, and occipital cortices. Also, some evidence indicates
that the configuration of γ-aminobutyric acid (GABA)A receptors in the fron-
tal cortex of subjects with bipolar disorder is altered (Dean et al. 2001) com-
pared with nonbipolar subjects, but the significance of this finding remains
unclear. Similarly, changes in various neurotransmitter receptor–G-protein
interactions (which modulate neurotransmission at the intracellular level)
and certain “downstream” signal transduction components (e.g., inositol) also
have been described in subjects with bipolar disorder (Dean 2004), but no co-
herent theory has yet emerged from these findings.
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4
Mood Disorders—Treatment
T reatment of mood disorders in the elderly generally follows the same prin-
ciples that apply to young and middle-aged adults but is typically complicated
by one or more of the confounding factors listed in Table 4–1. To avoid rep-
etition and redundancy, treatment trials should be conducted in a systematic
and logical sequence. For purposes of discussion, in the first part of this chapter,
we focus mainly on nonpsychotic major depression, but the treatment principles
apply, with modifications as indicated, to all of the depressive variants discussed
in Chapter 3 (“Mood Disorders—Diagnosis”). Treatment of bipolar depres-
sion is discussed at the end of the chapter in the “Bipolar Disorder” section.
127
128 Clinical Manual of Geriatric Psychiatry
assets or roles, and demands of caregiving, and these problems often form the
content of psychotherapy. For persons with high levels of disability or recurrent
mental and physical problems, appropriate clinical goals may be to manage,
rather than eliminate, symptoms and to sustain as high a level of independence
as possible. Higher-functioning older adults often do well with the usual forms
of individual, group, or family therapies that are provided in outpatient settings.
Depressed elders with cognitive impairment may benefit more from systematic
adjustments in the social or physical environment to maximize functional skills,
behavior modification (e.g., to increase participation in pleasurable activities), or
specialized cognitive training techniques (see Chapter 6, “Other Dementias and
Delirium”). For individuals with chronic health problems or significant physical
disabilities, techniques for addressing specific medical comorbidities (e.g., pain
or insomnia) can be especially beneficial. Helping with a specific, tangible prob-
lem can strengthen the provider-patient relationship and increase the likelihood
that other issues can be successfully addressed.
Problem solving and learning new behaviors may progress more slowly with
older adults than with young or middle-aged patients (Gallagher-Thompson
and Thompson 1996). Home visits may be needed for older patients with lim-
ited mobility. For patients with memory impairment, a simple written sum-
mary of topics covered in a session can help to support continuity from one
session to the next (see Chapter 6, “Other Dementias and Delirium”). Adjust-
ments for sensory losses (e.g., amplification for hearing-impaired patients and
large-print homework or educational materials) may be required, and as dis-
cussed in Chapter 1 (“Introduction”), current cohorts of older adults may lack
familiarity with psychotherapy or may have negative attitudes toward mental
illness that need to be addressed in initial sessions.
The best-studied psychotherapeutic interventions with older adults are be-
havior therapy, cognitive-behavioral therapy, and problem-solving therapy
(Areán and Cook 2002; Gatz et al. 1998). All share a common theoretical
framework that emphasizes the importance of learning adaptive responses.
These interventions have been examined in well-controlled studies in relatively
diverse populations by several independent investigators, and clear benefits
have been shown relative to no-intervention and wait-list control subjects. In
major depression, benefits for those who respond to such therapies have been
shown to persist for at least 1–2 years. Most studies have found little difference
in efficacy between these procedures. Cognitive-behavioral therapy has been
Mood Disorders—Treatment 129
Source. Adapted from Rush AJ: “Overview of Treatment Options in Depressed Elderly,” in Di-
agnosis and Treatment of Depression in Late Life. Edited by Schneider LS, Reynolds CF, Lebowitz
BD, et al. Washington, DC, American Psychiatric Press, 1994, pp. 171–180. Copyright © 1994,
American Psychiatric Press. Used with permission.
adapted for use over distance (e.g., with homebound elderly) through use of
written materials and periodic telephone contacts (Landreville 1998).
Interpersonal psychotherapy, which combines elements of psychodynamic
therapy with cognitive-behavioral approaches, also has been shown to be effec-
tive in alleviating geriatric depression, but it has been studied less often than
130 Clinical Manual of Geriatric Psychiatry
(e.g., in the 5 years preceding the 2002 review by Areán and Cook, only 9 psy-
chotherapy trials had been published, compared with 700 medication trials).
Additional studies of psychotherapy and combined medication and psychoso-
cial approaches are clearly needed.
One promising line of research is examining the effectiveness of brief, struc-
tured psychotherapeutic interventions for treating depression within primary
care. The multisite IMPACT (Improving Mood: Promoting Access to Collabora-
tive Treatment) project has been providing either medication, psychotherapy, or
combined therapies to depressed older adults identified in primary care (Unützer
et al. 2003). Choice of treatment is determined jointly by the patient, the primary
care provider, a depression care manager (either a nurse or a psychologist), and a
consulting psychiatrist. Problem-Solving Treatment in Primary Care (PST-PC) is
the principal psychotherapeutic intervention being studied, and it is provided by
a nurse, generally a nurse clinical specialist or psychiatric nurse practitioner. Spe-
cific problems are identified, and a seven-stage approach to problem solving is in-
troduced and practiced for each problem. Typically, one problem is addressed per
session for a total of four to eight sessions, followed by less frequent maintenance
sessions as needed. Areán and colleagues (2001) provide a more detailed descrip-
tion of PST-PC procedures suitable for older adults, and Haverkamp et al. (2004)
present a case example of its application with a chronically depressed older person.
Individuals participating in the IMPACT intervention program have experienced
significantly lower depression for at least 12 months compared with patients in
usual care, for black and Latino elderly as well as white patients (Areán et al.
2005), and despite the presence of multiple medical comorbidities (Harpole et al.
2005). Such collaborative models for intervention offer the hope of access to ef-
fective treatments for depression to a broader range of older adults and offer op-
portunities for psychiatrists with geriatric expertise to educate about depression
and other mental health conditions within a general medical context.
Other studies have been examining methods for countering older adults’
negative attitudes toward depression and its treatment and for increasing ad-
herence to recommended therapies. Dropout rates in therapeutic studies of
antidepressant medications run as high as 33%, and in clinical practice, discon-
tinuation rates of psychoactive medications are even higher (Pampallona et al.
2002). Studies of interventions aimed at helping older people adhere to medi-
cation regimens have tended to be small scale and of poor methodological qual-
ity (Higgins and Regan 2004), but most suggest that one-time, education-only
132 Clinical Manual of Geriatric Psychiatry
that met their criteria: 12 trials studied tricyclics, 5 studied selective serotonin
reuptake inhibitors (SSRIs), 2 studied bupropion, and 1 studied mirtazapine.
They concluded that
Source. Based on data from Richelson E: “The Pharmacology of Antidepressants at the Synapse: Focus on Newer Compounds.” Journal of Clinical Psy-
chiatry 55 (suppl A):34–39, 1994; Kent JM: “SnaRIs, NaSSAs, and NaRIs: New Agents for the Treatment of Depression.” Lancet 355:911–918, 2000;
Fawcett J, Barkin RL: “Review of the Results From Clinical Studies on the Efficacy, Safety and Tolerability of Mirtazapine for the Treatment of Patients
With Major Depression.” Journal of Affective Disorders 51:267–285, 1998; and Thase ME, Tran PV, Wiltse C, et al: “Cardiovascular Profile of Duloxetine,
a Dual Reuptake Inhibitor of Serotonin and Norepinephrine.” Journal of Clinical Psychopharmacology 25:132–140, 2005.
Mood Disorders—Treatment
135
Table 4–3. Advantages and disadvantages of major categories of antidepressants
First-line agents
SSRIs Benign side effects Sexual side effects
Once-daily dosing Interact with many medications prescribed for elderly patients
Bupropion Benign side effects Three-times-daily dosing required
Relatively unlikely to cause Contraindicated in patients with seizures, eating disorder
rapid cycling
Venlafaxine Benign side effects Sexual side effects
Mirtazapine Stimulates appetite Weight gain may be a problem in the long run.
Benign side effects
Duloxetine Benign side effects Sexual side effects
Second-line agents
Tricyclics May be more effective than Dangerous side effects:
nontricyclics in severe depression Orthostatic hypotension
Inexpensive Delayed cardiac conduction
Once-daily dosing
Trazodone Inexpensive Dangerous side effects:
Orthostatic hypotension
Can cause priapism, although rare
Table 4–3. Advantages and disadvantages of major categories of antidepressants (continued)
Category Advantages Disadvantages
Third-line agents
MAOIs Inexpensive Dietary and medication restrictions required
Effective in atypical depression Potentially fatal interaction with meperidine, sympathomimetics,
SSRIs
Lithium Inexpensive Only two-thirds as effective as above agents
Psychostimulants Immediately effective No controlled studies
(methylphenidate, Benign side effects Development of tolerance common
amphetamines)
Note. MAOIs= monoamine oxidase inhibitors; SSRIs =selective serotonin reuptake inhibitors.
Mood Disorders—Treatment
137
138 Clinical Manual of Geriatric Psychiatry
do cause tend to be less dangerous than those caused by tricyclics, the SSRIs
(including fluoxetine, sertraline, paroxetine, fluvoxamine, citalopram, and
escitalopram) and the nonselective amine inhibitors bupropion, venlafaxine,
and mirtazapine are generally preferable to the TCAs and are therefore re-
garded here as first-line agents. It must be noted that some authorities still pre-
fer TCAs in patients with severe, melancholic depression; however, even these
experts avoid the tertiary tricyclics (e.g., amitriptyline, imipramine, doxepin,
trimipramine) because of their greater sedating, anticholinergic, and cardiac
side effects and their relatively greater tendency to cause orthostatic hypo-
tension than their demethylated counterparts, the secondary tricyclics (e.g.,
desipramine, nortriptyline, protriptyline). All TCAs have type 1 antiarrhyth-
mic effects and are relatively contraindicated in patients with ischemic heart
disease or preexisting cardiac conduction disturbance (increased P-R interval,
bundle-branch block, increased QRS). Trazodone is an effective and safe an-
tidepressant in the elderly, but it is sedating enough to be difficult for many
elderly patients to tolerate in effective doses and thus is regarded along with
the tricyclics as a second-line agent in the discussion below and in the sum-
mary presented in Table 4–3.
Because the tetracyclic agent maprotiline has a relatively strong associa-
tion with seizures and has no advantages that are not matched by other less
risky agents, it is not recommended for elderly patients. Similarly, the diben-
zoxazepine amoxapine has mixed neuroleptic-antidepressant properties and
attendant risks of extrapyramidal symptoms and tardive dyskinesia and is not
recommended.
ceutical agents (Table 4–4); the SSRIs can therefore cause clinically significant
increases in serum levels of other medications if administered concurrently. In
this regard, paroxetine is the most potent, followed by fluoxetine, sertraline,
citalopram, escitalopram, and fluvoxamine. SSRIs all have an elimination
half-life of about 1 day, except fluoxetine, which has a significantly longer
half-life (discussed in the following subsection). Fluoxetine, paroxetine, and,
to a lesser extent, fluvoxamine (but not citalopram, escitalopram, or sertra-
line) inhibit their own metabolism, producing nonlinear increases in plasma
concentrations with dosage increases. SSRIs also attenuate platelet activation
by depleting serotonin storage and have been shown in at least one study
(Sauer et al. 2003) to reduce the risk of myocardial infarction, although the
effect is modest.
Citalopram is metabolized predominantly by the CYP isoenzymes 2C19
and 3A4, and at least six polymorphisms of 2C19 that result in slowed me-
tabolism of citalopram have been identified. Patients with these phenotypes
will have higher blood levels of citalopram at any given dose than will patients
with the wild-type allele, and dosages must be adjusted accordingly. Although
there is no practical way to determine any given patient’s 2C19 phenotype,
the “slow metabolizer” variant is present in about 13%–23% of individuals of
Asian descent and in only 2%–5% of non-Asian persons (Yu et al. 2003).
All of the SSRIs can produce serious, potentially fatal interactions with
monoamine oxidase inhibitors (MAOIs) and should not be administered
within 2 weeks of discontinuation of an MAOI; similarly fatal interactions
have been reported with the antihistamines terfenadine and astemizole, both
of which have been withdrawn from the U.S. market but are still available in
other countries.
Fluoxetine
Advantages. Fluoxetine has mild psychostimulant-like effects and is very
weakly anticholinergic. As is true of the other SSRIs, the final dosage of
20 mg/day (for the vast majority of patients) is only twice the recommended
starting dosage of 10 mg/day, which vastly simplifies the process of dosage ad-
justment in the induction phase of therapy.
Disadvantages. Stimulant-like properties may interfere with sleep and appe-
tite, particularly in the first few weeks of therapy. Fluoxetine has a long elimi-
Table 4–4. Psychotropic medications that inhibit or induce cytochrome P450 (CYP)
Inducers (continued)
Antidepressants 1A2 May lower levels of
Citalopram Antidepressants: Amitriptyline, imipramine, fluvoxamine
Fluvoxaminea Antipsychotics: Phenothiazines, haloperidol, clozapine
Others: Acetaminophen, caffeine, ciprofloxacin, estradiol, theophylline, warfarin
Antidepressants 2C9 May lower levels of
Fluoxetinea Diclofenac, ibuprofen, naproxen, phenytoin, warfarin
Fluvoxaminea
Sertraline
Mood Disorders—Treatment
Antidepressants 2C19 May lower levels of
Fluoxetine Antidepressants: Amitriptyline, clomipramine
Fluvoxaminea Proton pump inhibitors: Omeprazole, lansoprazole, pantoprazole
Others: Diazepam, phenytoin, progesterone
Note. ACE =angiotensin-converting enzyme.
a
Relatively more potent inhibitor.
bAdministration of nefazodone (or other nonpsychotropic inhibitors of CYP isoenzyme 3A4) with these agents may lead to potentially fatal torsades de
141
142 Clinical Manual of Geriatric Psychiatry
nation half-life (more than 24 hours) and has at least one active metabolite
(norfluoxetine) with a half-life of up to 15 days. Therefore, at least 5 weeks must
elapse after discontinuing fluoxetine therapy before an MAOI can be safely ad-
ministered.
Sertraline
Advantages. Sertraline has a relatively low potential for competitive inhibi-
tion of any of the CYP isoenzymes and is therefore a good choice for patients
taking complex multidrug regimens. It is also a relatively potent reuptake inhib-
itor of dopamine, at least in vitro, and may have theoretical advantages in pa-
tients with Parkinson’s disease, although several authorities recommend against
the use of SSRIs in such patients because of the risk of confusion. Sertraline has
the most linear dose–plasma level relation of the SSRIs.
Disadvantages. Possibly because of its dopaminergic properties, sertraline is
somewhat stimulating and may interfere with sleep if administered late in the
day.
Paroxetine
Advantages. Paroxetine has no active metabolites and is less activating than
either fluoxetine or sertraline and therefore may be given at bedtime.
Disadvantages. Paroxetine causes relatively potent inhibition of CYP2D6 and
therefore may pose a problem for patients taking multidrug regimens. It also has
mild anticholinergic effects, but a study conducted by Nebes and colleagues
(1999) showed that “the slight increase in serum anticholinergicity seen in some
elderly patients treated with paroxetine did not significantly impair cognitive
function, even in patients with a preexisting cognitive impairment” (p. 26).
Fluvoxamine
Advantages. Fluvoxamine is the most sedating of the SSRIs and may be ad-
ministered at bedtime.
Disadvantages. Fluvoxamine causes potentially clinically significant inhibition
of CYP1A2 and CYP2C19 (and probably a third, CYP3A3/4) and therefore may
elevate serum levels of propranolol and omeprazole, as well as citalopram and ven-
lafaxine. It has been studied relatively little in geriatric depression.
Mood Disorders—Treatment 143
Citalopram
Advantages. Citalopram is a very weak inhibitor of all the CYP isoenzymes
and therefore is the SSRI of choice for patients with complex multidrug reg-
imens. It has mild gastrointestinal side effects associated with all of the SSRIs
(nausea, diarrhea), which appear to be less frequent in elderly than in middle-
aged patients; a weak tendency to cause bradycardia (in about 2%–3% of pa-
tients) appears to increase with age.
Disadvantages. Citalopram is contraindicated in patients receiving pimozide.
An incompletely understood interaction results in significant increases in the
QTc interval, with consequent risk of serious arrhythmia.
Escitalopram
Advantages. Escitalopram, the S-enantiomer of citalopram, is similar to ci-
talopram but more selective and may cause side effects less frequently than
does citalopram.
Disadvantages. Few studies on escitalopram have been done to date in el-
derly patients.
Duloxetine
Advantages. Duloxetine is an inhibitor of norepinephrine and serotonin re-
uptake and has been shown to be effective for depression, neuropathic pain,
and stress urinary incontinence in women.
Disadvantages. Data on duloxetine in elderly depressed subjects are lacking
to date.
Second-Line Agents—Nontricyclics
Trazodone
Advantages. Trazodone has no anticholinergic effects and is extremely se-
dating, so it may have a role in the treatment of patients with significant sleep
disturbance.
Disadvantages. Trazodone may cause mild gastrointestinal upset and ortho-
static hypotension. Its sedative properties limit its usefulness in many patients.
Mood Disorders—Treatment 147
MAO and therefore requires only a 1-week washout period before sympatho-
mimetic agents or diet ad libitum can be administered safely.
Disadvantages. Because of its psychostimulant effects, tranylcypromine
may have greater abuse potential than phenelzine.
Selegiline
Advantages. As mentioned, selegiline is selective for MAO B and will not
interact with dietary tyramine in low dosages. However, it is probably not, by
itself, an antidepressant at these dosages.
Disadvantages. Selegiline is poorly studied at antidepressant dosages and,
like all MAOIs, is prone to potentially dangerous interactions with other
drugs.
Moclobemide
Advantages. Moclobemide is selective for MAO A and does not require di-
etary restriction. It has been well studied as an antidepressant, including in
elderly subjects, and has been shown to be comparable to TCAs and SSRIs in
efficacy (Amrein et al. 1997). Reversibility of MAO inhibition makes it less
likely to pose a problem interacting with other agents.
Disadvantages. Like all MAOIs, moclobemide is prone to potentially dan-
gerous interactions with other drugs.
General Principles of Treatment With MAOIs
Pretreatment physical and laboratory examinations should be conducted as
described earlier for cyclic antidepressants, including determination of pre-
treatment orthostatic changes in blood pressure and, based on the medical
history and physical examination, assessment of the patient’s likelihood of re-
quiring sympathomimetic agents. Elderly patients with chronic asthma or
bronchitis who must take indirect-acting bronchodilators and patients with
Parkinson’s disease who may require treatment with levodopa are not candi-
dates for MAOI therapy. The patient’s reliability vis-à-vis dietary and medi-
cation restrictions must be assessed carefully. Specifically, patients who have
dementia and who are monitoring their own diet and medications are poor
candidates for MAOI therapy.
152 Clinical Manual of Geriatric Psychiatry
wear MedicAlert bracelets indicating that they are taking MAOIs and speci-
fying that they should not receive meperidine. Similarly, dental procedures
should be performed with local anesthetics that do not contain epinephrine.
Third-Line Agents—Psychostimulants
Although controlled studies in elderly patients are lacking, a relatively large
body of clinical literature supports the use of psychostimulants in elderly de-
pressed patients, particularly those in whom medical illness precludes the use
of cyclic antidepressants or MAOIs (Emptage and Semla 1996). Both am-
phetamines and methylphenidate have been administered, although meth-
ylphenidate is generally preferred because of its relatively lower cardiovascular
side-effect profile. Dosages range from 5 to 20 mg administered orally twice
a day, generally immediately before breakfast and lunch so as not to interfere
with appetite or sleep. Cardiovascular side effects are typically limited to very
minor increases in blood pressure and heart rate. The most common side ef-
fect is mild jitteriness, which may be managed with small doses of benzodiaz-
epine anxiolytics, but severe dysphoria and agitation, appetite disturbance,
and insomnia requiring discontinuation of treatment may occur rarely. One
retrospective comparison of methylphenidate and nortriptyline found that
both medications produced comparable rates of remission in patients with
poststroke depression but that the time to peak response for methylphenidate
was 2.4 days compared with 27 days for nortriptyline (Lazarus et al. 1994). A
double-blind, placebo-controlled study of poststroke depression found that
3 weeks of treatment with methylphenidate (in dosages up to 15 mg twice
daily) produced statistically significant but mild improvement in mood and
was well tolerated (Grade et al. 1998). Modafinil, a more recently developed
wake-promoting agent with psychostimulant properties, has been proposed
as an adjunct to antidepressant therapy, and results from several open-label
studies in nongeriatric subjects are encouraging (DeBattista et al. 2004; Ni-
nan et al. 2004).
Combining Antidepressants
Combination therapy involves the simultaneous administration of two or
more agents in dosages that would be expected to have antidepressant effects
if administered alone. Combinations that appear, on the basis of largely un-
controlled, small studies, to be safe and to provide some enhanced effective-
ness over either agent administered alone include a TCA plus an MAOI, a
TCA plus an SSRI, an SSRI plus trazodone, an SSRI plus another SSRI,
moclobemide (a reversible MAOI) plus an SSRI, bupropion plus an SSRI,
bupropion plus venlafaxine, mirtazapine plus an SSRI, venlafaxine plus an
SSRI, and reboxetine plus an SSRI (Lam et al. 2002). Combinations chosen
to produce reuptake inhibition of both serotonin and norepinephrine may be
most effective. One double-blind, random-assignment study of middle-aged
adults with nonpsychotic major depression found that desipramine (norepi-
nephrine reuptake blocker) and fluoxetine (SSRI) together were significantly
more effective than either drug alone in inducing remission after 6 weeks of
treatment. Side effects (orthostatic hypotension, tachycardia) were those typ-
ical for desipramine (Nelson et al. 2004).
Maintenance Treatment
It is now well established that relapse and recurrence are best prevented by
maintaining patients on the same dose of antidepressant required to induce
remission. Reynolds (1994) used this approach with nortriptyline (titrating
blood levels between 80 and 120 ng/mL) and reported that 80% of remis-
sions were sustained for a year or more.
Electroconvulsive Therapy
ECT remains the single most effective treatment for major depression with or
without psychosis in elderly patients. Remission rates in the range of 75%–
90% or greater can be obtained in “naïve” patients (i.e., those who have not
tried and failed other treatments), but in the more typical elderly patient who
has had an inadequate response to other treatments, response rates (defined
as a decline of 50% or more in pretreatment depression ratings) are in the
80%–90% range, even in the “old-old” (i.e., older than 75), and side effects
are usually limited to transient memory impairment (Tew et al. 1999). ECT
is about equally effective in psychotic and nonpsychotic depression; however,
because psychopharmacological therapy has relatively limited effectiveness in
psychotic depression, this condition is the strongest indication for ECT as a
first-line therapy. Other indications for ECT as the treatment of first choice
include
158 Clinical Manual of Geriatric Psychiatry
• Active suicidality
• Severe anorexia
• High likelihood of inability to tolerate antidepressant side effects
• High likelihood of medication noncompliance
seems to produce a more enduring response, at least in the first several weeks
after treatment, than that reported by most investigators. Prophylactic anti-
depressant treatment is initiated immediately after the last ECT treatment.
The associated anterograde memory impairment, which is cumulative
over the course of treatment, typically reaches the level of mild disorientation
to time and mild to moderate anterograde and retrograde memory loss. All of
these symptoms usually clear rapidly and are clinically undetectable a week or
so after the last treatment, but in some cases, they may persist for as long as 3
or 4 weeks. Retrograde memory loss, especially for events occurring during
the course of treatment, may persist much longer, and memory for some in-
trahospitalization events may be permanently lost. Given this information,
along with the recovery statistics mentioned earlier, and the extremely low
mortality rate of ECT (less than 1 death per 10,000 patients), the great ma-
jority of patients are willing to accept this degree of memory loss as part of the
cost of treatment.
Experimental Therapies
book Feeling Good (Burns 1999); however, many other self-help depression
books on the market have not been systematically studied.
Bipolar Disorder
The site of treatment of bipolar disorder depends on the urgency of the clin-
ical situation. In the acute manic phase, inpatient treatment is indicated,
whereas outpatient management is often sufficient for hypomania or bipolar
depression without suicidality.
ated from friends, family, treating physicians, and other caregivers. Generally,
insight-oriented therapies are avoided during the acute phase of illness but
may be quite effective when the most severe symptoms are under control.
Both individual and family therapy approaches can be used, whereas group
settings may not provide enough structure to allow the elderly bipolar patient
to benefit. Psychosocial treatment of bipolar depression is similar to the treat-
ment of unipolar depression but calls for more psychoeducation of the patient
and family regarding the early signs of a switch into mania, which can occur
spontaneously or be provoked by antidepressant therapy.
glomerular filtration rates (by 30%–50%) compared with young adults, and
the elimination half-life of lithium may be increased up to 36 hours. There-
fore, elderly patients generally require smaller dosages of lithium to reach
therapeutic serum levels; a typical starting dosage may be as low as 150 mg/
day. The increased half-life allows once-a-day dosing, which is also believed
to reduce side effects compared with divided doses (Hardy et al. 1987). After
6–7 days at a steady daily dosage, serum for determination of lithium level is
drawn, and an approximately linear dose–serum level relation is assumed
within therapeutic dosage ranges.
Divalproex is an acceptable alternative to lithium in manic elderly pa-
tients, particularly in those who develop deterioration of cognitive perfor-
mance during lithium treatment (Young et al. 2004). Dosages of divalproex
range from 400 to 1,000 mg/day (in divided doses) and are adjusted to pro-
duce serum levels between 50 and 120 µg/mL. Divalproex may be of partic-
ular value in rapid-cycling patients and those with mixed mania (i.e., with
depressive symptoms and manic symptoms). Side effects are usually minimal
and include sedation, nausea, and ataxia.
Other agents that have been proposed for acute and maintenance treat-
ment of geriatric bipolar disorder include the anticonvulsants carbamazepine,
oxcarbazepine, lamotrigine, topiramate, and gabapentin, but none has been
studied in elderly bipolar patients per se. Studies in middle-aged subjects sug-
gest that carbamazepine and lamotrigine both have acute (i.e., phase two)
antimanic effects and also may be effective for prophylaxis of mania and hy-
pomania (Ichim et al. 2000; Sachs et al. 2000).
Carbamazepine may be most effective in manic patients who cycle rapidly
and who have predominantly irritable rather than euphoric mood, features that
have been reported to occur relatively commonly in elderly manic patients.
Dosages of carbamazepine (typically beginning at 200 mg orally twice a day) are
adjusted to produce blood levels in the range of 4–12 ng/mL, and antimanic
effects appear after 4–7 days. Because carbamazepine induces its own metab-
olism, dosage increase is commonly required after 4–6 weeks of therapy to
maintain therapeutic blood levels. Side effects of and adverse reactions to car-
bamazepine include sedation, dizziness, ataxia, nausea and vomiting, mild an-
ticholinergic effects, skin rash (rarely including Stevens-Johnson syndrome and
toxic epidermal necrolysis), and worsening of congestive heart failure, hyperten-
sion, and hypotension. Rare cases of aplastic anemia and agranulocytosis also
Mood Disorders—Treatment 165
have been reported; thus, baseline blood studies and periodic reevaluations are
necessary for patients taking this drug. Carbamazepine undergoes hepatic mi-
crosomal metabolism, so the general pharmacokinetic and pharmacodynamic
considerations discussed in Chapter 2 (“Normal Aging”) apply.
Lamotrigine in nonelderly manic patients is as effective as lithium for
phase two management, and one study in elderly patients found that lamo-
trigine added to lithium or divalproex led to remission (Robillard and Conn
2002). To reduce the risk of rash, a rigid schedule of dosage increases is re-
quired: for nonelderly adults, it is 25 mg once daily for 1 week, 50 mg once
daily for the second week, and 100 mg once daily for the last 2 weeks. Elderly
patients may require even smaller dosages at each step.
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173
174 Clinical Manual of Geriatric Psychiatry
Mini-Mental State 11-item, 30-point scale 5–10 Brief; examines several Insensitive to mild or focal
Examination (MMSE; assesses orientation, functions; wide deficit; high false-
Folstein et al. 1975) registration and delayed application; good norms positive rate with poorly
recall, language, educated patients
attention,
visuoconstruction
Cognitive Abilities 20 items from modified 10–15 100-point scoring range May not be more sensitive
175
Table 5–1. Cognitive mental status examinations and brief screening tools (continued)
Dementia Rating Scale Scales assess attention, 30–45 May detect subcortical or Take too much time to
(DRS; Mattis 1976) conceptualization, frontal brain deficit; administer in some
DRS-2 (Jurica et al. 2001) memory, initiation and sensitive to wider range of situations; limited data
perseveration, dementia than are briefer on use with diverse
visuoconstruction scales samples
Animal Naming task Naming animals as quickly 1 Extremely brief; will detect Insensitive to mild deficit
(e.g., Duff Canning et al. as possible for 60 seconds moderate to severe or conditions affecting
2004) dementia; may be useful nonlanguage skills;
as an initial screen when cutoff scores likely to
time is very limited vary by education level
and ethnicity
Clock Drawing Test Drawing the face of a clock 2–5 Very brief; well accepted by Insensitive to mild deficit;
(e.g., Shulman 2000) and setting hands to a patients; sensitive to no generally accepted
specified time parietal function and method of
some aspects of frontal or administration and
executive function; will scoring; does not assess
detect moderate to severe memory processes most
dementia directly affected by
Alzheimer’s disease
Table 5–1. Cognitive mental status examinations and brief screening tools (continued)
Administration Advantages and
Measure Description time (min) applications Limitations
Mini-Cog Three-word learning and 2–4 Very brief; will detect Insensitive to mild deficit;
(Borson et al. 2000) recall task plus clock moderate to severe relatively new test, and
drawing dementia; developed for independent validation
use with ethnically and studies are needed
linguistically diverse
populations
Orientation-Memory- Six items assess temporal 3–5 Very brief; will detect Insensitive to mild deficit
177
178 Clinical Manual of Geriatric Psychiatry
ranged within sections, so that the first item serves as a screen for intact ability
in each domain. This scale provides more extensive assessment of language,
memory, and praxis than do most mental status examinations and includes
items that may be sensitive to frontal-lobe impairment (initiation and perse-
veration sections). The DRS is recommended for use in patients who have
mild impairment when a detailed assessment of abilities is desired and when
time permits complete administration.
A Closer Look at the MMSE
Table 5–2 presents sample items from the popular MMSE. The widespread use
of this test with diverse populations is likely to ensure its continued popularity,
despite some recognized limitations. The MMSE, initially validated with el-
derly psychiatric groups and nonpsychiatric community control subjects, has
been translated into several languages, and a modified form suitable for hearing-
impaired patients is also available. The MMSE has high interrater reliability
and adequate retest reliability in stable conditions. Folstein and colleagues
(1975) have emphasized that the MMSE does not establish a diagnosis of de-
mentia; instead, as with all screening instruments, it identifies individuals with
possible cognitive impairment that may warrant further assessment.
Initially, a score of 23 or fewer correct items was recommended as a cutoff
to screen for cognitive impairment. However, subsequent studies have shown
that this cutoff score is likely to overidentify poorly educated persons as im-
paired and fail to detect true decline in well-educated individuals. Table 5–3
presents median values and scores at the twenty-fifth percentile for several age
and educational groups, based on an epidemiological survey of more than
18,000 persons from several areas within the United States. Scores at the
twenty-fifth percentile are above typical cutoffs for impairment, but if the his-
tory or other observations raise a question of decline, a score at this level may
warrant further assessment or monitoring. It is obvious from the values shown
in the table that both age and education influence MMSE scores and that a
specific score for a particular individual must be interpreted in light of these
characteristics and other historical and medical information.
Although the MMSE was not specifically designed to screen for Alzheimer’s
disease, certain items—most notably, delayed recall and copying of penta-
gons—are likely to be failed by patients with Alzheimer’s disease. Recalling of
only two of three words, or even one word, may fall within normal limits for
Dementia and Alzheimer’s Disease 179
some older persons, but inability to recall any words, particularly when prompts
are provided, strongly suggests a problem with retention characteristic of
Alzheimer’s disease or other disorders producing amnesia. Many patients with
Alzheimer’s disease will have forgotten that they were asked to remember some
words when delayed recall is requested. Other items on the MMSE that are sen-
sitive to early or mild Alzheimer’s disease are design copying and temporal ori-
entation. This scale is not sensitive to executive or psychomotor changes, and as
a result, it is less useful in screening for frontotemporal dementia or subcortical
dementia (see Chapter 6, “Other Dementias and Delirium”).
Despite careful attempts at translation, research suggests that some
MMSE items may be biased for use with populations whose primary lan-
guage is not English or whose cultural identification differs from that of
normative samples, which are largely white and middle class. Several items
showed significant ethnicity or language differences in a comparison of white
Table 5–3. Mini-Mental State Examination scores by age and educational level
0–4 years
Median 22 22 22 22 21 21 19 20
25th percentile 20 20 19 19 19 18 16 15
5–8 years
Median 27 27 27 27 26 26 25 24
25th percentile 25 25 24 24 24 22 22 21
9–12 years
Median 29 29 28 28 28 27 26 26
25th percentile 27 27 27 27 26 25 23 23
Some college or higher
Median 30 29 29 29 29 28 28 28
25th percentile 28 28 28 28 27 27 26 25
Source. Adapted from Crum RM, Anthony JC, Bassett SS, et al.: “Population-Based Norms for the Mini-Mental State Examination by Age and Ed-
ucational Level.” Journal of the American Medical Association 269:2386–2391, 1993. Copyright © 1993, American Medical Association. All rights re-
served.
Dementia and Alzheimer’s Disease 181
and Hispanic adults, and another study found that the MMSE misclassified
more nonimpaired Hispanic elderly persons as cognitively impaired than did
a memory test based on learning and recall of 10 common objects (Loewen-
stein et al. 1995). However, some of the items most sensitive to Alzheimer’s
disease (delayed recall and design copying) are minimally affected by ethnicity
and educational differences. The CASI (Teng et al. 1994) (see Table 5–1) in-
cludes items from the MMSE and the Hasegawa Dementia Scale (Tsai and
Gao 1989) that have been modified to accommodate translation problems
and differential difficulty across various countries as suggested by pilot test-
ing. Developed initially for patients in Japan and the United States, this test
has now been used in several large-scale studies that provide normative refer-
ence points (e.g., McCurry et al. 1999). Performance on the CASI, like the
MMSE, is influenced by age and education in older adults without dementia.
Abbreviated Cognitive Screens
There has been an emphasis in recent research on the development and vali-
dation of very brief cognitive assessment tools that might be suitable for de-
mentia screening in primary care settings or other situations when time is very
limited (Lorentz et al. 2002).
Category fluency measures, especially Animal Naming, have long been
included in neuropsychological testing batteries to evaluate retrieval from se-
mantic memory, and recent studies examining the diagnostic accuracy of such
tasks suggest that they could play a role as brief, initial screens for dementia
of several types. In two independent cohorts of older adults being followed up
for dementia, a 60-second Animal Naming task performed as well in detect-
ing Alzheimer’s disease as did the MMSE, and when the Animal Naming task
was combined with recall of a five-item name and address (“John Brown 42
Market Street Chicago”), sensitivity and specificity surpassed those of the
MMSE (Kilada et al. 2005). Another study (Duff Canning et al. 2004) that
examined well-diagnosed cases of Alzheimer’s disease and vascular dementia
found the Animal Naming task to be the best of several verbal fluency tasks
in differentiating patient groups from control subjects; sensitivity to dementia
was high, even among persons with MMSE scores greater than 24. In that
study, which mainly included well-educated older adults, a cutoff score of less
than 14 animals in 60 seconds was highly effective in detecting dementia.
However, optimal verbal fluency cutoff scores are likely to vary by education
182 Clinical Manual of Geriatric Psychiatry
level and, possibly, ethnic and linguistic background, and care must be taken
to use appropriate normative reference points. Animal Naming is not recom-
mended as a stand-alone cognitive screen, but it may be useful as part of a
multistep screening procedure in which persons with low fluency scores are
then given additional screens or tests.
Clock drawing tests also have been widely used for very brief cognitive
screening. Attempting to re-create such a familiar item is generally acceptable
to patients, and the visual outcomes can be useful in showing undetected cog-
nitive problems to patients or their family members. Administration time varies
depending on the version used and the patient’s psychomotor skills, but many
patients can complete the task in 1 or 2 minutes. A recent review of clock draw-
ing procedures for dementia screening (Shulman 2000) found fairly high sensi-
tivities and specificities (about 85%), and outcomes usually were not affected
by linguistic background. However, very old persons, or those with little or no
education, are likely to perform less well. A practical drawback to clock drawing
is the lack of standard procedures for administration and scoring. Some meth-
ods require the patient to draw the circle for the clock face, whereas others
present a predrawn circle. Scoring ranges from a simple pass-or-fail method to
relatively elaborate systems of 20 or more points (see Appendix for references to
scoring systems). Another limitation is that clock drawing does not directly test
for impaired memory, which is the core early deficit in Alzheimer’s disease and
certain other dementias. Because of these drawbacks, the Clock Drawing Test
is generally not used as a stand-alone screening measure.
The Mini-Cog (Borson et al. 2000) is composed of a three-item word
learning and recall task and a simple clock drawing task. By combining the
most sensitive item used in the MMSE and CASI (i.e., word-list recall) with
a visual task that can detect parietal dysfunction and some aspects of frontal
and executive deficits, the Mini-Cog has been shown to perform as well as or
slightly better than the full MMSE in identifying probable Alzheimer’s disease
and some other dementias. Administration time runs from 2 to 4 minutes,
and scoring is relatively simple and straightforward. An additional advantage
is that this test was designed for and has been validated with multiethnic el-
derly populations (black, Asian American, and Hispanic) and appears less
likely to be biased by low education and literacy than is the full MMSE (Bor-
son et al. 2005). A recent review of the performance of cognitive screening
tests in diverse groups (Parker and Philp 2004) concluded that, in general,
Dementia and Alzheimer’s Disease 183
short tests yield more consistent data across varying cultures and education
levels and may be better accepted by patients compared with lengthier and
more demanding measures.
The Orientation-Memory-Concentration Test (OMCT), a six-item ver-
sion of the Blessed Information Memory Concentration Test (Katzman et al.
1983), takes approximately 5 minutes to administer. It taps several skills often
affected in dementias of various types, including temporal orientation, men-
tal control (counting backward and reciting months backward), and memory
for verbal narrative (a spoken phrase). The OMCT correlates highly with the
MMSE, but in at least one study, it was found to be more sensitive to mild or
subclinical dementia (Brooke and Bullock 1999). Advanced age and very low
education adversely affect scores.
The Memory Impairment Screen (Buschke et al. 1999) looks in a brief but
well-designed way at a single skill: the ability to learn and retrieve new informa-
tion. The patient is shown four large-print words on a page and is asked to read
each word and then point to and name each word again in response to a cate-
gory cue (e.g., the cue word for “apple” would be “fruit”). After a delay of about
2 minutes filled with an unrelated task (counting forward and backward from
1 to 20), both free and cued recall are assessed. Administration time is about
4 minutes, and the total score combines both free and cued recall. For popula-
tions with different base rates of disease, the authors provide recommended cut-
off scores for use in screening for dementia and for Alzheimer’s disease.
Preliminary data from a small number of patients suggested that the Memory
Impairment Screen may be more sensitive to mild dementia than are most other
screens. The Memory Impairment Screen is more effective in identifying
Alzheimer’s disease than is the three-word recall task from the MMSE (Kuslan-
sky et al. 2002), has been adapted for telephone screening, and has been trans-
lated into Spanish. Although the Memory Impairment Screen is a promising
screening tool, it has not been used widely yet, and the relative lack of indepen-
dent validation data is a limitation.
Laboratory Evaluation
Laboratory evaluation is aimed at identifying illnesses known to cause de-
mentia and generally begins with a selected standardized battery of tests with
relatively high sensitivity and low specificity. The screening battery presented
in Table 5–4 was recommended by Reichman (1994).
Neuropsychological Tests
Neuropsychological tests are often performed to corroborate an impression of
dementia and to identify specific cognitive strengths and weaknesses that may
affect treatment or placement. Table 5–5 summarizes some of the tests that we
have found useful in diagnostic assessment for possible dementia. Each of these
tests has been developed for measures applicable to geriatric populations or has
been studied extensively with older patients. Other measures may be useful as
well, but any battery for dementia evaluation should tap a full range of cognitive
abilities, including general intelligence, attention, language, learning and mem-
ory, visuospatial performance, and reasoning or problem solving. If coexisting
psychiatric disturbance is suspected, psychodiagnostic measures also should be
included (see Chapter 3, “Mood Disorders—Diagnosis”).
Neuropsychological testing alone is generally not sufficient to establish a
particular etiology of dementia. However, the pattern of performance on
these tests can either strengthen or weaken the case for certain types of de-
mentia. For example, on tests of learning and memory, a very shallow learning
curve, sharply reduced delayed recall, and impaired recognition are com-
monly observed in dementia of the Alzheimer’s type but are less often noted
in subcortical dementia (e.g., Huntington’s chorea or Parkinson’s disease), in
frontotemporal dementia, or in major depression.
Wechsler Adult General adult Verbal and nonverbal IQ scores lower than Influenced by education
Intelligence Scale— intelligence battery skills, including estimated baseline or
Third Edition with 14 subtests; vocabulary, attention, low age-scaled subtest
(WAIS-III) normed to age 89 reasoning, perceptual scores may indicate
organization, and impairment
processing speed
Wechsler Memory Battery of verbal and Orientation; mental Low scores on immediate Sensitive to mild
Scale—Third Edition nonverbal memory control; memory span; or delayed memory amnesia, dementia
187
Table 5–5. Examples of neuropsychological assessment instruments (continued)
Consortium to Establish Memorization of a list of Verbal learning and Slow rate of learning or Sensitive to mild
a Registry for 10 words; developed delayed recall impaired delayed recall dementia of the
Alzheimer’s Disease and normed for older suggests amnestic Alzheimer’s type; easier
(CERAD) Word List adults deficit than CVLT
Learning
Object Memory Memorization of 10 Storage and retrieval Delayed recall <50% or Good test of secondary
Evaluation common objects; from secondary very low rate of learning memory for patients
normed for ages 70–90 memory, delayed recall suggests amnestic with low education level
and recognition deficit
Boston Naming Test Naming of drawings of Confrontation naming, Cutoff scores vary with More sensitive to mild
(BNT) objects; normed to age access to semantic age and education anomic aphasia than is
90+ memory mental status
examination
Controlled Oral Word Naming of words Verbal fluency, access to Cutoff scores vary with Intrusions may be noted
Association Test beginning with semantic memory, age and education in early Alzheimer’s
(COWAT) specified letters; ability to organize rapid disease, perseverations
normed to age 90+ retrieval or loss of set in
subcortical dementias
Table 5–5. Examples of neuropsychological assessment instruments (continued)
Test Description Functions assessed Interpretation Comment
Trail Making Test (TMT) Lines drawn to connect Composite index of Cutoff scores vary with Failure on alternating
number and letter visual scanning speed, age and education sequence noted in mild
sequences; normed to sequencing, mental brain impairment of
age 80+ flexibility, visuomotor various types; slowing
integration in subcortical dementia
Wisconsin Card Sorting Sorting of Inferring concepts, Cutoff scores vary with May be more sensitive
Test (WCST) multidimensional cognitive flexibility age and education than memory tests to
patterns into frontotemporal and
Note. For references to tests and further discussion, see La Rue A: “Geriatric Neuropsychology: Principles of Assessment,” in Handbook of Assessment in
Clinical Gerontology. Edited by Lichtenberg PA. New York, Wiley, 1999, pp. 381–416; Spreen O, Strauss E (eds): A Compendium of Neuropsychological
Tests, 2nd Edition. New York, Oxford University Press, 1998; and Lezak M, Howieson D, Loring D: Neuropsychological Assessment, 4th Edition. New
York, Oxford University Press, 2004.
189
190 Clinical Manual of Geriatric Psychiatry
Substances
Medications
Antihypertensives
Corticosteroids
Digitalis
Opiates and synthetic narcoticsa
Psychoactive agents with anticholinergic propertiesa
Other chemicals
Carbon disulfide
Carbon monoxide
Lead
Manganese
Mercury
Most drugs of abuse
a
Common offender.
bPatient
may present as having “frontotemporal dementia.”
192 Clinical Manual of Geriatric Psychiatry
Alzheimer’s Disease
Alzheimer’s disease, including both early-onset (age 65 or younger, account-
ing for about 1% of all Alzheimer’s disease cases) and late-onset (older than
65) subtypes, accounts for about 50% of all cases of primary dementia and
may combine with other conditions, primarily vascular dementia, in another
10%–20% (Langa et al. 2004). Because the definitive diagnosis of Alzhei-
mer’s disease requires direct visualization of characteristic neuropathology
(i.e., amyloid β-peptide–containing senile plaques, neurofibrillary tangles
[NFTs] consisting of hyperphosphorylated tau protein, neuritic degeneration
and loss) in brain tissue of affected patients and brain biopsy is prohibitively
risky, Alzheimer’s disease is at best a probable diagnosis in the living patient.
Age (years)
in part by earlier onset of Alzheimer’s disease in those who are APOE4 posi-
tive, and it is attenuated in black and Hispanic individuals (Harwood et al.
2004). APOE4 is also associated with the presence of concomitant Lewy bod-
ies in autopsy studies of patients with Alzheimer’s disease (Tsuang et al. 2005),
decreased longevity, increased plasma cholesterol levels, and prevalence of car-
diovascular disease and tends to worsen response to head trauma, age-related
cognitive decline, and several other disorders (Smith 2000).
In a meta-analysis of 11 retrospective and prospective studies, Szekely et al.
(2004) concluded that long-term exposure to nonsteroidal anti-inflammatory
drugs (NSAIDS) is associated with a reduced risk for developing Alzheimer’s
disease. The literature reviewed did not allow any conclusions regarding which
194 Clinical Manual of Geriatric Psychiatry
NSAIDs are best, and the most effective duration of treatment or dosage of
medication is unknown. Hormone replacement therapy (estrogen with or with-
out progestins) in postmenopausal women was reported to reduce the risk of
developing Alzheimer’s disease (LeBlanc et al. 2001). This observational report
was contradicted by the Women’s Health Initiative Memory Study, a random-
ized, double-blind, placebo-controlled primary prevention trial in women age
65 years or older, which found that estrogen with or without progestin increased
the risk of developing both Alzheimer’s disease and mild cognitive impairment
(Shumaker et al. 2004). A possible explanation for these discrepant findings was
reported by Henderson et al. (2005), who found that hormone replacement
therapy was protective against the development of Alzheimer’s disease, but only
in women ages 50–63; older subjects did not sustain the same benefit.
The risk of developing Alzheimer’s disease also appears to be reduced in
people who ingest adequate amounts of the antioxidants vitamin E and vita-
min C, in food or supplement form, according to several investigators. Engel-
hart et al. (2002) reported findings from the Rotterdam study and concluded
that “high intake of vitamin C and vitamin E from food may be associated
with a lower incidence of Alzheimer disease after a mean follow-up period of
6 years” (p. 3228, emphasis added). In this study, vitamin E and C supple-
ments did not reduce the risk of Alzheimer’s disease. However, Zandi et al.
(2004) did find a significantly lower incidence and prevalence of Alzheimer’s
disease in individuals who ingested the combination of supplemental vitamin
E (400 IU/day or more) and vitamin C (at least 500 mg/day of ascorbic acid),
but not either vitamin alone, over a 3-year follow-up period.
Morris and colleagues (2005) reported data that may partially resolve the dis-
agreement between the two studies discussed in the prior paragraph. They fol-
lowed up 1,041 subjects age 65 or older for a median of 3.9 years and found that
dietary α-, γ-, and δ-tocopherols were significantly and inversely associated with
incident Alzheimer’s disease, with reductions in risk of 34% per 5-mg/day in-
crease in α-tocopherol, 40% per 5-mg/day increase in γ-tocopherol, and 25% per
1-mg/day increase in δ-tocopherol. There was no evidence of an association be-
tween intake of β-tocopherol and Alzheimer’s disease risk. The authors concluded
that “various tocopherol forms rather than α-tocopherol alone may be important
in the vitamin E protective association with Alzheimer disease” (p. 508).
Several cross-sectional observational studies raised the possibility that
statins, which reduce cholesterol, might reduce the risk of Alzheimer’s disease.
Dementia and Alzheimer’s Disease 195
To examine this relation, Zandi et al. (2005) followed up with 4,895 partici-
pants in the Cache County Study, an investigation of the genetic and envi-
ronmental antecedents of dementia among the elderly population of Cache
County, Utah, which began in 1995 with the enrollment of 5,092 individuals
age 65 or older. Statin use was less frequent in subjects with prevalent dementia,
but the authors found no association between statin use and subsequent onset
of dementia or Alzheimer’s disease. This finding is surprising given the known
relation between atherosclerosis and cerebrovascular disease. The authors ac-
knowledged several methodological and statistical factors that may have ob-
scured a real association, among them the short duration (about 3 years) of
exposure to statins, the small number of subjects who reported taking statins,
and the small number who developed Alzheimer’s disease. The role of statins in
the prevention of dementia and Alzheimer’s disease remains to be determined.
Diagnostic Criteria
In DSM-IV-TR (American Psychiatric Association 2000), the term dementia
of the Alzheimer’s type is applied to patients whose condition meets clinical and
laboratory criteria for probable Alzheimer’s disease; dementias associated with
other neurological diseases (e.g., Pick’s disease or Creutzfeldt-Jakob disease)
are coded separately. General criteria for dementia must be met, and a history
of insidious onset and gradual progression must be present; if all other causes
of dementia are ruled out by the history, physical examination, and laboratory
tests, dementia of the Alzheimer’s type is diagnosed (Table 5–7).
NINCDS Criteria
The National Institute of Neurological and Communicative Disorders and
Stroke (NINCDS) published a set of diagnostic criteria for research purposes
that are somewhat more narrow than the DSM-IV-TR criteria (McKhann et
al. 1984). Separate standards are listed for the clinical diagnosis of probable
and possible Alzheimer’s disease (Table 5–8).
Neuropathological Criteria
At present, at least three pathological criteria for Alzheimer’s disease are inter-
nationally acceptable: 1) Braak’s criteria (Braak and Braak 1991); 2) Consor-
tium to Establish a Registry for Alzheimer’s Disease (CERAD) criteria (Mirra
et al. 1991) and their combination; and 3) National Institute on Aging and
196 Clinical Manual of Geriatric Psychiatry
Source. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of
Mental Disorders, 4th Edition, Text Revision. Washington, DC, American Psychiatric Associa-
tion, 2000. Copyright © 2000, American Psychiatric Association. Used with permission.
level of the caudate-putamen complex, 2) the first temporal gyrus at the level
of the amygdala, and 3) the supramarginal gyrus with parieto-occipital sulcus.
Density is rated as follows: stage A =less than 2, stage B =approximately 6, and
stage C = more than 30 neuritic plaques per 100× light microscopic field.
Alzheimer’s disease is diagnosed when stage A is identified in patients younger
than 50 years, when stage B is seen in patients between 50 and 75 years, and
when stage C occurs in patients older than 75 years, along with a definite clin-
ical history of dementia (Murayama and Saito 2004).
Clinical Presentation
As is true for all dementing illnesses, the clinical presentation of Alzheimer’s
disease depends on the stage of illness and may be obscured or complicated
by symptoms related to concomitant physical and psychiatric illness, in-
cluding depressive or anxiety disorders, psychosis, and delirium. Table 5–9
summarizes the clinical and laboratory findings typically observed in uncom-
plicated cases as the disease progresses (Group for the Advancement of Psy-
chiatry 1988). Functional symptoms nearly indistinguishable from those of
concomitant psychiatric illness are part of the presentation of Alzheimer’s dis-
ease, even in the early stages, and patients may present to general psychiatric
clinical settings. Gormley and Rizwan (1998) reported that one-third of
Alzheimer’s disease patients had delusions, and 11% had hallucinations
within the month before evaluation, and this prevalence was not affected by
severity of dementia or of depressive symptoms. Farber and colleagues (2000)
found that 63% of patients with Alzheimer’s disease had psychosis at some
point in the course of illness and that those with psychosis had 2.3 times the
density of neocortical NFTs than did those without psychosis. In some pa-
tients with Alzheimer’s disease, the psychosis is clinically prominent enough
to obscure the underlying cognitive impairment and delay accurate diagnosis.
Delusions are usually persecutory in nature and are typically fragmented
and inconsistent, unlike those seen in the common functional disorders (e.g.,
schizophrenia, delusional disorder, or mood disorder with psychosis). Com-
mon delusional content includes the belief that one is being threatened,
deprived, or abused by caregivers or that possessions are being stolen; hypo-
chondriacal delusions and Capgras’ syndrome are also common (Migliorelli
et al. 1995). Delusions in Alzheimer’s disease typically do not have the elab-
orate “connectedness” seen in functional delusions (i.e., the myriad ways in
198 Clinical Manual of Geriatric Psychiatry
Subtypes
Familial
Onset before age 65
Presence of trisomy 21
Other relevant disorders (e.g., parkinsonism)
Note. ADRDA =Alzheimer’s Disease and Related Disorders Association; NINCDS= National
Institute of Neurological and Communicative Disorders and Stroke.
Source. Adapted from McKhann et al. 1984.
which the patient is able to tie the delusional belief to all aspects of his or her
experience), and hallucinations—usually auditory but sometimes visual, ol-
factory, or tactile—are intermittent and of varying and usually trivial content,
lacking the ordered, meaningful quality typical of functional hallucinations.
Depressive symptoms and apathy occur in about 20%–25% of Alzhei-
mer’s disease patients at any given time (Lyketsos et al. 2000b), but full de-
pressive syndromes (e.g., major depression) are relatively rare.
History
The history of Alzheimer’s disease is typically one of insidious onset and
gradual progression of cognitive and functional impairment, with few of the
Table 5–9. Natural history of Alzheimer’s disease: clinical and laboratory findings
Complex or new tasks Decreased performance Decreased performance; may Cannot perform
withdraw from challenging
situations
Personality Possible apathy, depression, Denial common; apathy and Agitation or anxiety, psychosis,
or irritability indifference abulia, obsessiveness
CT scan Normal Normal to atrophic cortices and Cortical atrophy and ventricular
dilated ventricles enlargement
EEG Normal Background slowing Diffuse slowing
Note. CT=computed tomography; EEG= electroencephalogram; PET=positron emission tomography; SPECT= single photon emission computed to-
mography.
Source. Copyright 1988 from The Psychiatric Treatment of Alzheimer’s Disease by Group for the Advancement of Psychiatry. Reproduced by permission
of Routledge/Taylor & Francis Group, L.L.C.
201
202 Clinical Manual of Geriatric Psychiatry
Neuropsychological Tests
In probable Alzheimer’s disease, multiple neuropsychological impairments
are seen, including anomic or mixed aphasia, apraxia, deficits in reasoning,
and prominent learning and memory impairment. Patients with Alzheimer’s
disease rapidly forget new information and often do not benefit from cueing
Dementia and Alzheimer’s Disease 203
Laboratory Evaluation
Laboratory evaluation of Alzheimer’s disease is the same as that described ear-
lier in this chapter for dementia (Table 5–4). Despite the promise of the ex-
perimental diagnostic procedures discussed in the following subsection, the
laboratory evaluation of patients with possible Alzheimer’s disease is primarily
aimed at ruling out other causes of dementia. If this evaluation does not iden-
tify another cause of dementia, and either DSM-IV-TR or NINCDS–Alzhei-
mer’s Disease and Related Disorders Association clinical criteria are applied,
the diagnosis of “probable Alzheimer’s disease” has reasonable sensitivity (ap-
proximately 80%) and specificity (approximately 70%), as confirmed by sub-
sequent neuropathological diagnosis (Knopman et al. 2001).
Delirium
Alzheimer’s disease is usually easily differentiated from delirium, which has a
much more acute onset and progression and entails more severe impairment
of attention and concentration and more disorganization of thought. How-
ever, delirium superimposed on Alzheimer’s disease may be more difficult to
diagnose, often requiring reevaluation after potential causes of delirium have
been eliminated and the underlying dementia has been allowed to emerge.
activities such as bathing or walking (Gatz et al. 1998). More recent work ad-
dressing behavior problems has used cued recall procedures adapted from the
cognitive rehabilitation literature; Bird and colleagues (1995) provide good
examples of successes and failures of this approach.
Reminiscence therapy, which involves the discussion of past activities,
events, and experiences, usually with the aid of tangible prompts such as pho-
tographs or music, has become an increasingly popular intervention. It can be
used by staff at activity centers and long-term-care facilities and lends itself to
involvement of family members. A recent review of the literature on reminis-
cence therapy in dementia found four controlled trials, all of which reported
beneficial effects on cognition or mood in comparison with no-treatment or
social-contact control subjects. However, studies were small in size, and all
used different types of reminiscence procedures (Woods et al. 2005).
Early studies of memory training for patients with dementia used tech-
niques developed for normal older adults (e.g., group or individual practice
of mnemonics such as visual imagery), and results showed either no benefit
or very circumscribed benefit. Recently, more promising results have been
demonstrated with the use of specialized training techniques (e.g., spaced re-
trieval) that have proven effective in work with memory-impaired brain-
injured populations. These interventions typically involve a relatively intense
initial encoding phase in which the person with dementia is asked to say or
do a to-be-remembered action repeatedly, with the interval between the cue
and the desired response gradually lengthened from immediately to over an
hour or more. In an interesting case study, Clare and colleagues (2001) de-
scribed how a 74-year-old man with mild but progressive dementia (MMSE
score decreased from 26 to 22 across the study period) was able to learn
name–face associations for 11 members of his social club, sustain recall of
nearly all these names with daily self-practice over 9 months, and still retain
7 or 8 names over the next 2 years with only weekly club visits to rehearse the
associations. Individualization of the training and selecting objectives that
meet a real-life need are thought to be important by many contemporary
researchers studying the limits and benefits of a cognitive rehabilitation
approach for dementia patients. However, there are also ongoing new inves-
tigations of the effects of predetermined training regimens for persons with
early Alzheimer’s disease, especially as an adjunct to cholinesterase inhibitor
therapies (e.g., Loewenstein et al. 2004).
210 Clinical Manual of Geriatric Psychiatry
parts (Coon et al. 2004). It is unclear whether such findings reflect cultural
differences in filial roles and obligations or limited knowledge of or access to
alternative means of care (Aranda and Knight 1997). In any family that has a
relative with dementia, the therapist must assess the possibility of caregiver
distress and provide information about in-home, community, and institu-
tional resources.
Organizations such as the Alzheimer’s Association offer information and
help-line support for dementia caregivers, and many self-help books and Web
sites are available. Examples of resources that can be helpful to caregivers, es-
pecially when used in conjunction with family therapy or other interventions,
are included at the end of this chapter, following the references.
tor and appears to exert its effects at the cellular level by reducing glutamate-
mediated excitotoxicity, which leads to neuronal injury or death. Unlike the
cholinesterase inhibitors, memantine is effective in patients with moderate to
severe Alzheimer’s disease and seems to exert at least additive effects when com-
bined with cholinesterase inhibitors (Tariot et al. 2004). Improvement in agita-
tion and mood has been observed in several clinical trials, but cognitive and
functional decline in Alzheimer’s disease remains the main indication. The ini-
tial dose is 5 mg/day, which is increased in 5-mg/day increments over 4 weeks
to the final dose of 10 mg twice per day. Side effects are minimal, with dizziness,
confusion, headache, and constipation being most often reported. Memantine
undergoes little metabolism, and adverse drug-drug interactions have not been
reported and are unlikely. Table 5–10 shows the clinical pharmacology of the
cholinesterase inhibitors and memantine.
Other Agents
NSAIDS, hormones, statins, and ginkgo biloba have been studied in patients
with Alzheimer’s disease, and some positive results have been reported, but to
date definitive evidence of the efficacy of any of these agents remains unpub-
lished. Sano et al. (1997) reported that patients with Alzheimer’s disease who
were taking 2,000 IU of vitamin E showed no improvement in cognitive
function but did take significantly longer to require institutionalization than
did those receiving either placebo or 10 mg/day of selegiline. Although this
finding has not been replicated, it has stimulated some clinicians to add high-
dose vitamin E to the treatment regimen of patients with Alzheimer’s disease.
215
216 Clinical Manual of Geriatric Psychiatry
data also suggested a similar increase in mortality for these agents. Accord-
ingly, clinicians should consider this risk before recommending antipsychotic
medications for agitation in elderly individuals with dementia. (The FDA ad-
visory is available at http://www.fda.gov/cder/drug/infopage/antipsychotics/
default.htm.)
Typical dosage ranges of neuroleptic medications are 0.5–3 mg/day of
haloperidol, 1–3 mg/day of risperidone, 5–10 mg/day of olanzapine, and 25–
200 mg/day of quetiapine, administered in two or three doses orally or, with
conventional agents, by intramuscular injection. Low-potency, high-dose
conventional agents such as thioridazine are generally avoided because of their
greater anticholinergic potency, which can increase confusion in patients with
Alzheimer’s disease, and their propensity to cause other side effects such as
orthostatic hypotension. High-potency agents are also effective when agita-
tion is accompanied by hallucinations, delusions, belligerent and hostile be-
havior, or physical aggressiveness. In one unreplicated double-blind, random-
assignment study, Sultzer and associates (1997) found that trazodone (50–
250 mg/day) was as effective as haloperidol (1–5 mg/day) for agitation and
somewhat more effective in the subgroup of patients with repetitive, verbally
aggressive, and oppositional behaviors. Street and associates (2000) found
that olanzapine (in dosages of 5 and 10 mg/day) was superior to placebo for
control of agitation or aggression and psychosis in nursing home residents
with Alzheimer’s disease; side effects were limited to somnolence and gait dis-
turbance, and no extrapyramidal or anticholinergic symptoms were seen.
If symptoms of agitation do not respond to neuroleptic therapy at dosages
low enough to avoid significant side effects, switching to trazodone or aug-
menting with lorazepam, 0.5–1 mg administered orally or by intramuscular
injection, may be effective. A typical daily regimen would include a standing
order for 2 mg of haloperidol or risperidone orally at bedtime and either
1) 0.5 mg of lorazepam orally every 4–6 hours as a standing order or as
needed or 2) 25–50 mg of trazodone orally every 4–6 hours as a standing or-
der or as needed. Refractory symptoms may require treatment with neurolep-
tics and trazodone.
Several rating scales, including the Behavior Pathology in Alzheimer’s Dis-
ease Rating Scale (BEHAVE-AD; Reisberg et al. 1987), the Cohen-Mansfield
Agitation Inventory (Cohen-Mansfield et al. 1989), and the Agitated Behavior
in Dementia scale (Logsdon et al. 1999), are available to track treatment effect.
218 Clinical Manual of Geriatric Psychiatry
Anxiety
Patients with Alzheimer’s disease are also susceptible to anxiety in various
forms and degrees of severity. Although treatment with anxiolytics is generally
guided by the same principles that apply to elderly patients without dementia
(see Chapter 7, “Anxiety Disorders and Late-Onset Psychosis”), patients with
Alzheimer’s disease may be unable to articulate subjective feelings of appre-
hension, psychomotor tension, or fear, and the clinician may be forced to rely
on more objective signs. In this regard, mild agitation as described earlier can
reflect an anxiety state and may respond to anxiolytics alone.
Depression
Although authorities disagree on the prevalence of clinical depressive disor-
ders in patients with Alzheimer’s disease, such disorders do occur and can be
quite disabling, often leading to increased cognitive impairment (a syndrome
that has been termed pseudodementia). Tricyclics and selective serotonin re-
uptake inhibitors have been studied in this regard, with mixed results (Katona
et al. 1998; Lyketsos et al. 2000a; Taragano et al. 1997). In general, the prin-
ciples that guide treatment of depression in elderly patients without dementia
apply (see Chapter 4, “Mood Disorders—Treatment”), with the following
modifications:
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Epidemiology
Because of the histopathological heterogeneity of this syndrome (see “Pathol-
ogy” below), and the overlap of its clinical features with those of Alzheimer’s
disease and vascular dementia, it is difficult to estimate its prevalence. One
Swedish study (Andreasen et al. 1999) found a prevalence of 3.2% in a clini-
cally diagnosed sample of 619 patients referred for diagnostic evaluation
(compared with 36.9% with Alzheimer’s disease), whereas Gustafson and col-
leagues (1992) estimated the prevalence as close to 10%. Ratnavalli and col-
leagues (2002) analyzed records from a university hospital in Cambridge,
England, and found that frontotemporal dementia and Alzheimer’s disease
had the same prevalence (15 per 100,000) in patients ages 45–64; the average
age at onset of the frontotemporal dementia was 52.2 years.
Diagnostic Criteria
Consensus criteria for diagnosing frontotemporal dementia were published in
1998 (Neary et al. 1998) and are presented in Table 6–1.
229
230 Clinical Manual of Geriatric Psychiatry
The typical age at onset of frontotemporal dementia is in the 50s and 60s, and
a family history of dementia is present in about half of cases, with a dominant
pattern of inheritance found in the majority (Chow et al. 1999). Some au-
thorities subdivide frontotemporal dementia into three clinical subsyndromes
based on its initial presentation: 1) frontal variant frontotemporal dementia
(often called dementia of frontal type), 2) semantic dementia, and 3) progres-
sive nonfluent aphasia. In the frontal variant, the main presenting feature is
progressive personality change, with disinhibition, loss of empathy, change in
eating patterns, ritualized or stereotypical behavior, and apathy (Bozeat et al.
2000). Semantic dementia is characterized by progressive loss of knowledge
of people, objects, facts, and word meanings and is associated with primarily
temporal lobe pathology. Progressive nonfluent aphasia is associated with pri-
marily frontal (perisylvian) pathology, presents with deficits in the phonolog-
ical and syntactic components of language (Grossman 2002), and may
progress to corticobasilar degeneration (Gorno-Tempini et al. 2004). A recent
longitudinal study (Seeley et al. 2005) found that after an average of 3 years,
patients who initially presented with the semantic (left temporal) variant of
frontotemporal dementia also developed the symptoms of right frontotempo-
ral deficit (especially emotional flatness, irritability, and disruption of physi-
ological drives such as sleep and appetite), and those with initially prominent
behavioral symptoms developed semantic language deficits. Disinhibition,
compulsions, altered food preferences, and weight gain emerged in both
groups later in the disease, about 5–7 years after onset.
232 Clinical Manual of Geriatric Psychiatry
structured caregiver interview. Items for this scale were based on behaviors de-
scribed in diagnostic consensus reports (e.g., Neary et al. 1998) for fronto-
temporal dementia. The Frontal Behavioral Inventory has good reliability
and appears effective in discriminating clearly diagnosed frontotemporal de-
mentia from Alzheimer’s disease or vascular dementia. However, norms for
clinical use are lacking. The Neuropsychiatric Inventory (NPI; see Chapter 5,
“Dementia and Alzheimer’s Disease,” and Appendix) is another behavior rat-
ing scale completed by professionals on the basis of a caregiver interview. It
taps several behaviors that are often affected in frontotemporal dementia and
has been used in clinical trials. A caregiver-completed form of the NPI has
been developed (Kaufer et al. 2000), but data are limited on the clinical use-
fulness of this version.
The symptoms of frontotemporal dementia, especially the frontal variant,
are often very distressing to family members, and education is needed to help
with understanding the avolitional nature of specific behavior changes and
with developing management strategies. A systematic survey of affected be-
haviors, whether based on direct informant ratings or interviews, can provide
a good starting point for tailoring interventions for caregivers.
Neuropsychological Tests
On neuropsychological examination, frontotemporal dementias can be dis-
tinguished in early stages from dementia due to Alzheimer’s disease by the rel-
ative salience of executive function deficits as opposed to memory disorder or
by the emergence of progressive alterations in speech (e.g., dysfluency, stereo-
typy) before notable memory deficits emerge. Neuropsychological tests sensi-
tive to frontal executive dysfunction include motor programming tasks,
cognitive speed and flexibility measures (e.g., the Trail Making Test), and rea-
soning tasks (e.g., the Similarities subtest of the Wechsler Adult Intelligence
Scale—Third Edition), as well as naming and verbal fluency tests (see Table
5–5 in Chapter 5, “Dementia and Alzheimer’s Disease,” for test descriptions).
The heterogeneity that has been noted in frontotemporal dementia is also
234 Clinical Manual of Geriatric Psychiatry
Laboratory Evaluation
Depending on the underlying pathology, frontal and temporal hypoperfusion
(on single photon emission computed tomography), reduced glucose metab-
olism (on positron emission tomography with fluorodeoxyglucose), and atro-
phy (on computed tomography or magnetic resonance imaging) may be seen
in frontotemporal dementia.
Differential Diagnosis
The other degenerative dementias (Alzheimer’s disease and dementia with
Lewy bodies); vascular dementia; the dementias associated with Huntington’s
disease, Parkinson’s disease, Creutzfeldt-Jakob disease, human immunodefi-
ciency virus (HIV) infection, and head trauma; and those associated with
other general medical conditions all must be ruled out before a diagnosis of
frontotemporal dementia is made. Because of the lack of differentiating phys-
ical signs, and the tendency for Alzheimer’s disease to include signs and symp-
toms of frontal lobe involvement, the most challenging distinction is between
frontotemporal dementia and Alzheimer’s disease. Table 6–2 summarizes the
main differentiating features of these two conditions. Knopman et al. (2005)
reviewed 433 cases that went to autopsy and found that frontotemporal de-
mentia was correctly identified on the basis of clinical and laboratory findings
in 29 of 34 autopsy-verified cases. This finding represents 85% sensitivity; the
authors also reported 99% specificity.
Pathology
The typical gross pathological finding is of frontal and anterotemporal atrophy.
Microscopic findings have been subdivided according to the profile of immu-
nohistochemical staining and the pattern of intracellular inclusions, as follows:
Other Dementias and Delirium 235
The second and third subdivisions above include cases with tau-negative,
ubiquitin-positive inclusions in the dentate gyrus and in the brain-stem mo-
tor nuclei (frontotemporal dementia with motor neuron inclusions) and de-
mentia lacking distinctive histology (Hodges et al. 2004).
Treatment
There is no specific treatment for the personality or cognitive changes seen in
the frontotemporal dementias, but several aspects of disturbed behavior have
been reported to respond to psychopharmacological treatment. Trazodone
improved symptoms of irritability, agitation, depression, and eating disorders
in one randomized, double-blind, placebo-controlled crossover study (Lebert
et al. 2004), and similar results have been observed in open-label studies with
moclobemide (Adler et al. 2003), rivastigmine (Moretti et al. 2004), and par-
oxetine (Moretti et al. 2003). However, a double-blind, placebo-controlled
crossover study with paroxetine resulted in worsening cognition and no im-
provement in behavior (Deakin et al. 2004), suggesting that open-label treat-
ment studies in frontotemporal dementia may be misleading.
Symptom
Behavior Socially correct Early disinhibition
Affect Normal Remote, bizarre
Apathy Mild Severe
Delusions Simple Bizarre
Compulsions Mild Severe
Eating Weight loss Weight gain
Neuropsychological test performance
Drawing Impaired Spared
Memory Impaired Variable
Executive function Impaired Severely impaired
Generation Impaired Severely impaired
Anomia Lexical Semantic (often)
Neuropathology
Plaques Yes No
Tangles Yes No (except for familial
tauopathy)
Gliosis Proportional to neuronal Out of proportion to
loss neuronal loss
Abnormal genes Amyloid precursor protein,
presenilin 1 and 2;
apolipoprotein ε4;
tau mutations
Neurochemistry
Cholinergic deficit Presynaptic cholinergic Postsynaptic cholinergic;
and serotonergic presynaptic and
postsynaptic serotonergic
Positron emission Temporoparietal Frontotemporal
tomography hypometabolism hypometabolism
Source. Adapted from Miller BL, Gustavson A: “Alzheimer’s Disease and Frontotemporal De-
mentia,” in American Psychiatric Press Textbook of Geriatric Neuropsychiatry, 2nd Edition. Edited
by Coffey CE, Cummings JL. Washington, DC, American Psychiatric Press, 2000, p. 521. Copy-
right © 2000, American Psychiatric Press. Used with permission.
Other Dementias and Delirium 237
Epidemiology
The prevalence and incidence of dementia with Lewy bodies are not well es-
tablished, but autopsy series have found it to account for 15%–36% of cases
of dementia (Hansen et al. 1990; Holmes et al. 1999), which would make it
the second most common cause of dementia, after Alzheimer’s disease.
Diagnostic Criteria
Consensus criteria published originally by McKeith et al. (1996) and recently
revised (McKeith et al. 2005) require dementia and two of the following three
core features to make a diagnosis of probable dementia with Lewy bodies:
“fluctuating cognition with pronounced variations in attention and alertness;
recurrent visual hallucinations that are typically well formed and detailed; and
spontaneous motor features of parkinsonism” (McKeith et al. 2005, p. 1864).
If one or more of the following suggestive features are present, a diagnosis
of probable dementia with Lewy bodies can be made in the presence of only
one core feature: “REM [rapid eye movement] sleep behavior disorder [“vivid
and often frightening dreams during REM sleep, but without muscle atonia,”
McKeith et al. 2005, p. 1866]; severe neuroleptic sensitivity; and low dopa-
mine transporter uptake in basal ganglia as demonstrated by [single photon
emission computed tomography] SPECT or [positron emission tomography]
PET imaging” (McKeith et al. 2005, p. 1864).
Supportive features include “repeated falls and syncope; transient unex-
plained loss of consciousness; depression; systematized delusions; hallucina-
tions in other modalities; relative preservation of medial temporal lobe
structures on computed tomography/magnetic resonance imaging scan; gen-
eralized low uptake on SPECT/PET perfusion scan with reduced occipital ac-
tivity; abnormal (low uptake) MIBG (metaiodobenzyl guanidine—a measure
of postganglionic sympathetic cardiac innervation) myocardial scintigraphy;
and prominent slow wave activity on electroencephalogram with temporal
lobe transient sharp waves” (McKeith et al. 2005, p. 1864).
The diagnosis of dementia with Lewy bodies is less likely if “cerebrovascular
disease evident as focal neurological signs or on brain imaging is present; in the
presence of any other physical illness or brain disorder sufficient to account in
part or in total for the clinical picture; and if parkinsonism only appears for the
first time at a stage of severe dementia” (McKeith et al. 2005, p. 1864).
238 Clinical Manual of Geriatric Psychiatry
History
The history of dementia with Lewy bodies is typically of a gradual, progres-
sive decline in intellectual function that is almost always eventually accompa-
nied by parkinsonism. Although marked day-to-day fluctuations in cognitive
function and well-formed, silent visual hallucinations that typically appear as
animals, objects, or people that the patient insists are real may turn out to be
accidental features of the illness, their occurrence should be considered at least
supportive, if not diagnostic. The history is likely to include repeated falls,
syncope, transient loss of consciousness, neuroleptic sensitivity, systematized
delusions, and hallucinations in other modalities, as well as extrapyramidal re-
actions to conventional neuroleptics (severe) and atypical neuroleptics (severe
in comparison to patients with other conditions), all of which are also re-
garded as supportive of the diagnosis of dementia with Lewy bodies. REM
sleep behavior disorder also may be present early in the disease (Ferman et al.
2002).
Neuropsychological Tests
Cognitive profiles of patients with dementia with Lewy bodies overlap with
those of Alzheimer’s disease patients in that both show deficits in multiple areas,
including memory dysfunction. Compared with patients with uncomplicated
Alzheimer’s disease, however, individuals with dementia with Lewy bodies may
have disproportionate problems with attention and working memory, visuoper-
ceptual processing, and executive function. In dementia with Lewy bodies, low
scores are likely to be seen on nearly all types of attention tasks, whereas simple
attention (e.g., forward digit span) is usually preserved in Alzheimer’s disease.
Similarly, persons with dementia with Lewy bodies often have more difficulty
than do patients with Alzheimer’s disease on relatively simple visuoperceptual
tasks such as recognizing fragmented letters or extracting meaning from pic-
tures (Calderon et al. 2001). By contrast, delayed recall tends to be better pre-
served in dementia with Lewy bodies than in Alzheimer’s disease, especially if
the newly learned information is organized in a natural way (e.g., stories) (Cal-
deron et al. 2001); there may also be greater benefit from cues and recognition
testing formats. Typically, more psychomotor slowing occurs early in the course
of dementia with Lewy bodies, and patients have greater difficulty with motor
programming and executive functions such as shifting from one thought or ac-
tion to another.
A recent study comparing autopsy-verified cases of Alzheimer’s disease,
dementia with Lewy bodies, and combined Alzheimer’s disease and dementia
with Lewy bodies (Kraybill et al. 2005) provided further support that neuro-
psychological testing may help in diagnostic differentiation. Participants in
this study were tested early in the course of illness (about 1 year after the onset
of memory problems), and at that point, no significant differences were seen
between diagnostic groups on mental status examinations (either the MMSE
or the Dementia Rating Scale; see Table 5–1). However, individuals later
240 Clinical Manual of Geriatric Psychiatry
Differential Diagnosis
The differential diagnosis of dementia with Lewy bodies includes essentially
all of the dementing diseases, including Alzheimer’s disease, frontotemporal
dementia, vascular dementia, Parkinson’s disease and Alzheimer’s disease, and
Parkinson’s disease with dementia.
Treatment
Because of the relatively severe loss of cholinergic innervation found in demen-
tia with Lewy bodies, cholinesterase inhibitors such as donepezil and rivastig-
mine have been studied in this condition. A double-blind, placebo-controlled,
double-crossover study of just seven subjects found donepezil to be statistically
significantly superior to placebo, as measured by the MMSE and the Alzhei-
Other Dementias and Delirium 241
Vascular Dementia
Epidemiology
The prevalence of vascular dementia is difficult to estimate because no gener-
ally accepted and validated neuropathological criteria have been established
to date, and this has impeded definitive validation of clinical diagnostic crite-
ria for vascular dementia (Jellinger 2005). Still, community-based studies
suggest that 1) the prevalence of clinical vascular dementia is age dependent,
with prevalence rates doubling every 5 years; 2) the frequency of vascular de-
mentia is higher in men; and 3) the prevalence differs substantially from na-
tion to nation. Overall, the prevalence of vascular dementia ranges from 2.2%
in 70- to 79-year-old women to 16.3% in men older than 80 (Leys et al.
1998).
Diagnostic Criteria
The nosological status of vascular dementia has been called into question by au-
topsy studies indicating that the underlying neuropathology in clinical vascular
dementia is commonly a “mixture” of vascular lesions and other degenerative
conditions, usually Alzheimer’s disease. A report by Hulette and colleagues
242 Clinical Manual of Geriatric Psychiatry
(1997) indicated that only 6 of nearly 2,000 brains of individuals with demen-
tia that were surveyed by pathologists had “pure” vascular pathology. If this fig-
ure is at all representative, clinical vascular dementia should be thought of as
a “vascular complication” superimposed on another dementing illness in many,
if not most, cases. This view was supported by Chui (2005), who reviewed the
status of cerebrovascular brain injury (CVBI) in relation to dementia and
stated, “An emerging database suggests that CVBI contributes significantly to
mild cognitive impairment and can precipitate the appearance of dementia in
early stages of AD [Alzheimer’s disease] pathology. However, the effects of
CVBI may become submerged once AD-pathology arrives at the isocortical
stages” (p. 51). Korczyn (2005) came to a similar conclusion, stating that
History
The history of the current illness in vascular dementia is classically one of a
more abrupt, stepwise course of cognitive impairment than the more gradual
onset and decline typical of “pure” Alzheimer’s disease and other degenerative
dementias. Risk factors identified by the history in vascular dementia are
those associated with stroke—that is, arterial hypertension, atherosclerotic
disease, low education level, alcohol abuse, and heart disease.
Other Dementias and Delirium 243
Source. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of
Mental Disorders, 4th Edition, Text Revision. Washington, DC, American Psychiatric Associa-
tion, 2000. Copyright © 2000, American Psychiatric Association. Used with permission.
Abrupt onset 2
Stepwise deterioration 1
Somatic complaints 1
Emotional incontinence 1
History or presence of hypertension 1
History of strokes 2
Focal neurological symptoms 2
Focal neurological signs 2
Note. A score of 4 or more is consistent with vascular dementia.
Source. Adapted from Rosen et al. 1980.
dysarthria, impaired gag reflex, extensor plantar reflex, and signs of “frontal re-
lease” such as grasp or snout reflex. Evidence of systemic atherosclerosis (e.g.,
bruits) and signs of poor peripheral circulation (e.g., diminished pulses, atro-
phic skin changes) also may increase the probability that dementia is at least
partly of vascular origin. Physical and neurological examination may show ab-
normal findings associated with Parkinson’s disease (tremor, cogwheel rigidity,
and akinesia), Huntington’s disease (choreoathetoid movements), head trauma
(motor or sensory deficits), HIV infection (tremor, ataxia, atonia and hyperre-
flexia, frontal release signs), or Creutzfeldt-Jakob disease (ataxia, myoclonus).
Neuropsychological Tests
Neuropsychological test findings in vascular dementia vary with the nature and
severity of cerebrovascular illness. For patients who have had single or multiple
large infarcts, deficits commensurate with the location and extent of infarction
should be expected. For those whose cerebrovascular impairment is limited to
lacunar infarcts or who have extensive deep white matter disease, deficits are
more consistent with subcortical dementia, with impairments expected on tests
of psychomotor speed and dexterity, frontal executive functions (e.g., difficul-
ties with divided attention, attentional shifting, working memory, or behavioral
planning and sequencing), and motor aspects of speech (e.g., dysarthria or re-
duced verbal output may be present) (Roman et al. 1993). Subtle frontal-sub-
cortical deficits may precede clinically significant dementia in patients with
Other Dementias and Delirium 245
deep white matter disease (leukoaraiosis) or lacunar infarcts, and abrupt change
in mood and personality, with or without clear cognitive impairment, also may
be observed in vascular dementia. A high rate of intertest scatter is not specific
to vascular dementia and cannot be used to identify this condition or to differ-
entiate it from Alzheimer’s disease or other dementias.
Laboratory Evaluation
Laboratory evaluation generally begins with a selected standardized battery of
tests with relatively high sensitivity and low specificity, as presented in Chapter 5
(“Dementia and Alzheimer’s Disease”; Table 5–4). As indicated in Table 6–3, to
establish a diagnosis of vascular dementia in the absence of neurological signs and
symptoms, laboratory evidence of cerebrovascular disease is required. Computed
tomographic or magnetic resonance brain imaging that shows brain infarction is
sufficient, if the number and location of infarcts are judged to account for the ob-
served cognitive deficits.
Differential Diagnosis
As is true of all of the dementing illnesses, the differential diagnosis of vascular
dementia includes Alzheimer’s disease; frontotemporal dementia; dementia
with Lewy bodies; the dementias associated with HIV disease, head trauma,
Parkinson’s disease, Huntington’s disease, and Creutzfeldt-Jakob disease; de-
mentia due to other medical conditions, such as brain tumor, normal-pressure
hydrocephalus, and hypothyroidism; delirium; and functional disorders (see
Table 5–6 in Chapter 5, “Dementia and Alzheimer’s Disease”). As discussed
earlier, the history, clinical presentation, mental status examination, physical
and neurological examination, and laboratory evaluation, including neuropsy-
chological tests, have been considered to be adequate to differentiate vascular
dementia from other dementing illnesses (which are discussed in detail below),
but some studies have cast doubt on this claim. Reed et al. (2004) studied 18
individuals with autopsy-defined cerebrovascular disease and found that
clinical features were quite variable; only 40% of cases with high CVD [cere-
brovascular disease] levels had elevated Hachinski Ischemia Scale scores and
neither abrupt onset nor stepwise progression was found in most high CVD
cases, even when AD [Alzheimer’s disease] changes were essentially absent.
The presence of dementia was predictably related to the level of neurofibril-
lary pathology, but was not related to the severity of CVD. (p. 63)
246 Clinical Manual of Geriatric Psychiatry
Pathogenesis
Vascular dementia is caused by varying combinations of vascular insults to the
brain, including arterial territory infarcts, distal field (watershed/borderzone)
infarcts, small and medium-sized lesions mainly in functionally important
brain areas, lacunar infarcts and scars, white matter lesions, incomplete is-
chemic injury, hippocampal lesions, and sclerosis (Jellinger 2005). Several
subtypes of vascular dementia have been described, based on either the num-
ber and distribution of lesions or the size of vessels involved (large vs. small
vessels). An emerging consensus suggests that the “subcortical” pattern of
damage is sufficiently homogeneous in terms of clinical, radiographic, and
pathophysiological features to constitute a meaningful subtype, particularly
with respect to treatment trials. Generalized arteriosclerosis secondary to hy-
pertension, cerebral atherosclerosis, and diabetes usually are cited as the most
common causes of thrombotic infarction, and cardiac disease and carotid ath-
erosclerosis as the most common causes of embolic infarction. Increasing ev-
idence suggests that the vascular lesions of vascular dementia may affect
Other Dementias and Delirium 247
tion of microglial cells and reactive astrocytes (Kittner et al. 2000), has been
effective in early Phase II trials and warrants watching.
Mixed Dementia
In a review, Langa et al. (2004) defined mixed dementia as “cognitive decline
sufficient to impair independent functioning in daily life resulting from the
coexistence of AD [Alzheimer’s disease] and cerebrovascular pathology, docu-
mented either by clinical criteria or by neuroimaging findings” (p. 2902). As
discussed earlier, the amyloid plaques and neurofibrillary tangles of Alzhei-
mer’s disease and the large infarctions, multiple lacunar infarctions, and is-
Other Dementias and Delirium 249
Alzheimer’s disease Gradual onset and Typically none until Language deficits early Cortical atrophy,
progression; ± family middle to late stages (word finding, anomia, ventricular
history fluent aphasia); clues enlargement on CT,
not helpful with MRI; temporal/parietal
retrieval; visuospatial hypometabolism on
deficits early PET; hypoperfusion on
SPECT
Vascular dementia Abrupt onset, stepwise Neurological signs and Patchy impairment; Stroke; lacunae in basal
decline; history of symptoms (e.g., gait depression, relative ganglia, white matter;
hypertension, abnormalities, falls, preservation of periventricular lesions
atherosclerosis incontinence) personality common very common, required
for diagnosis if focal
neurological signs
absent
HIV dementia HIV-positive blood test; Neurological signs and Forgetfulness, apathy, Elevated CSF protein;
gradual onset of symptoms may be slowness, poor mild lymphocytosis
cognitive changes present (e.g., ataxia, concentration common may be present;
tremor, “frontal release” neuroimaging
signs) nonspecific; HIV
usually present in CSF
Table 6–5. Differentiating the common dementias (continued)
Cognitive and Imaging and
Type History Physical findings behavioral function laboratory findings
Head trauma Head injury Depends on location of Memory impairment Depends on location,
injury; dysarthria, usually present; impulse extent of injury
hemiparesis common dyscontrol, irritability,
personality change may
be seen; nonprogressive
unless head trauma
repeated (e.g., in
dementia pugilistica)
Parkinson’s disease Dementia in later stages Extrapyramidal signs Cognitive slowing, poor Subcortical atrophy on
251
affected parent 50% psychosis common
likely to be affected
Table 6–5. Differentiating the common dementias (continued)
Pick’s disease Onset in 50s–60s Frontal release signs (e.g., Personality change, CT or MRI may show
snout, grasp reflex) emotional blunting, frontal and temporal
common deterioration of social atrophy; PET may show
skills, language deficits frontal
early; memory hypometabolism
impairment, dyspraxia
later
Creutzfeldt-Jakob Onset in 40s–60s; 5%– Myoclonus early, seizures Nonspecific symptoms CT and MRI may be
disease 15% have family later; ataxia, visual (e.g., fatigue, normal; EEG may show
history; rapid symptoms, gait diminished sleep and sharp, triphasic
progression (i.e., 1-year disturbance variably appetite early; global synchronous discharges
course) typical; can be present cognitive deficits late) at 0.5–2 Hz
transmitted by corneal
transplant or contact
with infected brain
tissue or CSF
Note. CSF= cerebrospinal fluid; CT= computed tomography; EEG =electroencephalogram; HIV=human immunodeficiency virus; MRI=magnetic
resonance imaging; PET= positron emission tomography; SPECT= single photon emission computed tomography.
Other Dementias and Delirium 253
progressive neurological disorders may benefit from some of the same inter-
ventions as caregivers of patients with Alzheimer’s disease (see Chapter 5,
“Dementia and Alzheimer’s Disease”), including psychotherapy for marked
caregiver strain (e.g., Secker and Brown 2005).
Reversible Dementia
Some dementias (mainly those due to a general medical condition), at least in
principle, can be arrested or reversed if the underlying condition is success-
fully treated before significant brain damage occurs. Clarfield (1988) re-
256 Clinical Manual of Geriatric Psychiatry
viewed several studies and found that 13% of dementias were potentially
reversible, but only 11% partially and 3% fully reversed. With more con-
servative criteria (excluding the dementia syndrome of depression), only 8%
reversed at all. Clarfield found that other than the dementia syndrome of de-
pression, substance-induced persisting dementia; metabolic dementia (in-
cluding thyroid and vitamin B12 [cobalamin] deficiency); and dementia
secondary to normal-pressure hydrocephalus, subdural hematoma, or brain
tumor were reversible. Osimani and colleagues (2005) confirmed the revers-
ibility of the dementia due to vitamin B12 deficiency and suggested that neu-
ropsychological evaluation could distinguish this syndrome from Alzheimer’s
disease. They found more frequent psychosis, minimal language disturbance,
and absence of ideomotor apraxia in dementia due to vitamin B12 deficiency
as compared with Alzheimer’s disease.
In 2003, Clarfield updated his meta-analysis and found that of more than
5,000 cases reviewed, potentially reversible causes were seen in 9%, and only
0.6% of the dementia cases actually reversed (0.29% partially, 0.31% fully).
Clarfield attributed the decline to improved selection criteria and more rigor-
ous methodology, resulting in the proportion of truly reversible dementias de-
clining toward its “true” very low value. Since Clarfield’s last review, cases of
reversible dementia also have been reported involving cerebral Whipple’s dis-
ease (Rossi et al. 2005); cryptococcal meningitis (Ala et al. 2004); bromide in-
toxication (Yu et al. 2004); systemic lupus erythematosus (Lee et al. 2004);
cerebral amyloid inflammatory vasculopathy (Harkness et al. 2004); and du-
ral arteriovenous fistula of the right transverse sinus and torcula, with occlu-
sion of the right sigmoid sinus (Bernstein et al. 2003). In general, the list of
organic etiologies that can cause dementia increases with the age of the pa-
tient, as declining functional brain reserve reduces the individual’s ability to
tolerate physiological derangement.
Delirium
Epidemiology
The prevalence of delirium depends on the population at risk and the diagnostic
criteria used. Bucht and associates (1999) reviewed the literature and found that
about 15% of elderly inpatients on acute medical-surgical services have delirium
at any time, and the rate is even higher among nursing home patients. The high-
Other Dementias and Delirium 257
Diagnostic Criteria
DSM-IV-TR diagnostic criteria for delirium due to a general medical condi-
tion are summarized in Table 6–6.
Source. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of
Mental Disorders, 4th Edition, Text Revision. Washington, DC, American Psychiatric Associa-
tion, 2000. Copyright © 2000, American Psychiatric Association. Used with permission.
Source. Adapted from Butler C, Zeman AZ: “Neurological Syndromes Which Can Be Mis-
taken for Psychiatric Conditions.” Journal of Neurology, Neurosurgery, and Psychiatry 76:i31–i38,
2005. Reproduced with permission from the BMJ Publishing Group.
Laboratory Evaluation
Proper evaluation of delirium requires comprehensive medical evaluation, in-
cluding a complete physical and neurological examination and laboratory
260 Clinical Manual of Geriatric Psychiatry
Source. Adapted from Wise MG, Trzepacz PT: “Delirium (Confusional States),” in The Amer-
ican Psychiatric Press Textbook of Consultation-Liaison Psychiatry. Edited by Rundell JR, Wise MG.
Washington, DC, American Psychiatric Press, 1996, p. 267. Copyright © 1996, American Psy-
chiatric Press. Used with permission.
Differential Diagnosis
In addition to identifying the primary illness underlying delirium, the clini-
cian must rule out other psychiatric illnesses that have signs and symptoms
similar to those of true delirium. As mentioned earlier, dementia can mimic
delirium, particularly when agitation, psychosis, or anxiety is superimposed. In
these circumstances, the clinical picture of a disorganized, aroused, confused
patient with poor attention and concentration is virtually indistinguishable
262 Clinical Manual of Geriatric Psychiatry
from that of delirium, and even when the clinician knows that the patient has
dementia, he or she is often obliged to conduct a rapid “mini-evaluation” in
which potential causes of delirium, particularly medications with central
anticholinergic effects and infection, are ruled out. This “pseudodelirium” is
usually self-limited and of very brief duration (minutes to hours), is not ac-
companied by alterations in the level of consciousness, and may be rapidly re-
sponsive to simple reassurance or other behavioral interventions. Functional
disorders, including mania, hypomania, depression, hysteria, and schizophre-
nia, particularly in the severe manifestations known as manic delirium and
catatonic excitement, also can present with a clinical state that can be difficult
to distinguish from delirium caused by a general medical condition or a psy-
choactive substance.
Pathogenesis
Treatment
Specific Psychopharmacotherapy
Two subtypes of delirium call for specific pharmacological therapy. First, with-
drawal of alcohol, benzodiazepines, or barbiturates can produce a charac-
teristic delirium (delirium tremens, in its most severe form) that is rapidly
responsive to replacement therapy with any of the three agents. Practically,
benzodiazepines are the treatment of choice and are usually administered
parenterally until symptoms are under control, at which time oral administra-
tion can be initiated. Lorazepam, a benzodiazepine with the most reliable ab-
sorption after intramuscular injection, has the additional advantages in elderly
patients of having no active metabolites and undergoing one-step hepatic me-
tabolism (i.e., conjugation) that is relatively insensitive to the presence of liver
disease. Lorazepam may be administered in doses of 0.5 mg every hour until
symptoms are under control; in more acute situations, intravenous administra-
tion provides more rapid onset of action. The second type of delirium respon-
sive to specific psychopharmacotherapy is that caused by centrally acting
anticholinergic agents. When withdrawal of the offending agent and support-
ive therapy are ineffective, further amelioration of symptoms can be attained
with oral administration of cholinesterase inhibitors such as donepezil or
parenteral administration of physostigmine, a more rapidly acting cholines-
264 Clinical Manual of Geriatric Psychiatry
Nonspecific Psychopharmacotherapy
In most other situations in which rapid control of symptoms of delirium is
desired, a growing body of case reports suggests that empirical administration
of oral cholinesterase inhibitors (donepezil, rivastigmine, galantamine)
should be followed by administration of a high-potency neuroleptic agent
such as haloperidol, risperidone, or olanzapine as necessary. Although neuro-
leptics may not correct the pathophysiology underlying delirium, they can
control agitation and thereby reduce the danger of self-inflicted injury, ex-
haustion, or disconnection from vital extracorporeal supports and render the
patient more cooperative with appropriate diagnostic and therapeutic inter-
ventions. Dosages and routes of administration vary depending on the sever-
ity of the clinical situation. Intravenous or intramuscular administration of
0.5–2.0 mg of haloperidol or intramuscular administration of 2.5–5.0 mg of
olanzapine is appropriate when rapid control of symptoms is required. In a
less acute situation, 0.5–1.0 mg of haloperidol or risperidone administered
orally is effective (Han and Kim 2004). When symptoms are refractory, aug-
mentation with 0.5 mg of lorazepam is usually very effective.
Prognosis
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7
Anxiety Disorders and
Late-Onset Psychosis
Anxiety Disorders
Epidemiology
The Epidemiologic Catchment Area survey found anxiety disorders to be the
most common mental illnesses, with a 1-month prevalence of 7.3% in adults
of all ages (Regier et al. 1988). However, a lower prevalence of 5.5% was
found in adults older than 65; within this group, phobic disorders (4.8%),
obsessive-compulsive disorder (OCD; 0.8%), and panic disorder (0.1%) were
the most prevalent specific disorders. Generalized anxiety disorder (GAD)
was not surveyed in the first wave of this study, but the second wave found a
6-month prevalence of GAD of 1.9% in adults age 65 or older, in whom only
3% of the cases began after age 65 (Blazer et al. 1991). Subsequent studies
converge on higher prevalence rates than those reported by Regier and col-
leagues. Krasucki et al. (1998) and Ritchie et al. (2004) reported an overall
prevalence of anxiety disorders of between 12% and 20%, depending mainly
on how agoraphobia was defined.
Accurate diagnosis of anxiety disorders in elderly patients can be particu-
larly difficult because of the great overlap between symptoms of anxiety dis-
orders and anxiety symptoms seen in other Axis I conditions, particularly
depression, dementia, and late-onset psychosis. A Dutch study of 3,056 indi-
viduals ages 55–85 found that 47.5% of those with major depressive disorder
also met criteria for anxiety disorders, whereas 26.1% of those with anxiety
273
274 Clinical Manual of Geriatric Psychiatry
disorders also met criteria for major depressive disorder (Beekman et al.
2000). In some cases, it can also be difficult to distinguish anxiety symptoms
from symptoms of physical illnesses such as cardiac and pulmonary condi-
tions (e.g., palpitations, shortness of breath, chest pain) that are common in
elderly persons.
Clinical Presentation
Whether anxiety occurs in reaction to a transient situation, in reaction to a per-
manent or semipermanent life change, or as part of an anxiety disorder or
other Axis I disorder, patients with anxiety present with a subjective state of
dysphoric apprehension or expectation, accompanied by various combinations
of the signs and symptoms listed in Table 7–1 (which includes features listed
in DSM-IV-TR [American Psychiatric Association 2000] criteria for panic at-
tack and for GAD). Because the current generations of elderly individuals are
especially disinclined to complain of mental distress, anxious elderly patients
often focus on these physical features rather than on the subjective state of ap-
prehension or dysphoria per se. Unfortunately, their complaints often mislead
the general practitioner or internist into an extensive medical evaluation before
the correct diagnosis is established.
Recognition and treatment of anxiety disorders is important because of
the effect these disorders have on quality of life and because they are associ-
ated with a significantly increased risk of suicide attempts and completed sui-
cide, even in the absence of other mental disorders (Khan et al. 2002).
Geriatric depression is often slower to remit when the clinical picture is com-
plicated by comorbid general anxiety symptoms, panic disorder, or posttrau-
matic stress disorder (Hegel et al. 2005; Steffens and McQuoid 2005).
Anxiety also may be a predictor of cognitive decline, especially when accom-
panied by complaints of loss of memory (Sinoff and Werner 2003).
derly patients (J.G. Beck et al. 1996). The Spielberger scale includes items
that assess both current (“state”) and habitual (“trait”) anxiety symptoms. It
has proved useful as an outcome measure in studies of psychological interven-
tions to reduce anxiety in both young adult and elderly subjects but has been
less widely applied in pharmacological research. The Worry Scale was specif-
ically developed for use with older adults; the 35 items reflect severity of
worry about financial, health, and social concerns. It is useful in assessing se-
verity of anxiety symptoms in both the general population of older adults and
those with GAD (J.G. Beck et al. 1996). Other self-rated anxiety scales that
have been used in clinical geriatric research include the Beck Anxiety Inven-
276 Clinical Manual of Geriatric Psychiatry
tory (A.T. Beck et al. 1988) and the Penn State Worry Questionnaire (Hopko
et al. 2003). Additional information on anxiety assessment procedures appro-
priate for older adults can be found in Carmin et al. (1999).
Laboratory Evaluation
Laboratory evaluation of the elderly patient with anxiety is aimed at ruling
out physical, chemical, and iatrogenic factors that can cause or exacerbate
anxiety and related symptoms. When laboratory evaluation results in a diag-
nosis of a physical illness (e.g., hyperthyroidism) that can explain the anxiety
symptoms, anxiety disorder due to a general medical condition is the correct
diagnosis. If a medication or other chemical (e.g., aminophylline) is identified
as the cause, substance-induced anxiety disorder is diagnosed. A functional
anxiety disorder may be exacerbated, but not caused, by medical illness or
substance use; thus, clinical judgment regarding the relative contribution of
the medical illness or medication is required to determine the correct diagno-
sis. Table 7–2 lists common medical conditions, chemicals, and medications
that can cause anxiety.
Differential Diagnosis
Situational Anxiety
Common situations in which elderly patients experience anxiety are very sim-
ilar to those that affect adults of all ages. These situations include those con-
ventionally acknowledged to provoke anxiety, such as a visit to the dentist or
doctor or an airplane flight, as well as those that may seem more idiosyncratic,
such as being asked simple mental status examination questions, conducting
a transaction with an accountant or a bank teller, or being asked to drive an
unfamiliar car. Unlike specific phobia, situational anxiety may not signifi-
cantly interfere with the person’s normal routine and, in that sense, may be
considered nonpathological; in fact, it does not appear in DSM-IV-TR. It is
mentioned here as a “subsyndromal” complaint for which medications may
be requested and may be effective.
Adjustment Anxiety
In elderly persons, adjustment reactions with anxiety may occur during or af-
ter periods of obvious personal crisis and in relation to crises that may not
seem particularly stressful to evaluating professionals. For example, a simple
Anxiety Disorders and Late-Onset Psychosis 277
move from one apartment to another, even within the same neighborhood,
or from one room in a retirement hotel or nursing home to another may pre-
cipitate significant anxiety. Similarly, development of a new physical illness,
even one that is not life threatening or particularly disabling, may precipitate
significant anxiety. Other events that commonly elicit adjustment anxiety in-
clude divorce or illness in the family, business or financial reversals, marital
strife, or even a long-awaited retirement.
Generalized Anxiety Disorder
GAD is the second most common anxiety disorder in the elderly (after phobic
disorders) and the one most commonly comorbid with depressive illness.
DSM-IV-TR diagnostic criteria for GAD are summarized in Table 7–3. As it
is for phobic disorders, the female-to-male ratio for GAD is about 2:1. Lenze
278 Clinical Manual of Geriatric Psychiatry
and colleagues (2000) found that 27% of 182 elderly patients with depressive
disorder also met criteria for GAD and that symptoms of GAD were associ-
ated with a higher level of suicidality. In a follow-up study, Lenze and col-
leagues (2005a) found that the average age at onset of GAD in 103 elderly
subjects was 48.8. Although 47% had onset “later in life,” few differences
were found between early- and late-onset cases. GAD tended to be a single,
chronic episode, whereas subjects with comorbid major depressive disorder
tended to have recurrent depressive episodes. The most common lifetime pat-
tern of comorbidity was GAD preceding major depressive disorder, and Lenze
et al. (2005a) found that GAD tends to persist, with spontaneous remission
(without treatment) unlikely even if comorbid major depressive disorder re-
mits. The authors interpreted this finding as enhancing the rationale for long-
term treatment of GAD. In another recent study (Le Roux et al. 2005), older
adults with onset of GAD before age 50 years were found to have a higher rate
of psychiatric comorbidity, greater psychotropic use, and more severe worry
compared with GAD patients with later ages at onset, whereas late-onset pa-
tients reported more functional limitations resulting from physical problems.
An earlier report based on the same sample compared frequency of DSM-IV
(American Psychiatric Association 1994) anxiety symptoms for older adults
with GAD, subsyndromal anxiety, or no mental disorder (Wetherell et al.
2003b). Frequency and uncontrollability of worry, degree of distress or im-
pairment associated with worry, muscle tension, and sleep disturbance were
the symptoms most likely to distinguish GAD from the other conditions.
Worrying about family members was common in all groups (endorsed by
69% of control subjects with no mental disorder, 91% with subsyndromal
anxiety, and 90% with GAD), whereas worries about oneself were elevated in
the GAD group, with health concerns, worries about minor matters, and fi-
nancial concerns predominating. About one-third of older individuals in each
group reported worries about community or world affairs.
Phobias
Phobias include the DSM-IV-TR categories of specific phobia, social phobia,
and agoraphobia without history of panic disorder. Taken together, phobias
constitute the most common anxiety disorder among elderly individuals, with
a reported prevalence between 0.7% and 12%, with results of most studies fall-
ing in the 3%–12% range, depending on inclusion criteria and the period of
Anxiety Disorders and Late-Onset Psychosis 279
Source. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of
Mental Disorders, 4th Edition, Text Revision. Washington, DC, American Psychiatric Associa-
tion, 2000. Copyright © 2000, American Psychiatric Association. Used with permission.
Source. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of
Mental Disorders, 4th Edition, Text Revision. Washington, DC, American Psychiatric Associa-
tion, 2000. Copyright © 2000, American Psychiatric Association. Used with permission.
Source. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of
Mental Disorders, 4th Edition, Text Revision. Washington, DC, American Psychiatric Associa-
tion, 2000. Copyright © 2000, American Psychiatric Association. Used with permission.
quent stress and enable elderly people to develop the coping strategies to
adapt successfully to traumatic events. However, data from a more recent
study of 148 survivors of two traumatic events, an airplane crash and a train
crash (Chung et al. 2004), suggest that neither the vulnerability hypothesis
Anxiety Disorders and Late-Onset Psychosis 283
Source. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of
Mental Disorders, 4th Edition, Text Revision. Washington, DC, American Psychiatric Associa-
tion, 2000. Copyright © 2000, American Psychiatric Association. Used with permission.
Source. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of
Mental Disorders, 4th Edition, Text Revision. Washington, DC, American Psychiatric Associa-
tion, 2000. Copyright © 2000, American Psychiatric Association. Used with permission.
als, many of whom are uncomfortable with introspection and unfamiliar with
conventional terms for subjective states. In most cases, neurovegetative signs
and symptoms of mood disorder and the autonomic and psychomotor fea-
tures of anxiety disorder facilitate accurate diagnostic classification.
Schizophrenia With Anxiety
Although the characteristic hallucinations, delusions, thought disorder, and
bizarre behavior typical of schizophrenia and delusional disorder are clearly
not a part of uncomplicated anxiety disorder, elderly patients with these con-
ditions may be quite secretive about their psychotic experiences and can ap-
pear to have anxiety alone. Extra effort to establish rapport and develop the
patient’s trust can be very important in this situation; hospitalized elderly pa-
tients often connect with a particular staff member (usually on the night shift)
whom they trust and with whom they share their inner psychic content. If
doubt persists, projective psychological tests (e.g., the Thematic Appercep-
tion Test, the Rorschach Inkblot Test; see Chapter 3, “Mood Disorders—
286 Clinical Manual of Geriatric Psychiatry
Pathogenesis
Psychodynamic Theories
The general psychodynamic literature on the pathogenesis of anxiety is too
voluminous to attempt to summarize here, although relatively little consider-
ation has been given to anxiety in late life. In addition to intrapsychic conflict
between libidinal impulses and emotions, the demands of conscience, and the
limitations imposed by circumstances, which are postulated to account for
anxiety throughout the life span, elderly individuals face anxiogenic circum-
stances unique to senescence. These include the growing discrepancy between
past and present capabilities, the increasing likelihood of mental and physical
incompetence, and the encroaching reality of death. Anxiety related to these
concerns may emerge directly into consciousness, wherein it can be relatively
easily identified, or may remain unconscious and be expressed indirectly as
somatic dysfunction, memory impairment, or nonspecific illness. In support
of this hypothesis, improved emotional well-being is often associated with in-
creased conscious awareness of, and ability to come to terms with, these as-
pects of aging (Gurian and Miner 1991).
Neurobiological Theories
Contemporary hypotheses about neurobiological substrates of anxiety and
fear focus on several interconnected subsystems of the central nervous system.
One subsystem is composed of noradrenergic innervation arising from cell
bodies in the locus coeruleus, a bilateral nucleus of cell bodies located in the
central gray matter of the isthmus on the floor of the fourth ventricle. Axons
from these cells provide the main noradrenergic input to the ipsilateral cortex,
cingulate gyrus, hippocampus, and cerebellum. They also impinge on cells in
the hypothalamus, thalamus, septal nuclei, and other subcortical structures,
Anxiety Disorders and Late-Onset Psychosis 287
levels of GABA are reduced in older subjects, which could result in an in-
creased propensity to anxiety with age (Sunderland et al. 1991).
Finally, a key role for serotonin receptors in the development of “normal”
anxiety behavior in humans has been delineated by Gross et al. (2002). They
noted that agonists of the serotonin type 1A (5-HT1A) receptor have anxiolytic
properties in both humans and animal models and that mice lacking this re-
ceptor (5-HT1A receptor knockout) show increased anxiety-like behavior in a
variety of conflict tests. The 5-HT1A receptor is expressed in two distinct neu-
ronal populations in the brain: as an autoreceptor on serotonin-containing
neurons of the raphe nuclei and as a heteroreceptor on nonserotonin-contain-
ing neurons of the forebrain (mainly the hippocampus, septum, and cortex).
Gross and colleagues used a tissue-specific and conditional 5-HT1A receptor
rescue mouse and found that restoration of the forebrain 5-HT1A receptor
alone was sufficient to reverse the anxiety-like phenotype of the knockout mice
and argued that this particular receptor population critically modulates anxi-
ety-like behavior. They also showed that receptor expression during the early
postnatal period is needed to establish normal anxiety-like behavior in the
adult. Despite these findings, no “unified” neurobiological theory of anxiety or
anxiety disorders in the elderly is widely accepted at this time.
Treatment
Psychosocial-Behavior Therapy
Although definitive studies in geriatric patients are lacking, there is little clin-
ical basis to doubt the efficacy of traditional psychotherapeutic approaches to
anxiety in the elderly. However, cost considerations often favor use of more fo-
cused, time-limited techniques such as cognitive-behavioral therapy (CBT),
which has been shown to be effective in nonelderly patients with anxiety dis-
orders, including OCD (Simpson et al. 1999), social phobia (Cottraux et al.
2000), and panic disorder (Barlow et al. 2000). The more purely behavioral
therapies are also preferred for reasons of cost and include relaxation tech-
niques aimed at generalized reduction of muscle tension and anxiety; desensi-
tization techniques that typically pair a state of induced relaxation with a real
or imagined feared situation or object; and graded exposure approaches that
attempt to extinguish anxiety, fear responses, or compulsive rituals gradually
by increasingly prolonged and intense exposure to feared situations.
Anxiety Disorders and Late-Onset Psychosis 289
nificant reductions in subjective anxiety have been reported for elderly pa-
tients in response to both progressive and imaginal relaxation procedures
(Scogin et al. 1992). Following specific procedures for relaxation training
(Bernstein and Borkovec 1973) is important to ensure an effective interven-
tion and to compare results for a given patient with results of clinical investi-
gations. Several rating scales have been designed to assess the effectiveness of
relaxation interventions (Crist et al. 1989). Most therapists who use behavior
techniques in the treatment of anxiety advocate the adjunctive use of anti-
anxiety agents with behavior therapy; similarly, when phobic or obsessive-
compulsive behaviors emerge as part of a depressive syndrome, pharmacolog-
ical treatment of depression should be initiated before or during the applica-
tion of behavior therapy.
Psychopharmacotherapy
Benzodiazepines remain the treatment of choice for anxiety of acute or sub-
acute duration (Table 7–8). For very short-term anxiety associated with spe-
cific situations such as airplane travel, the longer-acting agents such as
diazepam can be used safely; when treatment is required on a daily or near-
daily basis for up to 4–6 weeks, such as in adjustment disorder with anxiety
or in acute GAD, daily use of the longer-acting agents in elderly patients will
lead to accumulation of clinically significant blood levels of long-acting active
metabolites, most of which have half-lives of several days or longer. Therefore,
in these situations, the shorter-acting benzodiazepines such as lorazepam or
oxazepam, which undergo single-step conjugation in the liver and have no ac-
tive metabolites, are generally preferable. These agents have the additional ad-
vantage of being relatively well tolerated by patients with even fairly advanced
liver disease. However, some elderly patients experience acute withdrawal
symptoms between doses of short-acting benzodiazepines; these symptoms
are severe enough to render these agents intolerable. In this situation, one au-
thor of this book (J.E.S.) has had excellent results with clonazepam, which is
long-acting but does not give rise to clinically significant amounts of active
metabolite, making it the only long-acting benzodiazepine free of this disad-
vantage. Typical dosages are 0.5–1.0 mg by mouth twice daily (Calkin et al.
1997).
Chronic GAD and the other anxiety disorders generally require continu-
ous therapy beyond 4–6 weeks, at which point the effectiveness of benzo-
Table 7–8. Pharmacological properties of benzodiazepines
Therapeutic
Rate of Duration Active Elimination dosage range
Drug Trade name absorption of action metabolites half-life (hours) (mg/day)a
291
292 Clinical Manual of Geriatric Psychiatry
diazepines may diminish and more reliable results may be obtained with
heterocyclic antidepressants such as nortriptyline, sertraline, paroxetine, ci-
talopram, escitalopram, mirtazapine, or venlafaxine. Dosages are similar to
those required for treatment of depression, and peak effects on anxiety tend
to occur sooner than peak antidepressant effects; otherwise, prescription fol-
lows the guidelines for treatment of mood disorder outlined in Chapter 4
(“Mood Disorders—Treatment”). Controlled trials in the elderly are scant;
Lenze et al. (2005b) administered citalopram, 20–30 mg/day, in a double-
blind, placebo-controlled, random-assignment design to 34 subjects (average
age=69.4). In each group, 15 subjects had GAD; the remaining 4 had panic
disorder (3) and PTSD (1). In the citalopram group, 11 of 17 responded,
whereas only 4 of 17 in the placebo group did.
Buspirone is another nonbenzodiazepine that has been shown to be an ef-
fective anxiolytic agent in elderly patients (Goldberg 1994). It has several ad-
vantages over benzodiazepines: no sedative effects, no interaction with alcohol,
and no tendency to produce dependence or withdrawal symptoms; therefore,
buspirone has little or no abuse potential. A disadvantage is that it has little or
no acute efficacy, and usually several weeks of daily dosage are required before
effects are observed. Buspirone is contraindicated in patients taking mono-
amine oxidase inhibitors (presumably because of its serotonergic properties)
and is less effective in patients who have been treated with benzodiazepines. In
general, neuroleptics have a very minimal role in the treatment of uncompli-
cated GAD, but Morinigo et al. (2005) reported excellent results with low-
dose risperidone (i.e., average dosage of about 1.3 mg/day) in a small study of
15 subjects (average age=74) with mixed anxiety disorders (including 10 with
GAD) who had failed treatment with other agents.
Treatment of panic disorder and OCD is somewhat more specific. Al-
though efficacy of alprazolam in nonelderly adults with panic disorder has
been reported, in general, benzodiazepines and buspirone are both relatively
ineffective in inhibiting panic attacks. Heterocyclic antidepressants (includ-
ing selective serotonin reuptake inhibitors, serotonin-norepinephrine re-
uptake blockers, and monoamine oxidase inhibitors) have been shown to be
effective in nonelderly patients, and one small, open-label study of 10 subjects
(average age =72.5) who had panic disorder, with or without agoraphobia,
found that 25–200 mg/day of sertraline (average dosage= 92.5 mg) elimi-
nated panic attacks in 9 of 10 subjects by the end of the 12-week study
Anxiety Disorders and Late-Onset Psychosis 293
(Sheikh et al. 2004a). Similarly, the adult literature has convincingly docu-
mented the efficacy of selective serotonin reuptake inhibitors for the treat-
ment of OCD, and although they are generally well tolerated and should be
effective in the elderly, definitive studies are lacking. Generally, dosages of an-
tidepressants are similar to those used for depressive disorders, and cautions
listed in Chapter 4 (“Mood Disorders—Treatment”) for treatment of depres-
sion apply.
Late-Onset Psychosis
Epidemiology
The prevalence of late-onset psychosis is difficult to estimate because of a lack
of diagnostic consistency across investigations. DSM-IV recognized the possi-
bility of late onset in all psychotic illnesses, including schizophrenia, delu-
sional disorder, mood disorder with psychotic features, substance-induced
psychotic disorder, and psychotic disorder due to a general medical condition.
Besides these “functional” disorders, DSM-IV also allowed dementia, includ-
ing Alzheimer’s type and vascular dementia, to be coded as “with delusions.”
(DSM-IV-TR, following ICD-9-CM [World Health Organization 1978]
convention, has a codable subtype of “with delusions” for vascular dementia
only.) In the National Institute of Mental Health Epidemiologic Catchment
Area Program (Regier et al. 1988), 0.1% of individuals age 65 or older were
given a diagnosis of schizophrenia with DSM-III (American Psychiatric Asso-
ciation 1980) criteria, which did not allow onset of schizophrenia after age 45.
Leuchter and Spar (1985) reported that first onset of psychosis after age 65
was recognized in 8% of 880 patients admitted to a university hospital–based
geropsychiatric unit. The diagnostic breakdown was as follows: 3.4% had or-
ganic mental disorder (mainly primary degenerative or vascular dementia)
with psychosis, 2.8% had mood disorder with psychosis, and 1.7% had disor-
ders that would be diagnosed by DSM-III-R (American Psychiatric Associa-
tion 1987) criteria as schizophrenia (10 of 15 patients) or delusional disorder
(4 of 15 patients). A similar diagnostic distribution was found by Webster and
Grossberg (1998), who reported on 1,700 consecutive admissions to a psycho-
geriatric unit. In their group, 10% had onset of psychotic symptoms after age
65, and the most common diagnoses were dementia of the Alzheimer’s type,
294 Clinical Manual of Geriatric Psychiatry
Risk Factors
Risk factors for development of VLOSLP include age (the incidence increases
by 11% with each 5-year increase in age [van Os et al. 1995]), female gender,
and ethnic minority immigrant status. British investigators found that the in-
cidence of VLOSLP was significantly higher in African- and Caribbean-born
elders than in indigenous elders (Reeves et al. 2001). Compared with early-
onset schizophrenia patients, patients with VLOSLP are less likely to have a
family history of schizophrenia, more commonly have sensory deficits (par-
ticularly conductive hearing loss), and less commonly have negative symp-
toms. Rodriguez-Ferrera et al. (2004) and Barak et al. (2002) found that
patients with VLOSLP had higher levels of education and were more likely to
be married than were members of a comparison group of early-onset schizo-
phrenia patients. Despite the age association, VLOSLP appears to be a stable
entity and not merely the harbinger of a progressive dementing condition, as
indicated by follow-up studies conducted by Mazeh and colleagues (2005),
Palmer et al. (2003), and Rabins and Lavrisha (2003).
Diagnostic Criteria
DSM-IV-TR diagnostic criteria for schizophrenia and delusional disorder are
summarized in Tables 7–9 and 7–10, respectively.
Clinical Presentation
The clinical presentation of late-onset psychosis depends in large part on the
underlying diagnosis. Mood disorder with psychosis is described in Chapter
3 (“Mood Disorders—Diagnosis”), and dementia with psychosis is discussed
in Chapter 5 (“Dementia and Alzheimer’s Disease”); the typical picture of
VLOSLP follows DSM-IV-TR diagnostic criteria for schizophrenia: there are
Anxiety Disorders and Late-Onset Psychosis 295
Source. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of
Mental Disorders, 4th Edition, Text Revision. Washington, DC, American Psychiatric Associa-
tion, 2000. Copyright © 2000, American Psychiatric Association. Used with permission.
296 Clinical Manual of Geriatric Psychiatry
Source. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of
Mental Disorders, 4th Edition, Text Revision. Washington, DC, American Psychiatric Associa-
tion, 2000. Copyright © 2000, American Psychiatric Association. Used with permission.
Neuropsychological Tests
Most patients with schizophrenia spectrum disorders have neuropsychological
deficits, with severity ranging from mild frontal executive deficits to clinical de-
mentia. In a study of community-residing outpatients with schizophrenia
(Heaton et al. 2001), the average global neuropsychological score was 1.62 stan-
Anxiety Disorders and Late-Onset Psychosis 297
dard deviations (SDs) lower for patients compared with control subjects, and
about 30% of the patients had “very impaired” cognitive scores (>3 SDs below
the level of nonschizophrenic control subjects). Deficits of this magnitude con-
tribute in significant ways to the functional and social limitations associated with
schizophrenia-like conditions. However, in contrast to neurodegenerative disor-
ders such as Alzheimer’s disease and dementia with Lewy bodies, most studies
have found schizophrenia-related cognitive deficits to be stable over time. In the
Heaton et al. study, for example, mean changes over time and test-retest reliabil-
ities were the same for schizophrenic patients and control subjects across a wide
range of cognitive measures. Both older and younger patients had this stable pat-
tern. A related study compared performance on cognitive mental status exami-
nations (the Mini-Mental State Examination and Dementia Rating Scale; see
Chapter 5, “Dementia and Alzheimer’s Disease”) for older early-onset schizo-
phrenia spectrum patients, late-onset schizophrenia-like psychosis patients (on-
set after age 45 years), patients with Alzheimer’s disease, and control subjects
without mental disorders across retest intervals of 1–2 years. In this study, retest
scores also remained stable or even slightly improved for both early- and later-
onset schizophrenic-like disorder groups, whereas significant decline was noted
for patients with Alzheimer’s disease, with and without psychotic symptoms.
Longitudinal neuropsychological data for VLOSLP patients (e.g., age 75
and older) are scant, however, and more research is needed. Also, although
most cross-sectional studies have not shown excess rates of dementia among
patients with schizophrenia spectrum disorders when appropriate control
comparisons have been made, a few studies, mainly with older institutional-
ized samples, have found higher dementia rates. For example, in a retrospec-
tive chart review study (Dwork et al. 1998) that examined brain autopsy
findings for patients who had been institutionalized for severe mental disor-
der or dementia, a higher proportion of schizophrenic patients than those
with severe depression were rated as having significant cognitive impairment
prior to death (68% vs. 19%). The cognitively impaired schizophrenic pa-
tients had higher rates of Alzheimer-type brain changes (especially neocortical
neuritic plaques) than did those without cognitive deficit, but the extent of
these changes generally fell short of pathological criteria for Alzheimer’s dis-
ease. The investigators speculated that individuals with schizophrenia may
have lowered cognitive reserve, which predisposes them to clinically signifi-
cant cognitive changes at lesser levels of Alzheimer’s disease pathology.
298 Clinical Manual of Geriatric Psychiatry
Differential Diagnosis
The major diagnostic entities to be ruled out before diagnosing VLOSLP in-
clude mood disorder with psychosis and dementia with psychosis. Delirium,
particularly if induced by medications, also should be considered. In psy-
chotic mood disorder, sadness, dysphoria, anhedonia, and irritability are usu-
ally apparent enough to lead diagnostic efforts in the right direction; when
these features are obscured by psychotic manifestations, the diagnosis may
rest on identification of the characteristic neurovegetative signs and symp-
toms of depression and careful determination of a sequence of onset of symp-
toms in which mood and neurovegetative changes occur before delusions and
hallucinations. Late-onset hypomania and mania can present a clinical
picture very similar to that of VLOSLP (Spar et al. 1979). Again, correct di-
agnosis may require a detailed history obtained from multiple sources, in-
cluding medical records, along with inpatient observation. Dementia with
psychosis may be identified by mental status examination supplemented with
neuropsychological tests (see Chapter 5, “Dementia and Alzheimer’s Dis-
ease”). It is important to remember that performance on neuropsychological
tests may be impaired in the absence of organic brain disease if attention, con-
centration, and motivation are negatively affected by functional illness (i.e.,
pseudodementia). Accordingly, retesting after these symptoms are at least
partly controlled may avoid false-positive findings suggestive of degenerative
or vascular disease. Finally, delirium is rarely mistaken for VLOSLP, but med-
ications or combinations of medications that produce psychomotor slowing
and toxic hallucinations (e.g., low-potency neuroleptic medications with po-
tent central anticholinergic effects) can lead to this potentially hazardous
misdiagnosis.
Pathogenesis
Psychodynamic Theories
Several plausible psychodynamic theories have been proposed to explain the
development of delusions in mental illness, although none has focused on
late-onset disorders. These hypotheses assume that delusions are “secondary,”
functioning to help maintain psychic equilibrium threatened by peculiar or
frightening experiences. For instance, the common delusion expressed by pa-
Anxiety Disorders and Late-Onset Psychosis 299
tients with dementia that people are stealing things from them becomes an
“explanation” for the disappearance and reappearance of items that are actu-
ally moved around by the patient, who has no recall of the events. The delu-
sion enables the individual to avoid the awareness of severely impaired
memory function. Similarly, mood-congruent delusions of bodily malfunc-
tion (“I can’t eat because the food doesn’t go into my stomach anymore”) and
delusional guilt (“The president has lost his veto power, and the Communists
are going to take over because of me”), commonly seen in psychotic major de-
pression, help the individual to explain and understand his or her pervasive
sense of dysphoria, degradation, and helplessness. In late-onset schizophrenia
and delusional disorder, in which intellectual deficits and mood disturbance
are absent, both internal and external stimuli for the development of persecu-
tory delusions have been described. Schwartz (1963) proposed that an inner
sense of meaninglessness or insignificance results in a self-aggrandizing delu-
sion of “centrality” (e.g., “The ill-intended actions of many other people are
oriented around me, so I must be a powerful and important person”). Arnold
(1999) proposed that in schizophrenia, a dysfunction in a “phylogenetically
old apparatus of a memory of situations” results in familiar perceptions being
experienced as novel, uncertain, vague, and alien. Psychic equilibrium is sus-
tained by explaining these changes as the results of the covert hostile actions
of others. Similarly, delusional beliefs often seem designed to explain halluci-
natory experiences; for example, “The neighbors are pumping poison gas into
my apartment” is a belief that might accompany olfactory hallucinations. Psy-
chodynamic explanations of hallucinations, catatonic behavior, and flat af-
fect, each of which is a feature of DSM-IV-TR schizophrenia, are generally
inadequately articulated in the literature.
Neurobiological Theories
Neurobiological explanations of delusions and hallucinations are partly based
on analogy with well-known drug-induced mental changes. The psychoses as-
sociated with long-term ingestion of dopaminergic agents such as amphet-
amine or cocaine have led to the hypothesis that “endogenous” dopaminergic
hyperactivity causes functional psychosis, whereas psychotic symptoms asso-
ciated with ingestion of serotonergic hallucinogens such as lysergic acid
diethylamide (LSD) have implicated serotonergic dysfunction. More recent
attention has been paid to the role of glutamate.
300 Clinical Manual of Geriatric Psychiatry
Treatment
Psychosocial-Behavior Therapy
Tarrier (2005) reviewed 20 controlled studies of CBT in schizophrenic patients
and found an overall effect size of 0.37 (SD=0.39), which is modest at best. He
Anxiety Disorders and Late-Onset Psychosis 301
Rector and Beck (2002) described in detail how cognitive therapists con-
ceptualize and treat positive and negative symptoms of schizophrenia. The
Beck Cognitive Insight Scale (Beck et al. 2004), which measures the ability to
observe and question one’s own cognitive processes, provides a method for
tracking the cognitive effect of CBT or other therapies that has been validated
with older patients with psychotic disorders (Pedrelli et al. 2004).
Besides CBT, individual supportive psychotherapy aimed at building
trust, facilitating the flow of clinical data from the patient, and maximizing
compliance with somatic therapy can be an effective component of the overall
treatment program for VLOSLP. A recommended therapeutic stance toward
the patient’s delusional belief is “respectful disagreement,” wherein the thera-
pist does not claim to share the patient’s false belief but avoids confrontation
or argument with its content. Psychotic patients usually realize that others do
not agree with their beliefs, and they may become suspicious and distrustful
of the treating professional who does. However, open disagreement invites the
patient to incorporate the therapist into the delusion, thereby thwarting ef-
302 Clinical Manual of Geriatric Psychiatry
ranges. However, long-term side effects of significant weight gain, insulin re-
sistance and diabetes, and dyslipidemia are seen in varying degrees of severity
with all of the atypical antipsychotic agents. Accordingly, the experts surveyed
by Alexopoulos et al. (2004) would avoid clozapine, olanzapine, and conven-
tional antipsychotics (especially low- and mid-potency) for patients with dia-
betes, dyslipidemia, or obesity. Moreover, Alexopoulos et al. stated the
following:
Typical agents
Chlorpromazine 100 +++ ++ ++ +++ (im)
Thioridazineb,c 100 +++ +++ + ++
Perphenazine 8 ++ 0/+ +++ +
Trifluoperazine 5 + + ++ +
Thiothixene 5 + 0/+ ++ ++
Haloperidol 2 + 0 +++ 0/+
Fluphenazine 2 + 0/+ +++ +
Atypical agents
Risperidone 1.5 + 0 + +
Clozapined 100 +++ +++ 0/+ ++
Olanzapine 5 ++ ++ 0/+ +
Quetiapine 75 + + 0/+ +
Ziprasidonec 40 ++ + 0/+ +
Aripiprazole 15 + 0 0/+ +
Table 7–11. Antipsychotic drugs, dose equivalences, and side-effect profiles (continued)
Note. 0/+ =absent or very weak effect; += weak effect; ++= moderate effect; +++= strong effect; im=intramuscular.
aInclude acute dystonia, pseudoparkinsonism, akathisia, and perioral tremor (“rabbit syndrome”).
bMaximal dosage is 800 mg/day; higher dosages may cause pigmentary retinopathy.
c
Causes increase in QT/QTc interval; is contraindicated in patients with preexisting QTc interval>500 msec or various forms of cardiac illness.
dHypersalivation is common, especially at night.
Source. Adapted from Wise MG, Rundell JR: “Delirium (Acute Confusional States) and Dementia,” in Concise Guide to Consultation Psychiatry, 2nd
Edition. Washington, DC, American Psychiatric Press, 1994, p. 41. Copyright © 1994, American Psychiatric Press. Used with permission.
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Differential Diagnosis
Almost half of the 29 million Americans age 65 and older complain of inad-
equate amount or quality of sleep (Monane 1992). The differential diagnosis
of insomnia in the elderly includes the conditions listed below.
Normal Aging Changes
In general, with advancing age, sleep becomes more fragmented, more time
is required to fall asleep, more awakenings occur, relatively less deep (Stage
IV) sleep is experienced, and people tend to spend more time in bed. The sub-
jective impression produced by these changes is unsatisfying sleep, which may
be reported as insomnia; it is not uncommon for elderly hospitalized patients
to report not sleeping at all, despite nursing observations of 6–8 hours of ap-
parent sleep, complete with snoring.
313
314 Clinical Manual of Geriatric Psychiatry
Source. Adapted from Trevorrow T: “Assessing Sleep Functioning in Older Adults,” in Hand-
book of Assessment in Clinical Gerontology. Edited by Lichtenberg P. New York, Wiley, 1999, pp.
331–350. Copyright © 1999 John Wiley & Sons, Inc. Reprinted with permission of John Wiley
& Sons, Inc.
Source. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of
Mental Disorders, 4th Edition, Text Revision. Washington, DC, American Psychiatric Associa-
tion, 2000. Copyright © 2000, American Psychiatric Association. Used with permission.
Source. Adapted from American Sleep Disorders Association: The International Classification of
Sleep Disorders: Diagnostic and Coding Manual, Revised. Rochester, MN, American Sleep Disor-
ders Association, 1997.
Treatment—Psychopharmacotherapy
Benzodiazepine anxiolytic and hypnotic medications and the nonbenzodiazepine
medications zolpidem, zaleplon, and eszopiclone (see Table 8–4) are the drugs of
choice for elderly patients with primary insomnia.
Benzodiazepine Hypnotics
Although Table 8–4 includes only three benzodiazepines that are specifically
marketed for inducing sleep, all agents of this class have hypnotic activity
and are essentially interchangeable, even though minor interindividual dif-
ferences in susceptibility to one or more of their effects are the rule. For oc-
casional use, almost any of the available agents are effective, but most elderly
patients will experience less morning “hangover” with the short-acting
agents, such as temazepam, lorazepam, or oxazepam, than with the long-act-
ing agents, such as diazepam or flurazepam. In this regard, alprazolam is in-
termediate in duration of action and in desirability, whereas triazolam is very
318 Clinical Manual of Geriatric Psychiatry
Benzodiazepine hypnotics
Flurazepam (Dalmane) 15–30 Long
Temazepam (Restoril)a 15–30 Short
Triazolam (Halcion) 0.125–0.250 Ultrashort
Benzodiazepine anxiolytics
Lorazepam (Ativan)a 0.5–2 Short
Oxazepam (Serax)a 15–30 Short
Diazepam (Valium) 2.5–5 Long
Alprazolam (Xanax) 0.5–1 Intermediate
Barbiturates
Pentobarbital (Nembutal) 50–100 Intermediate
Secobarbital (Seconal) 50–500 Intermediate
Others
Chloral hydrate (many) 500–1,000 Intermediate
Glutethimide (Doriden) 25–250 Intermediate
Methyprylon (Noludar) 100–200 Intermediate
Zolpidem (Ambien)a 5–10 Short
Zaleplon (Sonata)a 5–10 Ultrashort
Eszopiclone (Lunesta)a 1–2 Short
a
Agents recommended for use in elderly persons.
short acting but should be avoided because of its propensity to cause ataxia,
paradoxical agitation, and mild but sometimes disturbing amnesia in some
elderly patients. For long-term use, the short-acting agents named above
(temazepam, lorazepam, or oxazepam) are much preferred over long-acting
agents (diazepam or flurazepam) because of the risk with the latter of build-
ing up potentially intoxicating blood levels of very long-acting active metab-
olites. The following case is illustrative:
after sleep onset, unlike the newest entry in the nonbenzodiazepine hypnotic
category, eszopiclone, which is a single-isomer cyclopyrrolone agent.
Eszopiclone is rapidly absorbed, with a time to peak concentration of ap-
proximately 1 hour and a half-life of 5–6 hours. It has been shown to produce
improvement in all four domains of insomnia—including sleep onset, sleep
maintenance, sleep duration, and restorative sleep—and studies in the elderly
suggest that it is safe and effective at dosages up to 2 mg/night.
Trazodone
Trazodone is not marketed as a hypnotic, but in low doses (i.e., 50–75 mg) it
is well tolerated and effective in inducing sleep and has the theoretical advan-
tage over several of the agents listed above of maintaining or actually increas-
ing delta sleep (Stages III and IV) (Scharf and Sachais 1990), which some sleep
researchers believe are the most refreshing stages of sleep. It has been shown to
be an effective hypnotic in patients with selective serotonin reuptake inhib-
itor–induced insomnia (Kaynak et al. 2004). However, trazodone, like the
benzodiazepine hypnotics, is associated with next-day somnolence and mild
impairment on some measures of cognitive function. It should also be noted
that insomnia remains an “off-label” (i.e., not approved by the U.S. Food and
Drug Administration), although widely recognized, indication for use of tra-
zodone.
trasted alcohol abuse prevalence rates from two comparable national surveys,
one done in 1991–1992 and the other in 2001–2002, and found a 4.8-fold
increase in the rate of alcohol abuse in people age 65 and older, from 0.25%
in 1991–1992 to 1.21% in 2001–2002.
All studies find that men are much more likely to be problem drinkers
than are women, and several patterns of relation to age at onset have been
identified. Most elderly alcoholic patients began drinking in young adult-
hood, but a significant proportion (up to 30%) do not develop a problem
with alcohol until late life.
Risk Factors
Risk factors for development of alcohol abuse or dependency in late life have
been difficult to pin down, but one survey (Moos et al. 2005) found that in-
creased health problems in elderly individuals predicted reduced alcohol con-
sumption but more drinking problems. The authors stated, “Older adults
with several health problems who consume more alcohol are at elevated risk
for drinking problems and should be targeted for brief interventions to help
them curtail their drinking” (p. 49).
Diagnostic Criteria
DSM-IV-TR distinguishes substance (alcohol) dependence, which is defined
in Table 8–5, from the generally less severe syndrome of substance (alcohol)
abuse, which is defined in Table 8–6.
Source. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of
Mental Disorders, 4th Edition, Text Revision. Washington, DC, American Psychiatric Associa-
tion, 2000. Copyright © 2000, American Psychiatric Association. Used with permission.
Source. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of
Mental Disorders, 4th Edition, Text Revision. Washington, DC, American Psychiatric Associa-
tion, 2000. Copyright © 2000, American Psychiatric Association. Used with permission.
and, unlike subjects with Alzheimer’s disease, vascular dementia, or mixed de-
mentia, did not show declines in cognitive or physical functioning over a 24-
month follow-up period, during which they were abstinent from alcohol.
The relation between depressive symptoms and syndromes and alcohol
use and abuse is similarly complex. However, it is well established that depres-
sive symptoms are usually self-limited and spontaneously resolve if the elderly
individual is able to abstain for 3–4 weeks; persistent depressive symptoms
should be regarded as not directly related to the alcohol problem. Factors that
predict persistent depression include poor social support, major life problems
(both of which may be indirect effects of alcohol abuse), a history of depres-
sion or suicidality, and a family history of depression (Atkinson 1999).
Assessment
Accurate histories of alcohol use in adults can often be augmented by embed-
ding alcohol-related questions in the context of a general interview about
health behaviors. Several short questionnaires—for example, the CAGE
Questionnaire (Buchsbaum et al. 1992), the Michigan Alcoholism Screening
Test—Geriatric Version (Blow et al. 1992), the Alcohol Use Disorders Iden-
tification Test (AUDIT; Saunders et al. 1993), and the five-item AUDIT-5
324 Clinical Manual of Geriatric Psychiatry
Source. Adapted from Oslin and Cary 2003; Oslin et al. 1998.
(Philpot et al. 2003)—have been used to screen for problematic alcohol use.
Conigliaro and colleagues (2000) found each of these instruments to have
shortcomings when used in an elderly primary care population, and O’Con-
nell et al. (2004) reported that the CAGE Questionnaire “performed poorly
Other Common Mental Disorders of the Elderly 325
Treatment—Pharmacology
Oslin and associates (1997) studied a group of older veterans ages 50–70 years
in a double-blind, placebo-controlled randomized trial of naltrexone (50 mg/
day). The results were similar to those found with middle-aged adults: no im-
provement was seen in total abstinence, but half as many naltrexone-treated
subjects relapsed to significant drinking compared with those who received pla-
cebo. The medication was well tolerated and had few side effects beyond nausea
and dizziness. Acamprosate (calcium acetylhomotaurinate) is the newest phar-
macological agent approved for the treatment of alcoholism. It is a derivative of
the essential amino acid taurine and is structurally similar to GABA. Acam-
prosate is believed to enhance GABA neurotransmission and interfere with
glutamate action at the N-methyl-D-aspartate receptor. Bouza and colleagues
(2004) reviewed the research literature, which does not include any studies in
the elderly, and concluded that acamprosate was effective as adjuvant treatment
326 Clinical Manual of Geriatric Psychiatry
abuse is also seen in young people. Other studies suggest that drug misuse
could affect as many as 14%–25% of elderly outpatients seen in psychiatric
settings (Jinks and Raschko 1990; Whitcup and Miller 1987). Medications
that are not in themselves psychoactive, and therefore not usually thought of
as abusable, may pose problems when they are combined with addicting sub-
stances. In this regard, acetaminophen-containing compounds, such as hy-
drocodone bitartrate–acetaminophen preparations. are of particular concern
because of renal (Elseviers and De Broe 1998) and hepatic (McClain et al.
1999) toxicity. Hepatic damage from long-term use may be severe; one author
of this book (J.E.S.) has consulted on several cases in which liver transplanta-
tion was necessitated by addiction to opioid-acetaminophen preparations.
Treatment
The key to treatment of substance abuse in elderly patients is preventing the
problem in the first place; Table 8–9 lists factors that Juergens (1994) recom-
mends physicians consider before prescribing potentially addictive medica-
Other Common Mental Disorders of the Elderly 329
Sexual Dysfunction
Source. Adapted from Juergens SM: “Prescription Drug Dependence Among Elderly Persons.”
Mayo Clinic Proceedings 69:1215–1217, 1994.
Because normal aging is associated with reduced function in all three areas,
particularly in men, diagnosis of the above sexual dysfunctions in elderly pa-
tients requires that the clinician take normal aging changes into account. The
Massachusetts Male Aging Study found that the probability of complete erectile
dysfunction tripled from 5% to 15%, and that of moderate erectile dysfunction
doubled from 17% to 34%, between ages 40 and 70 years. The probability of
minimal erectile dysfunction was constant at 17% throughout the age range,
however (Levine 2000). This study also surveyed changes in male sexual activity
over a 9-year follow-up period. The investigators reported consistent declines in
frequency of intercourse, frequency of erections, sexual desire, and satisfaction
with sex in all age groups, but the largest declines were in men ages 60–70 at
entry into the study (Araujo et al. 2004). Similar results were found in the Glo-
bal Study of Sexual Attitudes and Behaviors (Laumann et al. 2005). These data
indicated that as men age, they should expect that sexual desire will gradually
diminish, sexual arousal will take more time and more stimulation, erections
Other Common Mental Disorders of the Elderly 331
will be softer and not last as long, ejaculation may be diminished in vigor, and
orgasm may not occur during every episode of intercourse. Because of the nat-
ural lengthening of the plateau phase of arousal, premature ejaculation is some-
what less likely to occur late in life but can occur in men at any age. Despite
these age-related changes, in one survey, almost 74% of the married men older
than 60 reported being sexually active, with the percentage declining to 43% in
men older than 75 (Diokno et al. 1990).
Women may notice several changes with advancing age: reduced desire
for sex, less vaginal lubrication (which can contribute to the development of
the sexual pain disorders dyspareunia and vaginismus), reduced clitoral and
breast sensitivity, and reduced intensity of the muscular phase of orgasm (due
to reduced perineal muscle tone). The ability to have orgasm per se is more
inconsistently affected, with some reporting increased ease of orgasm with
age. Despite these possible problems, the Global Study of Sexual Attitudes
and Behaviors found that increased age among women was not reliably asso-
ciated with any sexual dysfunction except lubrication difficulties (Laumann
et al. 2005). This relative “immunity” to age-related problems notwithstand-
ing, the reported prevalence of sexual activity in older women is somewhat
lower than in elderly men and appears to be influenced more by the availabil-
ity of a secure partner (Mooradian and Greiff 1990).
Treatment
Adjustment of offending medications, treatment of underlying physical and
mental illnesses, and optimization of general health are the treatments of first
choice for diminished libido and anorgasmia in elderly men and women.
When these steps are ineffective, treatment with testosterone may be effective.
According to a review by Bolour and Braunstein (2005),
85% have been reported, the rate of treatment discontinuation is high, and side
effects include prolonged erection, penile pain, penile fibrosis, and hematoma
or ecchymosis. Because of the high dropout rate, a transurethral preparation of
alprostadil was developed that does not require needle injections into the penis.
In the medicated urethral system for erection, the patient uses a polypropylene
applicator to insert a semisolid pellet containing alprostadil into the urethra.
The medicated urethral system for erection produced erections sufficient for in-
tercourse in 65.9% of patients, and efficacy was similar regardless of age or the
cause of erectile dysfunction. The most common complaint was mild penile
pain, which was reported after 10.8% of alprostadil administrations in the
home setting and by 32.7% of men (Padma-Nathan et al. 1997).
The third-line intervention for treatment-resistant erectile dysfunction is sur-
gical implantation of a penile prosthesis. The three types of implants are semi-
rigid, positionable, and multicomponent inflatable. Each has advantages and
disadvantages, and consultation with a urologist experienced with these devices is
recommended. Treatment of erectile dysfunction is summarized in Table 8–10.
Source. Adapted from Process of Care Consensus Panel: “Position Paper: The Process of Care
Model for Evaluation and Treatment of Erectile Dysfunction.” International Journal of Impotence
Research 11:59–74, 1999.
Source. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of
Mental Disorders, 4th Edition, Text Revision. Washington, DC, American Psychiatric Associa-
tion, 2000. Copyright © 2000, American Psychiatric Association. Used with permission.
Chronic Pain
Half of the community-dwelling elderly and 60%–80% of those living
in nursing homes have been reported to have persistent pain complaints
(Schneider 2005); these complaints can be exacerbated by depression and
338 Clinical Manual of Geriatric Psychiatry
provide reliable information about the pain. Several visual analogue scales
have been shown to be useful in this situation (Pautex et al. 2005), and Rubey
(2005) provides a good overview of chronic pain management in elderly pa-
tients with dementia.
Personality Disorders
Agronin and Maletta (2000) reviewed the literature on personality disorders
in late life and found not more than “several dozen articles”; most were cross-
sectional prevalence studies in community and treatment populations that
used variable diagnostic criteria and inconsistent methodology, thereby allow-
ing few reliable generalizations. Studies that used structured interviews sug-
gested that the prevalence of personality disorders tends to decline with age
in community-dwelling subjects. However, personality disorders are as prev-
alent among elderly patients in geropsychiatric inpatient units as in a young
adult comparison sample (Ames and Molinari 1994; Molinari et al. 1994).
Studies typically report a higher prevalence of DSM-IV-TR Cluster C person-
ality disorders (avoidant, dependent, and obsessive-compulsive) among older
adults than either Cluster A disorders (paranoid, schizoid, and schizotypal) or
Cluster B disorders (antisocial, borderline, histrionic, and narcissistic) (Kunik
et al. 1994). Personality disorder as a comorbid condition appears to be sig-
nificantly more common in patients hospitalized for depression than in those
hospitalized for disorders of cognition (Kunik et al. 1994), and older de-
pressed patients with personality disorder have more persistent declines in
function and quality of life despite treatment (Abrams et al. 2001).
Regarding the natural history of personality disorders, Agronin and Mal-
etta (2000) found that published studies generally agreed with the prognostic
scheme proposed by Solomon (1981), which claimed that
more of the younger patient groups” (p. 447), provided further support for
Solomon’s scheme. For an excellent overview of the effects of personality fac-
tors on mental disorders in later life, see Seidlitz (2001).
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9
Competency and Related
Forensic Issues
347
348 Clinical Manual of Geriatric Psychiatry
Decisional Competency
Competency to Give Informed Consent for Medical Care
Four components of decisional competency in the medical setting were dis-
tinguished by Appelbaum and Grisso (1988) and have been accepted by most
authors. The four components involve the ability to
1. Communicate a choice
2. Understand relevant information
3. Appreciate the situation and its consequences
4. Manipulate information rationally (i.e., “to reach conclusions that are
logically consistent with the starting premises. This requires both weigh-
ing the risks and benefits of a single option and the usually more complex
process of weighing multiple options simultaneously.” [p. 1636])
Informed consent is generally not required for the great majority of medical
interventions, which are performed on the basis of “simple consent,” usually
obtained at the time a patient engages a new physician or during the admis-
sion process (the “Terms and Conditions of Admission” typically include sim-
ple consent). Simple consent similarly requires that the patient be competent
and that the consent be voluntary but does not require the provision of a pre-
determined body of information to the patient by the physician. Neither in-
formed nor simple consent is required in an emergent situation, in which
significant harm would come to a patient (or to others, in the case of a violent
patient) if the intervention were delayed so that consent could be obtained.
Under these circumstances, the principle of implied consent applies: that is, the
physician may perform the intervention to which a reasonable, self-interested
patient would consent, given the opportunity. Similarly, if the patient is un-
conscious or otherwise incompetent to participate in the consent process, and
no substitute decision maker (e.g., guardian or conservator, attorney-in-fact
for health care, or, in some jurisdictions, next of kin) or advance directive is
available, the physician may administer appropriate emergency treatment un-
til the patient is able to consent. In California, a nonemergent situation in
which no competent decision maker is available requires a specific court order
for medical intervention (Cal Prob. Code §3201).
Some states have enacted similar laws creating the health care proxy.
A living will is a document that is created by an individual when he or she
is of sound mind, specifying the limits of care to be given by health care pro-
viders if the individual “cannot make or communicate a choice regarding a
particular health care decision.” The version available through the American
Medical Association directs the attending physician to withhold or withdraw
treatment “when the treatment will not give me a meaningful quality of life”
and provides a choice of three levels of quality of life, including “permanent
unconsciousness,” “some consciousness and in an irreversible condition of
complete, or nearly complete, loss of ability to think or communicate with
others,” and “no more than some ability to think or communicate with oth-
ers, and the likely risks and burdens of treatment outweigh the expected ben-
efits.” It also has a section in which the individual can specify particular
treatments that he or she does not want, as well as particular preferences re-
garding treatment and the end of his or her life (e.g., the preference to die at
home), and a section containing instructions regarding organ donation.
There are clear advantages and disadvantages to both types of directives.
A proxy has much more flexibility than an “instructive” has, and a proxy can
Competency and Related Forensic Issues 351
respond to circumstances that may not have been anticipated by the princi-
pal. Conversely, a proxy also can betray the trust of the principal by making
decisions that the principal would not have endorsed. In some states, a living
will and durable power of attorney for health care or health care proxy can be
combined, resulting in an instrument that requires the attorney-in-fact or
proxy to follow the provisions of the living will and authorizes the exercise of
his or her judgment in circumstances not covered by the will.
Because advance directives are intended to be executed when the principal
is competent to give or withhold consent for medical care, one might think
that the standard for competency to execute an advance directive would be
the same as the standard for competency to consent to medical care. Yet Cal-
ifornia law states, “A natural person having the capacity to contract may exe-
cute a power of attorney” (Cal. Prob. Code §4120). However, different
standards for competency to execute an advance directive may obtain in other
states.
In a similar vein, the powers of the attorney-in-fact differ from state to
state. California law prohibits the attorney-in-fact from consenting to place-
ment in a mental health treatment facility, convulsive treatment, psychosur-
gery, sterilization, or abortion (Cal. Prob. Code §4722) and also prohibits the
attorney-in-fact from consenting to health care or consenting to the with-
holding or withdrawal of health care “necessary to keep the principal alive, if
the principal objects to the health care or to the withholding or withdrawal
of the health care. In such a case, the case is governed by the law that would
apply if there were no durable power of attorney for health care” (Cal. Prob.
Code §4724). This section appears to reflect the will of the California legis-
lature that individuals retain the authority to make end-of-life decisions, even
if they are incompetent to make other medical decisions.
Much has been written about the question of which rules should govern
the decisions of substitute decision makers such as attorneys-in-fact. The pre-
vailing view is known as the doctrine of “substituted judgment,” according to
which the substitute decision maker should act, as much as possible, in accor-
dance with the wishes, values, and goals of the principal. The alternative “best
interests” approach calls on the substitute decision maker to perform an “ob-
jective assessment of the burdens and benefits for this patient” as the basis for
his or her decision (Fellows 1998, p. 924). The court in a New Jersey case (In
re Conroy 1985) spelled out a three-step protocol for analyzing the patient’s
352 Clinical Manual of Geriatric Psychiatry
wishes: First, consider any statements or other directives made by the patient.
If these are not conclusive, then attempt to deduce the patient’s wishes from
his or her more generally held values, religious beliefs, and so on. Finally, if
these steps leave the issue in doubt, revert to what a person in the patient’s
situation might reasonably choose.
Source. President’s Commission for the Study of Ethical Problems in Medicine and Biomedical
and Behavioral Research 1982.
affected by the will.” Some states require only one or two of these criteria to be
met, and many states require that “the testator [be] also free of…delusions or
hallucinations [that] result in the person’s devising his or her property in a way
which, except for the existence of the delusions or hallucinations, he or she
would not have done” (Cal. Prob. Code §6100.5). In general, if lack of testa-
mentary capacity is proved, the entire will or codicil (modification to an exist-
ing will) is invalid. Testamentary capacity is generally recognized as “only a
modest level of competence (‘the weakest class of sound minds’)” (Estate of
Rosen 1982), and legal presumptions relating to this competency have tradi-
tionally also helped to set the bar fairly low. Besides the general presumption
that the testator was competent at the time the will was executed, it has also
been stated that “when one has a mental disorder in which there are lucid pe-
riods, it is presumed that his will has been made during a time of lucidity” (Es-
tate of Goetz 1967). The trend of more recent cases, however, has been toward
increasing recognition that at least in the case of progressive illnesses, such as
Alzheimer’s disease and vascular dementia, once testamentary capacity has
been lost, it is unlikely to return, even for brief periods.
Despite the fact that testamentary capacity is a low standard, wills are vulner-
able to challenge if an aggrieved party can produce any evidence of mental im-
pairment in the testator, and a medical record containing the mere diagnosis of a
neuropsychiatric illness is almost always enough, all things else being equal, to en-
courage contestants to proceed. Although it is common knowledge among psy-
chiatrists that a diagnosis alone does not imply any particular level of intellectual
function or automatically determine the presence or absence of any type of com-
petency, many judges, attorneys, and juries are not in possession of this insight
and may need to be educated through expert testimony. In many will contests,
the allegation that the testator lacked testamentary capacity at the time the will
was executed is accompanied by the allegation that the will, or parts of it, is the
product of undue influence. Because testamentary capacity is such a low stan-
dard, and because prospective evaluation of the testator is rarely performed (and
if it is, it is almost always at the request of a competent testator or of his or her
anticipated beneficiaries), it is usually very difficult to prove that a testator did not
possess testamentary capacity at the precise moment that the contested will was
signed (executed). Accordingly, allegation of undue influence often proves to be
the stronger case for the contestant. Any part of a will that is proved to be a result
of undue influence is overturned, but the remainder remains valid if the will
356 Clinical Manual of Geriatric Psychiatry
without the influenced provisions still makes sense and the testator otherwise had
testamentary capacity. Undue influence is discussed later in this chapter.
trustee(s), successor trustees, and beneficiaries were selected; and what events
and considerations led to the decision to amend the trust. The discussion of a
proposed medical intervention should cover the risks and benefits of the pro-
posed intervention and the most reasonable alternatives and should include in-
quiries of the subject that allow her or him to paraphrase and manipulate the
information provided and ask whatever questions that arise. By the end of this
discussion, it should be clear to the examiner whether the subject has the requi-
site understanding and appreciation of the consequences of the decision for the
subject and all others affected, the extent to which the decision was influenced
by interactions with others, how the decision comports with previously held val-
ues and goals, and whether delusional thinking affected the decision. The con-
clusion that the subject is or is not competent to make the decision at issue then
depends on what the examiner regards as evidence of minimally acceptable abil-
ity to “understand and appreciate,” “recall and recollect,” and so forth. That is,
does the examiner require that the subject produce key information from mem-
ory, either spontaneously or in response to inquiry, or is the ability merely to rec-
ognize information acceptable (e.g., a description of a parcel of real property or
of a proposed surgical procedure)? What level of detail is acceptable? How much
error is acceptable? This interrater variability in threshold accounts, in part, for
the often observed lack of agreement between examiners in published studies of
decisional competency (e.g., Marson et al. 1997; Vellinga et al. 2004) and for the
fact that equally qualified experts often provide conflicting opinions under oath.
Tests of Cognitive Function
To help mitigate the effects of the interrater variables described earlier, the ex-
aminer is advised to administer a battery of standardized tests of cognitive func-
tion along with the clinical interview. Impairment in other domains of mental
function (e.g., abnormal mood, anxiety, thought disorder) can, in principle,
negatively affect competency, but cognitive ability is the most consistent corre-
late of decisional competence (Palmer et al. 2005), and scores on tests of cogni-
tive function provide support for the examiner’s conclusions and allow the
cross-examining attorney and the trier of fact to place the expert’s opinion in
something approximating an “objective” context. One author of this book
(J.E.S.) routinely administers a Folstein Mini-Mental State Examination
(MMSE), a 12-item Boston Naming Test, general information items from the
Wechsler Adult Intelligence Scale, tests of remote memory (list the presidents,
358 Clinical Manual of Geriatric Psychiatry
describe key news events such as “What happened on 9/11/01?” and “What
was unusual about the 2000 presidential election?”), and tests of frontal execu-
tive function, including similarities, word-list generation, proverb interpreta-
tion, alternating design copying, and clock drawing. When indicated, this
battery is augmented with a “shopping list” test of new learning, tests of verbal
comprehension, and other more focused tests as indicated.
Standardized Tests of Decisional Competency
The literature on competency generally agrees that standardized tests have had a
limited role in competency determination, in part because of their inability to ad-
just to unique situational factors, including the consequences of the decision at is-
sue. As Grisso and Appelbaum (1998) indicated, the threshold for competence
should be adjusted according to the degree of harm associated with the subject’s
choice. For example, a lower level of understanding would be acceptable when a
patient is consenting to a medical procedure with a high benefit-risk ratio, as com-
pared with one that has a low ratio. Similarly, a lower threshold for concluding
that a testator has the ability to “understand and recollect the nature and situation
of his or her property” would be appropriate if there is only one natural heir, the
testator had no previous intention to leave the estate to anyone else, and the tes-
tator now intends to leave his or her estate entirely to that heir, as compared with
a situation in which a will contest is likely.
Several of the more recently developed standardized tests of competency al-
low the rater to adjust the threshold and may be useful as adjuncts to the clinical
interview. They include the MacArthur Competence Assessment Tool—Treat-
ment (Grisso et al. 1997) and the Competence Assessment Tool for Psychiatric
Advance Directives (Srebnik et al. 2004). These instruments assess a patient’s
capacity for understanding, appreciation, and reasoning by providing a body of
information and then requiring the patient to respond to questions about that
information. The result is several subscale scores that can be incorporated into
a competency determination.
claim of undue influence, but such a diagnosis is rarely more than just one con-
sideration of many. Singer (1992) identified six additional factors that “are
prominent in undue influence situations.” They are
the production of isolation, the creation of the ‘siege mentality,’ the fostering
of dependence, the creation of powerlessness, the use of fear and deception,
and keeping the victim unaware of the manipulative program put into place
to influence and control the person and to obtain the signing of documents
which benefit the manipulators at the cost of the signer. (p. 8)
competent to care for themselves or manage their finances. Criteria vary for
appointment of a conservator of a person (this conservator is called a guardian
in many states) and conservator of an estate (both conservator roles may be as-
sumed by the same person). This competency may be regarded as a form of
decisional capacity, at least in those states that use the Uniform Probate Code
(e.g., Alaska, Colorado, Montana), which defines an incapacitated individual
as someone who is “impaired by reason of mental illness, mental deficiency,
physical illness or disability, chronic use of drugs, chronic intoxication, or
other cause (except minority) to the extent that he lacks sufficient understand-
ing or capacity to make or communicate responsible decisions concerning his
person or which cause has so impaired the person's judgment that he is inca-
pable of realizing and making a rational decision with respect to his need for
treatment” (for an example, see http://data.opi.state.mt.us/bills/mca/72/5/
72-5-101.htm). However, in California, “a conservator of the person may be
appointed for a person who is unable to provide properly for his or her per-
sonal needs for physical health, food, clothing, or shelter” (Cal. Prob. Code
§1801a), and “a conservator of the estate may be appointed for a person who
is substantially unable to manage his or her own financial resources or resist
fraud or undue influence” (Cal. Prob. Code §1801b). Functional criteria such
as these subsume simple decisional capacity and, as mentioned earlier, add the
requirements of sustained motivation, judgment, and other executive func-
tions. Other than at the extremes of cognitive function (i.e., a perfectly normal
individual or one with severe, end-stage dementia), everyday function is diffi-
cult to predict from an office interview. Accordingly, the evaluation of the need
for a conservator of a person and/or an estate in California typically includes
interviewing individuals familiar with the proposed conservatee’s everyday
level of function; given that such informants are subject to bias and may them-
selves not be perfectly reliable (Wadley et al. 2003), multiple sources are desir-
able. In addition to this ancillary information, measures of frontal executive
function are also more critical in the assessment of these “downstream” func-
tions than are the simpler tests of language, memory, and comprehension that
are typically used in the assessment of decisional capacity (Brekke et al. 1997;
Chen et al. 1998).
In general, the powers of the conservator of person and the conservator of
estate are quite broad: the conservator of person has the power to make deci-
sions regarding place of residence and administration of medical care, and the
362 Clinical Manual of Geriatric Psychiatry
conservator of estate has the power to manage property, assets, and income
(this includes the power to enter into contractual arrangements on behalf of
the principal). In California, the conservator of person can consent to medical
care, but not over the objection of the conservatee, unless the court has
granted general or specific medical power—that is, the power to consent to
all medical care (general power) or to consent to a specific treatment (specific
power) even over the objection of the conservatee. The establishment of a
conservator of estate automatically renders the conservatee legally incompe-
tent to contract or to transfer property but does not establish lack of testa-
mentary capacity (i.e., the conservatee can still execute a will).
Conservatorship and guardianship are clearly radical solutions to the
competency problems occasioned by psychiatric and other illnesses. The pro-
cess of appointment of a guardian or conservator is often demeaning and
embarrassing to the conservatee, and disagreement over the need for conser-
vatorship and the motivations of those who support or resist it may lead to
long-lasting intrafamilial conflict and resentment. The appointment is also
expensive and time-consuming. In response to these shortcomings, most
states have provision for limited conservatorship and guardianship, wherein
only some of the powers discussed earlier are granted to the conservator, and
the rest remain with the conservatee, as determined by the court on a case-by-
case basis. But even this approach is costly and demeaning to the patient and,
despite court oversight, is sometimes conducive to fiduciary and even physical
abuse by guardians. And the process of adjudication of conservatorship and
guardianship itself has been criticized.
Personal decision-
making
Durable power of Contractual Yes Makes medical May revoke DPAHC Agent may not make
363
Table 9–3. Surrogate decision-makers available to older persons in California
Personal decision-
making (continued)
Probate None Yes May determine May refuse civil Conservator may not respect
conservatorship of residence, make commitment conservatee’s values and
person with general medical decisions (psychiatric wishes; court is recourse
medical powers hospitalization),
certain treatments
(e.g., psychosurgery,
abortion, sterilization)
Probate None Yes May determine May refuse civil Conservator may not respect
conservatorship residence, make commitment conservatee’s values and
for persons with medical decisions (psychiatric wishes; court is recourse
dementia hospitalization),
certain treatments
Mental health None Yes May consent to May refuse physical but Conservator may not respect
conservatorship mental health care not mental health care conservatee’s values and
of person only, including (including civil wishes; court is recourse
civil commitment commitment).
Table 9–3. Surrogate decision-makers available to older persons in California
(may vary in other states) (continued)
Capacity necessary Survives Powers of agent Powers retained by
to establish incapacity or conservator individual Risks and recourse
Financial decision-
making
Power of attorney Contractual No May expend funds, May revoke as long as Principal must monitor use
365
a
Typically is a “springing power” that comes into effect after the principal becomes incompetent.
bAuthor
(J.E.S.) opinion.
366 Clinical Manual of Geriatric Psychiatry
sources other than the testator. Here it may be prudent to elicit testimony on di-
rect examination that clinical assessment and diagnosis of psychiatric illness in
the elderly are commonly reliant on information from sources (such as spouses,
relatives, caregivers, and medical records) other than direct examination of the
patient, especially if the patient is severely cognitively impaired, uncooperative,
mute, or catatonic. This explanation may be important testimony if the court is
inclined to believe, as some clearly are, that retrospective evaluation is not part of
reasonable clinical practice, is therefore not “protected” by Rule 703, and is of
highly questionable probative value. Anticipating and correcting this mispercep-
tion can be of great value in preserving the proper weight of expert testimony.
However it is performed, the expert role is substantially different from the
role of clinician, and somewhat different ethical principles pertain. The clini-
cian’s obligation to act in the best interests of the patient is replaced by the
consultant’s mandate to provide an honest and objective opinion and, in the
testimonial context, to express that opinion in a convincing manner. Because
the two obligations can easily conflict, it is usually not recommended for one
individual to assume both roles for the same patient.
Competency to Drive
The fraction of the American population that drives is rapidly aging, and it is
estimated that by the year 2024, one in four drivers in the United States will
be older than 65. Motor vehicle injuries are the leading cause of injury-related
deaths among drivers ages 65- to 74-years old and are the second leading cause
(after falls) among drivers ages 75- to 84-years old. Older drivers have a higher
fatality rate per mile driven than any other age group except drivers under age 25.
By age 80, male and female drivers are, respectively, 4 and 3.1 times more likely
than 20-year-olds to die as a result of a motor vehicle crash. On the basis of esti-
mated annual travel, the fatality rate for drivers 85 years and older is 9 times
higher than the rate for drivers ages 25–69 years old (Wang et al. 2003). Mul-
tiple age-related factors are likely to contribute to this phenomenon, including
declining visual and auditory acuity, effects of physical and neuropsychiatric
illnesses and their treatments, and declining decisional competence resulting
from slowing of cognitive processes and reaction time and deficits in attention,
concentration, and visuospatial and executive functions.
368 Clinical Manual of Geriatric Psychiatry
White 2003), was examined for its predictive value. It uses color drawings of
a road scene from the perspective of sitting behind the steering wheel of the
car and correctly classified 66% of the subjects into the three driving safety
categories of “safe,” “marginal,” and “unsafe.” It may have advantages over the
other tests discussed here in ease and convenience of administration and ac-
ceptableness to older adult examinees.
Physicians who make judgments about patients’ driving based on clinical
data appear to be comparably accurate at predicting the on-road performance
of patients with dementia. Ott et al. (2005) found that physician accuracy
(percentage of correct classifications) in categorizing patients as safe or unsafe
(as subsequently determined by on-road testing) ranged from 62% to 78%,
with the accuracy of the general practitioners ranging from 62% to 64% and
that of the dementia specialists ranging from 72% to 78%. Participating phy-
sicians based their predictions on almost 20 clinical variables, but those whose
predictions were most accurate placed more weight on duration of dementia,
measures of dementia severity (CDR and MMSE scores), and specific tests of
visuospatial ability, praxis, and executive function. In a similar study by
Brown et al. (2005), the single physician rater was an experienced neurologist
and specialist in dementia. His judgments, based on an extensive clinical in-
terview that included specific questions about any recent history of driving
problems, and the tests included in his diagnostic dementia evaluation were
74% accurate in predicting which patients would be classified as safe, mar-
ginal, or unsafe after an on-road driving test. In this study, the physician was
more accurate than either a family member “informant” or the patient in pre-
dicting driving safety. Subjects with very mild dementia (CDR score=0.5) or
mild dementia (CRD score=1.0) did not differ significantly in driving per-
formance, but both groups were significantly worse than control subjects
without dementia.
On-road evaluation remains the gold standard for assessing the safety of
drivers with dementia. Fitten et al. (1995) found that subjects with demen-
tia not only performed significantly more poorly on a driving test than did
control subjects but also committed more serious driving errors, particularly
during the more complex stages of the course. A. R. Dobbs (1997) studied
cognitively impaired seniors who were all still driving and observed three
types of driving errors. The most serious errors, which “could have resulted
in a crash had the driving instructor not taken control of the vehicle or the
370 Clinical Manual of Geriatric Psychiatry
traffic adjusted” (p. 10), were made almost exclusively by subjects with de-
mentia, and three of the four control subjects who made errors of this type
were subsequently determined, on the basis of cognitive testing, to have de-
mentia or other cognitive impairments. In this study, 25% of the subjects
with dementia showed driving competence within the range of the normal
drivers. Dobbs concluded that diminished driving competence among sub-
jects with dementia is most likely to be picked up by a test protocol (course
and scoring procedure) that focuses on the very serious errors that were most
discriminating in the experimental situation. Uc and colleagues (2005)
studied subjects with mild Alzheimer’s disease (average MMSE score= 26;
average age = 76.1 years) using several measures of cognitive function, the
UFOV, and visual acuity and then had subjects drive along a 1-mile stretch
of four-lane divided highway. The task was to identify and verbally report
traffic signs and restaurants along the route. Subjects with Alzheimer’s dis-
ease identified a significantly smaller percentage of restaurant and traffic
signs than did neurologically normal control subjects and made significantly
more at-fault driving errors.
Older drivers are at risk for other medical conditions that can impair driv-
ing ability. McCloskey et al. (1994) found that retinal disorders, macular de-
generation, myopia and presbyopia, and monocular vision, which all would
seem likely to increase crash risk, in fact did not. Glaucoma, however, was as-
sociated with an increased relative risk (odds ratio) of 1.5. Foley et al. (1995)
found that having cataracts severe enough to preclude reading a newspaper or
recognizing a friend across the street was associated with a relative risk of only
0.9, which did not reach statistical significance, and McCloskey et al. (1994)
found that hearing impairment did not increase crash risk, but wearing a
hearing aid while driving increased the risk of crashing by a relative risk of 1.9.
Koepsell et al. (1994) looked at stroke; coronary disease, including heart at-
tack, angina, and coronary surgery; chronic obstructive pulmonary disease;
cancer; asthma; osteoarthritis; rheumatoid arthritis; and diabetes and found
that only coronary disease in general (odds ratio=1.4) and diabetes (odds
ratio=2.6) were associated with increased crash risk.
Certain medications, as expected, are also important contributors to crash
risk. Ray et al. (1992) found that current use of benzodiazepines was statisti-
cally significantly associated with injurious crashes among older drivers in
Tennessee, at a relative risk of 1.5, whereas current use of cyclic antidepres-
Competency and Related Forensic Issues 371
sants was associated with a twofold increased risk. Foley et al. (1995) reported
the surprising finding that the use of opioids or antihistamines was not asso-
ciated with increased crash risk but use of nonsteroidal anti-inflammatory
agents was (relative risk =1.4).
Despite the evidence that dementia is a major contributor to crash risk,
as of this writing, few states have laws mandating that physicians report driv-
ers with dementia or other neuropsychiatric conditions that could impair
driving. In 2002, only 28 states had laws providing immunity for breach of
confidentiality for physicians who report medically unfit drivers.
Responding to evidence that a patient has become a dangerous driver may
be fraught with conflicts for the physician. A physician’s official report to au-
thorities of the patient’s impairment may result in an angry patient who
chooses another physician. Conversely, and more seriously, a physician’s deci-
sion not to report impairment may result in adverse legal consequences for
the physician. Physicians practicing in states with laws mandating reporting
of impaired drivers would seem somewhat better off in this regard, as would
physicians in states that do not provide immunity for a breach of confidenti-
ality. But every physician has the right and the obligation to attempt to con-
vince dangerously impaired drivers to stop driving, even if these admonitions
are not always effective. B.M. Dobbs (1997) found that 26% of the patients
evaluated as unsafe to drive continued to do so despite being instructed by
their physician to stop. Even here, though, there are conflicts of obligation,
because many patients perceive the loss of “the right to drive” as an intolerable
deprivation of autonomy and freedom, and the physician is obligated to pro-
tect the patient from that loss whenever it is reasonable to do so. But the phy-
sician is also obliged to protect the patient and others from the possible
consequences of the patient’s impairment. Improvements in the ability to pre-
dict dangerous driving on the basis of office evaluations are likely to exacer-
bate this aspect of the physician’s dilemma.
Elder Abuse
Epidemiological and clinical studies suggest that for every 100 older adults,
between 2 and 10 individuals are victims of abuse (Lachs and Pillemer 2004).
These figures may well be underestimates, because most cases are likely to go
undetected. In the National Elder Abuse Incidence Study, for example, 84%
372 Clinical Manual of Geriatric Psychiatry
of the cases were not reported to adult protective service agencies (Adminis-
tration on Aging 1998).
Elder abuse can occur in several forms, including the following generally
recognized categories:
that all health care professionals need to be alert to the possibility of elder abuse
and to adopt methods for its detection in the United States and worldwide (Bon-
nie and Wallace 2002; World Health Organization 2002).
In their tutorial for physicians, Lachs and Pillemer (2004) emphasize the
need for in-depth but flexible examinations when elder abuse is suspected,
given the diverse forms and circumstances that may give rise to concern. In
the context of a comprehensive geriatric assessment, direct inquiries about
abuse and neglect are recommended, in addition to functional, cognitive,
physical, and social assessment. Psychiatrists and other physicians must be
able to differentiate normal aging changes and symptoms of disease from
signs of mistreatment and must be alert to both their own biases and those of
patients and family members with regard to acknowledging mistreatment.
Many older patients are reluctant to divulge abuse, and those with cognitive
impairment may be unable to recall or report their experiences. In most cases,
it is recommended that the patient be interviewed separately from caregivers
or family members whenever abuse is suspected. A home interview can also
yield valuable information.
Interventions for abused older adults need to be tailored to the symptoms
and situation. Medication to reduce agitation in an older person with demen-
tia may help to control triggers for abuse by a caregiver, or in the case of a
mentally ill perpetrator, treatment focused on the abuser may have the great-
est effect. Excellent case examples illustrating issues in intervention can be
found in a recent edited volume by Anetzberger (2004).
The National Center on Elder Abuse (http://www.elderabusecenter.org/)
provides links to bibliographies on detection and management of elder abuse,
as well as state-specific guidelines for case substantiation and reporting re-
quirements. Bergeron (2004) provides a thoughtful and practical discussion
of obligation to report issues for mental health professionals.
References
Administration on Aging: The National Elder Abuse Incident Study. Prepared by the
National Center on Elder Abuse in collaboration with Westat. Final Report,
September 1998. Available at http://www.aoa.gov/eldfam/Elder_Rights/
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Competency and Related Forensic Issues 375
Clinical Assessment
Instruments
379
380 Clinical Manual of Geriatric Psychiatry
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sion Screening Scale: A Preliminary Report.” Journal of Psychiatric Research 17:37–49, 1983. See
also Yesavage JA: “The Use of Self-Rating Depression Scales in the Elderly,” in Handbook for Clin-
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logical Association, 1986, pp. 213–217.
382 Clinical Manual of Geriatric Psychiatry
383
384 Clinical Manual of Geriatric Psychiatry
Frequency Reaction
1. Asking the same question over and over 012349 012349
2. Trouble remembering recent events
(e.g., items in the newspaper or on TV) 012349 012349
3. Trouble remembering significant past events 012349 012349
4. Losing or misplacing things 012349 012349
5. Forgetting what day it is 012349 012349
6. Starting, but not finishing things 012349 012349
7. Difficulty concentrating on a task 012349 012349
8. Destroying property 012349 012349
9. Doing things that embarrass you 012349 012349
10. Waking you or other family members up at night 012349 012349
11. Talking loudly and rapidly 012349 012349
12. Appears anxious or worried 012349 012349
Appendix: Clinical Assessment Instruments 387
Source. Adapted from Teri L, Truax P, Logsdon R, et al.: “Assessment of Behavior Problems in
Dementia: The Revised Memory and Behavior Problems Checklist.” Psychology and Aging
7:622–631, 1992. Used with permission.
388 Clinical Manual of Geriatric Psychiatry
Abbreviated cognitive screens, 181–183 Age and aging. See also Age of onset;
Abraham, Karl, 108, 115 Older adults; Very old people
Acamprosate, 325–326 biological factors in, 48–61
Accidents, and motor vehicles, 367– conceptual issues in, 21–23
368 delirium and, 262
Acetaminophen, 327, 328, 338 diversity in patterns of, 12–15
Acetazolamide, 78 elder abuse and, 372
Acetylcholinesterase, 207 general trends in, 25–28
Acquired immunodeficiency syndrome increase in older adults as
(AIDS), and dementia, 249 percentage of population, 1–2
Activated or hyperactive subtype, of influence on mental disorders of
delirium, 258 early onset, 339–341
Activities of daily life Mini-Mental State Examination
Alzheimer’s disease and, 202 and, 180
cognitive changes of normal aging personality and emotional changes
and, 32–34 in, 38–43
rating scales and, 183–184, 384– prevalence of Alzheimer’s disease by,
385 193
Acute treatment, for bipolar disorder, processing resource model of
163–165 cognitive abilities and,
Adjustment 23–38
anxiety and, 276–277 psychosis and, 294
bereavement and, 69 sexual dysfunction and, 329–331
Advance directives, and competency, sleep and advancing, 313
349–352 social context of, 43–48
African Americans. See Black Age-associated memory impairment
Americans (AAMI), 35–36, 37
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390 Clinical Manual of Geriatric Psychiatry